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 Chapter 14

Biology and Diseases of Ruminants:

Sheep, Goats, and Cattle
Margaret L. Delano, Scott A. Mischler, and Wendy J. Underwood

I. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 519
A. Taxonomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 520
B. Comments about and Examples of Use in Research . . . . . . . . . . . . . . 520
C. Availability and Sources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 522
D. Laboratory Management and Husbandry . . . . . . . . . . . . . . . . . . . . . . 524
II. Biology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 525
A. Unique Physiological Characteristics and Attributes,
with Emphasis on Comparative Physiology . . . . . . . . . . . . . . . . . . . . 525
B. Normal Values: Growth, Longevity, Hematology, Clinical Chemistry 525
C. Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 526
D. Reproduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529
E. Behavior . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 535
III. Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 537
A. Infectious Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 537
B. Genetic, Metabolic, Nutritional, and Management-Related Diseases. 598
C. Traumatic Disorders (Wounds, Bites, and Entrapped
Foreign Bodies) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 610
.... D. Iatrogenic Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 610
E. Neoplastic Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 611
F. Miscellaneous . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 611
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 611

I. INTRODUCTION neering, and b i o t e c h n o l o g y for basic science, agricultural, and

clinical applications. C o n c e r n and interest for the welfare for
these species and i m p r o v e d u n d e r s t a n d i n g of their b i o l o g y and
Since the first edition of this book, the use of r u m i n a n t s as re- b e h a v i o r have c o n t i n u e d during this time, and these are
search subjects has c h a n g e d dramatically. Formerly, large ani- reflected in s o m e respects in the c h a n g i n g h u s b a n d r y and m a n -
mals were p r i m a r i l y used for agricultural research or as m o d e l s a g e m e n t . This c h a p t e r addresses the basic biology, husbandry,
of h u m a n diseases. O v e r the past decade, r u m i n a n t s have con- and m o r e c o m m o n and i m p o r t a n t diseases of three r u m i n a n t
tinued in their traditional agricultural research role but are n o w species m sheep, goats, and c a t t l e - - c o m m o n l y used in the lab-
extensively used for studies in m o l e c u l a r biology, genetic engi- oratory. O n e chapter is s i m p l y not adequate, however, to address

LABORATORYANIMALMEDICINE,2ndedition Copyright2002,ElsevierScience(USA).Allfightsreserved.
ISBN0-12-263951-0
520 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

the many details and complexities of these species' biology, British stock with Egyptian and Indian goats. This breed is rel-
management, and diseases. References noted in the text offer atively heat tolerant and produces milk with the highest butter-
more information to the interested reader. fat (about 4-5%). Fiber breeds include the Angora and the
Cashmere. The Angora, the source of mohair, originated in Tur-
key. The Cashmere breed is found primarily in mountainous ar-
A. Taxonomy eas of Central Asia. The La Mancha, a newer breed of dairy goat
first registered in the United States in 1958, has rudimentary
Sheep, goats, and cattle are ungulates, "hooved" animals that ears that are a genetically dominant distinguishing characteris-
are members of the order Artiodactyla (even-toed ungulates, or tic of the breed. The meat breeds include the Boer, Sapel, Ma
animals with cloven hooves), suborder Ruminantia (ruminants, Tou, Kambling, and Pygmy. The Pygmy goat is small and is
or cud-chewing animals) and family Bovidae. Members of the sometimes used for both meat and milk. The Mubend of
Bovidae group of mammals are distinguished by characteristics Uganda and the Red Sokoto of West Africa produce quality
such as an even number of toes, a compartmentalized forestom- skins for fine leather (Smith and Sherman, 1994).
ach, and horns. These animals are obligate herbivores and, as Most breeds of cattle are classified as "dairy" or "beef"; a few
adults, derive all their glucose from gluconeogenesis. The sub- breeds are considered "dual-purpose." Common dairy breeds in
family Caprinae includes sheep and goats. The genus and sub- the United States include Holstein-Friesian, Brown Swiss, Jer-
genus Ovis includes domestic sheep as well as wild Asian and sey, Ayrshire, Guernsey, and Milking Shorthorn. Holsteins have
European sheep species. Domestic sheep are Ovis aries. The the largest body size, whereas Jerseys have the smallest. Of
subgenus Pachyceros includes the wild North American species breeds in temperate regions, Jerseys have been considered to be
as well as snow sheep (O. nivicola) of northeastern Siberia. the most heat tolerant, but Holsteins have been found to adapt to
Capra hircus is the domestic goat that originated from western warmer climates. There are many beef breeds. The more com-
Asian goats. Capra pyrenaica (Spanish goat), C. ibex (goats of mon in the United States include Angus (also called Aberdeen-
the Red Sea and Caucasus area), and C. falconiere (wild goat of Angus), Hereford (both polled and horned), and Simmental
Afghanistan and Pakistan) are other members of the genus. The (Briggs and Briggs, 1980; Schmidt et al., 1988). Breeds indige-
subfamily Bovinae and genus Bos include all domestic and wild nous to other continents, such as the Cape Buffalo, have been
cattle. The subgenus taurus contains all of today's domestic cat- found to have unique innate immune characteristics that protect
tle. Common genus and species terminology for modern-day them from endemic trypanosomiasis (Muranjan et al., 1997).
cattle includes Bos taurus and B. indicus. Bos taurus (domestic More detailed information regarding these and other ruminant
cattle), originally from the European continent, have no hump breeds is available in Briggs and Briggs (1980). "Rare" or "mi-
over the withers. Bos indicus, also known as Zebu cattle, have a nor" breeds of sheep, goats, and cattle are studied for their ge-
hump over the withers and drooping ears. These cattle include netic and production characteristics. Discussions of these and
breeds found in the tropics and are extremely heat tolerant, and efforts at conservation are described in detail elsewhere (Na-
some breeds are known for parasite resistance. Bos taurus and tional Research Council, 1993).
B. indicus have been crossed, and new breeds have been devel- Several terms are unique to ruminants. In relation to sheep, a
oped during this century (Briggs and Briggs, 1980; Walker ewe is the female, and a ram is the adult intact male. A lamb is
et al., 1983). the young animal, and ram lamb and ewe lamb are commonly
There are several hundred breeds of sheep worldwide that are used terms. A wether is a castrated male. The birthing process
distinguished as "meat," "wool" or "hair," or "dual-purpose." is referred to as lambing. With respect to goats, a doe or nanny
Some wool or hair breeds have varying coat colors. Some is the female. A buck or billy is the adult intact male. A kid or
breeds are raised for milk (cheese) production. Common breeds goatling is a young goat. A young male may be referred to as a
of European origin that are raised for meat in the United States buckling, and a young female may be referred to as a doeling. A
include the larger breeds such as Dorset, Columbia, Suffolk, castrated male in this species is also called a wether. The
and Hampshire. Slightly smaller breeds include Southdown and birthing process is called kidding. With respect to cattle, an
Border Cheviot. Wool breeds include Merino, Rambouillet, adult female is a cow, and an adult male is a bull. A calf is a
Lincoln, and Romney; wool breeds are subclassified according young animal. A heifer is a female who has not had her first calf.
to the properties of the wool. The Barbados is known as a "hair" A steer is a castrated male. Calving refers to the act of giving
breed. Newer breeds that have been developed in the United birth.
States include Polypay and Targhee (Briggs and Briggs, 1980).
Goat breeds are numerous and are usually classified accord-
ing to use as dairy, meat, fiber, or skin-type breeds. The major B. Comments about and Examples of Use in Research
dairy breeds are the Alpine, Nubian, Toggenburg, La Mancha,
Saanen, and Oberhaslie; all have origins on the European con- Ruminants have been used as research models since the in-
tinent. The Nubian breed was developed from crossbreeding ception of the land grant college system, first in production
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 521

agriculture and now also in basic and applied studies for the fits over the use of cattle in research from the standpoint of size,
anatomic and physiologic sciences and in biomedical research ease of handling, cost of maintenance, and docile behavior.
for a variety of purposes. Healthy, normal young ruminants Sheep are also widely used models for basic and applied fetal
serve as models of cardiac transplantation and as preclinical and reproductive research (Buttar, 1997; Rees et al., 1998; Ross
models for evaluation of cardiac assist or prosthetic devices, and Nijland, 1998). The species is used for investigating circa-
such as vascular stents and cardiac valves (Salerno et al., 1998). dian rhythms related to day length (Lehman et al., 1997), and
For many years, ruminants have been useful research subjects the interaction between olfactory cues and behavior (Kendrick
for reproductive research, such as research on embryo transfer, et al., 1997). The number and diversity of natural- and induced-
artificial insemination, and control of the reproductive cycle disease research models in sheep are great and increasing.
(Wall et al., 1997). Several important milestones in gene trans- Natural models include congenital hyperbilirubinemia/hepatic
fer, cloning, nuclear transfer, and genetic engineering tech- organic anion excretory defect (Dubin-Johnson syndrome) in
niques have been developed or demonstrated using these spe- the Corriedale breed, congenital hyperbilirubinemia/hepatic
cies (Ebert et al., 1994; Schnieke, 1997; Cibelli et al., 1998a,b) organic anion uptake defect (Gilbert syndrome) in the South-
(see Fig. 1). One of many proposed uses of genetically engi- down breed, glucose-6-phosphate dehydrogenase deficiency in
neered ruminants is the production of proteins that will be se- the Dorset breed, GM~ gangliosidosis in the Suffolk breed, and
creted in the milk and later isolated (Ebert et aL, 1994; Memon pulmonary adenomatosis (jaagsiekte) in many breeds (Hegre-
and Ebert, 1992). Healthy sheep and goats are also often used berg, 198 l a). Induced models include arteriosclerosis, hemor-
for antibody production (Hanly et al., 1995). Genome mapping rhagic shock, copper poisoning (Wilson's disease), and meta-
developed rapidly during the 1990s; extensive information is bolic toxocosis (Hegreberg, 198 lb).
available and is increasing for sheep and cattle (Broad et al., Goats are used in a wide variety of agricultural and biomed-
1998; Womack, 1998). ical disciplines such as immunology, mastitis, nutrition, and
Sheep are often selected for studying areas such as ruminant parasitology research. Vascular researchers select the goat be-
physiology and nutrition. These animals provide obvious bene- cause of the large, readily accessible jugular veins. Goats with

Fig. 1. The production of cloned cattle reflects the changing use of ruminants in research.
522 SCOTT A. MISCHLER,WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

inherited caprine myotonia congenita ("fainting goats") have housed as biosecure or closed flocks. Animal health programs
been used as a model for human myotonia congenita (Thom- are in place, and health reports or other quality assurance re-
sen's disease) (Kuhn, 1993). A line of inbred Nubians serves as ports are usually available on request. Agricultural sources of
models for the genetic disease [3-mannosidosis and prenatal either small ruminant may be acceptable, but specific research
therapeutic cell transplantation strategies (Lovell et al., 1997). needs may not have been addressed or may not be understood.
(These disorders are discussed in more detail in Section Lambs, kids, and milking goats may be difficult to locate in fall
III,B,1.) Goats are used as a model for osteoporosis research and winter months because most breeds of sheep and goats are
(Welch et al., 1996). seasonal breeders. Management practices exist, however, to ex-
Cattle are often used as a source of ruminal fluid for research, tend the breeding and milking seasons.
teaching, or treatment of other cattle, by placing a permanent Most cattle used as animal models in research in the United
fistula in the left abdominal wall to allow sampling of ruminal States are from one of the dairy breeds, usually Holstein, be-
fluid (Dougherty, 1981). Cattle also serve as models of many in- cause this breed is now the most common. Purpose-bred,
fectious diseases, including zoonoses, and several inherited specific pathogen-free research cattle are not typically avail-
metabolic diseases. This species is useful for the basic and com- able. Because of selection and the management of dairy pro-
parative research on the pathogenesis and immunology of in- duction units, calves and young stock are available year-round.
herited and infectious diseases. Bovine trichomoniasis, caused Availability of young beef cattle is more seasonal, according to
by Tritrichomonas (Trichomonas)fetus, has been identified as a production cycles typically followed by that industry.
useful model for the human infection by Trichomonas vaginalis Auction barns or sales are not appropriate sources for re-
(Corbeil, 1995). Inherited cardiomyopathies have been found in search ruminants. Many of these animals are culls and will be
the Holstein-Friesian, Simmental-Red Holstein, Black Spot- poor-quality research subjects. They may be in poor body con-
ted Friesian, and Polled Hereford with woolly coat (Weil et al., dition and stressed, may be sources of disease, and may con-
1997). Lipofuscinosis has been identified in Ayrshires and taminate other healthy animals, as well as the research facility.
Friesians, and glycogenesis in Shorthorns and Brahmans. Selection of the suppliers should be made only after research
Metabolic diseases such as hereditary orotic aciduria and hered- needs have been carefully considered. Consistently working
itary zinc deficiency have been characterized in Holstein- with and buying directly from as few sources as possible are
Friesian or Friesian cattle. Holstein cattle also serve as a model best. Certain types of research (i.e., agricultural nutrition stud-
for leukocyte adhesion deficiency syndrome (AFIP, 1995). ies) may better be served by selecting animals from local agri-
cultural suppliers rather than commercial vendors located in a
different geographical area.
C. Availability and Sources The selection of sources for research ruminants includes scru-
tiny of flock or herd record keeping; health monitoring, vac-
Common breeds of normal, healthy ruminants are usually cination, and preventive medicine programs (including hoof
readily available, although seasonality may play a role, as noted care); production standards and management practices consis-
below. Agricultural sources and reputable farms may be located tent with the industry; management of the breeding flock or
through land-grant universities or agricultural schools, cooper- herd; sanitation and waste handling programs; vermin and in-
ative extension and 4-H networks, regional ruminant breeders' sect control measures (especially for flies and other flying in-
associations, and farm bureaus. Commercial sources of purpose- sects); rearing programs for and condition of young stock; the
bred animals are found in technical publications and annual list- location, health, and condition of the other animals on the prem-
ings of research animal vendors. Breeds carrying genetic traits ises; intensity of housing; and animal housing facilities.
of interest, either as animal models or as valuable production Preliminary and periodic visits to the source farms should
characteristics, may be located through literature or Internet be conducted. It is important to establish a good relationship
searches, animal science societies, breed or livestock conserva- with the local attending large-animal veterinarians, who will be
tion associations, and information resources such as the Armed valuable resources for current approved therapies and practices.
Forces Institute of Pathology. Organizations such as the Insti- They may need to be oriented on the specific requirements of
tute for Laboratory Animal Research (ILAR), National Center animal research. Creative ways can be used to initiate and fos-
for Research Resources (NCRR), or the Animal Welfare Infor- ter a good working relationship between the agricultural sup-
mation Center (AWIC) may also serve as information sources plier and the research facility. Supplying the vaccines or de-
about the animals needed. wormers required for flock health programs, providing services
Purpose-bred research sheep and goats are available from such as quarterly serological testing or fecal examinations for
commercial vendors and are usually maintained in registered fa- the herd or flock, and paying a premium (rather than market
cilities under federal standards that are also acceptable to re- price) for animals that meet the quality criteria established for
search animal accrediting agencies. These commercial animals the research animals are often helpful.
are frequently described as specific pathogen-free (SPF) and A set of testing standards can be developed based on one
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 523

high-quality supplier, and then flocks or herds can be "quali- tinal worms; and external parasitism such as sheep keds. Each
fied" based on those standards. Qualifying entails evaluations supplier should be queried about vaccination programs for blue-
utilizing the facility and management aspects mentioned above tongue, Brucella ovis, Campylobacter spp., Chlamydia (enzo-
and testing either a percentage of the herd or flock or the entire otic abortion of ewes), clostridial diseases, pneumonia complex
herd or flock for a number of infectious agents. The testing reg- (parainfluenza 3, Pasteurella haemolytica, and P. multocida),
imen itself should be carefully developed and evaluated. ovine ecthyma, rabies, Dichelobacter (Bacteroides) nodosus,
Once qualified, each source farm should be reevaluated peri- Arcanobacterium pseudotuberculosis, Bacillus anthracis, and
odically to maintain its status. Slaughter checks may be appro- Fusobacterium necrophorum. Because of the limited number of
priate; otherwise necropsy of sentinel animals may be required. biologics approved for small ruminants, products licensed for
Selected animals undergoing screening tests should be quaran- cattle have been used with success in sheep, and some licensed
tined from the rest of flock or herd while awaiting test results. for sheep are used in goats ("Council report," JAVMA, 1994).
Vaccination and deworming regimens can be instituted during In some cases, approved feed additives, such as coccidiostats,
these quarantine periods. A second quarantine should occur are fed to sheep.
when animals arrive at the research facility. The animal screen- The basic screening profile for goats should include Q fever
ing process also depends on the origin of the animal (state, (Coxiella burnettii), caprine arthritis encephalitis (CAE), bru-
country) and the scientific program. Federal and state regula- cellosis, tuberculosis, and Johne's disease (Mycobacterium
tions must be followed. paratuberculosis). Goats may also be tested for caseous lym-
Socialization of the animals at the source facility should also phadenitis, contagious ecthyma, or Mycoplasma as needed.
be considered in terms of ease of handling and safety for per- Herd vaccination programs may include immunizations against
sonnel in the confinement of the research lab, barn, or farm. For tetanus and other clostridial diseases, Chlamydia, Campylobac-
example, frequently handled calves will be easier to manage, ter, contagious ecthyma, caseous lymphadenitis, Corynebac-
and adult dairy goats that have been acclimated to human con- terium pseudotuberculosis, and Escherichia coli.
tact are preferable. Cattle herds should be screened for Johne's disease, brucel-
Several texts provide information on industry standards for losis, tuberculosis, respiratory diseases, internal and external
flock and herd management and preventive medicine strategies parasitism, and foot conditions such as hairy heel warts and foot
that can provide helpful orientation to those unfamiliar with rot. Determination of the status of the herd with respect to
these aspects. These references also provide information re- bovine leukemia virus (BLV) may be worthwhile. Herd pro-
garding vaccination products licensed for use in ruminants and grams may include essential or highly recommended vaccines
typical herd and flock vaccination parasite control schedules against bovine viral diarrhea virus (BVDV), infectious bovine
("Current Veterinary Therapy," 1986, 1993, 1999; "Council re- rhinotracheitis virus (IBRV), bovine respiratory syncytial virus
port," 1994; "Large Animal Internal Medicine," 1996; Smith (BRSV), parainfluenza 3 (PI-3), Leptospira pomona, Tritri-
and Sherman, 1994) chomonas fetus, rotavirus, coronavirus, Campylobacter (Vi-
When designing a vaccination program during qualification brio), Pasteurella haemolytica and P. multocida, and Brucella
of a source or at the research facility, it is important to evaluate abortus. Other vaccination programs, dependent on herd status,
the local disease incidence and the potential for exposure. Vac- endemic diseases, or geographic location, may include immu-
cination programs should be conducted with an awareness of nizations against the Clostridial diseases, Moraxella bovis
duration of passive immunity and stresses in ruminants' lives (pinkeye), Fusobacterium necrophorum (foot rot), Staphylo-
(e.g., weaning, grouping, management changes, and shipping) coccus aureus (mastitis), Haemophilus somnus, rabies, tetanus,
that may impair immunity or increase susceptibility to infec- Bacillus anthracis, enterotoxigenic E. colL Anaplasma, and
tious diseases. It is also prudent to evaluate the cost-effective- other Leptospira species. Some products considered to have
ness of vaccination; labor and vaccine expenses may be much limited efficacy include vaccines against Salmonella dublin and
higher than the potential animal morbidity or mortality for dis- S. typhimurium. Some autogenous vaccines may be more effec-
eases in a particular locality. Not all of the vaccines mentioned tive than the commercially available products--for example,
subsequently will be necessary in all herds or flocks. Vaccina- the bovine papillomavirus (warts) vaccines.
tion needs for research animals will also depend on the local Rearing programs for dairy calves differ from those for the
disease history, intent of the research, the age of the animals smaller ruminants, including the withdrawal of calves from
needed for research, and the length of time the animals will be their dams immediately or by 24 hours after birth. In the cattle
housed. industry, antibiotics, ionophores (antibiotics that control se-
Typical health screening programs for sheep include Q fever lected populations of ruminal organisms), coccidiostats, probi-
(Coxiella burnetii); contagious ecthyma; caseous lymphadeni- otics, and other approved additives may be part of the milk
tis (Corynebacterium pseudotuberculosis); Johne's disease (My- replacers, grain and concentrate formulations, and/or creep
cobacterium paratuberculosis); ovine progressive pneumonia; feeding regimens. Use varies by the segment of the indus-
internal parasitism such as nasal bots, lungworms, and intes- try, and regulations vary by country. Subcutaneous hormonal
524 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

implants (such as estradiol benzoate and progesterone com- preciation for ruminant behaviors has grown in recent years,
bined, zeranol, or 17[~-estradiol) are administered, especially to and refined ruminant handling techniques have been published
beef calves destined for market rather than breeding, to promote (Houpt, 1998; Grandin, 1998).
growth. When ruminants are confinement-housed, care should be
Transportation of the animals from the source to the research taken to provide adequate but draft-free ventilation. Ammonia
facility must be carefully planned, and all applicable livestock buildup and other waste gases may induce respiratory problems.
travel regulations followed. It is best to have the animals trans- In cold weather, if the ceiling, walls, or water pipes condense
ported in vehicles regularly utilized by the source farm. If com- water, then the ventilation should be increased even at the ex-
mercial haulers are used, then disinfecting trucks, trailers, and pense of lower temperatures. Even adult goats and younger
associated equipment, such as ramps and chutes, beforehand is cattle are quite comfortable in cold, even subfreezing tempera-
particularly important. The loading, footing, and distribution of tures, if provided with adequate amounts of dry dust-free bed-
the animals in the trailers and trucks, as well as environmental ding and draft protection. Sheep, because of their wool, are
conditions during shipping, are important to consider to mini- remarkably tolerant to both hot and cold extremes. Newborn
mize stress and injury to the animals. Sufficient time for accli- lambs and recently shorn adults are susceptible to hypothermia,
mation to the facility, pens, handlers, feed, and water must be hyperthermia, and sunburn. Therefore, in outside housing areas,
allowed once at the destination ("Livestock Handling and sheep should be provided with shelters to minimize exposure to
Transport," 1998). sun and inclement weather.
Animals housed under intensive confinement should be kept
clean, and excreta should be removed from the pens or enclo-
sures daily. Feed and water equipment should be maintained
D. LaboratoryManagement and Husbandry in sound, clean condition and should be constructed to pre-
vent fecal contamination. Waterers should not create a muddy
Recent publications address many general considerations as environment in paddocks or pens. There should be sufficient
well as specifics about the facilities, husbandry, space require- continuous-access waterers placed around the area to prevent
ments, and standard practices for research and production ru- competition or fighting. Feeders should be constructed to con-
minants. Institutions, private entities, researchers, and facility form to species size and feeding characteristics and to prevent
staff must also be aware of the recent adoption by the U.S. De- entrapment of head and limbs. Pens, other enclosures, passage-
partment of Agriculture (USDA) of specific guidelines for reg- ways, chutes, and floors must be very sturdy to withstand such
ulation of farm animals, such as ruminants, that are used in bio- factors as the frequent cleaning; the strength, weight, and cu-
medical and other nonagricultural research. The USDA Animal riosity of all ages of animals; and the investigative and climbing
Care Policy 29 notes that the "Guide for the Care and Use of behaviors of goats. Chain-link fences are dangerous because
Agricultural Animals in Agricultural Research and Teaching" goats (as well as some breeds and ages of sheep) are curious and
and the "Guide for the Care and Use of Laboratory Animals" tend to stand on their hind legs against fencing or walls. Fore-
provide additional information to supplement the existing Ani- limbs may be caught easily in the mesh. Floors in any areas
mal Welfare Act regulations (CFR, 1985; FASS, 1999; Hays where animals will be housed, led, or herded must ensure secure
et al., 1998; NRC, 1996a; USDA, 2000). footing at all times to prevent slipping injuries. All ruminants
In all cases, stress should be considered and minimized in the are social and herding animals. Therefore, they should be
husbandry and handling of ruminants. Animals need to be pro- housed in groups or at least within eyesight and hearing of other
vided adequate time to adapt to new surroundings. Stress de- animals. Singly housed animals should have regular human
creases feed intake, and the resulting energy, vitamin, and min- contact. Environmental enrichment should be governed by the
eral deficiencies will affect the growth and development in experimental protocol or standard operating procedures, and
younger animals. Reproductive soundness and rumen function durable play objects should be supplied to those animals that are
are affected by transport and similar stresses. Standard practices housed in confinement. Calves, in particular, that must be singly
such as weaning, castration, dehorning, vaccinations, deworm- housed or that have been recently weaned, need play objects
ing and treatments for external parasites, shipping and the asso- (Morrow-Tesch, 1997).
ciated feed and water deprivation, introduction to a new hous- Because sheep and goats are sensitive to changes in light
ing environment and new personnel, and intercurrent disease cycle (especially reproductive parameters), photoperiod must
are all stressors (Houpt, 1998). Animals should be acclimated to be taken into account. Normally, sheep and goats should be
the use of halters and leads, temporary restraint devices, and maintained on a cycle comparable to natural conditions. Light
other handling equipment associated with the research program. intensity should be maintained at about 220 lux (ILAR, 1996;
Personnel in the research facility who are unfamiliar with rumi- FASS, 1999). Light cycles can be manipulated for experimental
nants should be trained in appropriate handling techniques. Ap- reasons.
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 525

lI. BIOLOGY man (HLA) and murine (H-2) systems in terms of depth of
knowledge (Lewin, 1996). Cattle are considered free of autoim-
mune diseases (Schook and Lamont, 1996).
A. Unique Physiological Characteristics and Attributes, The complexity of the immunobiology of the bovine mam-
with Emphasis on Comparative Physiology mary gland is being studied extensively because mastitis is
the most prevalent disease in the dairy industry. Several innate
The development of the digestive system and the unique func- immune mechanisms and cellular defenses, and their variation
tion of the rumen are among the most notable comparative throughout lactation, have been described (Sordillo et al.,
anatomic and physiologic characteristics of ruminants. There is 1997).
a three-compartment forestomach (rumen, reticulum, and oma-
sum) and a true stomach (abomasum). The mature rumen func-
tions as an anaerobic fermentation chamber in which the en- BO Normal Values: Growth, Longevity,
zymes, such as cellulase, of the resident bacteria allow the Hematology, Clinical Chemistry
animals to prosper as herbivores. Digestion is also aided by
other microorganisms, such as protozoa (105-106/ml) and bac- Hematology and clinical reference texts are available for the
teria (109-101~ that contribute to rumen fermentation. The ruminant species and include overviews of normal values for
result is the production of volatile fatty acids (acetic, propionic, age, sex, and breed-specific ranges, as well as discussions re-
and butyric). Unlike in the monogastrics, fermentative diges- garding the influences on the hemogram of many management,
tion and volatile fatty acid absorption also occur in the large in- nutritional, geographic, metabolic, physiologic (including lac-
testines. The main sources of energy for ruminants are volatile tation), medication, and iatrogenic variables (Duncan and
fatty acids (VFAs) rather than glucose. Glucose is formed from Prasse, 1986; Jain, 1986; Kaneko et al., 1997). These references
propionic acid (or from amino acids) for metabolism in the should be consulted when preparing to include blood collection
central nervous system (CNS), uterus, and mammary glands. data in research protocols and when reviewing hematologic
Plasma glucose in ruminants is much lower than and is regu- findings. In addition, most veterinary diagnostic laboratories
lated differently from that in nonruminants. The rumen mi- have also developed databases for normal ranges for hemato-
croorganisms also synthesize vitamins, such as B and K, and logic and clinical chemistry values based on subjects from their
provide protein that is used by the animals' systems. Large service areas, and these may be useful as local and breed refer-
amounts of fermentation gases such as CO2 and methane, and ences. Appropriate control groups must be incorporated into
small amounts of nitrogen, are naturally eructed (Hecker, 1983; each research plan, however, to establish the normal values (see
Schimdt et al., 1988). Table I) for the particular locale, diagnostic facilities, breed,
Intestinal immunoglobulin absorption by pinocytosis in the age, sex, and research circumstances. Normal hematologic and
neonates is crucial to the success of passive transfer. This trans- clinical biochemistry data are presented in Tables II and III.
fer mechanism is functional for approximately the first 36 hr af- Some general statements apply to most ruminants. Most ru-
ter birth. Neonatal ruminants are immunocompetent, however, minants have fewer neutrophils than lymphocytes. The blood
and this condition is used to advantage for vaccinations against urea nitrogen (BUN) values cannot be used as an indicator of re-
some common diseases of the neonatal and later juvenile peri- nal function because of the metabolism of urea nitrogen by ru-
ods, such as infectious bovine rhinotracheitis (IBR) vaccine men microflora. Because of the large volume of rumen water,
(using modified live virus vaccines) to calves when their dams' ruminants can generally go several days without drinking be-
colostrum is lacking antibody against this virus. fore significant dehydration occurs. Erythrocytes may become
Unlike hepatic lipogenesis in humans, lipogenesis in sheep more fragile during rehydration, resulting in some degree of
primarily occurs in adipose tissue and the mamrnary gland hemolysis and hemoglobinuria. Severe dehydration can occur
(Hecker, 1983). In addition to normal lymph node Chains, and quickly, however, in animals that are ill. Urine pH is generally
as in other ruminants, sheep have small red "nodes" associated alkaline in adult ruminants.
with blood vessels. Inadvertently named hemal "lymph nodes," Ruminant erythrocytes are smaller than those in other mam-
they contain numerous red blood cells. Sheep have a relatively mals, and hematocrits tend to be overestimated unless blood
large pituitary gland, and accessory adrenal medullary tissue samples are centrifuged for longer amounts of time for packing
may be interspersed throughout the abdominal cavity. of the cell pellet. Increased red-cell fragility is also associated
Three major ovine histocompatability classes have been with the smaller erythrocyte. Rouleau formation does not occur
identified and designated as OVAR (Ovis aries) classes I, II, and in cattle but does to a limited extent in sheep and goats. In ad-
III (Franz-Werner et al., 1996). Bovines are recognized as hav- dition to fetal hemoglobin, sheep are reported to have at least six
ing several unique aspects involving their immune systems. The different hemoglobins (Hecker, 1983). Blood coagulation in
bovine lymphocyte antigen (BoLA) system ranks after the hu- sheep is similar to that in humans.
526 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

Table 1
Normal Values for Sheep, Goats, and Cattle:
Vital Signs, Life Spans, and Weightsa

Parameter and age Sheep Goats Cattle

Chromosome number 54 60 60
Body temperature(o C)
Young 39.5-40.5 39-40.5 39-40.5
Adult 39-40 38.5-39.5 38-39
Heart rate (beats/min)
Young 140 (120-160) 140 (120-160) 120 (100-140)
Adult 75 (60-120) 85 (70-110) 60 (40-80)
Respiration rate (breaths/min)
Young 50 (30-70) 50 (40-65) 48 (30-60)
Adult 36 (12-72) 28 (15-40) 24 (12-36)
Life span (years) 10-15 8-12 20-25
Body weights (lb)
Birth 3-25
1 month 25
3 months 55 400
6 months 110 85
9 months 110
12 months 130 720
18 months 155
24 months 300 (ram), 200 (ewe) 170 1100
36 months 205
Deciduous dental formula 2(Di 0/3, Dc 0/1, Dp 3/3) = 20 2(Di 0/3, Dc 0/1, Dp 3/3) = 20 2(Di 0/3, Dc 0/1, Dp 3/3) = 20
Permanent dental formula 2(10/3, C 0/1, M 3/3) = 32 2(10/3, C 0/1, M 3/3) = 32 2(10/3, C 0/1, M 3/3) = 32

aVital sign data for goats are from "Large Animal Internal Medicine" (1996). Sheep weight data representweights of feeder lamb and adult dry ewe (Federa-
tion of Animal Science Societies [FASS], 1998). Goat weight data are for a large-breedmale goat. Cattle weight data represent weights of female Holstein or
Guernsey dairy cattle (FASS, 1998). Life span data for sheep and cattle are from Brooks et al. (1984).

Erythrocytes in Pygmy and Toggenburg goats tend to be C. Nutrition

more fragile than erythrocytes from other goat breeds. Nor-
mal caprine erythrocytes lack central pallor because they are The nutritional needs of ruminants vary considerably accord-
fiat and lack biconcavity. Normal caprine erythrocytes may ex- ing to the species, breed type, different phases of development,
hibit poikilocytosis. At least five blood groups have been re- the use of the animals, location, and different stresses in their
ported in goats: B, C, M, R-O, and X. Because transfusion lives. For example, mineral requirements and other nutritional
reaction rates may be as high as 2 - 3 % , cross-matching is requirements vary even among breeds of cattle. Several refer-
advisable although not always practical (Smith and Sherman, ences are available that describe the varying requirements and
1994). Blood loss of up to 25% of the red cell mass at a single are useful for determining the requirements of ruminants con-
time point can be tolerated by healthy goats. Blood may safely sistent with the parameters noted above and the type of feeds
be obtained in volumes of 10 m l / k g body weight and given available (Jurgens, 1988; "Large Animal Clinical Nutrition,"
in volumes Of 1 0 - 2 0 ml/kg. In general, aspartate aminotrans- 1991; NRC, 1981, 1989, 1993, 1996b; "Large Animal Internal
ferase (AST) and lactate dehydrogenase (LDH) are not liver- Medicine," 1996).
specific in goats, and alanine aminotransferase (ALT; formally Preformulated commercial feeds, concentrates, and supple-
serum glutamic-pyruvic transaminase, or SGPT) cannot be ments are available specifically for the different species of ru-
used to evaluate hepatic disease in goats. ~,-Glutamyltransferase minants. Some of these provide complete energy and protein re-
(GGT) and alkaline phosphatase (AP) are associated with bil- quirements or may be used as supplements for what cannot be
iary stasis, and elevations in GGT are generally associated with provided entirely by pasture, forage, hay, or silage. Concentrate
hepatic damage. mixtures contain salt, minerals, and other elements. Concen-
trates should contain a protein source such as soybean meal,
cottonseed meal, or linseed meal. Computer programs are also
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 527

Table II
Normal Values for Sheep, Goats, and Cattle: Hematology

Parameter (units) Sheep Goats Cattle

Packed cell volume (%) 27-45 22-38 24-46

Hemoglobin (g/dl) 9-15 8-12 8-15
Red blood cells (RBC) (x 106/~tl) 9-15 8-18 5-10
White blood cells (WBC) (x 103) 4-12 4-13 4-12
Total protein (g/dl) 6.0-7.5 6-7.5 7-8.5
Mean corpuscular volume (fL) 28-40 16-25 40-60
Mean corpuscular hemoglobin (pg) 8-12 5.2-8 11-17
Mean corpuscular hemoglobin
concentration (g/dl) 31-34 30-36 30-36
Reticulocytes (%) 0 0 0
RBC diameter (~tm) 3.2-6 2.5-3.9 4.8
RBC life (days) 140-150 125 160
Myeloid: Erythroid ratio 0.77-1.68:10 0.69:10 0.31-1.85:10
Platelets (x 103/~tl) 250-750 300-600 100-800
Fibrinogen (mg/dl) 100-500 100-400 300-700
WBC differential: absolute count/~tl (% of total)
Stabs, bands Rare Rare 0-250 (0-2)
Segmented neutrophils 400-6000 (10-50) 1200-6250 (30-48) 600-5400 (15-45)
Lymphocytes 1600-9000 (40-75) 2000-9100 (50-70) 1800-9000 (45-75)
Monocytes 0-750 (0-6) 0-550 (0-4) 80-850 (2-7)
Eosinophils 0-1200 (0-10) 50-1050 (1-8) 80-2400 (2-20)
Basophils 0-350 (0-3) 0-150 (0-1) 0-250 (0-2)
Coagulation tests (sec)
Prothrombin time 13.5-15.9 9.0-14.0 6.8-8.4
Partial thromboplastin time 27.9-40.7 11.0-17.4
Thrombin time 4.8-8.0 20.9-33.4 4.3-7.1

readily available for those who may need to formulate and bal- particles in mixes. Generally, goats do not prefer "sweet" feeds
ance rations. The palatability of feeds should be taken into ac- that contain molasses and do not need supplemental concen-
count. Mineral deficiencies and supplementation have been trates if a good-quality pasture or hay is fed. When given access
shown to influence several physiologic parameters such as im- to a salt block, goats generally are self-regulating. Grass-fed
mune function. Introduction of young stock should include con- goats and lactating goats may need supplementation with
tinuation of the feeding program of the source or gradual tran- calcium and phosphorus, whereas alfalfa-fed goats do not
sition to appropriate feed for the animals available in the region (Bretzlaff et al., 1991). Horse and sheep feeds may be fed to
of the research facility (NRC, 1996). goats provided that the feed does not contain much molasses
Good-quality pasture can support ruminants under certain (Bretzlaff et al., 1991). The copper content of horse feed is not
circumstances. Lush spring pastures, especially pastures con- excessive for goats, as it is for sheep. Pelleted horse feeds with
taining alfalfa, can induce bloat, diarrhea, grass tetany, or ni- 2 5 - 2 8 % fiber and 12-14% protein are good goat rations.
trate poisoning. Ruminants not acclimated to lush pasture Goats will consume 5 - 8 % of body weight in dry-matter intake
should be fed good-quality hay and slowly introduced to pasture (whereas cattle will usually consume only 4% of body weight).
environments. Goats enjoy human contact, and small alfalfa cubes make tasty
When ruminants have access to pasture, it is important to be treats for the goat.
aware of different eating habits. Sheep and cattle are grazers. Rations that have excessive calcium-phosphorus ratios or el-
Goats are browsers and will readily eat grasses, as well as seeds, evated magnesium levels may induce urinary calculi in male ru-
nuts, fruit, and woody-stemmed plants. Goats, however, can also minants. These may also occur when forage grasses are high in
be selective eaters and will only eat the leafy, more nutritious silicates and oxalates.
parts of the plant. Therefore, goats have a tendency to "waste" To increase ovulation rate in does, some producers "flush" fe-
hay. Other eating habits should also be considered. Finely males by feeding 0.5-1 lb concentrate per head per day for sev-
ground concentrates are not tolerated well by goats; pelleted eral weeks before and after the initiation of the breeding season.
concentrates are preferred because the goat will pick out large Thin pregnant dairy goats should be fed 1 lb concentrate per
528 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

Table IIl
Normal Values for Sheep, Goats, and Cattle: Clinical Biochemistry a

Parameter (units) Source Sheep Goat Cattle

Alanine aminotransferase (ALT, SGPT; U/liter) s, hp 30 ___4 6-19 11-40 (27 _ 14)
Albumin (g/liter) 24-3.0 (27 ___1.9) 27.0-39.0 (33.0 _ 3 . 3 ) 30.3-35.5 (32.9 _ 1.3)
Alkaline phosphatase (AP; U/liter) 68-387 (178 ___102) 93-387 (219 ___76) 0-488 (194 ___126)
Aspartate aminotransferase (AST, SGOT; U/liter) s, hp 60-280 (307 ___43) 167-513 78-132 (105 +__27)
Bicarbonate (HCO3; mmol/liter) 20-25 17-29
Bilirubin
Conjugated (mg/dl) s, p, hp 0-0.27 (0.12) 0.04-0.44 (0.18)
Unconjugated (mg/dl) 0-0.12 0.03
Total (mg/dl) 0.1-0.5 (0.23 ___0.01) 0.01 0.01-0.5 (0.2)
Blood urea nitrogen (BUN; mg/dl) s, p, hp 8-20 10-20 (15 __+2.0) 20-30
Calcium, total (mg/dl) s, hp 11.5-12.8 8.9-11.7 9.7-12.4
Carbon dioxide, total (mmol/L) s, hp 21-28 (26.2) 25.6-29.6 (27.4 ___1 . 4 ) 21.2-32.2 (26.5)
Chloride (C1; mmol/liter) s, hp 95-103 99-110.3 (105.1 _+ 2 . 9 ) 97-111 (104)
Creatine kinase (CK) U/liter) s, hp 8.1-12.9 (10.3 ___1.6) 0.8-8.9 (4.5 ___2.8) 4.8-12.1 (7.4 __+2.4)
Creatinine (mg/dl) s, p, hp 1.2-1.9 1.0-1.8 1.0-2.0
y-Glutamyltransferase (GGT; U/liter) s, p 20-52 (33.5 ___4.3) 20-56 (38 ___13) 6.1-17.4 (15.7 ___4.0)
Globulin (g/liter) s 35.0-57.0 (44.0 +_ 5 . 3 ) 27.0-41.0 (36.0 ___5 . 0 ) 30.0-34.8 (32.4 _ 2.4)
Glucose (mg/dl) s, p, hp 50-80 (68.4 _ 6.0) 50-75 (62.8 ___7.1) 45-75 (57.4 _+ 6.8)
Lactate dehydrogenase (U/liter) s, hp 238-440 (352 ___59) 692-1445 (1061 ___222)
Magnesium (mg/dl) s 2.2-2.8 2.8-3.6 1.8-2.3
Phosphorus (P; mg/dl) hp 5.0-7.3 (6.4 ___0.2) 4.2-9.1 (6.5) 5.6-6.5
Potassium (K; mmol/L) hp 3.9-5.4 (4.8) 3.5-6.7 (4.3 ___0.5) 3.9-5.8 (4.8)
Sorbitol dehydrogenase (SDH; U/liter) hp 5.8-27.9 (15.7 ___7 . 5 ) 14.0-23.6 (19.4 __+3 . 6 ) 4.3-15.3 (9.2 ___3.1)
Sodium (Na; mmol/liter) hp 139-152 142-155 (150 ___3.1) 132-152 (142)
Total protein (TP, g/liter) s 60.0-79.0 (72.0 + 5 . 2 ) 64.0-70.0 (69.0 ___4 . 8 ) 67.4-74.6 (71.0 ___1.8)

aData presented as ranges with mean and standard deviation in parentheses, s, Serum; p, plasma; hp, heparinized plasma. Clinical biochemistry data from
Kaneko et al. (1997).

day, with the amount increasing to 1.5 lb per head per day dur- In typical m a n a g e m e n t situations, dairy calves either are sepa-
ing the last 6 weeks of gestation. Forage should be fed a d libi- rated from their dams immediately after birth and bottle-fed
t u m during this time. colostrum, or they remain with their dams for only about 24 hr
All newborn ruminants must receive passive immunity from and suckle fresh colostrum during this time. Dairy producers
colostrum, the first postpartum milk of a dam that contains con- then refrigerate and/or freeze the colostrum that cannot be con-
centrated protective maternal antibodies (most as IgG1), func- sumed by the calf during that time and then feed this diluted
tional leukocytes, cytokines, vitamins, minerals, and protein. 5 0 : 5 0 with warm water 3 times a day to the calves during the
Colostrum also has laxative properties. Trypsin inhibitors in the next 2 - 3 days. Extra frozen colostrum for emergencies may
colostrum allow the passage of intact antibody molecules, by be obtained from dairy farmers; it is advantageous to obtain
pinocytosis, through the neonate's gut wall and into the blood- colostrum from well-managed herds and from the multiparous
stream during the first few days after birth. The quality of the cows in the herd (not heifers) in the same geographic locale.
colostrum is directly related to herd or flock management, vac- Holstein calves, for example, should receive a m i n i m u m of 3 -
cination programs, and the dam's overall condition and nutri- 5 liters within 12 hr of birth and then be fed about 1 0 - 1 5 % of
tion throughout gestation and at the time of parturition. Ensur- body weight in colostrum by 24 hr of age. After 3 days, calves
ing effective colostrum transfer is also dependent on the timing are then placed on milk replacers.
and amount taken by the neonate. Most neonatal ruminants can Although young ruminants generally do well receiving their
suckle well within 3 hr of birth. Those that do so have been dams' milk, commercially available milk replacers are available
shown to have significantly less diarrhea (Naylor, 1996). Neo- and should generally be prepared and fed according to the man-
nates weakened by dystocia or hypothermia, for example, ufacturer's recommendations. Containers used to prepare and
should be hand-fed or tube-fed colostrum. If necessary, the dam feed these replacers should be sanitized daily. The fat content of
should be hand-milked and the newborn fed colostrum (for ex- both calf and lamb milk replacers is excessive; however, calf milk
ample, 2 0 - 4 0 ml for kids) every 2 - 4 hr for the first 1 - 2 days. replacers can be used for kids if care is taken not to overfeed.
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 529

Young ruminants can be offered good-quality hay (such as from about 3 - 4 lb up to 25 lb. Factors that affect birthweight in-
second cutting) to nibble on by 1 week of age. Calves may be clude parental size, number of lambs in the litter (fewer lambs
provided with calf starter, a commercially available concentrate or singlets tend to be larger), age of the ewe (younger ewes have
with appropriate levels of energy and protein, fed according to smaller lambs), lamb gender (males tend to be heavier), nutri-
the manufacturer's recommendations at 2 - 3 weeks of age. They tion, and season or temperature (spring lambs tend to be larger
can be weaned off milk replacer by 4 - 7 weeks of age. Young than fall lambs).
ruminants (4-12 months of age) need good-quality forage as Goats are seasonally polyestrous in temperate regions, so that
well as grain and concentrate supplementation to promote de- young are born in favorable times of the year. They are short-
velopment of the rumen. In farm management situations, forage day breeders, in that estrus (heat) is brought about by the de-
can be silage, pasture, and hay. In a confinement situation like a creasing light of shorter days. In temperate climates of the
research unit, good-quality hay, such as second cutting, is desir- Northern Hemisphere, goats are normally anestrous during
able. Animals should not be overfed and should be offered a the summer and begin cycling in the fall. The actual length of
mineral mix free-choice. the sexual cycle depends on day length, breed, and nutrition.
In contrast to dairy calves, beef calves remain with their Most dairy goats cycle between August and February or March.
mother cows until weaning at 7 months of age. Calves tend to Nubians often have extended breeding cycles, and the sexual
suckle many times per day. As they mature, calves are creep- season of some breeds, including the Alpine, can be extended
fed, with the energy and protein content of the ration deter- by artificial means. The caprine gestation length averages 150
mined by the milk production of the dams and by the available days with a variation of 145-155 days. Does bear singletons,
forage, such as pasture. twins, and triplets, with slightly shorter gestation when the doe
is carrying triplets.
D. Reproduction Cows are polyestrous. Domestication of cattle has included
selection against seasonality of the breeding season, particu-
Several useful references addressing ruminant reproduction larly in dairy breeds but to some extent also in the beef breeds.
in detail are available ("Current Veterinary Therapy: Food Ani- In spite of this, cattle have been found to be still sensitive,
mal Practice," 1986, 1993, 1999; "Large Animal Internal Med- in varying manifestations, to photoperiodicity. Reproductive
icine," 1996; "Current Therapy in Large Animal Theriogenol- physiology in cattle is influenced by many factors. The repro-
ogy," 1997; Hafez, 1987). ductive programs in source herds and at well-managed facilities
will be production-related. Extensive coverage of both physio-
1. Reproductive Physiology logic basics and specific industry-related criteriamfor retention
of a cow as a breeder, for examplenare addressed in detail in
Sheep are seasonally polyestrous; most breeds will express texts and references oriented toward herd and production man-
estrus in the fall (Northern Hemisphere) and subsequently lamb agement ("Current Veterinary Therapy," 1986). Gestation in
in the spring. Some breeds of sheep may cycle in both the fall cattle is approximately 280 days, with a range of 270-292 days.
and the spring. Between seasonal periods of receptivity, the The length of gestation in cattle is influenced by fetal sex; fetal
females undergo a long period of sexual quiescence called numbers; age and parity of the cow; breed; genotype of cow,
anestrus. In a research environment, ewes can be artificially bull, or fetus; nutrition; and local environmental factors. As
stimulated to progress from anestrous to estrous cyclicity by noted, these factors are also important in sheep and goats. Cows
maintaining the females in 8 hr of light and 16 hr of dark for 8 - usually bear single calves, although twin births do occur. When
10 weeks. Puberty is reached at about 7-8 months (or earlier) in twins are combinations of male and female calves, the female
both rams and ewes; rams will typically reach puberty before should be evaluated for freemartinism.
their female counterparts. Ewes will display signs of estrus for
about 2 4 - 3 0 hr and will ovulate spontaneously at the end of es- 2. Detection of Estrus and Pregnancy
trus. The estrous cycle length is 14-19 days, with an average of
about 17 days. Following breeding, the average length of gesta- Ovine estrus detection is usually accomplished by the ram.
tion is 147-150 days. Slightly longer gestations are observed in Nonetheless, because artificial insemination is achievable in
animals carrying single lambs (singlets), in animals carrying ewes, clinical signs of estrus are important. Typically, ewes in
rams, and in certain breeds such as those derived from Merinos. heat will show a mild enlargement of the vulva, with slight in-
Prolificacy, or the number of lambs produced per gestation, creases of mucus secretion. Ewes may isolate from the flock and
tends to be dependent on the maturity of the dam (older dams appear anxious. It is often better and clearly more reliable to
tend to have multiple lambs) and on breed characteristics (some employ the help of a sterile ram to mark females when they are
fine-wool breeds have fewer multiple births). The Finn and in standing heat. Two mating systems commonly employed in-
Dorset breeds are especially prolific. Lambs vary in size at birth clude hand mating and group mating. With hand mating, ewes
530 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

are placed either singly or in small groups with the ram of season (with winter delaying), and the level of nutrition (with
choice. Ewes are removed as serviced. Group mating involves higher levels hastening puberty). In some cases, the presence of
placement of a mature ram with approximately 5 0 - 6 0 ewes for mature cycling cows influences heifer puberty. With adequate
the entire 6-week breeding season. In either mating system, it is nutrition, dairy breeds will reach puberty at 10-12 months and
best to attach a marking harness to the male so that individual beef breeds at 11-15 months, and estrous cycles will occur reg-
ewes can be identified as serviced. This is important so that par- ularly after the pubertal (first) estrus, Maturing heifers will of-
turition dates can be calculated. ten have one or more ovulations before showing overt signs of
An easy, natural way to estimate pregnancy is by placing ster- estrus. Only one follicle usually ovulates per estrous cycle
ile teaser rams with the ewes at the end of the breeding season. (Hafez, 1987) Estrus, or standing heat, in cattle averages 12-
Any animal marked by the ram probably has not conceived. 16 hr in length, with a range of 6 - 2 4 hr ("Large Animal Inter-
Ultrasound scanners are also used for pregnancy detection. The nal Medicine," 1996). Detection of standing heat is important
ultrasound transducer is placed against the right abdomen; pres- because it is closely related to the time of ovulation. Ovulation
ence of a fetus is indicated on the machine. Claims of 98% ac- occurs approximately 25-32 hr after estrus. Detection of estrus
curacy at 6 weeks postbreeding have been made, although ac- is usually accomplished by visual observation of vaginal mu-
curacy is generally best beyond 60 days of gestation. Interrectal cous discharge, mounting behavior by other females (i.e., the
Doppler ultrasound probes detect fetal pulses. Fetal heart rate is cow standing to be mounted is the individual in estrus), and re-
in the range of 130-160 beats per minute, whereas maternal ceptivity to a bull (willingness to stand). Successful visual de-
heart rates tend to be 90-110 beats per minute. Accuracy is best tection of standing heat is dependent on observation skills of
beyond 60 days of pregnancy. Rectal-abdominal palpation is an handlers, knowledge of the herd, stresses (e.g., detection de-
inexpensive alternative. A plastic probe is introduced intrarec- creased in Bos taurus during heat stress), barn and yard surfaces
tally into the ewe, which is restrained on her back in a cradle. (estrus detected better on dirt than on concrete), and maintain-
The plastic probe is then manipulated toward the abdomen ing a consistent observation schedule. Teaser animals outfitted
while palpating for the fetus with the opposite hand. with marking devices are also used. Other methods of detecting
The age of the doe when she first expresses heat varies with estrus include monitoring progesterone levels; glass slide and
breed. Some does will express signs of heat between 3 and 4 other evaluations of cervical mucus; change in vaginal pH; and
months old. However, does should be 7-10 months old or at body temperature changes (Hafez, 1987). Estrous cycles are
least 8 0 - 9 0 lb in weight before being bred. The caprine estrous usually 21 days in length, with a range of 17-25 days. It is rec-
cycle lasts 18-24 days. The duration of estrus is 2 4 - 9 6 hr but ommended that a heifer deliver her first calf by 2 years of age.
averages about 40 hr. The estrous cycle can be more erratic in After successful conception, progesterone levels in the cow
the beginning than in the end of the breeding season (Smith, remain elevated for most of the pregnancy, as the result of the
1997). "Standing heat" is usually 12-24 hr but can be as short 9corpus luteum of pregnancy, and they decline only during the
as a few hours. Signs of estrus in goats include uneasiness, tail final month. Conceptus implantation occurs beginning at about
switching or "flagging," redness and swelling of the vulva, clear day 17. If the pregnancy fails before this time, the cow will be-
vaginal discharge that becomes white by the end of estrus, vo- gin to cycle again between days 18-24, but if the pregnancy
calization such as continuous bleating, and occasionally riding ends after day 17, there may be a delayed return to estrus. Real-
and standing with other does. A doe that is not in heat will not time ultrasonography can be used to determine pregnancy as
stand to back pressure or for attempts to hold her tail. Does can early as 9 days after insemination, with embyros seen by days
be induced to show signs of heat by buck exposure and will ovu- 26-29. Fetal gender can also be determined by experienced
late within 7-10 days after introduction of the buck. Goats ovu- personnel by this method by about day 55. Detection of preg-
late during the later part of the estrous cycle, most between 2 4 - nancy can be successful by 2 5 - 4 0 days after conception by ob-
36 hr after the onset of estrus. Nevertheless, goats should be servation of failure to return to estrus or by palpation per rec-
mated once signs of estrus are recognized and every 12 hr until tum (detecting fetal membrane slip by days 30-35 and/or
the end of estrus. amniotic vesicle by days 28-35). Palpation of the fetus is pos-
Most goats kid only once a year, although some goats near the sible by day 65 and placentomes by approximately days 100-
equator may kid twice. Once bred successfully, a goat will only 110. Palpation later in presumed pregnancy will provide infor-
rarely show signs of heat again. In fact, the first sign of preg- mation based on differences in size of the two uterine horns,
nancy is usually a failure to return to heat, so animals should be changes in the uterine wall, and fremitus in the miduterine ar-
carefully watched. Pregnancy can be affirmed by a variety of tery. Pregnancy can also be determined with reasonable success
means. Goats will generally decrease milk production with rates by determining if progesterone levels are elevated at days
pregnancy and should have at least a 6- to 8-week dry period 2 0 - 2 4 after insemination. Levels of bovine pregnancy-specific
for the udder to fully involute and prepare for the next milking protein B may also be measured; this is produced by tro-
period. phoblastic cells and is detectable by days 15-24 and elevated
In cattle, age of first estrus is dependent on the breed, the throughout pregnancy.
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 531

Placentation in sheep, goats, and cattle is epitheliochorial and 10 ft. Evaluation of a cow's udder prior to breeding and espe-
cotyledonary, in contrast to the diffuse or microcotyledonary cially as parturition approaches is important in order to assure
placentas of horses and pigs. The placentomes, the infolded adequate nutrition and success of passive transfer by the
functional units of the placenta, are formed as the result of fu- neonate. If the udder is edematous or if mastitis is present, for
sion of the villi of the fetal cotyledons projecting into the crypts example, an alternate source of colostrum (such as frozen re-
of the maternal caruncles (specialized projections of uterine " serves) must made be available. Poor udder conformation may
mucosa). Caruncles of sheep and goats are concave in shape, also be problematic; contingency plans should be made to en-
whereas those of cows are convex. The placentomes are dis- sure adequate support for the young if they cannot suckle from
tributed between the pregnant and nonpregant horns of the those udders. Inexperienced heifers may react indifferently or
uterus in sheep, and there are 90-100. In cattle, although the aggressively to their offspring and should be monitored more
placentomes initially develop around the fetus, they will even- closely than older, multiparous cows with uneventful calving
tually be distributed to the limit of the chorioallantoic mem- histories.
brane even in the nongravid horn. The placentomes in the non-
gravid horn will be smaller than in the gravid horn. The total 4. Parturition
number will be 70-120.
Ewes approaching parturition generally isolate themselves
3. Husbandry Needs from the flock, become restless, stamp their feet, blat, and peri-
odically turn and look at their abdomen. The pelvic region
The best birthing preparation for all dams is to ensure a proper will appear relaxed, and milk will be present in the udder.
plane of nutrition (not overnutrition) and adequate exercise. If Once hard labor contractions begin, lambs will usually be born
possible, the dam should be confined to a birthing pasture or quickly. Animals that do not appear to be progressing correctly
sanitized maternity pen a few days prior to parturition. The should be examined for dystocia. Most cases of fetal malpre-
birthing environment will be very important in the overall sentation or malpositioning can be corrected via vagino-uterine
health of the dam and offspring; stress minimization and a clean manipulation. Occasionally cesarean sections will be necessary.
environment will benefit the immune health of both in the short Sanitation, cleanliness, and adequate lubrication are of utmost
and long term. Outdoor parturition in a small birthing pasture importance when performing obstetrical procedures.
has advantages. There is less stress and less intensity of patho- For about a week before parturition, rectal temperature of the
gens. Indoor maternity pens should be clean, dry, warm, well doe will be above normal, or about 103~ depending on envi-
bedded, well ventilated but draft-free, and well lighted. Ade- ronmental temperatures. Approximately 24 hr prior to birth,
quate space per pen minimizes losses of neonates from being rectal temperature will fall to slightly below normal. Many
stepped and sat on by the dam. Management of these pens, es- large dairy-goat facilities attempt to control the onset of partu-
pecially if concentrated in an area, is important to minimize rition in order to assist birthing. The drug of choice to induce
pathogens to which dam and young are exposed. Water troughs parturition in the goat is prostaglandin F2~ (PGF2~) (Ott, 1982).
or buckets should be elevated or placed outside the pen, because On day 144 of gestation, goats given PGF2~ (2.5-5 mg) will de-
lambs and kids have a tendency to fall or be pushed into them. liver kids within 28-57 hr. Most goats prefer to kid alone and
Soiled bedding should be removed from the birthing pen be- do so unaided. Human interaction can actually interfere with
tween dams, the area sanitized and allowed to dry, and fresh normal birthing, especially in young or nervous does. Some
bedding installed for the next occupant. Moving the female im- does may reject kids if extensive human interference occurs.
mediately before or during parturition may delay the birthing Does nearing parturition have an obviously swollen udder and
process. In goats, furthermore, in utero death may occur if par- a red, swollen vulva. Pelvic ligaments at the base of tail relax.
turition is unduly delayed. Dams should be monitored closely The doe may circle to make a bed, get up and down, look at her
during parturition for dystocias; these may result in loss of tail or sides, push other goats away, and bleat softly. Signs of im-
young or in young severely weakened from the prolonged pending parturition include restlessness; vocalization (bleating
birthing process. softly); uneasiness, including getting up and down, pawing, and
Prior to parturition, ewes should be sheared or crutched. bedding; and a mucous discharge, leading to a moist tail. Eight
Crutching refers to removing wool around the perineal and to 12 hr prior to parturition, the cervix will dilate and the cervi-
mammary areas; this minimizes fetal contamination during the cal mucous plug will be evident as a tan, smeared substance on
birth process. Foot trimming can be done at this time as well. the tail and perineum of the dam. Kids should present within 1-
The tail and perineal area of the doe should be clipped and 6 hr in either anterior or posterior position. A posterior presen-
cleaned to improve postbirth sanitation. In general, the pregnant tation can be recognized by the presence of upward-pointing
doe needs a 14 ft 2 (1.2 m X 1.2 m) area for the birthing process, feet. Most does will rest between fetuses and are best left alone.
and area needs to be increased after birthing to allow spacing However, if labor is prolonged more than 1 hr, a vaginal exam
for kids. Each cow should have a minimum pen area of 10 ft x is indicated.
532 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

If the pregnant goat is housed with other goats, then herd- should be identified by the application of an ear tag or ear notch.
mates will express great interest in the dam. Unless moved prior It is extremely important that the lamb be supplied with high-
to parturition, it is best to leave the dam with the group until af- quality colostrum within the first 12 hr of birth. Lambs that are
ter parturition, because removal may delay parturition. Goats not nursing on their own should be tube-fed with colostrum that
are not prone to retained placenta. Normal kids will be quite ac- has been collected and saved previously (i.e., frozen in ice cube
tive and will quickly attempt to stand and nurse. Weak kids trays) or collected from the mother after parturition. Passive
should be towel-dried, warmed (via heat lamp, heat pad, or transfer can be assessed by measuring serum y-glutamyltrans-
warm water bottle), and assisted to nurse or fed colostrum. ferase (GGT) levels (Tessman et al., 1997). After the first few
The goat is one of the few ungulate species that will exhibit days, colostrum changes over to milk. Nursing lambs will ingest
"false pregnancy," or pseudopregnancy. This is a fairly common increasing amounts of milk as they grow. If the ewe cannot pro-
condition. Does may have characteristically distended ab- duce sufficient milk, the lamb should be "grafted" onto another
domens and may develop hydrometra and "deliver" large vol- ewe or fed artificially with a baby bottle. Powdered milk re-
umes of cloudy fluid at expected due dates. Subsequent preg- placers are commercially available; the content of ewe milk is
nancies can be normal. Goats should be tested for pregnancy by much different from that of cow's milk; thus lamb milk replacer
40 days of age. Veterinary use of prostaglandins has been suc- should specifically be used. One report notes that 5 0 - 7 0 % of
cessful in treating this condition. lamb deaths occur during the first week of life and up to 90%
As in other species, parturition in cattle results from a combi- occur within the first month. Good management of ewes during
nation of hormonal changes associated with the maturity of the gestation, care of the lamb at parturition, application of an ap-
fetus, notably ACTH (adrenocorticotropic hormone) and subse- propriate vaccination program, and observation and interven-
quent increases in fetal corticosteriods within 2 days of birth. tion within the first several weeks of a lamb's life will minimize
Administration of ACTH to a fetus, or administration to the losses (Ross, 1989).
dam, results in premature birth. Pregnancy is extended if fetal Immediately after birth, the placenta and any birthing materi-
pituitary or adrenal glands are removed surgically. The fetal als should be removed from the doe's pen. Kids do not usually
cortisol probably affects placental steroid production, account- need assistance. If kids are to be raised by the dam, they can be
ing for sharp increases in the estrogens and estrogen precursors. left alone; otherwise, kids should be towel-dried and removed
Coincident with this, maternal progesterone levels fall. The ris- from the dam. Kids are cold-sensitive and may require a heat
ing levels of estrogen cause release of maternal PGF2~ and in- lamp or other source of added warmth in cold weather. Navel
duction of oxytocin receptors. Most cows will separate them- cords should be dipped in tincture of iodine, and kids should be
selves from the rest of the herd. A cow will lift her tail and arch dehorned and castrated within the first several days of life.
her back when she is within a few hours of delivering the calf, To control caprine arthritis encephalitis (CAE), kids should
and most cows are recumbent when delivering the calf. Typi- be immediately removed from the dam and hand-fed heat-
cally, the whole birthing process takes about 100 min. The treated colostrum. Colostrum should be heat-treated for 1 hr at
length of labor of cows carrying larger calves also will be 131 ~E The first feeding can be up to 125 ml of colostrum. Kids
longer. Nervous heifers will take longer to deliver, and if they should receive a total of 250 ml colostrum within the first 3 6 -
are disturbed, their labor may cease. All postparturient ani- 48 hr of birth. After day 3, kids can be placed on milk replacer.
mals should be monitored for successful passage of these fetal Milk replacers should contain 16-24% fat and 2 0 - 2 8 % milk-
membranes within 12 hr of birth. Veterinary intervention is re- based protein. By 14 days of age, kids should be consuming ap-
quired if not. Cows occasionally eat placentas, which may sub- proximately 1.1-1.4 liters of milk per day. Kids should be in-
sequently obstruct rumen outflow and require surgical correc- troduced to forages as soon as possible and may be weaned by
tion. For cattle, it is now recommended practice to remove 6 - 1 0 weeks or 18-25 lb body weight. Milk that is fed can be
membranes that have passed, in order to prevent ingestion. reduced by 4 weeks of age by decreasing either the volume fed
or the number of feedings.
5. Early Development of the Newborn As with other dams, a cow is usually very attentive to her new-
born calf, cleaning and softly vocalizing to the neonate. Calves
Following lambing, it is critical that the newborns be typically are standing by 1 hr after birth and are suckling within
"processed" so that they will have greatest survival chances. In 3 hr. As noted previously, dairy calves may be removed from the
a well-managed flock, many lambs and ewes will not need much cow even before suckling, and the colostrum milked from the
assistance. When assistance is given, the newborn lamb's nose dam and given to the calf. Assistance may be required for nerv-
and mouth should be wiped free of secretions; gently swinging ous heifers, after dystocias and in extreme circumstances such
the lambs, head down, aids in removal of these fluids. The lamb as severe cold. Cleaning the newborn's nose and mouth, rubbing
should be dried off and stimulated through rubbing to aid its down the neonate, assuring that the calf does not get chilled, and
breathing. The lamb's navel should be dipped in an iodine solu- assuring that it receives adequate colostrum are all important
tion to prevent subsequent navel infections. And the lamb under any of these circumstances. A stressed calf's umbilical
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 533

may be treated with an iodine or chlorhexidine solution, al- weaned as early as 4 weeks of age, although 6 - 8 weeks of age
though some authors note no benefit of navel treatment, speci- is more common. If ewes are of a breed that will cycle twice a
fying that successful transfer of passive immunity and sound year, and if it is expected that they will be rebred, then the lambs
sanitary management of birthing area are the most crucial fac- must be weaned as early as possible so that lactational anestrus
tors in preventing omphalitis (navel ill) (House, 1996; Kersting, will resolve and ewes will recycle. Another factor is the cost of
1997; Kasari and Roussel, 1999). Because newborn calves can lactation rations for the ewes; if lamb grain is more economical
be deficient in vitamin A and iron, these may be injected to im- than ewe grain, then lambs should be weaned. About 4 - 5 days
prove disease resistance (Wikse and Baker, 1996). In cases in prior to weaning, feeding of the lactation ration to the ewes
which the dams' colostrum is known to be deficient in antibod- should be discontinued, and only roughage fed. At weaning, the
ies against common diseases, vaccinations may be administered lambs should be removed in the creep, and the ewes removed to
at 1 day old and followed with boosters at regular intervals. De- an area that is not within sight (and preferably sound) of the
horning is performed when horn buds appear. Castration is per- lambs. The ewes should be monitored for postweaning mastitis
formed between 2 and 9 weeks of age or later. and treated as necessary. Ewes that have physical or disease
problems or that have not been productive at lambing or feeding
their lambs should be culled. The lambs should be monitored to
6. Sexing assure that they continue to gain weight and are eating the new
ration.
Sexing the young in any of the ruminant species is straight-
Kids should be introduced to forages within the first week of
forward. The vulva of the female young is located just ventral to
life because the natural curiosity of these animals will cause
the anus. The genitalia of the male include a penis, located
them to investigate sources of feed. Kids can be weaned by 6 -
along the ventral midline, and a scrotum, located in the inguinal
10 weeks or 18-25 lb. Hand-fed milk should be reduced by
region. The phenomenon of the freemartin, a genetic female
4 weeks of age by reducing the volume fed or by decreasing the
born as a twin to a male, is the result of anastomoses between
number of feedings.
placental circulations of the twin fetuses; the mixing of blood-
Dairy calves are now usually removed from their dams im-
forming cells and germ cells results in the X X / X Y chimeras.
mediately after birth. It is less common now to allow the calves
This occurs in 8 5 - 9 0 % of phenotypic bovine females born as
to remain with their dams for about 24 hr and suckle fresh
co-twins with males. The female will often have abnormal
colostrum during this time, because their intake will be inade-
vulva and clitoris, and the vagina will be a blind end because of
quate. Dairy producers refrigerate and/or freeze the colostrum
the lack of a cervix. Sometimes singleton freemartins are born
produced during the first 24 hr and feed this, diluted 50:50 with
if the male fetus is lost after 30 days' gestation. Multiple births
warm water, twice a day to the calves during the next 2 - 3 days.
are selected for and are common in sheep; the freemartin phe-
Holstein calves, for example, should receive a minimum of 3 -
nomenon is regarded as rare. Twinning is common in goats, and
5 liters within 12 hr of birth and then be fed about 10-15% of
freemartinism occurs in about 6% of male-female pairs of
body weight in colostrum by 24 hr of age. After 3 days, calves
twins. Intersexes are seen in some goat breeds and when polled
are then placed on milk replacers, preformulated powders re-
goats are mated. Proof is usually based on evidence of abnormal
constituted with water that provide complete nutrition. Milk re-
genital development and reports of abnormal sexual behavior.
placers are commercially available and should be fed according
to manufacturer's recommendations
7. Weaning Vaccination programs for calves vary with the preventive
medicine program for the overall herd. Passive immunity pro-
Prior to weaning, it must be established that lambs can nutri- vided by colostrum from cows on sound management programs
tionally survive without mother's milk. Thus, grain, and later will last until a calf is about 6 - 7 months old; normally vacci-
roughage, should be offered to lambs well in advance of the day nations are not necessary and are contraindicated during those
of weaning so that they can adjust to the feedstuff. To prevent first 6 months. The duration of passive immunity varies consid-
the ewes from ingesting the lamb ration, a "creep" should be set erably among calves, however; some producers choose to begin
up by building an area adjacent to the ewe-lamb pen and de- vaccinating calves at 1-2 months of age and continue with
vising a slatted entry for the lambs to enter but not the ewes. monthly booster immunizations until the animals are 7 months
Therefore, the lambs will be accustomed to the new ration old, when passive immunity is no longer a possibility.
through this creep-feeding process. If lambs and ewes will be
pastured later in the spring, it is still beneficial to creep-feed 8. Artificial Insemination
lambs until pasture growth is adequate enough to fulfill the re-
quirements of the growing lambs. Artificial insemination (AI) in sheep is more difficult than in
Lambs that are consuming 1.5-2 lb of creep feed per day may cattle because sheep are smaller and cannot be reproductively
be weaned. Depending on the individual program, lambs may be manipulated via the rectum and because the cervix of sheep is
534 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

more difficult to traverse with the insemination pipette. Breed- dairy breeds in order to produce milk throughout the year and
ing animals artificially with fresh semen produces pregnancy to reduce kidding labor. Goats in the luteal phase of the estrous
rates averaging 50% (not unlike that of cattle); artificial insem- cycle, days 4-16, are sensitive to PGF2~ (2.5-5 mg IM) and
ination with frozen semen is less successful. Several artificial will show estrus in 3 6 - 6 0 hr postinjection (Bretzlaff, 1997).
insemination techniques have been used. Laparoscopic AI in- Dosing cycling animals twice 11 days apart will synchronize
volves the surgical instillation of semen into the uterus through goats, and artificial insemination using this method has resulted
a small abdominal opening. The procedure is successful but is in 4 0 - 6 0 % conception rates (Bretzlaff, 1997; Greyling and Van
technically involved and costly. Cervical AI involves the trans- Niekerk, 1986). Programs for timed breeding have been de-
vaginal introduction of semen into the cervix. A modification of scribed and involve administering progestogens (Bretzlaff,
this technique (transcervical AI) allows for penetration through 1997). Vaginal pessaries of fluorogestone acetate left in place
the cervix into the uterus. This method (called the Guelph sys- for 21 days in the doe followed by an injection of pregnant mare
tem for transcervical AI) leads to successful penetration into the serum gonadotropin (PMSG) at the time of pessary removal
uterus in up to 75% of ewes when performed by an experienced have proven successful. Also, when primed by PGF2~, an 11-
inseminator. day regimen of fluorogestone acetate with PMSG given on day
Artificial insemination is now an integral part of dairy herd- 9 has been successful.
ing; natural insemination as a management practice is relatively Synchronization of cattle estrous cycles and superovulation
rare. Technicians performing the AI technique are available are used as management techniques in certain commercial
through commercial enterprises. Dairy production employees cattle and dairy production settings where estrus synchroniza-
are also trained. Information regarding the management of the tion or embryo transfer is advantageous to production and man-
donors and recipients, the storage and handling of the semen, agement. The methodology is also used in the research setting
and the skills and record keeping required is covered exten- for coordinating donors and recipients of embryos or other ge-
sively elsewhere (Nebel, 1997). netically manipulated tissues for implantation. The options and
dosing regimens are described in detail in veterinary clinical
9. Synchronization texts (Wenzel, 1997; Vanderboom et al., 1997). In synchroniza-
tion, the principle is lysis of the existing corpus luteum. The
Because sheep are hormonally similar to other ruminants, es- more common practices involve the use of products approved
trous synchronization techniques are comparable. Progesterone for use in cattle such as PGF2~, one of its analogs, or products
suppresses follicle-stimulating hormone (FSH) secretion, pre- containing estradiol valerate. Progestogens are also used in con-
venting animals from developing follicles and exhibiting estrus. junction with estradiol valerate. Other approaches, involving
Artificial or natural progesterone can be administered in the management techniques combined with pharmacologic inter-
feed, through parenteral injection, subcuticular implants, and ventions, are considered less successful. Superovulation regi-
vaginal pessaries. The progesterone is withdrawn in about 12- mens involve injections of FSH either alone or with PGF2~ at
14 days, after which the FSH secretion will initiate the process timed internals. Estrus is expected 48 hr after the final injection,
of follicle development (Trower, 1993). Estrus usually will oc- and two inseminations are performed at 12 hr intervals after es-
cur in 3 6 - 6 0 hr (average is 48 hr). A natural method of syn- trus detection. Preparation of recipients involves injection of
chronization, often applied to promote flock breeding within a PGF2~ or progestogens with gonadotropins such as PMSG. For
short period of time (and thus parturition will be within a nar- greatest success as management tools, these must be combined
row window as well), is the introduction of sterile rams with the with a consistent program that provides appropriate nutrition
ewes before the beginning of the normal fall mating period. for all cattle involved. Synchronization of animals is also in-
Pheromones released from males naturally stimulate the fe- fluenced by several other factors, however, such as time in the
males to cycle and to synchronize their heats. It should be noted cycle when hormones are administered, response by each indi-
that introduction of a male during late anestrus will often stim- vidual animal, whether the cow is a dairy or beef animal, parity
ulate ovulation in about 6 days; however, this cycle will gener- and maturity of the cows, success of heat detection after the lu-
ally be without clinical signs of estrus (silent heat). Vasectomy teolysis, and accurate record keeping.
of rams is one method of producing sterile "teaser rams."
Introduction of the buck to a group of does will induce ovula- 10. Embryo Transfer
tion and may even synchronize does. Does that are kept separate
from the buck will show signs of estrus, will ovulate within 6 - Embryo transfer involves the removal of multiple embryos
10 days, and will have normal pregnancies when introduced to from a superovulated embryo donor and transferring them to
a buck. Bucks with horns and intact scent glands are better able synchronized recipients. This method maximizes the genetic
to induce ovulation than dehorned bucks, whose scent glands potential of the donor animal. The donor animal is hormonally
often been removed. superovulated and inseminated. In sheep, about 1 week after
Control of breeding in the goat has been studied mostly in breeding, the embryos are surgically removed from the donor's
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 535

uterus. In cattle, the procedure is nonsurgical. About 75% of ex- tant to know the semen quality of the ram as one indicator of fer-
pected embryos (determined by counting corpora lutea) can be tility. Semen can be collected via electroejaculation or by use of
recovered; successful recovery is affected by factors such as age a teaser mount. Once semen is collected, it should be handled
of the donor, reproductive health, and experience of the surgeon carefully and kept warm to prevent sperm death, leading to im-
or technician. Furthermore, not all collected embryos are of proper conclusions about the male. Typically, the characteris-
transferable quality. Recipients are hormonally synchronized tics usually evaluated as a determinate of sperm quality are vol-
with the donor animals. On the day of embryo collection, trans- ume (normal between 0.7 and 2.0 ml); motility (% of sperm
ferable embryos are implanted into the uterus of the recipient; moving in a forward wave; high quality is associated with motil-
laparoscopy has been used in the past and is now being replaced ity of approximately 90%); concentration (sperm count per unit
by nonsurgical methods. Pregnancy rates average about 70%. If of volume as measured by a hemocytometer; high-quality se-
recipients are not available, embryos, like sperm, can be frozen men should contain 1.8 X 109 sperm per ml); morphology (live
and kept for later transfer. versus dead cells, as determined by special stains and the per-
Embryo transfer is commonly practiced in cattle as a herd im- centage of abnormal-appearing sperm; neither the abnormali-
provement technique and as a research technique for engineered ties nor the dead sperm should exceed 10% in high-quality
embyros. Disease screening programs for all animals involved semen).
are important because several pathogens can be transmitted di- The extensive use of artificial insemination in the dairy cattle
rectly or indirectly, such as bovine viral diarrhea virus, blue- industry has minimized the use of bulls on many farms, al-
tongue virus, infectious bovine rhinotracheitis virus, and my- though a farm may maintain a few bulls for heat detection and
coplasmal species. for "cleanup" breeding. Breeding bulls are maintained in beef
production establishments. Breeding bulls must be part of the
herd vaccination program, with special attention to appropriate
11. Miscellaneous Management Considerations timing of immunizations for the commonly transmitted vene-
real diseases campylobacteriosis and trichomoniasis.
a. Management of Male Animals
In sheep flocks and goat herds, as noted, male young are usu-
b. Cattle Tail Docking
ally castrated by 1 month of age. The elastrator method is the
more popular for animals less than 1 week of age. Other meth- Tail docking is a relatively recent development in dairy herd
ods include the emasculatome (crushing) and surgical removal management and is practiced in the belief that it will minimize
("knife method"). The distress associated with castration and bacterial contamination of the udder and therefore the milk.
tail docking in lambs is the subject of debate and has been re- Tails are typically docked to about 10 inches in length. The
searched recently (Kent et al., 1995). As noted, male calves are practice is more popular in certain regions in the United States.
usually castrated as early as possible and no later than 3 month To date, there is no published study indicating that this tech-
of age. In some production situations, however, where maxi- nique provides any distinctive advantage over keeping the tail
mum hormone responsive muscle development and grouping switch hair clipped short.
animals together for procedures dictate scheduling, the proce-
dure may be performed on older males. Open and closed tech-
niques are used, depending on the age of animals and on veteri- E. Behavior
nary or farm practice.
Breeding and vasectomized rams and bucks are usually main- Healthy ruminants have good appetites, chew cud, are alert
tained by medium to large production farms. Smaller farms and curious, have healthy intact coats, move without hindrance,
often borrow breeding males. Breeding males are typically se- and have clear, bright, clean eyes and cool dry noses. Even adult
lected by production record, pedigree, and/or breed. Vasec- animals, when provided sufficient space, will play. Sheep and
tomized males are often retired breeders and should be tattooed goats have tidy "pelleted" dark green feces. Cattle have pasty,
or identified clearly to avoid any wasted breeding time. The va- moist, dark green-brown feces. Ruminants normally vocalize,
sectomy technique for both species is comparable (Smith and and handlers will learn to recognize normal communication
Sherman, 1994). Rams may be housed together for most of the among the group or directed at caregivers in contrast to that
year, whereas bucks are penned separately. when animals are stressed. Excessive, strained vocalizations are
Because ewes will exhibit only a limited number of estrous often a sign of stress in cattle. "Bruxism," or grinding of the
cycles before becoming reproductively quiescent, it is critical teeth by a ruminant, is usually associated with discomfort or
that the male be capable of successfully breeding the female in pain. Other signs of discomfort, stress, or illness include de-
an expeditious manner. Any defects in the external genitalia, re- creased time spent eating and cud chewing, restlessness, pro-
productive diseases, or musculoskeletal abnormalities may pre- longed recumbency with outstretched neck and head, and
vent successful copulatory behaviors. Furthermore, it is impor- hunched back when standing. Unhealthy ruminants may be thin,
536 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

may arch their backs or favor a limb, or may have external and horns may also become entangled in fencing. Although less
lumps or swollen joints, an unusual abdominal profile, or rough strongly affected by flock behavior, goats are social animals.
or dull coats. Most goats raised in close human contact are personable and co-
All ruminants are herd animals to some extent and social in- operative and can easily be taught to stand for various proce-
dividuals; therefore, every effort should be made to allow con- dures, including blood collection.
tact among animals, in terms either of direct contact or of sound, An understanding of breed behaviors, sources of stress in cat-
smell, or sight. Human contact and handling should be initiated tle, play behaviors, calf behaviors, and dominance determinants
promptly and maintained regularly and consistently throughout will contribute to prevention of injuries to handlers and better
the animal's stay in the research facilities. Animals should be health and welfare of the animals. Ruminants of all ages, espe-
provided sufficient time to acclimate to handlers and research cially cattle of all ages, should be handled with an appreciation
staff. Cattle and sheep can hear at higher frequencies than hu- of the serious injury to human handlers that may result (Houpt,
mans can and may react to sounds not perceived by handlers. 1998). Cattle have a wide visual field, as sheep do, and a flight
Knowledge of the peculiarities of sheep behavior will in- zone that varies in size, according to previous handling experi-
crease the ease of handling and decrease stress-related effects in ences (gentle handling and animal tameness make the flight
research. Generally, fine-wooled breeds, such as Rambouillet, zone smaller) and the circumstances of the moment (Grandin,
are the most gregarious and are best handled in groups. The 1993). Groups of cattle are moved effectively around a facility
meat, or "downs," breeds tend to be less gregarious, and the by utilizing chute systems, with sequences of gates, that mini-
long-wooled breeds tend to be solitary (Ross, 1989; ASIA, mize chances of animals turning around.
1996). Nonetheless, movement of animals is simplified by Dairy cattle have been bred and selected over centuries for
proper facility design. Sheep have a wide-angle visual field and their docile, tractable characters and production characteristics.
are easily scared by activities that are taking place behind them. In contrast, beef breeds have not been selected for docility and
Sheep should be moved slowly and gently. To capture individu- are generally more difficult to handle and restrain. Beef breeds,
als within a flock, it is best to confine the flock to a smaller space such as Angus, are known for their independent natures and
and use a shepherd's crook or to gently catch the animal in front protective maternal instincts. All cattle respond well to feed as
of the neck/thorax. Grabbing the wool can injure the animals, a reward for desired behavior. Healthy cattle typically are very
as well as damage the wool and the underlying tissues. Sheep curious and watchful and are alert to sounds and smells. When
move best in chutes that have solid walls, and individual animals not grazing or eating, they hold their heads up. When sleeping,
will generally follow a lead animal. Any escape route will be the head and neck may be tucked back. Because of ruminant di-
challenged and, if successfully breached, will disrupt the entire gestive and metabolic needs, much of the day is spent eating or
flock movement. Sheep movement is also disrupted by contrasts cud chewing. Occasionally, adult cows sit upright like dogs.
such as light and shadows that impinge on a chute or corral. Fi- Cattle maintained inside tend to be more docile. In addition to
nally, like most animals, sheep have a flight zone (minimum forced isolation from other cattle, sources of stress include
zone of comfort), the penetration of which will result in sheep rough attitudes of handlers and unfamiliar visual patterns, rou-
scattering. This minimal flight distance can be modified by in- tines, or environments. These stressors may exacerbate signs of
creasing handling of the animals and working at the edge of the systemic illnesses.
zone, but it should always be considered when working with an- Calves are known for non-nutritive suckling, bar licking, and
imals in chutes, pens, or other confined areas. tongue rolling. Non-nutritive suckling behavior is greater in
Goats exhibit behavioral characteristics that make them quite hungry calves and also right after a milk meal. It is best to pro-
distinct from other ruminants. Their browsing activity makes vide nipples and other clean noninjurious materials for the ani-
them quite orally investigative. Goats will readily nibble or mals to suck. Non-nutritive suckling can be detrimental in
chew just about anything they come in contact with, so re- group-housed calves because it can result in disease transmis-
searchers should keep all paperwork and equipment out of sion and hair ball formation. Environmental enrichment devices
reach. A herd of goats will readily chew through wood gates and have been developed to cope with this behavior. The behavior
fencing, especially when confined in areas without alternatives diminishes as the animals are weaned onto solid food (Morrow-
for chewing behavior. Goats are also inquisitive, restless, agile Tesch, 1997).
jumpers and climbers, and quite mischievous. If maintained in Play activity and vocalizations of calves mimic adult domi-
paddocks, strong high fences are essential, as are adequate nance behaviors. Play activity by young adult cattle is more
spaces for exercise or boulders or rock piles for hoof mainte- common in males, can be quite rough, and is often triggered by
nance and recreational climbing. Goats are more tolerant of iso- a change in the environment. Dominance behaviors are depend-
lation and are more easily acclimated to human contact than ent on direct physical contact among the cattle, and dominance
sheep are, but goats will confront unfamiliar intruders and make hierarchies are established within a herd. Horns, age, and
sneezing noises. Goats with horns will use them to advantage, weight have been reported to be the most important determi-
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 537

nants. Aggressive behaviors in cattle may be triggered by newly food; may be anorexic, weak, unthrifty and depressed; and may
introduced animals or unfamiliar visual patterns and by feeding salivate excessively. Diagnosis is made based on clinical signs
when animals are very hungry. Aggression is more common and is confirmed by culture.
among intact adult males.
Epizootiology and transmission. The organism penetrates
wounds of the skin, mouth, nose, gastrointestinal tract, testicles,
and mammary gland. Rough feed material and foreign bodies
III. DISEASES may play a role in causing abrasions. Actino bacillus lignieresii
then enters into deeper tissues, where it causes chronic inflam-
mation and abscess formation. Lymphatic spread may occur,
This section focuses primarily on the more common diseases leading to abscessation of lymph nodes or infection of other
affecting sheep, goats, and cattle in the United States and else- organs.
where in North America and those that are reportable. For de-
tailed information not included in this limited overview and for Necropsy findings. Purulent discharges of white-green exu-
diseases of importance internationally, the authors recommend date drain from the tracts that often extend from the area of
several excellent comprehensive and focused veterinary clinical colonization to the skin surface. Exudates will also contain
texts and periodicals that address ruminant diseases, preventive characteristic small white-gray (sulfurlike) granules. The pus is
medicine, and individual and flock or herd management. These usually nonodorous.
are listed under "Major References" in the reference list at the
end of this chapter. Differential diagnosis. Contagious ecthyma and caseous lym-
Recommendations for current drug therapies, both approved phadenitis are the primary differentials. Diseases or injuries
and off-label use in ruminants, including withholding prior to causing oral pain and discomfort, such as dental infections, for-
slaughter, formularies, and related information can be found in eign bodies, and trauma, should be considered.
the references noted above and in formularies (Hawk and Leary,
1995; Plumb, 1999). In addition, the Food Animal Residue Treatment. Animals should be fed softer feeds. Antibiotics
Avoidance Databank (FARAD), accessible on the Internet such as sulfonamides, tetracyclines, and ampicillin are effec-
<http://www.farad.org>, should be used as a resource. FARAD tive, although high doses and long durations of therapy are
is a food safety project of the U.S. Department of Agriculture required. Penicillin is not effective. Weekly systemic adminis-
and is an information resource to prevent drug and pesticide tration of sodium iodide for several weeks is not as effective
residues in food animals and animal products. as antibiotic therapy. Surgical excision and drainage are not
recommended.

A. Infectious Diseases Prevention and control. Because the organism enters through
tissue wounds, especially those associated with oral trauma,
1. Bacterial, Mycoplasmal, and Rickettsial Diseases feedstuffs should be closely monitored for coarse material and
foreign bodies.
a. Actinobacillosis ("Wooden Tongue")
Etiology. Actinobacillus lignieresii is an aerobic, nonmotile,
b. Arcanobacterium Infection (Formerly actinomycosis,
non-spore-forming, gram-negative rod that is widespread in soil
or "Lumpy Jaw")
and manure and is found as normal flora of the respiratory, gas-
trointestinal, and reproductive tracts of ruminants. In sheep and Etiology. Arcanobacterium (formerly known as Actinomyces
cattle, A. lignieresii causes sporadic, noncontagious, and poten- or Corynebacterium) pyogenes and A. bovis are anaerobic, non-
tially chronic disease characterized by diffuse abscess and gran- motile, non-spore-forming, gram-positive, pleomorphic rods to
uloma formation in tissues of the head and occasionally other coccobacilli. Arcanobacterium bovis is a normal part of the ru-
body organs. This disease, called wooden tongue, has not been minant oral microflora and is the organism associated with
documented in goats. "lumpy jaw" in cattle; this syndrome is rarely seen in sheep and
goats. This organism has also been associated with pharyngitis
Clinical signs. Skin lesions are common. Tongue lesions are and mastitis in cattle.
more common in cattle than in sheep. Lip lesions are more com-
mon in sheep. Soft-tissue or lymph node swelling accompanied Clinical signs and diagnosis. Arcanobacterium bovis causes
by draining tracts is observed in the head and neck regions, as mandibular lesions primarily. The mass will be firm, non-
well as other areas. Animals may have difficulty prehending painful, and immovable. Draining tracts may develop over time.
538 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

If teeth roots become involved, painful eating and weight loss ious degrees of depression and anorexia, and purulent dis-
are evident. Radiographic studies are helpful for determining charges may be seen draining from the umbilicus. Involvement
fistulas. Diagnosis is based on clinical signs, and culture is re- of the urachus is usually followed by cystitis and associated
quired to confirm Arcanobacterium. The prognosis is poor for signs of dysuria, stranguria, hematuria, and so on. Severe se-
lumpy jaw. quelae may include septicemia, peritonitis, septic arthritis (joint
ill), meningitis, osteomyelitis, and endocarditis.
Epizootiology and transmission. These organisms are normal
flora of the gastrointestinal tracts of ruminants and gain entrance Research complications. Young stock affected by omphalo-
into the tissues through abrasions and penetrating wounds. phlebitis may be inappropriate subjects because of growth set-
backs and physiologic stresses from the infection. Affected
Necropsy. Draining lesions with sulfurlike granules (as with adult animals will not thrive and, even with therapy, may not be
actinobacillosis) are frequently observed. appropriate research subjects.

Pathogenesis. Arcanobacterium pyogenes is known to pro- d. Anthrax

duce an exotoxin, which may be involved in the pathogenesis.
Etiology. Bacillus anthracis is a nonmotile, capsulated, spore-
forming, aerobic, gram-positive bacillus that is found in alka-
Differential diagnosis. Actinobacillus lignieresii and caseous
line soil, contaminated feeds (such as bonemeal), and water.
lymphadenitis are important differentials for draining tracts. A
Common names for the disease anthrax include woolsorters'
major differential for omphalophlebitis is an umbilical hernia,
disease, splenic fever, charbon, and milzbrand.
which will typically not be painful or infected. There are many
differentials for septic joints and polyarthritis: Chlamydia spp., Clinical signs and diagnosis. Anthrax is a sporadic but very
Mycoplasma spp., streptococci, coliforms, Erysipelothrix rhu- serious infectious disease of cattle, sheep, and goats character-
siopathiae, Fusobacterium necrophorum, and Salmonella spp. ized by septicemia, hyperthermia, anorexia, depression, list-
Tumors, trauma to the affected area, such as the mandible, and lessness, depression, and tremors. Subacute and chronic cases
dental disease or oral foreign body should also be considered. may occur also and are characterized by swelling around the
shoulders, ventral neck, and thorax. The incubation period is
Prevention and control. Arcanobacterium bovis lesions can 1 day to 2 weeks. Bloody secretions such as hematuria and
be prevented or minimized by feeds without coarse or sharp bloody diarrhea often occur. Abortion and blood-tinged milk
materials. may also be noted. The disease is usually fatal, especially in
sheep and goats, after 1-3 days. Death is the result of shock, re-
Treatment. Penicillin or derivatives such as ampicillin or nal failure, and anoxia.
amoxicillin are treatments of choice. Sodium iodides (intra- Diagnosis is based on the clinical signs of peracute deaths and
venous) and potassium iodides (orally) have been utilized also. hemorrhage. Stained blood smears may show short, single to
Extended antibiotic therapy may be necessary. Surgical exci- chained bacilli. Blood may be collected from a superficial vein
sion is an option. In addition to medications noted above, isoni- and submitted for culture.
azid is somewhat effective for A. bovis infections in nonpreg-
nant cattle. Epizootiology and transmission. Cattle and sheep tend to be
affected more commonly than goats, because of grazing habits.
Research complications. The possibility of long-term infec- Older animals are more vulnerable than younger, and bulls are
tion and long therapy are factors that will diminish the value of more vulnerable than cows. Although the disease occurs world-
affected research animals. wide, and even in cold climates, most cases in the United States
occur in the central and western states, and outbreaks usually
c. Actinomycosis occur as the result of spore release after abrupt climatic changes
such as heavy rainfall after droughts or during warmer, dryer
Omphalophlebitis, omphaloarteritis, omphalitis, and navel months. Spores survive very well in the environment. The
ill are terms referring to infection of the umbilicus in young anthrax organisms (primarily spores) are generally ingested,
animals. sporulate, and replicate in the local tissues. Abrasive forages
Arcanobacterium pyogenes is the most common organism may play a role in infection. Transmission via insect bites or
causing omphalophlebitis, an acute localized inflammation and through skin abrasions rarely occurs.
infection of the external umbilicus. Most cases occur within
the first 3 months of age, and animals are presented with a Necropsy. Necropsies should not be done around animal pens
painful enlargement of the umbilicus. Animals may exhibit var- or pastures, and definitive diagnoses may be made without
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 539

opening the animals. Incomplete rigor mortis, rapid putrefac- commonly associated with ovine epididymitis or orchitis than
tion, and dark, uncoagulated blood exuding from all body abortion. In the United States, clusters of brucellosis are still
orifices are common findings. Blood collected carefully and found in western areas contiguous to Yellowstone National
promptly from peripheral veins of freshly dead animals can be Park. Bang's disease is the common name given to the disease
used diagnostically. Splenomegaly, cyanosis, epicardial and in ruminants.
subcutaneous hemorrhages, and lymphadenopathy are charac-
terisitic of the disease. Clinical signs and diagnosis. Brucella melitensis in the adult
ewe is generally asymptomatic and self-limiting within about
Pathogenesis. The rapidly multiplying organisms enter the 3 months. However, because the organism may enter and cause
lymphatics and bloodstream and result in a severe septicemia necrosis of the chorionic villi and fetal organs, abortion or still-
and neurotoxicosis. Encapsulation protects the organisms from births may occur. Abortion usually occurs in the third trimester,
phagocytosis. Liberated toxins cause local edema. after which the ewe will appear to recover. It has been reported
that up to 20% of infected ewes may abort more than once.
Differential diagnosis. Although anthrax Should always be Rams will also be infected and may develop orchitis or pneu-
considered when an animal healthy the previous day dies monia. The disease caused by B. ovis is manifested by clinical
acutely, other causes of acute death in ruminants should be or subclinical infection of the epididymis, leading to epididy-
considered, e.g., bloat, poisoning, enterotoxemia, malignant mal enlargement and testicular atrophy. Brucella ovis causes
edema, blackleg, and black disease. decreased fertility. Brucella melitensis is the more common
cause of brucellosis in goats. Brucella abortus has been shown
Prevention and control. Outbreaks must bereported to state to infect goats in natural and experimental infections, and B.
officials. Anthrax is of particular concern as a bioterrorism ovis has also been shown to infect goats experimentally. Does
agent. Any vaccination programs should also be reviewed with infected with B. melitensis will also abort during the third
regulatory personnel. Herds in endemic areas and along water- trimester. Infections with B. abortus in cattle produce few
ways are usually vaccinated routinely with the Sterne-strain clinical signs. There may be a brief septicemia during which
spore vaccine (virulent, nonencapsulated, live). Careful hygiene organisms are phagocytosed by neutrophils and fixed macro-
and quarantine practices are crucial during outbreaks. Dead an- phages in lymph nodes. In cows, the organism localizes in
imals and contaminated materials should be incinerated or supramammary lymph nodes and udders and in the endo-
buried deeply. Biting insects should be controlled. The disease metrium and placenta of pregnant cows. Infection may cause
is zoonotic and a serious public health risk. abortions after the fifth month, with resulting retained placen-
tas. Permanent infection of the udder is common and results in
Treatment. Treatment of animals in early stages with peni- shedding of organisms in milk. In bulls, the organism may cause
cillin and anthrax antitoxin (hyperimmune serum, if available) unilateral orchitis and epidydimitis and involvement of the sec-
may be helpful. Amoxicillin, erythromycin, oxytetracycline, ondary sex organs. Organisms may be in the semen. In infected
gentamicin, and fluoroquinolones are also good therapeutic herds, lameness may also be a clinical sign.
agents. During epidemics, animals should be vaccinated with Diagnosis of brucellosis can be made by bacterial isolation of
the Sterne vaccine. the Brucella organism from necropsy samples (especially the
fetal stomach contents), as well as by supportive serological ev-
Research complications. Natural and experimental anthrax idence. Many serological tests are available, such as the tube
infections are a risk to research personnel; the pathogen may be and plate agglutination tests, the card or rose bengal test, the ri-
present in many body fluids and can penetrate intact skin. The vanol precipitation test, complement fixation, enzyme-linked
organism sporulates when exposed to air, and spores may be in- immunosorbent assay (ELISA), polymerase chain reaction
haled during postmortem examinations. (PCR), and others. Test selection is often dependent on state re-
quirements in the United States.
e. Brucellosis
Epizootiology and transmission. The primary route of trans-
Etiology. Brucella is a nonmotile, non-spore-forming, nonen- mission of B. abortus is ingestion of the organism from infected
capsulated, gram-negative coccobacillus. Brucella abortus is tissues and fluids (milk, vaginal and uterine discharges) dur-
one of several Brucella species that infects domestic animals ing and for a few weeks after abortion or parturition; contami-
but cross-species infections occur rarely. Brucella abortus or B. nated semen is considered to be a minor source of infection.
melitensis may cause brucellosis in sheep, cattle, and goats. Exposure to the organism may occur via the gastrointestinal
Brucella melitensis (biovar 1, 2, or 3) is the primary cause of tract (contaminated feed or water), the respiratory tract (droplet
sheep disease (Garin-Bastuji et al., 1998). Brucella ovis is more infection), or the reproductive tract (contaminated semen) and
540 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

through other mucous membranes such as the conjunctiva. Bru- very successful when conducted on a herd basis to reduce like-
cella ovis is transmitted in the semen, as well as orally or nasally lihood of exposure. Strain 19 and the recently validated attentu-
through contaminated feed and bedding. ated strain RB51 are live vaccines and can be used in healthy
heifer calves 4 - 1 2 months old. Vaccination for older animals
Necropsy findings. A sheep fetus aborted due to Brucella will may be done under certain circumstances. Vaccination of bull
exhibit generalized edema. The liver and spleen will be swollen, calves is not recommended, because of low likelihood of spread
and serosal surfaces will be covered with petecchial hemor- through semen and possibility of vaccination-induced orchitis.
rhages. Peritoneal and pleural cavities often contain sero- The strain 19 vaccine induces long-term cell-mediated immu-
fibrinous exudates. The placenta will be leathery. nity, protects a herd from abortions, and protects the majority of
a herd from reactors during a screening and culling program.
Pathogenesis. Ruminants are considered especially suscepti- The vaccine will not, however, protect the animals from be-
ble to Brucella infection, because of higher levels of erythritol coming infected with B. abortus.
(a sugar alcohol), which is a growth stimulant for the organism. Strain 19 vaccine induces an antibody response in cattle. The
Brucella utilizes erythritol preferentially over glucose as an RB51 vaccine does not result in antibody titers and therefore is
energy source. Placentas and male genitalia also contain high advantageous because infection with Brucella can be deter-
levels of erythritol. Brucella organisms also evade lysis when mined serologically. The RB51 vaccine has been designated as
phagocytosed by macrophages and neutrophils and survive in- the official calfhood bovine brucellosis vaccine in the United
tracellularly in phagosomes. Abortion is the result of placenti- States by the U.S. Department of Agriculture's Animal and
tis, typically during the third trimester of gestation. Brucella Plant Health Inspection Service (APHIS) (Stevens et al., 1997).
ovis enters the host through the mucous membranes, then passes Brucella vaccine should be administered to unstressed,
into the lymphatics, causes hyperplasia of reticuloendothelial healthy cattle, with attention to particular side effects of the vac-
cells, and is spread to various organs via the blood. The organ- cination material and to prevention of compounding stresses as-
ism localizes in the epididymides, the seminal vesicles, the bul- sociated with weaning, regrouping, other management changes,
bourethral glands, and the ampullae. Orchitis may be a sequelae and shipping. The RB51 is regarded as less pathogenic and
of the disease. Epididymitis can be diagnosed by identifying abortigenic in cattle.
gross lesions by palpation of the epididymides, by serological
evidence of antibodies to B. ovis, and by semen cultures. Treatment. Definite confirmation of Brucella infection is
important from the standpoint of public and herd health.
Differential diagnosis. Differential diagnoses include all other Culling is considered the treatment of choice in cattle herds.
abortion-causing diseases. Many other agents, such as Acti- Rams infected with B. ovis should be isolated and treated with
nobacillus spp., Arcanobacterium (Actinomyces) pyogenes, Es- tetracyclines.
chericia coli, Pseudomonas spp., Proteus mirabilis, Chlamy-
dia, Mycoplasma, and others may be associated with ovine Research complications. Brucellosis represents a research
epididymitis and orchitis. A clinically and pathologically simi- complication as a cause of abortions and of infections in male
lar agent, Actinobacillus seminis, has been isolated from virgin ruminants. Impairment of the infected host's immune system,
rams. This organism has morphological and staining character- especially alteration of phagocytic cells where the bacteria stay
istics similar to those of B. ovis and complicates the diagnosis in membrane-bound vesicles, should be considered. The po-
(Genetzky, 1995). tential complications of needle sticks by large-animal veteri-
narians with the strain 19 vaccine and the public health risks
Prevention and control. The Rev 1 vaccine has been recom- (undulant fever) are well known. Less is known presently re-
mended for vaccination of ewe lambs in endemic areas, but this garding the RB51 vaccine effects in humans. Epidemiologic
vaccine is not used in the United States. Separating young rams and diagnostic methodologies are being developed to track and
from potentially infected older males, sanitizing facilities, and monitor these cases. There is also a risk of human infection
vaccinating them with B. ovis bacterin can prevent the disease. from handling infected materials during a dystocia or post-
Over the past 20 years, aggressive federal and state regulatory mortem. Worldwide, B. melitensis is the leading cause of hu-
and cattle herd health programs in the United States have pro- man brucellosis.
vided control and prevention mechanisms for this pathogen
through a combination of serological monitoring of herds,
f. Campylobacteriosis (Vibriosis)
slaughter of diseased animals, herd management, vaccination
programs, and monitoring of transported animals. Most states i. Campylobacter fetus subsp, intestinalis; C. jejuni infection
are considered brucellosis-free in the cattle populations; thus, (ovine vibriosis)
procurement of ruminants that have been exposed to this infec- Etiology. Campylobacter (Vibrio) fetus subsp, intestinalis, a
tious agent will be unlikely. Cattle vaccination programs can be pleomorphic curved to coccoid, motile, non-spore-forming,
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 541

gram-negative bacterium, causes campylobacteriosis, the most cycline. Aborting ewes should be isolated immediately from the
important cause of ovine abortion in the United States. There rest of the flock. After an outbreak, ewes will develop immunity
are few reports of campylobacteriosis in goats in the United lasting 2 - 3 years.
States. Vibriosis is derived from the name formerly given to the
genus; the term is still frequently used. Treatment. Infected animals should be isolated and pro-
vided with supportive therapy. Prompt decontamination of the
Clinical signs and diagnosis. Ovine vibriosis is a contagious area and disposal of the aborted tissues and discharges are
disease that causes abortion, stillbirths, and weak lambs. The important.
organism inhabits the intestines and gallbladder in subclinical
carriers. Abortion generally occurs in the last trimester, and Research complications. Losses from abortion may be con-
abortion storms may occur as more susceptible animals, such as siderable. Campylobacter ssp. are zoonotic agents, and C. fetus
maiden ewes, become exposed to the infectious tissues. It is re- subsp, intestinalis may be the cause of "shepherd's scours."
ported that 20-25% of the flock may become infected and up to
5% of the ewes will die (Jensen and Swift, 1982). Some lambs ii. Campylobacter fetus subsp, venerealis infection
may be born alive but will be weak, and dams will not be able (bovine vibriosis)
to produce milk. Etiology. Campylobacter fetus subsp, venerealis is the main
Diagnosis is achieved by microscopic identification or isola- cause of bovine campylobacteriosis abortions. It does not cause
tion of the organism from placenta, fetal abomasal contents, and disease in other ruminant species.
maternal vaginal discharges. Tentative identification of the or-
ganism can be made by observing curved ("gull-wing") rods in Clinical signs and diagnosis. Preliminary signs of a problem
Giemsa-stained or Ziehl-Neelsen-stained smears from fetal in the herd will be a high percentage of cows returning to estrus
stomach contents, placentomes, or maternal uterine fluids. after breeding and temporary infertility. This will be particu-
larly apparent in virgin heifers that may return to estrus by
Epizootiology and transmission. Campylobacteriosis occurs 40 days after breeding. Long interestrous intervals also serve an
worldwide. Campylobacter spp., such as C. jejuni, normally in- indication of a problem. Spontaneous abortions will occur in
habit ovine gastrointestinal tracts. Transmission of the disease some cases, typically during the fourth to eighth months of ges-
occurs through the gastrointestinal tract, followed by shedding, tation. Severe endometritis may lead to salpingitis and perma-
especially associated with aborted tissues and fluids. In abor- nent infertility.
tion storms, considerable contamination of the environment Demonstration or isolation of the organism, a curved rod with
will occur due to placenta, fetuses, and uterine fluids. Ewes may corkscrew motility, is the basis for diagnosis. The vaginal mu-
have active Campylobacter organisms in uterine discharges for cous agglutination test is used to survey herds for campylobac-
several months after abortion. The bacteria will also be shed teriosis. Serology will not be worthwhile, because the infection
in feces, and feed and water contamination serve as another does not trigger a sufficient antibody response. Culture from
source. There is no venereal transmission in the ovine. breeding animals may be difficult because Campylobacter will
be overgrown by faster-growing species also present in the
Necropsy. Aborted fetuses will be edematous, with accumula- specimens.
tion of serosanguinous fluids within the subcutis and muscle tis-
sue fascia. The liver may contain 2 - 3 cm pale foci. Placental Epizootiology and transmission. The bacteria is an obli-
tissues will be thickened and edematous and will contain serous gate, ubiquitous organism of the genital tract. Transmission
fluids similar to those of the fetus. The placental cotyledons is from infected bulls to heifers. Older cows develop effective
may appear gray. immunity.

Pathogenesis. The organism enters the bloodstream and Necropsy findings. Necrotizing placentitis, dehydration, and
causes a short-term bacteremia (1-2 weeks) prior to the local- fibrinous serositis will be found grossly. In addition, broncho-
izing of the bacteria in the chorionic epithelial cells and finally pneumonia and hepatitis will be seen histologically.
passing into the fetus.
Pathogenesis. Campylobacter organisms grow readily in the
Differential diagnosis. Toxoplasma, Chlamydia, and Listeria genital tract, and infection is established within days of expo-
should be considered in late gestation ovine abortions. sure. The resulting endometritis prevents conception or causes
embyronic death.
Prevention and control. A bacterin is available to prevent the
disease. Carrier states have been cleared by treating with a com- Differential diagnosis. The primary differential diagnosis for
bination of antibiotics, including penicillin and oral chlortetra- campylobacteriosis is trichomoniasis. Other venereal diseases
542 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

should be considered when infertility problems are noted in a Treatment. Severe infections should be treated with antibi-
herd. These include brucellosis, mycoplasmosis, ureaplasmo- otics based on culture and sensitivity. Severe lesions and lesions
sis, infectious bovine rhinotracheitis-infectious pustular vulvo- localized to the underbelly, thighs, and udder benefit by periodic
vaginitis (IBR-IPV), and bovine virus diarrhea (BVD). Lep- cleaning with an iodophor shampoo and spraying with an an-
tospirosis should also be considered. In addition, management tibiotic and an astringent (Smith and Sherman, 1994).
factors such as nutrition and age of heifers at introduction to the
herd should be considered.
h. Clostridial Diseases
Prevention and control. Killed bacterin vaccines are avail- i. Clostridium perfringens type C infection (enterotoxemia
able, either as oil adjuvant or as aluminum hydroxide adsorbed. and struck)
The former is preferred because of duration of immunity but Etiology. Clostridium perfringens is an anaerobic, gram-
causes granulomas. That vaccine also has specific recommen- positive, nonmotile, spore-forming bacterium that lives in the
dations regarding administration several months before the soil, in contaminated feed, and in gastrointestinal tracts of ru-
breeding season. The latter product is administered closer to the minants. The bacteria is categorized by toxin production. Tox-
breeding season, and the duration of immunity is not as pro- ins include alpha (hemolytic), beta (necrotizing), delta (cyto-
longed. In both cases, boosters should be given after the initial toxic and hemoltyic), epsilon, and iota. Types of C. perfingens
immunization and as part of the regular prebreeding regimen. are A, B, C, D, and E. This is a common and economically
Only one bacterin product is approved for use in bulls. Many significant disease of sheep, goats, and cattle.
combination vaccine products contain only the aluminum hy-
droxide adsorbed product. Artificial insemination (AI) is par- Clinical signs and diagnosis. The beta toxin associated with
ticularly useful at controlling the disease, but bulls used for AI overgrowth of this bacterium results in a fatal hemorrhagic en-
must be part of a screening program for this and other venereal terocolitis within the first 72 hr of a young ruminant's life. Many
diseases such as trichomoniasis. animals may be found dead, with no clinical presentation. Af-
fected animals are acutely anemic, dehydrated, anorexic, rest-
Treatment. Cows will usually recover from the infection, and less, and depressed and may display tremors or convulsions as
treatment with antibiotics such as penicillin, administered as well as abdominal pain. Feces may range from loose gray-brown
an intrauterine infusion, improve the chances of returning to to dark red and malodorous. Morbidity and mortality may be
breeding condition. nearly 100%.
A similar noncontagious but acutely fatal form of enterotox-
emia in adult sheep, called struck, occurs in yearlings and
g. Caprine Staphylococcal Dermatitis
adults. Struck is rare in the United States. The disease is also
Etiology. The most common caprine bacterial skin infection caused by the beta toxin of C. perfringens type C and is often
is caused by Staphylococcus intermedius or S. aureus and is associated with rapid dietary changes or shearing stresses in
known as staphylococcal dermatitis (Smith and Sherman, sheep. Although affected animals are usually found dead, clini-
1994). The Staphylococcus organisms are cocci and are catego- cal signs include uneasiness, depression, and convulsions. Mor-
rized as primary pathogens or ubiquitous skin commensals of tality is usually less than 15%.
humans and animals. Staphylococcus aureus and S. intermedius Diagnosis is usually based on necropsy findings, although
are classified as primary pathogens and produce coagulase, a confirmation can be made by culture of the organism. Identi-
virulence factor. fication of the beta toxin in intestinal contents may be difficult
because of instability of the toxin.
Clinical signs and diagnosis. Small pustular lesions, caused
by bacterial infection and inflammation of the hair follicle, oc- Epizootiology and transmission. Clostridial organisms are
cur around the teats and perineum. Occasionally, the infection ubiquitous in the environment as well as in the gastrointestinal
may involve the flanks, underbelly, axilla, inner thigh, and neck. tract and contaminated feeds. Confinement and poor sanitation
Staphylococcal dermatitis may occur secondary to other skin predisposes to infection with C. perfringens. Transmission is by
lesions. Diagnosis is based on lesions. Culture will distinguish ingestion of contaminated material.
S. aureus.
Necropsy findings. Necropsy findings include a milk-filled
Pathogenesis. Simple boredom may cause rubbing, followed abomasum, and hemorrhage in the distal small intestine and
by staphylococcal infection of damaged epidermis. throughout the large intestine. Petechial hemorrhages of the
serosal surfaces of many organs, especially the thymus, heart,
Differential diagnosis. The presence of scabs makes conta- and gastrointestinal tract, will be visible. Hydropericardium,
gious ecthyma a differential diagnosis, along with fungal skin hydroperitoneum, and hemorrhagic mesenteric lymph nodes
infections and nutritional causes of skin disease. will also be present. Pulmonary and brain edema may also be
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 543

seen. Histologically, the gram-positive C. perfringens organ- Clinical signs in chronic cases in older animals, such as adult
isms may be visible in excess numbers along the mucosal sur- goats, include soft stools, weight loss, anorexia, depression, and
face of the swollen, congested, necrotic intestines. severe diarrhea, sometimes with mucus and blood. Mature af-
In cases of struck, necropsy findings include congestion and fected sheep may be blind and anorectic and may head-press.
erosions of the mucosa of the gastrointestinal tract, serosal
hemorrhages, and serous peritoneal and pericardial fluids. In Necropsyfindings. Necropsy findings are similar to those seen
late stages of the disease and especially if prompt necropsy is with C. perfringens type C. Additionally, extremely necrotic,
not performed, the organism will infiltrate the muscle fascial soft kidneys ("pulpy kidneys") are usually observed immedi-
layers and produce serohemorrhagic and gaseous infiltration of ately following death. (This phenomenon is in contrast to what
perimysial and epimysial spaces. is normally associated with later stages of postmortem autoly-
sis.) Focal encephalomalacia, and petechial hemorrhages on
Pathogenesis. Hemorrhagic enterotoxemia is an acute, spo- serosal surfaces of the brain, diaphragm, gastrointestinal tract,
radic disease caused by the beta toxin of Clostridium perfrin- and heart are common findings. Diagnosis can be made from the
gens type C. Neonates ingest the organism, which then pro- typical clinical signs and necropsy findings as well as the ob-
liferates and attaches to the gastrointestinal microvilli and servation of glucose in the urine at necropsy.
elaborates primarily the beta toxins. The trypsin inhibitors pres-
ent in colostrum prevent inactivation of the beta toxin. The tox- Pathogenesis. The epsilon toxin causes neuronal death and
ins injure intestinal epithelial cells and then enter the blood, shock, probably through vascular damage. The noncontagious,
leading to acute toxemia. The intestinal injury may result in di- peracute form of enterotoxemia occurs in suckling, fast-grow-
arrhea, with small amounts of hemorrhage. Associated elec- ing animals, either nursing from their dams or on high-protein,
trolyte and water loss result in dehydration, acidosis, and shock. high-energy concentrates. The largest, fastest-growing animals
generally are predisposed to this condition; for example, lambs,
Differential diagnosis. Differential diagnoses include other fat ewe lambs, and usually singleton lambs tend to be most sus-
clostridial diseases such as blackleg and black disease, as well ceptible. The hyperglycemia and glucosuria seen in acute cases
as coccidiosis, salmonellosis, anthrax, and acute poisoning. are due to epsilon toxin effects on liver glycogen metabolism.

Prevention and control. A commercial toxoid is available and Differential diagnosis. Tetanus, enterotoxigenic E. coli, botu-
should be administered to the pregnant animals prior to parturi- lism, polioencephalomalacia, grain overload, and listeriosis are
tion. An alternative includes administration of an antitoxin to differentials.
the newborn lambs. The disease may become endemic once it is
on the premises. Prevention and control. Vaccination prevents the disease.
Maternal antibodies last approximately 5 weeks postpartum;
Treatment. Treatment is difficult and usually unsuccessful. thus young animals should be vaccinated at about this time.
Antitoxin may be useful in milder cases, and the antitoxin and Feeding regimens to young, fast-growing animals and feeding
toxoid can also be administered during an outbreak. of concentrates to adults should be evaluated carefully.

Research complications. This disease can be costly in losses Treatment. Treatment consists of support (fluids, warmth),
of neonates and younger animals. antitoxin administration, oral antibiotics, and diet adjustment.

ii. Clostridium perfringens type D infection (pulpy kidney iii. Clostridium tetani infection (tetanus, lockjaw)
disease) Etiology. Clostridium tetani is a strictly anaerobic, motile,
Etiology. Clostridium perfringens type D releases epsilon spore-forming, gram-positive rod that persists in soils and ma-
toxin that is proteolytically activated by trypsin. This disease nure and within the gastrointestinal tract. At least 10 serotypes
caused by C. perfringens tends to be associated with sheep and of C. tetani exist.
is of less importance in goats and cattle.
Clinical signs. Infection by C. tetani is characterized by a
Clinical signs. The peracute condition in younger animals sporadic, acute, and fatal neuropathy. After an incubation pe-
is characterized by sudden deaths, which are occasionally pre- riod of 4 days to 3 weeks, the animal exhibits bloat; muscular
ceded by neurological signs such as incoordination, opistho- spasticity; prolapse of the third eyelid; rigidity and extension
tonus, and convulsions. Because the disease progresses so rap- of the limbs, leading to a stiff gate; an inability to chew; and
idly to death (within 1-2 hr), clinical signs are rarely observed. hyperthermia. Erect or drooped ears, retracted lips, drooling,
Hypersalivation, rapid respirations, hyperthermia, convulsions, hypersensitivity to external stimuli, and a "sawhorse" stance
and opisthotonus have been noted. In acute cases, hypergly- are frequent signs. The animal may convulse. Death occurs
cemia and glucosuria are considered almost pathognomonic. within 3-10 days, and mortality is nearly 100%, primarily from
544 SCOTT A. MISCHLER, WENDY J. UNDERWOOD,AND MARGARET L. DELANO

respiratory failure. Diagnosis is based on clinical signs. Muscle- Prevention and control Like other ubiquitous clostridial dis-
related serum enzymes such as aspartate aminotransferase eases, tetanus is impossible to eradicate. The disease can be
(AST), creatinine kinase (CK), and lactate dehydrogenase controlled and prevented by following good sanitation mea-
(LDH) might be elevated. (Jensen and Swift, 1982). Serum cor- sures, aseptic surgical procedures, and vaccination programs.
tisol may also be elevated, and stress hyperglycemia may be ev- Tetanus toxoid vaccine is available and very effective for stim-
ident. Permanent lameness may result in survivors. ulating long-term immunity. Tetanus antitoxin can be adminis-
tered (200 IU in lambs) as a preventive or in the face of disease
Epizootiology and transmission. Clostridium tetani is a soil as an adjunct to therapy. Both the toxoid and the antitoxin can
contaminant and is often found as part of the gut microflora of be administered to an animal at the same time, but they should
herbivores. The organisms sporulate and persist in the environ- not be mixed in the syringe, and each should be administered at
ment. All species of livestock are susceptible, but sheep and different sites, with a second toxoid dose administered 4 weeks
goats are more susceptible than cattle. Individual cases may oc- later. Animals should be vaccinated 2 or 3 times during the first
cur, or herd outbreaks may follow castration, tail docking, ear year of life. Does and ewes should receive booster vaccinations
tagging, or dehorning. Mouth wounds may also be sites of within 2 months of parturition to ensure colostral antibodies.
entry.
Research complications. Unprotected, younger ruminants
Pathogenesis. Tetanus, or lockjaw, is caused by the toxins of may be affected following routine flock or herd management pro-
C. tetani. All serovars produce the same exotoxin, which is a cedures. Contaminated or inadequately managed open wounds
multiunit protein composed of tetanospasmin, which is neuro- or lesions in older animals may provide anaerobic incubation
toxic, and tetanolysin, which is hemolytic. A nonspasmogenic sites.
toxin is also produced. Contamination of wounds results in
anaerobic proliferation of the bacterium and liberation of the iv. Clostridium novyi infection (bighead; black disease;
tetanospasmin, which diffuses through motor neurons in a retro- bacillary hemoglobinuria, or red water) and C. chauvoei infec-
grade direction to the spinal cord. The toxin inhibits the release tion (blackleg)
of glycine and y-aminobutyric acid from Renshaw cells; this re-
suits in hypertonia and muscular spasms. Proliferation of C. Etiology. Clostridium novyi, an anaerobic, motile, spore-
tetani in the gut of affected animals may also serve as a source forming, gram-positive bacteria, is the agent of bighead and
and may produce clinical signs. The uterus is the most common black disease. Clostridium novyi type D (C. hemolyticum) is the
site of infection in postparturient dairy cattle with retained cause of bacillary hemoglobinuria, or "red water." Clostridium
placentas. chauvoei is the causative agent of blackleg.

Differential diagnoses. Early in the course of the infection, Clinical signs. Bighead is a disease of rams characterized by
differential diagnoses include bloat, rabies, hypomagnesemic edema of the head and neck. The edema may migrate to ventral
tetany, polioencephalomalacia, white muscle disease, entero- regions such as the throat. Additional clinical signs include
toxemia in lambs, and lead poisoning. Polyarthritis of cattle is a swelling of the eyelids and nostrils. Most animals will die
differential for the gait changes in that species. within 48-72 hours. Black disease, or infectious necrotic hep-
atitis, is a peracute, fatal disease associated with C. novyi. It is
Necropsy findings. Findings are nonspecific except for the more common in cattle and sheep but may be seen in goats. The
inflammatory reaction associated with the wound. Because of clinical course is 1-2 days in cattle and slightly shorter in sheep.
the low number of organisms necessary to cause neurotoxicosis, Otherwise healthy-appearing adult animals are often affected.
isolation of C. tetani from the wound may be difficult. Clinical signs are rarely seen, because of the peracute nature of
the disease. Occasionally, hyperthermia, tachypnea, inability to
Treatment. Treatment consists of cleaning the infected wound; keep up with other animals, and recumbency are observed prior
administering tetanus antitoxin (e.g., at least 500 IU in an adult to death. Bacillary hemoglobinuria is an acute disease seen pri-
sheep or goat); vaccinating with tetanus toxoid; administering marily in cattle and characterized by fever and anorexia, in ad-
of antibiotics (penicillin, both parenterally [potassium peni- dition to the hemoglobinemia and hemoglobinuria indicated by
cillin intravenously and procaine penicillin intramuscularly] the name. Animals that survive a few days will develop icterus.
and flushed into the cleaned wound), a sedative or tranquilizer Mortality may be high.
(e.g., acepromazine or chlorpromazine) and a muscle relaxant; Blackleg, a disease similar to bighead, causes necrosis and
and keeping the animal in a dark, quiet environment. Support- emphysema of muscle masses, serohemorrhagic fluid accumu-
ive fluids and glucose must be administered until the animal is lation around the infected area, and edema (Jackson et al.,
capable of feeding. If the animal survives, revaccination should 1995). Blackleg is more common in cattle than in sheep. The in-
be done 14 days after the previous dose. cubation period is 2 - 5 days and is followed by hyperthermia,
14. BIOLOGYAND DISEASESOF RUMINANTS: SHEEP, GOATS,AND CATTLE 545

muscular stiffness and pain, anorexia, and gangrenous myositis. diseases such as babesiosis, leptospirosis, and hemobartonel-
The clinical course is short, 2 4 - 4 8 hr, and untreated animals in- losis should be included as differentials.
variably die. Blackleg in cattle can be associated with subcuta-
neous edema or crepitation; these do not usually occur in sheep. Treatment. For C. chauvoei infection (blackleg), early treat-
Most lesions are associated with muscles of the face, neck, per- ment with penicillin or tetracycline may be helpful. Treatment
ineum, thigh, and back. for black disease is not rewarding even if the animal is found be-
fore death. Carcasses from bacillary hemoglobinuria losses
Epizootiology and transmission. Bighead is caused by the should be burned, buried deeply, or removed from the premises.
toxins of C. novyi, which enters through wounds often associ-
ated with horn injuries during fighting. The C. novyi type B or- Prevention and control. Vaccinating animals with multivalent
ganisms produce alpha and beta toxins, and the alpha toxins are clostridial vaccines can prevent these diseases. Subcutaneous
mostly responsible for toxemia, tissue necrosis, and subsequent administration of vaccine material is recommended over intra-
death. Clostridium novyi type D is endemic in the western muscular. Vaccinations may be useful in an outbreak. Careful
United States. It is hypothesized that the C. chauvoei organisms handling of ruminants during shipping and transfers will con-
enter through the gastrointestinal tract. Black disease and bacil- tribute to fewer muscular injuries. For bighead, mature rams
lary hemoglobinuria are associated with concurrent liver dis- penned together should be monitored for lesions, especially
ease, often associated with Fasciola infections (liver flukes); it during breeding season. Control of fascioliasis is very impor-
is sometimes seen as a sequela to liver biopsies. The diseases are tant in prevention and control of black disease and in the opti-
more common in summer months, and fecal contamination of mal timing of vaccinations.
pastures, flooding, and infected carcasses are sources of the or-
ganism. Birds and wild animals may be vectors of the pathogen. v. Clostridium septicum infection (malignant edema)
Ingested spores are believed to develop in hepatic tissue dam- Etiology. Clostridium septicum is the species usually associ-
aged and anoxic from the fluke migrations. ated with malignant edema, but mixed infections involving
other clostridial species such as C. chauvoei, C. novyi, C. sor-
Necropsy. Diagnosis of black disease is usually based on dellii, and C. perfringens may occur. Clostridium spp. are
postmortem lesions. Subcutaneous vessels will be engorged motile (C. chauvoei, C. septicum) or nonmotile, anaerobic,
with blood, resulting in dried skin with a dark appearance. Car- spore-forming, gram-positive rods.
casses putrefy quickly. In addition, hepatomegaly and endocar-
dial hemorrhages are common, and hepatic damage from flukes Clinicial signs. Malignant edema, or gas gangrene, is an acute
may be so severe that diagnosis is difficult. Blood coagulates and often fatal bacterial disease caused by Clostridium spp. The
slowly in affected animals. incubation period is approximately 2 - 4 days. The affected area
will be warm and will contain gaseous accumulations that can
Pathogenesis. The propagation of the clostridial organisms is be palpated as crepitation of the subcutaneous tissue around the
self-promoted by the damage caused by the toxins and the in- infected area. Regional lymphadenopathy and fever may occur.
creased local anaerobic environment created. Clostridium novyi The animal becomes anorexic, severely depressed, and possibly
proliferates in the soft tissues of the head and neck, and the re- hyperthermic. Edema and crepitation may be noted around the
sultant clostridial toxin causes increased capillary permeability wound; death occurs within 12 hr to 2 days.
and the liberation of serous fluids into the tissues. Mixed infec-
tions with related clostridial organisms may lead to increasing Epizootiology and transmission. The organisms are ubiqui-
hemorrhage and necrosis in the affected tissues. Diagnosis is tous in the environment and may survive in the soil for years.
based on clinical signs. In black disease and bacillary hemoglo- The disease is especially prevalent in animals that have had re-
binuria disease, the ingested clostridial spores are absorbed, en- cent wounds such as those that have undergone castration,
ter the liver, and cause hepatic necrosis. Associated toxemia docking, ear notching, shearing, or dystocia.
causes subcutaneous vascular dilatation; increased pericardial,
pleural, and peritoneal fluid; and endocardial hemorrhages. The Necropsy findings. The tissue necrosis and hemorrhagic
toxins produced by C. novyi, identified as beta, eta, and theta, serous fluid accumulations resemble those of other clostridial
and each having enzymatic or lytic properties or both, also con- diseases.
tribute to the hemolytic disease. Clostridium chauvoei spores
proliferate in traumatized muscle areas damaged by transporta- Pathogenesis. In most cases, the clostridial organisms cause
tion, rough handling, or injury. a spreading infection through the fascial planes around the area
of the injury; vegetative organisms then produce potent exotox-
Differential diagnosis. Differential diagnoses include other ins, which result in necrosis (alpha toxin) and/or hemolysis
clostridial diseases as well as photosensitization. Hemolytic (beta toxin). Furthermore, the toxins enter the bloodstream and
546 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

central nervous system, resulting in systemic collapse and high In ruminants, E. coli is is a less common cause of cystitis and
mortality. pyelonephritis. The cystitis is characterized by dysuria and
pollakiuria; gross hematuria and pyuria may be present. The
Necropsy. Spreading, crepitant lesions around wounds are infection may or may not be restricted to the bladder; in the
suggestive of malignant edema. Affected tissues are inflamed later presentation, and in cases of pyelonephritis, a cow will
and necrotic. Gas and serosanguineous fluids with foul odors be acutely depressed, have a fever and ruminal stasis, and be
infiltrate the tissue planes. Large rod-shaped bacteria may be anorexic. In chronic cases, animals will be polyuric and un-
observed on histopathology; confirmation is made through cul- dergo weight loss. Escherichia coli may also cause in utero dis-
ture and identification. Intramuscular inoculation of guinea pigs ease in cattle, resulting in abortion or weakened offspring.
causes a necrotizing myositis and death. Organisms can be cul-
tured from guinea pig tissues. Epizootiology and transmission. Escherichia coli is one of the
most common gram-negative pathogens isolated from ruminant
Treatment. Infected animals can be treated with large doses of neonates. Zeman et al. (1989) classify E. coli infections into
penicillin and fenestration of the wound is recommended. four groups: enterotoxigenic, enterohemorrhagic, enteropatho-
genic, and enteroinvasive. Enterotoxigenic E. coli (ETEC) at-
Prevention and control. Proper preparation of surgical sites, tach to the enterocytes via pili, produce enterotoxins, and are the
correct sanitation of instruments and the housing environment, primary cause of colibacillosis in animals and humans. Fimbrial
and attention to postoperative wounds will help prevent this dis- (pili) antigens associated with ovine disease include K99 and
ease. Multivalent clostridial vaccines are available. F41. Enterohemorrhagic E. coli (EHEC) attach and efface the
microviUus, produce verotoxins, and occasionally cause disease
Research complications. Morbidity or loss of animals from in humans and animals. Enteropathogenic E. coli (EPEC) colo-
lack of or unsuccessful vaccination and from contaminated sur- nize and efface the microvillus but do not produce verotoxins.
gical sites or wounds may be consequences of this disease. EPEC are associated with disease in humans and rabbits and
cause a secretory diarrhea. Enteroinvasive E. coli (EIEC) invade
the enterocytes of humans and cause a shigella-like disease.
i. Colibacillosis
Overcrowding and poor sanitation contribute significantly to
Etiology. Escherichia coli is a motile, aerobic, gram-negative, the development of this disease in young animals. The organism
non-spore-forming coccobacillus commonly found in the envi- will be endemic in a contaminated environment and present on
ronment and gastrointestinal tracts of ruminants. Escherichia dams' udders. The bacteria rapidly proliferate in the neonates'
coli organisms have three areas of surface antigenic complexes small intestines. The bacteria and associated toxins cause a se-
(O, somatic; K, envelope or pili; and H, flagellar), which are cretory diarrhea, resulting in the loss of water and electrolytes.
used to "group" or classify the serotypes. Colibacillosis is the If the bacteria infiltrate the intestinal barrier and enter the blood,
common term for infections in younger animals caused by this septicemia results.
bacteria. Diagnosis of the enteric form can be made by observation
of clinical signs, including diarrhea and staining of the tail
Clinical signs. Presentation of E. coli infections vary with the and wool.
animal's age and the type of E. coli involved. Enterotoxigenic
E. coli infection causes gastroenteritis and/or septicemia in Necropsy findings. Swollen, yellow to gray, fluid-filled small
lambs and calves. Colibacillosis generally develops within the and large intestines, swollen and hemorrhagic mesenteric lymph
first 72 hr of life when newborn animals are exposed to the or- nodes, and generalized tissue dehydration are common. Sep-
ganism. The enteric infection causes a semifluid, yellow to gray ticemic lambs may have serofibrinous fluid in the peritoneal,
diarrhea. Occasionally blood streaking of the feces may be thoracic, and pericardial cavities; enlarged joints containing
observed. The animal may demonstrate abdominal pain, evi- fibrinopurulent exudates; and congested and inflamed meninges.
denced by arching of the back and extension of the tail, classi- Isolation and serotyping of E. coli confirm the diagnosis.
cally described as "tucked up." Hyperthermia is rare. Severe ELISA and latex agglutination tests are available diagnostic
acidosis, depression, and recumbancy ensue, and mortality may tools.
be as high as 75%. The septicemic form generally occurs be-
tween 2 and 6 weeks of age. Animals display an elevated body Differential diagnosis. Differential diagnoses include the en-
temperature and show signs suggestive of nervous system in- terotoxemias caused by C. perfringens type A, B, or C; Campy-
volvement such as incoordination, head pressing, circling, and lobacter jejuni; Coccidia, rotavirus, coronavirus, Salmonella,
the appearance of blindness. Opisthotonos, depression, and and Cryptosporidia. Other contributing causes of abomasal
death follow. Occasionally, swollen, painful joints may be ob- tympany in young ruminants, such as dietary changes, copper
served with septicemic colibacillosis. Blood cultures may be deficiency, excessive intervals between feedings of milk re-
helpful in identifying the septicemic form. placer, or feeding large volumes should be considered.
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 547

Prevention and control. The best preventive measures are affected. Cranioventral lung consolidation with hemorrhage,
maintenance of proper housing conditions, limiting overcrowd- fibrin, and edema are seen histologically.
ing, and frequently sanitizing lambing areas. Attention to colos-
trum feeding techniques and colostral quality are important Pathogenesis. Corynebacterium pseudotuberculosis pro-
means of preventing disease. Treatment must include intra- duces an exotoxin (phospholipase D) that damages endothelial
venous fluid hydration and reestablishment of acid-base and and blood cell membranes. This process enhances the organ-
electrolyte abnormalities. isms' ability to withstand phagocytosis. The infection spreads
through the lymphatics to local lymph nodes. The necrotic
Treatment. Antibiotics such as trimethoprim-sulfadiazine, lymph nodes seed local capillaries and hematogenously and
enrofloxacin, cephalothin, amikacin, and apramycin may be lymphatically spread the organisms to other areas, especially
helpful; oral antibiotics are not recommended. Vaccines are the lungs.
available for prevention of colibacillosis in cattle.
Differential diagnosis.
Differentials include pathogens caus-
ing lymphadenopathy and abscessation.
Corynebacterium pseudotuberculosis Infection
(Caseous Lymphadenitis) Treatment. Antibiotic therapy is not usually helpful. Ab-
Etiology. Corynebacterium pseudotuberculosis (previously scesses can be surgically lanced and flushed with iodine-
C. ovis) are nonmotile, non-spore-forming, aerobic, short and containing and/or hydrogen peroxide solutions. Abscessing
curved, gram-positive coccobacilli. Caseous lymphadenitis lymph nodes can be removed entirely from valuable animals.
(CLA) is such a common, chronic contagious disease of sheep During warmer months, an insect repellent should be applied to
and goats that any presentation of abscessing and draining and around healing lesions. All materials used to treat animals
lymph nodes should be presumed to be this disease until proven should be disposed of properly. Because of the contagious na-
otherwise. The disease has been reported occasionally in cattle. ture of the disease, animals with draining and lanced lesions
should be isolated from CLA-negative animals at least until
healed. Commercial vaccines are available (Piontkowski and
Clinical signs and diagnosis. Abscessation of superficial
Shivvers, 1998).
lymph nodes, such as the superficial cervical, retropharyngeal,
subiliacs (prefemoral), mammary, superficial inguinals, and
Prevention and control. Minimizing contamination of the en-
popliteal nodes, and of deep nodes, such as mediastinal and
vironment, using proper sanitation methods for facilities and in-
mesenteric lymph nodes, is typical. Radiographs may be help-
struments, segregating affected animals, and taking precautions
ful in identifying affected central nodes. Peripheral lymph
to prevent injuries are all important.
nodes may erode and drain caseous, "cheesy," yellow-green-tan
secretions. The incubation period may be weeks to months.
Research complications. This pathogen is a risk for animals
Over time, an infected animal may become exercise-intolerant,
undergoing routine management procedures or invasive re-
anorexic, and debilitated. Fever, increased respiratory rates, and
search procedures, because of its persistence in the environ-
pneumonia may also be common signs. Exotoxin-induced he-
ment, its long clinical incubation period, and its poor response
molytic crises may occur occasionally. Morbidity up to 15% is
to antibiotics.
common, and morbid animals will often eventually succumb to
the disease.
Diagnosis is based on clinical lesions; ELISA serological test- Corynebacterium renale, C. cystitidis, and C. pilosum
ing is also available. Smears of the exudate or lymph nodes as- Infections (Pyelonephritis; Posthitis and Ulcerative
pirates can be Gram-stained. Lymph node aspirates may also be Vulvovaginitis)
sent for culturing.
Etiology. Corynebacterium renale, C. cystitidis, and C. pilo-
sum are sometimes referred to as the C. renale group. These are
Epizootiology and transmission. The organism can survive piliated and nonmotile gram-positive rods and are distinguished
for 6 months or more in the environment and enters via skin biochemically. Corynebacterium renale causes pyelonephritis
wounds, shearing, fighting, castration, and docking. Ingestion in cattle, and C. pilosum and C. cystitidis cause posthitis, also
and aerosolization (leading to pulmonary abscesses) have been known as pizzle rot or sheath rot, in sheep and goats. In many
reported as alternative routes of entry. references, all these clinical presentations are attributed to
C. renale.
Necropsy findings. Disseminated superficial abscesses as well
as lesions of the mediastinal and mesenteric lymph nodes will Clinical signs and diagnosis. Acute pyelonephritis is charac-
be identified. Cut surfaces of the affected lymph nodes may ap- terized by fever, anorexia, polyuria, hematuria, pyuria, and
pear lamellated. Lungs, liver, spleen, and kidneys may also be arched back posture. Untreated infections usually become
548 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

chronic, with weight loss, anorexia, and loss of production in tices must be reconsidered. Clipping long wool and hair also is
dairy animals. Relapses are common, and some infections are helpful.
severe and fatal. Diagnosis of pyelonephritis is based on urinal-
ysis (proteinuria and hematuria) and rectal or vaginal palpation Treatment. Long-term (3 weeks) penicillin treatment is effec-
(assessing ureteral enlargement). Urine culturing may not be tive for pyelonephritis. Reduction of dietary protein, clipping
productive. In chronic cases, E. coli and other gram-negatives and cleaning skin lesions, treating for or preventing fly-strike,
may be present. and topical antibacterial treatments are effective for pos-
Posthitis and vulvovaginitis are characteriazed by ulcers, thitis and vulvovaginitis; systemic therapy may be necessary for
crusting, swelling and pain. The area may have a distinct mal- severe cases. Surgical debridement or correction of scarring
odor. Necrosis and scarring may be sequelae of more severe in- may also be indicated in severe cases.
fections. Fly-strike may also be a complication. Diagnosis is
based on clinical signs and on investigation of feeding regimens. l. Erysipelas
Etiology. Erysipelothrix rhusiopathiae is a nonmotile, non-
Epizootiology and transmission. Ascending urinary tract in-
spore-forming, gram-positive rod that resides in alkaline soils.
fections with cystitis, ureteritis, and pyelonephritis are wide-
spread problems, but incidence is relatively low. The vaginitis
Clinical signs. Erysipelothrix causes sporadic but chronic
and posthitis contribute to the venereal transmission, but indi-
polyarthritis in lambs less than 3 months of age. In older goats,
rect transmission is possible because the organisms are stable in
erysipelas has been associated with joint infections.
the environment and present on the wool or scabs shed from af-
fected animals. Posthitis occurs in intact and castrated sheep
Epizootiology and transmission. The disease may follow
and goats.
wound inoculation associated with castration, docking, or im-
proper disinfection of the umbilicus. Following wound contam-
Necropsy findings. Pyelonephritis, multifocal kidney absces-
ination and a 1- to 5-day incubation period, the lamb exhibits a
sation, dilated and thickened ureters, cystitis, and purulent exu-
fever and stiffness and lameness in one or more limbs. Joints,
date in many sections of the urinary tract are common finding
especially the stifle, hock, elbow, and carpus, are tender but not
at gross necropsy.
greatly enlarged.
Pathogenesis. Corynebacterium renale is a normal inhabitant
Necropsy findings. Thickened articular capsules, mild in-
of bovine genitourinary tracts. The pilus mediates colonization.
creases in normal-appearing joint fluid and erosions of the ar-
Conditions such as trauma, urinary tract obstruction, and
ticular cartilage are usually found. The joint capsule is in-
anatomic anomalies may predispose to infection. In addition,
filtrated with mononuclear cells, but bacteria are difficult to
more basic pH urine levels may block some immune defenses.
find. Diagnosis is based on clinical signs of polyarthritis, and
Infections ascend through the urinary tract. The bacteria are
confirmation is made by culturing the organism from the joints.
urease-positive when tested in vitro, and the ammonia produced
in vivo during an infection damages mucosal linings, with sub-
Differential diagnosis. Differential diagnoses include poly-
sequent inflammation.
arthritis caused by chlamydia or other bacteria and stiffness
Corynebacterium cystitidis and C. pilosum are normally
caused by white muscle disease. Other bacteria causing septic
found around the prepuce of sheep and goats. High-protein di-
joints include Areanobacterium pyogenes and Fusobacterium
ets, resulting in higher urea excretion and more basic urine, are
necrophorum. Caprine arthritis encephalitis (CAE) should also
contributing factors. Posthitis and vulvovaginitis may develop
be considered.
within a week of change to the more concentrated or richer diet,
such as pasture or the addition of high-protein forage. The am-
Prevention and control. Proper sanitation and prevention of
monia produced irritates the preputial and vulvar skin, increas-
wound contamination are important in preventing the infection
ing the vulnerability to infection.
in lambs. Screening of goat herds for CAE is recommended.

Differential diagnosis. Urolithiasis is a primary consideration

Treatment. Erysipelas is sensitive to penicillin antibiotic
for these diseases. Contagious ecthyma should be considered
therapy.
for the crusting that is seen with posthitis and vulvovaginitis, al-
though the lesions of contagious ecthyma are more likely to de-
m. Dermatophilosis (Cutaneous Streptothricosis,
velop around the mouth. Ovine viral ulcerative dermatosis is
Lumpy Wool Strawberry Foot Rot)
also a differential for the lesions of posthitis and vulvovaginitis.
Etiology. Dermatophilus congolensis is an aerobic, gram-
Prevention and treatment. Because high-protein feed is of- positive, filamentous bacterium with branching hyphae. Der-
ten associated with posthitis and vulvovaginitis, feeding prac- matophilosis is a chronic bacterial skin disease characterized by
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 549

crustiness and exudates accumulating at the base of the hair or ing contagious foot rot in sheep and goats. Other organisms may
wool fibers (Scanlan et al., 1984). be involved as secondary invaders. Both Dichelobacter and
Fusobacterium are nonmotile, non-spore-forming, anaerobic,
Clinical signs. Animals will be painful but will not be pru- gram-negative bacilli. Foot rot is a contagious, acute or chronic
ritic. Two forms of the disease exist in sheep: mycotic dermati- dermatitis involving the hoof and underlying tissues (Bulgin,
tis (also known as lumpy wool) and strawberry foot rot. My- 1986). It is the leading cause of lameness in sheep. At least 20
cotic dermatitis is characterized by crusts and wool matting, serotypes of Dichelobacter are known. Arcanobacterium pyo-
with exudates over the back and sides of adult animals and genes may also contribute to the pathogenicity or to foot ab-
about the face of lambs. Strawberry foot rot is rare in the United scesses in goats. Foot scald, an interdigital dermatitis, is caused
States but is characterized by crusts and inflammation between primarily by D. nodosus alone.
the carpi and/or tarsi and the coronary bands. Animals will be
lame. In goats and cattle, similar clinical signs of crusty, suppu- Clinical signs. Varying degrees of lameness are observed in
rative dermatitis are seen; the disease is often referred to as cu- all ages of animals within 2 - 3 weeks of exposure to the organ-
taneous streptothricosis in these species. Lesions in younger isms. Severely infected animals will show generalized signs of
goats are seen along the tips of the ears and under the tail. weight loss, decreased productivity, and anorexia associated
Diagnosis is based on clinical signs as well as the typical mi- with an inability to move. The interdigital skin and hooves will
croscopic appearance on stained skin scrapings, cultures, and be moist, with a distinct necrotic odor. Morbidity may reach
serology. 70% in susceptible animals. Diagnosis is based on clinical
signs. Smears and cultures confirm the definitive agents. Clini-
Epizootiology and transmission. The disease occurs world- cal signs of the milder disease, foot scald, include mild lame-
wide, and the Dermatophilus organism is believed to be a sapro- ness, redness and swelling, and little to no odor.
phyte. Transmission occurs by direct or indirect contact and is
aggravated by prolonged wet wool or hair associated with in- Epizootiology and transmission. Fusobacterium necropho-
clement weather. Biting insects may aid in transmission. rum is ubiquitous in soil and manure, in the gastrointestinal
tract, and on the skin and hooves of domestic animals. In con-
Necropsy findings. Lymphadenopathy as well as liver and trast, Dichelobacter contaminates the soil and manure but
splenic changes may be observed. Histopathologically, su- rarely remains in the environment for more than about 2 weeks.
perficial epidermal layers are necrotic and crusted with serum, Some animals may be chronic carriers. Overcrowded, warm,
white blood cells, and wool or hair. Dermal layers are hyper- and moist environments are key elements in transmission. Out-
emic and edematous and may be infiltrated with mononuclear breaks are likely in the spring season. Shipping trailers and con-
cells. taminated pens or yards should be considered also as likely
sources of the bacteria.
Pathogenesis. Lesions typically begin around the muzzle and
hooves and the dorsal midline. Pathogenesis. Both organisms are transmitted to the suscepti-
ble animal by direct or indirect contact. The organisms enter the
Prevention and control. Potash alum and aluminum sulfate hoof through injuries or through sites where Strongyloides pa-
have been used as wool dusts in sheep to prevent dermatophilo- pillosus larvae have penetrated. Fusobacterium necrophorum
sis. Minimizing moist conditions is helpful in controlling and initiates the colonization and is followed by D. nodosus. The
preventing the disease. In addition, controlling external para- latter attaches and releases proteases; these cause necrosis of the
sites or other factors that cause skin lesions is important. Le- epidermal layers and separation of the hoof from the underlying
sions will resolve during dry periods. dermis. The pathogenicity of the serotypes of D. nodosus is cor-
related with the production of these proteases and numbers of
Treatment. Animals can be treated with antibiotics such as pili. Additionally, F. necrophorum causes a severe, damaging
penicillin and oxytetracycline. Treating the animals with povi- inflammatory reaction.
done-iodine shampoos or chlorhexidine solutions is also useful
in clearing the disease. Differential diagnosis. Foot abscesses, tetanus, selenium/
vitamin E deficiencies, copper deficiency, strawberry foot rot,
bluetongue virus infection (manifested with myopathy and
n. Dichelobacter (Bacteroides) nodosus and Fuso-
coronitis), and trauma are among the many differentials that
bacterium necrophorum Infection (Virulent Foot Rot;
must be considered.
Contagious Foot Rot of Sheep and Goats; Foot Scald)
Treatment. Affected animals are best treated by manually
Etiology. Two bacteria, Dichelobacter (Bacteroides) nodosus trimming the necrotic debris from the hooves, followed by appli-
and Fusobacterium necrophorum, work synergistically in caus- cation of local antibiotics and foot wraps. Systemic antibiotics
550 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

such as penicillin, oxytetracycline, and erythromycin may be Epizootiology and transmission. Cases may be sporadic, or
used. Goats have improved dramatically when given a single epizootics may occur. Bos taurus dairy breeds and animals with
dose of penicillin (40,000 U/kg) (Smith and Sherman, 1994). wide interdigital spaces are more commonly affected. The fac-
Footbaths containing 10% zinc sulfate, 20% copper sulfate, or tors here are comparable to those present in foot rot of smaller
10% formalin (not legal in all states) can be used for treatment ruminants.
as well as for prevention of the disease. Affected animals should
be separated from the flock. Vaccination has been shown to be
Necropsy findings. Findings at necropsy include dermatitis
effective as part of the treatment regimen. Some breeds of sheep
and necrosis of the skin and subcutaneous tissues. Although
and some breeds and lines of goats are resistant to infection. In-
necropsy would rarely be performed, secondary osteomyelitis
dividual sheep may recover without treatment or are resistant to
may be noted in severe cases by sectioning limbs.
infection.

Prevention and control. Prevention and control programs in- Pathogenesis. The bacteria enter through the skin of the inter-
volve scrutiny of herd and flock management; quarantine of in- digital area after trauma to the interdigital skin, from hardened
coming animals; vaccination; segregation of affected animals; mud, or from softening of the skin due to, for example, constant
careful and regular hoof trimming; discarding trimmings from wet conditions in pens. Colonization leads to cellulitis. In addi-
known or suspected infected hooves; maintaining animals in tion, F. necrophorum releases a leukocidal exotoxin that re-
good body condition; avoiding muddy pens and holding areas; duces phagocytosis and causes the necrosis, whereas the tissues
and culling individuals with chronic and nonresponsive infec- and tendons are damaged by the proteases and collagenases pro-
tions. Dichelobacter nodosus bacterins are commercially avail- duced by B. melaninogenicus. Zinc deficiency may play a role
able; cross protection between serotypes varies. Biannual vac- in the pathogenesis in some situations.
cinination in wet areas may be essential. Some breeds may
develop vaccination site lumps. Footbaths of 10% zinc sulfate, Differential diagnoses. The most common differentials for
10% formalin (where allowed by state regulations), or 10% sudden lameness include hairy heel warts and subsolar ab-
copper sulfate are also considered very effective preventive cesses. Bluetongue virus should also be considered. Grain en-
measures. Goats are less sensitive than sheep to the copper in gorgement and secondary infection from cracks caused by
the footbaths. selenium toxicosis should also be considered. The exotic foot-
and-mouth disease virus would be considered in areas where
Research complications. Treating and controlling foot rot is that pathogen is found.
costly in terms of time, initial handling and treatments and their
follow-up, housing space, and medications.
Prevention and control. As with foot rot in smaller ruminants,
management of the area and herd are important. Paddocks and
Fusobacterium necrophorum and Bacteroides
pens should be kept dry, well drained, and free of material that
melaninogenicus Infection (Foot Rot of Cattle,
will damage feet. Footbaths and chlortetracycline in the feed
Interdigital Necrobacillosis of Cattle)
have been shown to control incidence. Affected animals should
Etiology. Interdigital necrobacillosis of cattle is caused by the be segregated during treatment. Chronically affected or se-
synergistic infection of traumatized interdigital tissues by Fu- verely lame animals should be culled. New cattle should be
sobacterium necrophorum and Bacteroides melaninogenicus. quarantined and evaluated.
Like F. necrophorum, B. melaninogenicus is a nonmotile,
anaerobic, gram-negative bacterium. Dichelobacter nodosus,
Treatment. Successful treatment regimens that result in heal-
the agent of interdigital dermatitis, may be present in some
ing within a week include cleaning the feet and trimming
cases. This is a common cause of lameness in cattle.
necrotic tissue; parenteral antimicrobials, such as oxytetracy-
cline or procaine penicillin, or sulfonomethazine in the drinking
Clinical signs. Clinical signs include mild to moderate lame-
water or tetracyclines in feed; and footbaths (such as 10% zinc
ness of sudden onset. Hindlimbs are more commonly affected,
sulfate, 2.5% formalin, or 5% copper sulfate) twice a day. In se-
and cattle will often flex the pastern and bear weight only on the
vere cases, more aggressive therapy such as bandaging the feet
toe. The interdigital space will be swollen, as will be the coro-
or wiring the digits together may be needed. Animals can re-
net and bulb areas. Characteristic malodors will be noted, but
cover without treatment but will be lame for several weeks. Ac-
there will be little purulent discharge. In more severe cases, an-
quired immunity is reported to be poor.
imals will have elevated body temperature and loss of appetite.
The les~ons progress to fissures with necrosis until healing oc-
curs. The diagnosis is by the odor and appearance. Anaerobic Research complications. Research complications are compa-
culturing confirms the organisms involved. rable to those noted for foot rot in smaller ruminants.
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 551

p. Fusobacterium necrophorum infection (Foot Abscesses) Treatment. Antibiotic and antiseptic regimens have been used
successfully for this problem. Antibiotics include parenteral
Fusobacterium necrophorum is also associated with foot ab-
cephalosporins and pencillins, as well as topical tetracyclines
scesses, the infection of the deeper structures of the foot, in
with bandaging. Antiseptic or antibiotic solutions in footbaths
sheep and goats. Only one claw of the affected hoof may be in-
include tetracyclines, zinc sulfate, lincomycin, spectinomycin,
volved. The animals will be three-legged lame, and the affected
copper sulfate, and formalin. The footbaths must be well main-
hoof will be hot. Pockets of purulent material may be in the heel
tained, minimizing contamination by feces and other materials.
or toe.
Tandem arrangements, such as the cleaning footbaths and then
the medicated footbaths, and preventing dilution from pre-
Heel Warts (Bovine Digital Dermatitis, Interdigital cipitation are useful. Other treatments such as surgical debride-
Papillomatosis, Papillomatous Digital Dermatitis, Foot ment, cryotherapy, and caustic topical solutions have been
Warts, Heel Warts, Hairy Foot Warts, Mortellaro's successful.
Disease)
Etiology. Bacteria such as Fusobacterium spp., Bacteroides Research complications. Infectious, contagious PPD is one of
spp., and Dichelobacter nodosus have been isolated from the major causes of lameness among heifers and dairy cattle and
bovine heel lesions. Spirochete-like organisms have also been is a costly problem to treat. The outbreaks are generally worse
shown in the lesions of cows with papillomatous digital der- in younger animals in chronically infected herds. The immune
matitis (PDD), in the United States and Europe; these have cul- response is not well understood, and it may be temporary in
turing requirements similar to those of Treponema species. older animals.

Clinical signs. All lesions occur on the haired, digital skin. Haemophilus somnus infection (Thromboembolic
One or all feet may be affected. Most lesions occur on the plan- Menin goencephalitis)
tar surface of the hindfoot (near the heel bulbs and/or extending Etiology. Haemophilus somnus is a pleomorphic, nonencap-
from the interdigital space), but the palmar and dorsal aspect of sulated, gram-negative bacterium. Diseases caused by this or-
the interdigital spaces may also be involved. Progression of le- ganism include thromboembolic meningoencephalitis (TEME),
sions, typically over 2 - 3 weeks, includes erect hairs, loss of septicemia, arthritis, and reproductive failures due to genital
hair, and thickening skin. Moist plaques begin as red and remain tract infections in males and females. Haemophilus somnus is a
red or turn gray or black. Exudate or blood may be present also major contributor to the bovine respiratory disease com-
on the plaque. Plaques enlarge and "hairs" protrude from the plex. Haemophilus spp. have been associated with respiratory
roughened surface. Lesioned areas are painful when touched. disease in sheep and goats.
The lesions may or may not be malodorous.
Clinical signs. The neurologic presentation may be preceded
Epizootiology and transmission. Facility conditions and herd
by 1-2 weeks of dry, harsh coughing. Neurologic signs include
management are considered contributing factors. The following
depression, ataxia, falling, conscious proprioceptive deficits;
have been examined as contributing factors: nutrition, particu-
signs such as head tilt from otitis interna or otitis media,
larly zinc deficiency; poorly drained, low-oxygen, organic ma-
opisthotonus, and convulsions may be seen as the brain stem is
terial underfoot; poor ventilation; rough flooring; damp and
affected. High fever, extreme morbidity, and death within 36 hr
dirty bedding areas; and overcrowding. These interdigital le-
may occur. Respiratory tract infections are usually part of the
sions occur commonly in young stock and in dairy facilities
complex with infectious bovine rhinotracheitis virus, bovine
throughout the world. The disease is seen only in cattle.
respiratory syncytial virus, bovine viral diarrhea virus, para-
Pathogenesis. The organisms noted above, combined with influenza 3, Mycoplasma, and Pasteurella, and the synergism
poor facility and herd management, are critical in the patho- among these contributes to the signs of bovine respiratory dis-
genesis. ease complex (BRDC). In acute neurologic as well as chronic
pneumonic infections, polyarthritis may develop. Abortion,
Differential diagnosis. Differentials for lameness will include vulvitis, vaginitis, endometritis, placentitis, and failure to con-
sole abscesses, laminitis, and trauma. ceive are manifestations of reproductive tract disease. In all
cases, asymptomatic infections may also occur.
Prevention and control. Each facility and management condi- Diagnosis based on culture findings is difficult because H.
tion noted above should be addressed in conjunction with ap- somnus is part of the normal nasopharyngeal flora. Paired serum
propriate antibiotic and/or antiseptic treatment regimens. All samples are recommended; single titers in some animals seem
equipment used for hoof trimming must be cleaned and disin- to be high because of passive immunity, previous vaccination,
fected after every use. Trucks and trailers should also be sani- or previous exposure. In cases of abortion, other causes should
tized between groups of animals. be eliminated from consideration.
552 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

Epizootiology and transmission. Because the organism is times of stress to the cattle is worthwhile. Killed whole-cell
considered part of the normal flora of cattle and can be isolated bacterins are commercially available; these have been shown to
from numerous tissues, the distinction between the normal flora be effective in controlling the respiratory disease presentation.
and the status of chronic carrier is not clear. Outbreaks are as- Control of other clinical aspects of the H. somnus disease by
sociated with younger cattle in feedlots in western United these bacterins has not been well described.
States, but stresses of travel and coinfection with other respira-
tory pathogens are involved in some cases. Adult cattle have Treatment. Rapid treatment at the first signs of neurologic dis-
also been affected. Vaccination for viral respiratory pathogens ease is important in an outbreak. Haemophilus somnus is sus-
may increase susceptibility. Transmission is by respiratory ceptible to several antibiotics, such as oxytetracycline and peni-
and genital tract secretions. The organism does not persist in the cillin, and these are often used in sequence until the cattle are
environment. recovered.

Necropsy findings. Pathognomonic central nervous system le-

s. Leptospirosis
sions include multifocal red-brown foci of necrosis and inflam-
mation on and within the brain and the meninges. Many thrombi Etiology. Seven different species of the spirochete genus
with bacterial colonies will be seen in these affected areas. Oc- Leptospira are now recognized, and pathogenic serovars exist
ular lesions may also be seen, including conjunctivitis, retinal within each species; previously pathogenic leptospires were
hemorrhages, and edema. Usually animals with neurological all classified as members of the species L. interrogans. The
disease will not have respiratory tract lesions. The respiratory serovars pomona, icterohaemorrhagiae, grippotyphosa, inter-
tract lesions include bronchopneumonia and suppurative pleuri- rogans, and hardjo are recognized pathogens. Leptospira hardjo
tis. When combined with Pasteurella infection, the pathology and L. pomona are the serovars most commonly diagnosed in
becomes more severe. Aborted fetuses will not show lesions, cattle, with L. hardjo causing endemic infection. Leptospira
but necrotizing placentitis will be evident histologically. Pure hardjo is also the major sheep serovar. Goats are susceptible to
cultures of H. somnus may be possible from these tissues. several serovars.

Pathogenesis. Inhalation of contaminated respiratory secre- Clinical signs. Leptospirosis is a contagious but uncommon
tions from carrier animals is the primary means of transmission. disease in sheep and goats. The disease may cause abortion,
The anatomical location of bacterial residence within the carri- anemia, hemoglobinuria, and icterus and is often associated
ers has not been identified. After gaining access by way of the with a concurrent fever. After a 4- to 10-day incubation period,
respiratory tract, the bacteria proliferate, and a bacteremia de- the organism enters the bloodstream and causes bacteremia,
velops. The bacteria are phagocytosed by neutrophils but are fever, and red-cell hemolysis. Leptospiremia may last up to
not killed. The thrombosis formation is due to the adherence by 7 days. Immune stimulation is apparently rapid, and antibodies
the nonphagocytosed organisms to vascular endothelial cells, are detectable at the end of the first week of infection; cross-
degeneration and desquamation of these cells, and exposure of serovar protection does not occur. During active bacteremia, he-
subendothelial collagen, with subsequent initiation of the in- molysis may result in hemoglobin levels of 50% below normal.
trinsic coagulation pathway. Antigen-antibody complex for- Hyperthermia, hemoglobinuria, icterus, and anemia may be ob-
mation, resulting in vasculitis, is also correlated with high lev- served during this phase, and ewes in late gestation may abort.
els of agglutinating antibodies. Abortion usually occurs only once. Mortality rates of above
50% have been reported in infected ewes and lambs (Jensen and
Differential diagnosis. Differentials in all ruminants include Swift, 1982). Subclinical infection is more common in non-
other pathogens associated with neurological disease and respi- pregnant and nonlactating animals. Sheep infected with lep-
ratory disease such as Pasteurella hemolytica, P. multocida, and tospirosis may display a hemolytic crisis associated with IgM
P. aeruginosa. In smaller ruminants, Corynebacterium pseudo- acting as a cold-reacting hemagglutinin.
tuberculosis should be considered. Acute and chronic infections in cattle are more common than
infections in sheep and goats. Acute forms in cattle display
Prevention and control. Stressed animals or those exposed to signs similar to those in sheep. Acute infection in calves may
known carriers can be treated prophylactically with tetracycline progress to meningitis and death. Lactating cows will have se-
administered parenterally or orally (in the feed or water). The vere drops in production. Chronic cases may lead to abortion,
late-stage polyarthritis is resistant to antibiotic therapy, because with retained placenta, and weakened calves or animals that
of failure of the antibiotic to reach the site of infection. Planning carry the infection. Infertility may also be a sequela.
vaccination programs carefully will decrease chances of out-
breaks. For example, avoiding vaccinating animals for infec- Epizootiology and transmission. Leptospires are a large
tious bovine rhinotrachetitis and bovine viral diarrhea during genus, and leptospirosis is a complicated disease to prevent,
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 553

treat, and control. The organism survives well in the environ- t. Listeria (Circling Disease, Silage Disease)
ment, especially in moist, warm, stagnant water. Cattle, swine,
Etiology. Listeria monocytogenes is a pleomorphic, motile,
and other domestic and wild animals are potential carriers of
non-spore-forming, [3-hemolytic, gram-positive bacillus that in-
serovars common to particular regions. Wild animals often
habits the soil for long periods of time and has been often found
serve as maintenance hosts, but domestic livestock may be
in fermented feedstuffs such as spoiled silage. Of the 16 known
reservoirs also. Organisms are shed in urine, in uterine dis-
serovars, several produce clinical signs in ruminants. Listeria
charges, and through milk. Animals become carriers when they
ivanovii (associated with abortions in sheep) is serovar 5.
are infected with a host-adapted serovar; sporadic clinical dis-
ease is more commonly associated with exposure to a non-host-
adapted serovar (Heath and Johnson, 1994). Infection may oc- Clinical signs. Listeriosis is an acute, sporadic, nonconta-
cur via oral ingestion of contaminated feed and water, via gious disease associated with neurological signs or abortions in
placental fluids, or through the mucous membranes of the sus- sheep and other ruminants. The overall case rate is low. The
ceptible animal. Placental or venereal transmission may occur. disease may present as an isolated case or with multiple animals
As the organisms are cleared from the bloodstream, they chron- affected. Three forms of disease are described: encephalitis,
ically infect the renal convoluted tubules and the reproductive placentitis with abortion, and septicemia with hepatitis and
tract (and occasionally the cerebrospinal fluid or vitreous hu- pneumonia. The encephalitic form is most common in sheep;
mor). Chronically infected animals may shed the organism in septicemic forms may occur in neonatal lambs (Scarratt, 1987).
the urine for 60 days or longer. Clinically, the encephalitic form begins with depression, an-
orexia, and mild hyperthermia after an incubation period of 2 -
Necropsy. Diagnosis is confirmed by identification of lep- 3 weeks. As the disease progresses, animals exhibit nasal dis-
tospires in fetal tissues. The leptospires are visible in silver- or charges and conjunctivitis and begin to walk in circles, as if dis-
fluorescent antibody-stained sections of liver or kidney. Lep- oriented. Facial paralytic lesions, including drooping of an ear
tospires may also be seen under dark-field or phase-contrast mi- or eyelid, dilation of a nostril, or strabismus occur unilaterally
croscopy of fetal stomach contents. Fetal and maternal serology, on the affected side as the result of dysfunction of some or all
and diagnostic tests such as the microscopic agglutination test, the cranial nerves V-XII. The neck will by flexed away from
are useful; interpretation is complicated because of cross reac- the affected side. Facial muscle twitching, protrusion of the
tion of antibodies to many serovars. tongue, dysphagia, hypersalivation, and nasal discharges may
be noted. The hypersalivation may lead to metabolic acidosis in
Differential diagnosis. More than one serovar may cause in- advanced cases in cattle. Anorexia, prostration, coma, and death
fection in one animal, and each serovar should be considered as follow. The placental form usually results in last-trimester abor-
a separate pathogen. Because of the associated anemia, differ- tions in ewes and does, which typically survive this form of the
ential diagnoses should include copper toxicity and parasites, in disease. The affected females may be asymptomatic or may
addition to other abortifacient diseases. show severe clinical signs such as fever and depression, with
subsequent retained placenta or endometritis. Abortion usually
Prevention and control. Polyvalent vaccines, tailored to com- occurs within 2 weeks of Listeria infection. In cattle, abortion
mon serovars regionally, are available and effective for prevent- occurs during the last 2 months of gestation and has been in-
ing leptospirosis in cattle. Immunity is serovar specific. Because duced experimentally 6 - 8 days after exposure. Cows present
serological titers tend to diminish rapidly (40-50 days in sheep with the range of clinical signs seen in smaller-ruminant dams.
[Jensen and Swift, 1982]), frequent vaccination may be neces- There is no long-term effect on the fertility of affected dams.
sary. Other prevention measures such as species-specific hous-
ing, control of wild rodents, and proper sanitation should be
Epizootiology and transmission. The organism is transmitted
instituted.
by oral ingestion of contaminated feeds and water or possibly
Treatment. Antibiotic treatment is aimed at treating ill ani- by inhalation. By the oral route, the organism enters through
mals and trying to clear the carrier state. Treatment methods for breaks in the oral cavity and ascends to the brain stem by way
acute leptospirosis include oxytetracycline for 3 - 6 days. Ad- of nerves. When severe outbreaks occur, feedstuffs should be
dition of oxytetracycline or chlortetracycline to the feed for assessed for spoilage. Listeria organisms can be shed by asymp-
1 week may be helpful. These antibiotics are considered best for tomatic carriers, especially at the end of pregnancy and at
removal of the carrier state of some serovars. Vaccination and lambing.
antibiotic therapy can be combined in an outbreak.
Diagnosis and necropsy findings. Diagnosis is usually made
Research complications. Leptospirosis is zoonotic and may from clinical signs. Culture confirms the diagnosis (cold en-
be associated with flulike symptoms, meningitis, or hepatorenal richment at 20~ is preferable but not essential for isolation).
failure in humans. Impression smears will show the pleomorphic gram-positive
554 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

characterisitics of the pathogen. Tissue fluorescent antibody successful, and mortality is especially high in sheep. Recovered
techniques may also be utilized. Gross lesions are not observed animals tend to resist reinfection.
with the encephalitic form. Microscopic lesions include throm-
bosis, neutrophilic or mononuclear foci in areas of inflamma- Research complications. In addition to the loss of fetal ani-
tion, and neuritis. The pons, medulla, and anterior spinal cord mals, stress to the dams, and risks to other animals, any aborted
are primarily affected in the encephalitic form. Microabscesses tissue by a ruminant should be regarded as a potential zoonotic
of the midbrain are characteristic of Listeria encephalitis in risk. Listeria can cause mild to severe flulike symptoms in hu-
sheep. Aborted fetuses that are intact may show fibrinous poly- mans and may be a particular risk for pregnant women and for
serositis, with excessive serous fluids; small, necrotic foci of the older or immune-compromised individuals. Listeriosis in hu-
liver; and small abomasal erosions. Necrotic lesions of the fetal mans is a reportable disease.
spleen and lungs may also be seen. In goats, Listeria-induced
neurological lesions occur only in the brain stem. Placentitis,
focal bronchopneumonia, hepatitis, splenitis, and nephritis may Lyme Disease (Borrelia burgdorferi Infection,
be seen with other forms. Borreliosis)
Etiology. Lyme disease is caused by the spirochete Borrelia
Pathogenesis. With the encephalitic form, the organism pen- burgdorferi.
etrates mucosal abrasions and enters the trigeminal or hy-
poglossal nerves. The Listeria organisms then migrate along the Clinical signs and diagnosis. Reports in ruminants indicate
nerves and associated lymphatics to the brain stem (medulla and seroconversion to B. burgdorferi, but there are few definitive
pons). In the septicemic form, the organism penetrates tissues correlations to the arthritis that is present. Diagnosis requires
of the gastrointestinal tract and enters the bloodstream, to be culturing from the affected joints and diagnostic elimination of
distributed to the liver, spleen, lungs, kidneys, and placenta. Af- other causes of lameness and arthritis.
ter infection, organisms are shed in all body secretions (infected
milk is an important risk factor for zoonosis). A toxin produced Epizootiology and transmission. The organism is present
by Listeria monocytogenes is correlated with pathogenicity, but throughout much of the Northern Hemisphere and has been re-
the mechanism of the pathogenesis of this molecule has not ported in many mammals and also in birds. Ticks of the Ixodes
been elucidated. ricinus complex are the major vectors of the spirochete and
must be attached for 24 hr for successful transmission.
Differential diagnoses. Rabies, bacterial meningitis, brain ab-
scess, lead toxicity, and otitis media must be considered as dif- Pathogenesis. The Ixodes ticks have three life stages: larval,
ferentials. In sheep, the differentials include organisms that nymphal, and adult. Feeding occurs once during each stage, and
cause abortion, and neurological signs, such as enterotoxemia wild animals are the source of blood meals. The larval stages
due to Clostridium perfringens type D. In goats, the major dif- feed from rodents, such as the white-footed deer mouse, Pero-
ferentials include caprine arthritis encephalitis viral infection myscus leucopus, from which they acquire the spirochete. The
and chlamydial and mycoplasmal infections. In both species, nymphal stage is that which usually infects other animals. The
scrapie is a differential. In cattle, aberrant parasite migration or adult ticks are usually found on deer.
Hemophilus somnus infection must also be considered.
Differential diagnosis. Seroconversion to B. burgdorferi does
Prevention and control. Affected dams should be segregated not necessarily confirm the cause of arthritis. Other causes of
and treated. Other animals in the group may be treated with arthritis and lameness in ruminants include trauma, caprine
oxytetracycline as needed. Aborted tissues should be removed arthritis encephalitis virus, Mycoplasma spp., Chlamydia
immediately. Proper storage of fermented feeds minimizes this psittaci, Erysipelothrix spp., Arcanobacterium pyogenes, Bru-
source of contamination. When silage spoils, the pH increases, cella spp., and rickets.
producing a suitable growth environment for the organism.
Commercial vaccines are not available in the United States. Prevention and control. Control of the tick vector is the most
important factor in preventing the possibility of exposure or
Treatment. Affected animals can be treated aggressively with disease.
penicillin, ampicillin, oxytetracycline, or erythromycin. Excep-
tionally high levels of penicillin are required for treating af- Treatment. Antibiotic therapy, with tetracycline, penicillin,
fected cattle. Severely affected animals should receive appro- amoxicillin, and cephalosporins, is used for diagnosed or sus-
priate fluid support and other nursing care. Treatment is less pected Lyme arthritis.
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 555

Research complications. Lyme disease is zoonotic, and the der frequently; oxytocin injections preceding milking will im-
lxodes ticks transmit the disease to humans. prove gland evacuation. Because somatic cell counting is often
not routinely performed, treatment of subclinical mastitis is sel-
dom done. There is currently no treatment available for diffuse
v. Mastitis
chronic mastitis.
i. Ovine mastitis Mastitis in ewes may be acute, subclini-
cal, or chronic. Acute mastitis often results in anorexia, fever, ii. Caprine mastitis Lactating goats are subject to inflam-
abnormal milk, and swelling of the mammary gland. Pasteu- mation of mammary gland, or mastitis. The primary causative
rella haemolytica is the most common cause of acute mastitis. organisms are Staphylococcus epidermidis and other coagulase-
Additional isolates may include, in order of prevalence, Staphy- negative Staphylococcus spp. Clinical signs of mastitis include
lococcus aureus, Actinomyces (Corynebacterium) spp., and abnormal coloration or composition of milk, mammary gland
Histophilus ovis. Escherichia coli and Pseudomonas aerugi- redness, heat and pain, enlargement of the mammary gland, dis-
nosa have also been found to cause acute mastitis. As many as coloration of the mammary gland, and systemic signs of sep-
six serotypes of Pasteurella haemolytica have been isolated ticemia. Large abscesses may be present in the affected gland.
from the mammary glands of mastitic ewes. Furthermore, Staphylococcus aureus is also associated with caprine mastitis,
intramammary inoculation of these organisms isolated from and toxemia may be part of the clinical picture. This organism
ovine and bovine pulmonary lesions has resulted in clinical produces a necrotizing alpha toxin that can result in gangrenous
mastitis in ewes (Watkins.and Jones, 1992). mastitis. Caprine mastitis may be clinical or subclinical, and the
Subclinical mastitis is detected only indirectly, by count- first indication of mastitis may be weak, depressed, or thin kids.
ing somatic cells. The most common isolate from ewes with Diagnosis is based on careful culture of mastitic milk. Treat-
subclinical mastitis is coagulase-negative staphylococci. Other ment includes frequent stripping, intramammary antibiotics,
isolates include Actinomyces bovis, Streptococcus uberis, S. and nonsteroidal anti-inflammatory drugs. Oxytocin (5-10 U)
dysgalactiae, Micrococcus spp., Bacillus spp., and fecal strep- may help milk letdown for frequent strippings. Bovine mastitis
tococci. Most of these organisms are commonly found in the products can be used in the goat; however, care should be taken
environment. not to insert the mastitis tube tip fully, because damage to the
Diffuse chronic mastitis, or hardbag, results from interstitial protective keratin layer lining the teat canal may occur. In severe
accumulations of lymphocytes in the udder. Both glands are acute systemic cases, steroids, fluids, and systemic antibiotics
usually affected, but no inflammation is present. Serological may be necessary.
evidence suggests that diffuse chronic mastitis is caused by the Other less common causes of mastitis in goats include Strep-
retrovirus that causes ovine progressive pneumonia (OPP or tococcus spp. (S. agalactiae, S. dysgalactiae, S. uberis, and
maedi/visna virus). Other bacterial agents or Mycoplasma have zooepidemicus). Gram-negative causes of caprine mastitis in-
not usually been isolated from udders with this type of mastitis. clude Escherichia coli, Klebsiella pneumoniae, Pasteurella
Acute mastitis occurs in approximately 5% of lactating ewes spp., Pseudomonas, and Proteus mirabilis. Corynebacterium
annually, and it usually occurs either soon after lambing or pseudotuberculosis can cause mammary gland abscessation,
when lambs are 3 - 4 months old (Lasgard and Vaabenoe, 1993). whereas Mycoplasma mycoides may cause agalactia and sys-
Subclinical mastitis occurs in 4 - 5 0 % of lactating ewes (Kirk temic disease. "Hard udder" can be caused by caprine arthritis
and Glenn, 1996). Subclinical mastitis is more common in ewes encephalitis virus (CAEV). Brucellosis and listeriosis can cause
from high-milk-producing breeds. Skin or teat lesions and der- a subclinical interstitial mastitis (Smith and Sherman, 1994).
matitis increase the prevalence of disease. Acute mastitis can be
diagnosed in ewes with associated systemic signs of disease by iii. Bovine mastitis Mastitis is the disease of greatest eco-
physical examination of the udder and inspection of the milk. nomic importance for the dairy cattle industry. The majority of
Subclinical mastitis is often suggested by somatic cell counts the impact will be on the production and overall health of the
elevated above 1 x 106 cells/ml. When high somatic cell counts cows, but low-incidence herds also diminish the risk of calves'
are identified, subclinical mastitis can be diagnosed by milk ingesting or being exposed to pathogens. The most common
culture. The California mastitis test may also be helpful as an bovine mastitis pathogens include Staphylococcus aureus and
indicator of mastitis. Manual palpation of a hard, indurated ud- Streptococcus agalactiae, S. dysgalactiae, and S. uberis; col-
der as well as serological testing for the maedi/visna virus is iform agents such as Escherichia coli, Enterobacter aerogenes,
helpful in confirming the diagnosis of diffuse chronic mastitis. Serratia marcescens, and Klebsiella pneumoniae; mycoplasmal
Treatment for acute bacterial mastitis should include aggressive species such as Mycoplasma bovis, M. bovigenitalium, M. cali-
application of broad-spectrum antibiotics (intramammary and fornicum, M. canadensis, and M. alkalescens; and Salmonella
systemic) and supportive therapy such as fluids and anti-inflam- spp. such as S. typhimurium, S. newport, S. enteritidis, S. dublin,
matory drugs. It is may be helpful to milk out the infected ud- and S. muenster. Many of these agents such as Staphylococcus
556 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

spp., Salmonella spp., and the coliforms can cause both acute Clinical signs. Lacrimation, photophobia, and blepharospasm
and chronic mastitis, as well as severe systemic disease, includ- are seen initially. Conjunctival injection and chemosis develop
ing fever and anorexia. These must be regarded as herd and en- within a day of exposure, and then keratitis with corneal edema
vironmental pathogens in terms of treatment and prevention. and ulcers. Anterior uveitis may be a sequela within a few
The pathogenesis of staphylococcal infections is comparable to days, and thicker mucopurulent ocular discharge may be seen.
that in goats. Staphylococcus agalactiae can be cleared from Corneal vascularization begins by 10 days after onset. Reep-
udders because it does not invade other tissues, is an obligate ithelialization of the corneal ulcers occurs by 2 - 3 weeks after
resident of the glands, and is susceptible to penicillin. In con- onset. Diagnosis is usually based on clinical signs, but culturing
trast, S. uberis and S. dysgalactiae are environmental organisms is helpful and fluoroscein staining is useful for demonstrating
and can be highly resistant to pencillin. Mycoplasma bovis is the corneal ulceration.
more common of the mycoplasmal pathogens and can cause se-
vere infections. Transmission of the mycoplasmas is not well Epizootiology and transmission. The disease is more severe in
defined but may be related to their presence in other organ sys- younger cattle. The clinical signs of IBK tend to be more severe
tems. Treatments for mycoplasmal mastitis are not successful; in cattle that are also infected with infectious bovine rhinotra-
culling is recommended. cheitis (IBR) virus or those that have been vaccinated recently
There are many interrelated factors associated with preven- with modified live IBR vaccine. The bacteria are shed in nasal
tion and control of mastitis in a herd, including herd health secretions and cattle with no clinical symptoms may be carriers.
and dry cow management, order of animals milked, milking Transmission is by fomites, flies, aerosols, and direct contact.
procedures, milking equipment, condition of the teats, and the Incidence in winter months is very low. Nonhemolytic strains
condition of the environment. Management of the overall herd are associated with the winter epidemics, and hemolytic
includes aspects such as vaccination programs, nutrition, isola- strains are associated with summer epidemics.
tion of incoming animals, and quarantine and treatment of or
culling diseased individuals. Culturing or testing newly fresh- Necropsy findings. Necropsy is not typically performed on
ened cows and monitoring the bulk milk tank serve as indicators these cases. Corneal edema, ulceration, hypopyon, and uveitis
of subclinical mastitis. Herd management will diminish teat le- would be noted, depending on the stage of infection.
sions. Bacterin vaccines are available for preventing and con-
trolling coliform mastitis and S. aureus mastitis. At the time Pathogenesis. The pili ofM. bovis bind to receptors of corneal
of dry-off, all cows must be treated by intramammary route. epithelium. The virulent strains of the bacteria then release the
Some infections can be successfully cleared during this time. enzymes that damage the corneal epithelial cells. Other factors
Younger, disease-free animals should be milked first; any ani- contributing to infection include ultraviolet light and trauma
mals with diagnosed problems should be milked after the rest from dust and plant materials.
of the herd and/or segregated during treatment. Milkers' hands
easily serve as a means of pathogen transmission, and wearing Differential diagnoses. Infectious bovine rhinotrachetitis
rubber gloves is recommended. Teat and udder cleaning prac- virus causes conjunctivitis, but the central corneal ulceration
tices include washing and drying with single-service paper or that is characteristic of IBK is not seen with M. bovis infections.
cloth towels or pre- and postmilking dipping. Milking equip- Mycoplasma, Listeria, Branhamella (Neisseria), and adeno-
ment must be maintained to provide proper vacuum levels and virus may be cultured from affected bovine eyes but none has
pumping rates, and liners should be the appropriate size. Facil- been shown to produce the corneal lesions when inoculated into
ities that provide clean and dry areas for the animals to rest, susceptible animals.
feed, and move will diminish teat injuries and reduce exposures
to mastitis pathogens. In that regard, inorganic bedding such as Prevention and control. Cattle should not be immunized in-
clean sand harbors few pathogens in contrast to shavings and tranasally with modified live infectious bovine rhinotracheitis
sawdust. vaccine during IBK outbreaks; this will likely exacerbate the in-
fection. New animals should be quarantined and treated pro-
phylactically before introduction to herds. The available vac-
W. Moraxella bovis Infection (Infectious Bovine
cines, containing. M. bovis pili or killed M. bovis, help decrease
Keratoconjunctivitis, Pinkeye)
incidence and severity of disease; these preparations are not
Etiology. Moraxella bovis, a gram-negative coccobacillus, is completely effective, because the M. bovis strain may not be ho-
the most common cause of infectious bovine keratoconjunctivi- mologous to that used for the vaccine preparation. Other pre-
tis (IBK) in cattle. This organism is not a cause of keratocon- ventive measures include 10% permethrin-impregnated bilat-
junctivitis in sheep and goats. The disease includes conjunctivi- eral ear tags, pour-on avermectins, or dust bags or face rubbers
tis and ulcerative keratitis. The pathogenic M. bovis strain is containing insecticide (such as 5% coumaphos) to control flies
piliated, and at least seven serotypes exist. throughout the season and premises; mowing of high pasture
14. BIOLOGYAND DISEASESOF RUMINANTS: SHEEP, GOATS,AND CATTLE 557

grass to minimize ocular trauma; provision of shade; control of Epizootiology and transmission. Although M. bovis can be
dust and sources of other mechanical trauma; and segregation killed by sunlight, it otherwise survives a long time in the envi-
of animals by age. ronment and in cattle feces. Animals acquire the infection from
the environment or from other animals via aerosols, from con-
Treatment. Cattle can recover without treatment, but younger taminated feed and water, and from secretions such as milk,
animals should be treated as soon as the infection is detected. semen, genital discharges, urine, and feces. Clinically normal
Antibiotic treatments include topical, subconjunctival adminis- animals may serve as carriers. The bacilli stimulate an initial
tration and intramuscular dosing. Several standard topical an- neutrophilic tissue response. Neutrophils become necrotic and
tibiotics have been shown to be effective, including oxytetracy- are phagocytosed by macrophages, forming giant epithelioid
cline, gentamicin, and triple antibiotic combinations. These cells called Langhans' giant cells. An outer lymphocytic zone is
should be administered twice per day. Subconjunctival injec- formed, and fibrotic encapsulation creates the classical caseous
tions of antibiotics, such as penicillin G, provide higher corneal nodules. Vascular erosion and hematogenous migration of the
levels of drug; these are typically administered only once or organisms may lead to lesions throughout the body.
twice in severe cases. Intramuscular doses of long-acting oxy-
tetracycline, given on alternate days, are effective in larger Necropsy findings. Yellow primary tubercles (granulomas)
herds, and 2 doses 72 hr apart eliminate carriers. Third-eyelid with central areas of caseous necrosis and calcification are pres-
flaps, temporary tarsorrhaphy, or eye patches may be useful in ent in the lungs. Caseous nodules are also associated with gas-
certain cases. trointestinal organs and mesenteric lymph nodes.

Research complications. This pathogen does present a com- Prevention and control. Significant progress has been made
plication due to the carrier status of some animals, the likeli- in eradication programs in the United States during the past sev-
hood of herd outbreaks, the severity of disease in younger eral decades, but during the 1990s, infected animals continued
animals, and the morbidity, possible progression to uveitis, and to be found in domestic cattle herds and particularly in captive
time and treatment costs associated with infections. The overall deer herds in hunting preserves. The intradermal tuberculin test,
condition of the cattle will be affected for several weeks, and using purified protein derivative (PPD), is usually used as a di-
permanent visual impairment or loss, as well as ocular dis- agnostic indicator in live animals. This test should be performed
figurement, may occur. annually on bovine and caprine dairy herds (and bison herds);
the official tests are the caudal fold, comparative cervical, and
single cervical tests. Notification to state officials is required
x. Mycobacterial Diseases
following identification of intradermal-positive animals. Great
Mycobacterium bovis Infection (Tuberculosis) care must be exercised in any handling of tissue or necropsies
Etiology. Mycobacteria are aerobic, nonmotile, non-spore- of reactors, and state animal health officials should be consulted
forming, acid-fast pleomorphic bacteria. Most cases of tuber- regarding disposal of materials and cleaning of premises fol-
culosis in sheep are related to Mycobacterium bovis or M. lowing depopulation of positive animals.
avium. Cases in goats have been attributed to M. bovis, M.
avium, or M. tuberculosis. Mycobacterium bovis, or the bovine Treatment. No treatment is recommended, and treatment is
tubercle bacillus, is the cause in cattle but has been isolated usually not allowed, because of the zoonotic potential, chronic-
from many domestic and wild mammals. Other agents of mam- ity of the disease, and the treatment costs. Slaughter is preferred,
malian tuberculosis include M. microti and M. africanum. to prevent potential transmission to humans.

Clinical signs. Tuberculosis is a sporadic, chronic, contagious Research complications. The pathogen is zoonotic.
disease of ruminants and is zoonotic. The infection is often
asymptomatic later in the illness, and it may be diagnosed only Paratuberculosis, or Johne 's disease (Mycobacterium
at necropsy. The respiratory system (M. bovis) or the digestive paratube rculo sis)
system (M. avium) is the primary site of infection; other tissues Etiology. Mycobacterium paratuberculosis, the causative
such as mammary tissue and reproductive tract may be infre- agent of Johne's disease, is a fastidious, non-spore-forming,
quently involved. Locations of the characteristic tubercles will acid-fast, gram-positive rod. The organism is actually a sub-
determine whether clinical signs are seen. Respiratory signs species of M. avium, but M. paratuberculosis does not pro-
may include dyspnea, coughing, and pneumonia. Digestive tract duce the siderophore mycobactin (an iron-binding molecule) of
signs include diarrhea, bloat, or constipation; diarrhea is most M. avium.
common. Lymphadenopathy occurs in advanced cases. Fever
and generalized disease may be seen after calving. Infected Clinical signs and diagnosis. Johne's disease is a chronic,
goats lose weight and develop a persistent cough. contagious, granulomatous disease of adult ruminants and is
558 SCOTT A. MISCHLER,WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

characterized by unthriftiness, weight loss, and intermittent di- ileocecal lymph nodes provide the best samples for histology
arrhea. In sheep and goats, chronic wasting is usually seen, oc- and acid-fast staining.
casionally with pasty feces or diarrhea. In cattle, chronic diar-
rhea and rapid weight loss are the most common clinical signs Differential diagnosis. Diseases causing chronic wasting
of the disease. Usually older adult animals are infected, but over and poor coat and body condition of all ruminants should be
time in an infected herd, younger animals will become infected considered. These include chronic salmonellosis, peritonitis,
when sufficient doses of organisms are ingested. Although clin- severe parasitism, winter dysentery, and pyelonephritis. Deer
ical signs are nonspecific, Johne's disease should be considered can be infected, and the lesions can be confused with those of
if the affected diarrheic animals have a good appetite and are on tuberculosis.
a good anthelmintic program.
The disease is diagnosed based on clinical signs and labora- Treatment. Treatment is not worthwhile.
tory analyses, although none of the tests is more than 50% sen-
sitive. In addition, the sensitivity of the serological tests differs Prevention and control. Prevention is the most effective
between species. The standard is the fecal culture that takes 8 - method to manage this pathogen. Efforts should be focused on
12 weeks. Theenzyme-linked immunosorbent assay (ELISA) eliminating the disease through test and slaughter. Neonates
is now considered the most reliable serological test, but false should not be reared by infected dams. Some states have Johne's
negatives do occur. Other serological tests such as agar gel im- disease eradication programs. Facilities and pastures where an-
munodiffusion (AGID) and complement fixation are useful. imals testing positive for Johne' disease were maintained should
Herd screening may be done using the AGID or ELISA sero- be thoroughly cleaned and kept vacant for a year after culling.
logical tests. Identification of the organism on culture, or
the presence of acid-fast organisms on mucosal or mesenteric Other considerations. Mycobacterium paratuberculosis is
lymph node smears or from rectal biopsies, helps confirm the being investigated as a factor in the development of Crohn's dis-
diagnosis. Some animals serologically negative for Johne's dis- ease in humans.
ease, however, have been found to be positive on fecal culture.
Commercial AGID tests approved for use in cattle may be use-
Navel Ill (Omphalitis, Omphalophlebitis,
ful in diagnosing Johne's disease in sheep (Dubash et al., 1996).
Omphaloarteritis, Joint Ill)
Serological tests cross-react with other species of Mycobac-
terium, especially M. avium. Etiology. The most common organism causing infection of
the umbilicus is Arcanobacterium (formerly Actinomyces,
Epizootiology and transmission. The organism is prevalent in Corynebacterium) pyogenes; other bacteria may be present.
the environment and is transmitted to young animals by direct Arcanobacterium spp. are anaerobic, nonmotile, non-spore-
or indirect contact. Although vertical transmission has been re- forming, gram-positive, pleomorphic rods to coccobacilli.
ported, the organism more commonly enters the gastrointestinal Other environmental contaminants are also associated with this
tract and penetrates the mucosa of the distal small intestine, pri- disease, such as Escherichia coli, Enterococcus spp., Proteus,
marily the ileum. Chronic carriers may intermittently shed the Streptococcus spp., and Staplylococcus spp.
organisms.
Clinical signs and diagnosis. Navel ill is an acute localized
Pathogenesis. Mycobacteriumparatuberculosis is an obligate inflammation and infection of the external umbilicus. Animals
parasite that grows only in macrophages of infected animals. present with fever and painful enlargement of the umbilicus.
Nursing infected dams are a primary source of infection of Animals may exhibit various degrees of depression and an-
neonates. If the organism is not cleared, it proliferates slowly orexia, and purulent discharges may be seen draining from
in the tissue, leading to inflammatory reactions that progress the umbilicus. Involvement of the urachus is usually followed
through neutrophilic to mononuclear stages. The organism may by cystitis and associated signs of dysuria, stranguria, and
penetrate the lymphatics and proliferate in mesenteric lymph hematuria. Other common severe sequelae include septicemia,
nodes. After an incubation period of a year or more, some of the pneumonia, peritonitis, septic arthritis (joint ill), meningitis,
carriers will progress to clinical disease manifested by fibrotic osteomyelitis, uveitis, endocarditis, and diarrhea.
and hyperplastic changes in the ileum, leading to the classic
thickening in the region. Gut changes result in intermittent di- Epizootiology and transmission. Many cases occur in
arrhea, with subsequent dehydration, electrolyte imbalances, neonates, and most cases occur within the first 3 months of age.
and malnutrition, although this clinical sign is more common in Cleanliness of the birthing and housing environment and suc-
cattle than in sheep or goats. cessful transfer of passive immunity are important factors in the
occurrence of the disease. Dystocia resulting in weak neonates
Necropsy and diagnosis. The ileum from infected cattle is can be a factor predisposing to the development of the disease.
grossly thickened; this is not seen in sheep and goats. Ileal and Navel ill is diagnosed by typical clinical signs. The presence
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 559

of microabscesses and palpation of the umbilical area for firm may invade the bloodstream, causing disseminated septicemia.
intra-abdominal structures extending from the umbilicus are ab- Clinically, the lambs may exhibit nasal discharge of mucopuru-
normal. Assessment of colostral immunoglobulin transfer may lent to hemorrhagic exudate, hyperthermia, coughing, dyspnea,
contribute to determination of the prognosis. Navel ill should anorexia, and depression. With the respiratory form, ausculta-
always be considered for young ruminants with fever of un- tion of the thorax suggests dullness and consolidation of an-
known origin during the first week of life and for slightly older teroventral lobes; this will be confirmed by radiographs. The
lambs, kids, or calves that are not thriving. Arthrocentesis of af- disease is diagnosed by clinical signs, blood cultures from sep-
fected joints and culture of the fluid for identification of the ticemic animals, blood smears showing bipolar organisms, and
pathogen are also diagnostic options and essential for effective history of predisposing stressors. In cultures, P. hemolytica is
antimicrobial selection. distinguished from P. multocida by hemolysis on blood agar;
only P. multocida produces indole.
Differential diagnosis. The major differential is an umbilical
hernia, which will typically not be painful or infected and can Epizootiology and transmission. The organism is ubiquitous
often be reduced. Mycoplasmal arthritis is a differential in kids. in the environment and in the respiratory tracts of these animals.
In the past, Erysipelothrix rhusopathiae was a common navel ill Younger ruminants, between 2 and 12 months of age, are es-
pathogen in sheep. pecially prone to infection during times of stress, such as
weaning, transportation, dietary changes, weather changes,
Treatment. Omphalitis can be treated with a 10 to 14 day and overcrowding. The pneumonic form appears as a complex
course of broad-spectrum antibiotics such as ampicillin, amoxi- associated with concurrent infections such as parainfluenza 3,
cillin, penicillin, ceftiofur, florfenicol, and erythromycin. If an adenovirus type 6, respiratory syncytial virus, mycoplasmas,
isolated abscess is palpable, it should be surgically opened and chlamydia, Pasteurella multocida and Bordetella parapertussis
repeatedly flushed with iodine solutions. Surgical reduction of (Martin, 1996; Brogden et al., 1998). The organism is transmit-
the infected umbilicus is indicated if intra-abdominal structures ted between animals by direct and indirect contact, through in-
are involved. The prognosis for recovery is good if systemic in- halation or ingestion.
volvement has not occurred.
Necropsy findings. Necropsy lesions include areas of necrosis
Prevention and control. The disease is best prevented and and hemorrhage in the small intestines and multifocal 1 mm le-
controlled by providing clean birthing environments, ensuring sions distributed on the surfaces of the lungs and liver. With the
adequate colostral immunity, thoroughly dipping the umbilicus pneumonic form, serofibrinous exudates fill the alveoli; ventral
of newborns in tincture of iodine or strong iodine solution lung lobes are consolidated and are congested and purple-gray
(Lugol's), monitoring for dystocias, and maintaining young in color. Fibrinous pleuritis, pericarditis, and hematogenously
growing animals in noncontaminated environments. induced arthritis also may be evident..

Research complications. The disease can be costly to treat, Pathogenesis. A leukotoxin is considered to be a key factor in
and the toll taken on young animals due to the consequences of the pathogenesis of the P. hemolytica infection. Macrophages
systemic infection may detract from their research value. and neutrophils are lysed by the toxin as they arrive at the lung,
and the enzymes released by the neutrophils cause additional
damage to the tissue.
Pasteurellosis (Shipping Fever, Hemorrhagic
Septicemia, Enzootic Pneumonia)
Treatment. Treatment may include the use of antibiotics such
Etiology. Pasteurella hemolytica and P. multocida are aerobic, as penicillin, ampicillin, tylosin, sulfonamides, or oxytetracy-
nonmotile, non-spore-forming, bipolar, gram-negative rods. cline. Newer antibiotics, such as ceftiofur, tilmicosin, spectino-
Biotype A serotypes are associated with pneumonia and sep- mycin, and florfenicol, are very effective and approved for use
ticemia in all ruminants (Ellis, 1984). Serotype 1 of P. hemolyt- in cattle. In outbreaks, cultures from fresh necropsies are help-
ica is considered a major cause of pulmonary lesions of bovine ful for determining sensitivities useful for the remaining group.
bronchopneumonia and fibrinous bronchopneumonia.
Prevention and control. The incidence of disease can be de-
Clinical signs. Pasteurellosis is an acute bacterial disease creased by minimizing the degree of stress; by improving man-
characterized by bronchopneumonia, septicemia, and sudden agement, such as nutrition and control of parasitism; and, in
death. The organism invades the mucosa of the gastrointestinal cattle and sheep, by vaccinating for viral respiratory infections
tract or respiratory tract and causes localized areas of necrosis, such as parainfluenza. Early Pasteurella hemolytica bacterin
hemorrhage, and thrombosis. The lungs and liver are frequent vaccines for use in cattle are not considered effective, but newer
areas of formation of microabscesses. Acute rhinitis or pharyn- products based on immunizing against the leukotoxin and some
gitis often precedes the respiratory form. The organism also bacterial capsule surface antigens are effective. Pasteurella
560 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

multocida bacterins and live streptomycin-dependent mutant culturing fresh feces or at necropsy. Because of intermittent
vaccines are available. In young animals, passive immunity is shedding of organisms, culture may be difficult; repeated cul-
protective. Preventive measures also include maintaining good tures are recommended. Leukopenia and a degenerative shift to
ventilation in enclosures and barns. New animals to the flock the left are not uncommon hematological findings.
or herds should be quarantined for at least 2 weeks before
introduction. Epizootiology and transmission. Stresses associated with re-
cent shipping, overcrowding, and inclement weather may pre-
dispose the animal to enteric infection. Birds and rodents may
aa. Salmonellosis
be natural reservoirs of Salmonella in external housing envi-
Etiology. Salmonella typhimurium is a motile, aerobic to fac- ronments. Transmission is fecal-oral. After ingestion, the or-
ultatively anaerobic, non-spore-forming, gram-negative bacil- ganisms may proliferate throughout the gastrointestinal tract
lus and is the organism associated with enteric disease and some and may penetrate the mucosa of the intestines, invade the
abortions in ruminants. It is a common inhabitant of the gas- Peyer's patches and lymphatics, and migrate to the spleen, liver,
trointestinal tract of ruminants. Current nomenclature catego- and other organs. Animals that survive may become chronic
rizes S. typhimurium as a serovar within the species S. enteri- carriers and shedders of the organisms, and this has been
tidis (the other two species are S. typhi and S. choleraesuis). demonstrated experimentally (Arora, 1983). Fecal-oral trans-
Salmonella typhimurium, S. dublin, and S. newport are the mission is also associated with Salmonella abortion; veneral
common species seen in bovine cases. Salmonella typhimurium, transmission has not been reported.
S. dublin, S. anatum, and S. montevideo are seen in ovine and
caprine cases, although a host-adapted species has not been Necropsy findings and diagnosis. Animals will have notice-
identified in the goat. Ovine abortions due to various Salmo- able perineal staining. Intestines (particularly the ileum, cecum,
nella species are not reported in the United States but are en- and colon) may contain mucoid feces with or without hemor-
zootic in other countries. Salmonella serotypes have been asso- rhages. Petechial hemorrhages and areas of necrosis may be no-
ciated with aborted fetuses in all ruminant species. ticed on the surface of the liver, heart, and mesenteric lymph
nodes. The wall of the intestines, gallbladder, and mesenteric
Clinical signs and diagnosis. Salmonellosis causes acute gas- lymph nodes will be edematous, and a pseudodiphtheritic mem-
troenteritis, dysentery, and septicemia (Anderson and Blan- brane lining the distal small intestines and colon may be ob-
chard, 1989). Clinically, the animals become anorexic and hy- served. This membrane is not normally seen in the goat (Smith
perthermic. Diarrhea or dysentery develops; feces may contain and Sherman, 1994). Splenomegaly may be present. Aborted
mucus and/or blood and have a putrid odor. Animals become fetuses will often be autolysed. Placentitis, placental necrosis,
severely depressed and weak, losing a high percentage of their and hemorrhage are commonly seen. Serologic evidence of re-
body weight. Animals may die in 1-5 days because of dehydra- cent infection can be demonstrated in the dam. Salmonella can
tion associated with dysenteric fluid loss, septicemia, shock, be isolated from the aborted tissues.
and acidosis. Morbidity may be 25%, and mortality may be
high. Septicemia may result in subsequent meningitis, poly- Pathogenesis. After ingestion, the organism proliferates in
arthritis, and pneumonia. Chronically infected animals may the intestine. Damage to the intestines and the resulting diarrhea
have intermittent diarrhea. are due to the bacterial production of cytoxin and endotoxin.
In goats, salmonellosis may be recognized as diarrhea and Although the Salmonella organisms will be taken up by phago-
septicemia in neonates, as enteritis in preweaned kids and ma- cytic cells involved in the inflammatory response, they survive
ture goats, and, rarely, as abortion. Adult cases may be sporadic, and multiply further. Septicemia is a common sequela, with the
with intermittent bouts of diarrhea, subacute or even chronic. bacteria localizing throughout the body. In latently infected
Morbidity and mortality will be highest in neonates, and some animals, it is often shed from the gallbladder and mesenteric
may simply be found dead. The older animals generally tend to lymph nodes. Younger animals may be susceptible because of
fare better during the disease. Abdominal distension with pro- immature immunity and intestinal flora and higher intestinal
fuse yellow feces is common. Kids become severely depressed, pH. Carriers may develop clinical disease when stressed.
anorexic, febrile (with temperatures as high as 106~176
dehydrated, acidotic, recumbent, and comatose. Differential diagnoses. In young animals, differentials include
Salmonella abortions may occur throughout gestation. There other enteropathogens: Escherichia coli, rotavirus and coron-
may not be any other clinical signs, or abortion may be seen avirus, clostridia, cryptosporidia, and other coccidial forms.
with diarrhea, fever, and vulvar discharges. Hemorrhage, pla- These pathogens may also be present in the affected animals.
cental necrosis, and edema will be present. Metritis and placen- Differentials in adults include bovine viral diarrheas and winter
tal retention may occur. Some mortality of dams may occur. dysentery in cattle and parasitemia and enterotoxemia in all
Diagnosis is based on clinical signs and can be confirmed by ruminants.
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 561

Prevention and control. Affected animals should be isolated negative, rod-shaped bacterium. Type A is more virulent than
during herd outbreaks. Samples for culture should include herd- type B.
mates, water and feed sources, recently arrived livestock (other
species), and area wildlife, including birds and rodents. Re- Clinical Signs. Although tularemia is a disease of livestock,
peated cultures, culling of animals, intensive cleaning, and dis- pets, and wild animals, sheep are most commonly affected. The
infection of facilities are all important during outbreaks. The disease is characterized by hyperthermia, muscular stiffness,
bacteria survive for about a week in moist cow manure. Vacci- and lymphadenopathy. Infected animals move stiffly, are de-
nation using the commercially available killed bacterin or au- pressed, and are hyperthermic. Anemia and diarrhea may de-
tologous bacterins may be useful in outbreaks involving preg- velop, and infected lymph nodes enlarge and may ulcerate.
nant cattle, although the J-5 bacterin is now considered better. Mortality may reach 40%. Animals that recover will have im-
munity of long duration.
Treatment. Nursing care includes rehydration and correction
of acid-base abnormalities. Antibiotic therapy may be useful in Epizootiology and transmission. The disease is most com-
cases with septicemia, but it is controversial because it may in- monly transmitted by ticks or biting flies. The wood tick, Der-
duce carrier animals. Gentamicin, trimethoprim-sulfadiazine, macentor andersoni, is an important vector in transmitting the
ampicillin, enrofloxacin, and amikacin antibiotics may be disease in the western United States, and, as natural hosts, wild
successful. rodents and rabbits tend to be reservoirs of the pathogen.

Research complications. Salmonellosis is zoonotic, and some Pathogenesis. The organisms, entering the tick bite wound,
serotypes of the organism have caused fatalities even in im- move via lymphatics to lymph nodes and subsequently to the
munocompetent humans. Attempts should be made to identify bloodstream, where they cause septicemia. The organisms can
and cull carrier animals. also be transmitted orally through contaminated water.

Necropsy findings. Ticks may also be present on the car-

bb. Spirochete-Associated Abortion in Cattle
casses. Suppurative, necrotic lymph nodes are typical. Lungs
(Epizootic Foothill Abortion)
will be congested and edematous. Diagnosis is confirmed by
Etiology. Spirochete-like organisms are associated with this prompt culturing of the organism from lymph nodes, spleen, or
disease; it is now recognized that the agent is not a chlamydial liver where granulomatous lesions form; P. tularensis does not
organism. The disease has been reported only in the foothills survive for long periods in carcasses. Serological findings may
bordering the central valley of California. also be helpful.

Clinical signs. Cows that become infected with the causative Treatment. Infected animals can be treated with oxytetracy-
agent before 6 months of gestation abort or give birth to weak cline, aminoglycosides, or cephalosporins.
calves without any clinical sign of infection. Cows infected af-
ter 6 months of gestation give birth to normal calves. Affected Differential diagnosis. When tick infestations are heavy,
cows rarely abort in subsequent pregnancies. P. tularensis should be suspected. Pasteurella haemolytica
(sheep), Haemophilus somnus (cattle), and Mycoplasma my-
Epizootiology and transmission. The tick vector is Ornitho- coides (goats), and anthrax (all ruminant species) should be
dorus coriaceus. considered as differentials.

Necropsy. Fetuses show several pathological changes, in- Control and prevention. Eliminating the tick vectors can pre-
cluding enlargement of the cervical lymph nodes, spleen, and vent tularemia. Animals should be provided with fresh water
liver. The calf's thymus will be small, and histologically there frequently. The organism can survive in freezing conditions and
will be losses of thymic cortical lymphocytes. Histologic in water and mud for long periods of time. Caretakers, veteri-
changes in lymph nodes and spleen include vasculitis, necrosis, narians, and researchers should take special precautions before
and histiocytosis. handling the tissues of infected sheep, because this is a method
of zoonotic spread.
Treatment. Chlortetracycline treatment has been effective in
controlling this disease. Research complications. The disease is zoonotic, and trans-
mission to people may result from tick bites or from handling
contaminated tissues. Although not a major disease of concern
cc. Tularemia
in sheep, researchers using potentially infected animals from
Etiology. Tularemia is caused by Pasteurella (Francisella) western range states of the United States should be aware of it.
tularensis a nonmotile, non-spore-forming, aerobic, gram- The organism is antigenically related to Brucella spp.
562 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

dd. Yersinia Research complications. Yersinia is zoonotic. The risk of se-

vere enteric disease is considered particularly great for im-
Etiology. Yersiniosis is caused by infections with Yersinia en-
munocompromised persons.
terocolitica, a gram-negative, aerobic, and facultative anaerobe
of the family Enterobacteriaceae. There are 50 serotypes re-
ported for Y. enterocolitica. Yersinia pseudotuberculosis infec-
ee. Mycoplasmal Diseases
tions have also been seen in ruminants. Enteric infections pre- i. Mycoplasma bovigenitalium and M. bovis infections
dominate in the diseases caused by these bacteria.
Etiology. Mycoplasma bovigenitalium and M. bovis are asso-
Clinical signs and diagnosis. Clinical disease may be seen ciated sporadically with bovine infertility and abortions. This
rarely in many groups of ruminants. Goats of 1-6 months old pathogen has also been reported associated with similar clinical
suffer from the enteric form of the disease, which is character- signs in sheep and goats.
ized by sudden death or the acute onset of watery diarrhea last-
ing 1 or more days. Spontaneous abortions and weak neonates Clinical signs and diagnosis. Infertility is more commonly
are also clinical manifestations of infection. Lactating does may caused by M. bovigenitalium infections, and granular vulvo-
have mastitis that becomes chronically hemorrhagic. Bac- vaginitis and endometritis will be present. Granular vulvo-
teremia results in internal abscesses, abortion, and acute deaths. vaginitis is characterized by raised papules on the mucous
Yersinia pseudotuberculosis has been associated with labora- membranes and mucopurulent exudate. Abortions and mastitis
tory goat epizootics (Obwolo, 1976). Diarrhea in pastured are associated with M. bovis infections. Calves that are born
sheep, stressed by other factors, has also been reported. Diag- may be weak.
nosis is based on culture and serology. It is rare to have a definitive diagnosis of an abortion due to
Mycoplasma. After consideration of other causes of abortion
Epizootiology and transmission. The bacteria are carried by and evaluation of tissues for placentitis or fetal inflammation,
wild birds and rodents, and transmission is by ingestion of con- diagnosis is confirmed by isolation of Mycoplasma from the
taminated feed and water. genital tract or aborted tissues.

Necropsy findings. Edema of mesenteric lymph nodes is Epidemiology and transmission. Mycoplasmal species are
the most common postmortem finding. Liver abscesses, micro- considered ubiquitous, are carried in the genital tracts of males
absecesses in the intestines, and granuloma formation have also and females, and are transmitted during natural breeding or
been reported. Placentas are white, with opaque white foci through contaminated insemination materials. Aerosols also
found on cotyledons. Histologically, suppurative placentitis and serve as a means of transmission. In addition, transmission oc-
suppurative pneumonia are found in the fetal tissue. curs by passage through the birth canal, by direct contact, and
by contamination from urine of infected animals.
Pathogenesis. After ingestion, the bacteria cause an enteric
infection, and bacteremia follows. Pathophysiology. Experimental infections of M. bovis have
resulted in placentitis and fetal pneumonia.
Differential diagnoses. Other causes of abortions, including
abortion storms, acute deaths, enteritis, neonatal deaths, and Differential diagnoses. Acholeplasma, Ureaplasma, and Hae-
white foci on cotyledons, should be considered. In young ani- mophilus somnus are differentials for granular vulvovaginitis.
mals, differentials include coccidiosis and nematode parasitism.
Corynebacterium pseudotuberculosis and tuberculosis are dif- Treatment. Fluoroquinolone antibiotics may be useful for
ferentials for the internal abscesses. treating Mycoplasma-induced reproductive diseases.

Prevention and control. Control measure are not well defined, ii. Mycoplasma ovipneumoniae (ovine mycoplasmal
because the epidemiology of the disease is poorly understood pneumonia)
(Smith and Sherman, 1994). Tissues from affected goats must Etiology. Mycoplasma ovipneumoniae causes acute or
be handled and disposed of properly. Areas housing affected chronic pneumonia in lambs.
goats must be thoroughly sanitized.
Clinical signs. Mycoplasmas induce serious diseases in
Treatment. In case of an abortion storm, treatment of goats sheep, causing pneumonia, conjunctivitis, and genitourinary
with tetracycline has been useful. Other broad-spectrum antibi- disease. The disease may be coincidental with pasteurellosis.
otics may also be useful. Respiratory distress, coughing, and nasal discharge are ob-
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 563

served in infected animals. Bronchoalveolar lavage followed bidity and mortality characteristics of mycoplasmal infectious,
by culture is the best method for diagnosis (mycoplasmas are make these infections economically important diseases. Con-
fastidious organisms requiring special handling techniques). siderable attention is presently given to this genus as a source of
Mycoplasmas are isolated from the genitourinary tract of morbidity and mortality in goats.
sheep. Vulvovaginitis and reproductive problems are associated
conditions. iv. Mycoplasma conjunctivae (mycoplasmal keratoconjunc-
tivitis)
Treatment. Tylosin, quinolones, oxytetracycline, and genta- Etiology. Mycoplasma conjunctivae causes infectious con-
micin are good choices for therapy. junctivitis, or pinkeye, in sheep and goats with associated hy-
peremia, edema, lacrimation, and corneal lesions. Mycoplasma
Prevention. No vaccine is available. mycoides subsp, mycoides, M. agalactiae, M. arginini, and
Acholeplasma oculusi have also been associated with kerato-
iii. Mycoplasma mycoides biotype F38 (contagious caprine conjunctivitis in these species. Respiratory disease and other in-
pleuropneumonia, caprine pneumonia, pleuritis, and pleuro- fections, such as mastitis, may also be observed.
pneumonia)
Etiology. Mycoplasma mycoides biotype F38 is the agent of Clinical signs and diagnosis. All ages of animals may be af-
contagious caprine pleuropneumonia and is found worldwide. fected. Initially, lacrimation, conjunctival vessel injection, and
In the United States, caprine pneumonia is also caused by M. then keratitis and neovascularization are seen. Sometimes
ovipneumoniae, M. mycoides subsp, capri, and M. mycoides uveitis is evident. Although the presentation is usually unilat-
subsp, mycoides (large colony type). eral, bilateral involvement is possible. Recurring infections are
common. Culturing provides the better diagnostic information,
Clinical signs. Contagious caprine pleuropneumonia is char- and cultures will be positive even after clinical signs have
acterized by severe dyspnea, nasal discharge, cough, and fever diminished.
(McMartin et al., 1980). Infections with other Mycoplasma spe-
cies also have similar clinical signs. Septicemia without respi- Epizootiology and transmission. The infection is passed eas-
ratory involvement may also be a presentation. ily between animals by direct contact. Animals can become re-
infected, and carrier animals may be a factor in outbreaks.
Epizootiology and transmission. This disease is highly conta-
gious, with high morbidity and mortality. Transmission is by Necropsy. It is unlikely that animals would die or be eutha-
aerosols. Mycoplasma mycoides subsp, mycoides has become a nized and undergo necropsy for this problem. Conjunctival
serious cause of morbidity and mortality of goat kids in the scrapings would include neutrophils during earlier stages and
United States. lymphocytes during later stages. Epithelial cell cytoplasm
should be examined for organisms.
Necropsy. Large amounts of pale straw-colored fluid and
fibrinous pneumonia and pleurisy are typical. Some lung con- Differential diagnosis. The primary differential in sheep and
solidation may be present. Meningitis, fibrinous pericarditis, goats is Chlamydia, as well as Branhamella, Rickettsia (Cole-
and fibrinopurulent arthritis may also be found. Diagnosis is siota) conjunctivae, and infectious bovine rhinotracheitis in
usually made at necropsy by culture of the organism from lungs goats only. It is important to consider these differentials if
and other internal organs. arthritis, pneumonia, or mastitis is present in the group or the
individual.
Differential dagnosis. In the United States, the principal dif-
ferential for M. mycoides subsp, mycoides is caprine arthritis Treatment. Animals do recover spontaneously within about
encephalitis. 10 weeks. Tetracycline ointments and powders are also used.
Third-eyelid flaps may be necessary if corneal ulceration
Treatment. Tylosin and oxytetracycline are effective. Some develops.
infections are slow to resolve.
Prevention and control. New animals should be quarantined
Prevention and control. Vaccines are available in some areas. and, if necessary treated, before introduction to the flock or herd.
Infected herds are quarantined. New goats should be quaran-
tined before introduction to the herd.
ff. Rickettsial Diseases
Research complications. The worldwide distribution of the i. Eperythrozoonosis (Eperythrozoon, Haemobartonella)
F38 biotype, as well as the aerosol transmission and high mor- Etiology. Eperythrozoonosis is a rare, sporadic, noncontagious,
564 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

blood-borne disease in ruminants worldwide caused by the has resulted in transient hyperthermia, mild respiratory disease,
rickettsial agent Eperythrozoon. Host-specific species of im- and mastitis. Abortions, stillbirths, and births of weak lambs are
portance are E. ovis, the causative species in sheep and goats, also seen.
and E. wenyoni, E. tegnodes, and E. tuomii, the causative agents
in cattle. Although the disease is of minor importance, it can Epizootiology and transmission. Coxiella burnetii is ex-
cause severe anemia and debilitation in affected animals. Hae- tremely resistant to environmental changes as well as to disin-
mobartonella bovis is also rare, and is usually found only in as- fectants; persistence in the environment for a year or longer is
sociation with other rickettsial diseases. possible. The organism is associated with either a free-living or
an arthropod-borne cycle. Coxiella burnetii is found in a variety
Clinical signs and diagnosis. The disease is more severe in of tick species, such as ixodid or argasid, where it replicates
sheep. Following an incubation period of 1-3 weeks, infected and is excreted in the feces. Once introduced into a mammal,
animals exhibit episodic hyperthermia, weakness, and anemia. Coxiella may be maintained without a tick intermediate. The
Losses may be greater in younger lambs. Cattle are usually la- organism is especially concentrated in placental tissues, repli-
tently infected but may have swollen and tender teats and legs. cates in trophoblasts, and will be in reproductive fluids. Addi-
Fever, anemia, and depression will be present if the cattle are tionally, the organism is shed in milk, urine, feces, and oronasal
stressed by another systemic disease. Diagnosis is based on secretions.
clinical evidence of anemia and is confirmed by observing the
rickettsiae on the surface of red blood cells in a blood smear. Necropsy findings. No specific lesion will be seen in aborted
or stillborn fetuses, but necrotizing placentitis will be a finding
Epizootiology and transmission. The rickettsial organisms in cases of abortion. The placenta will contain white chalky
are transmitted typically to young sheep by biting insects, plaques and a red-brown exudate. The disease can be diagnosed
ticks, contaminated needles or blood-contaminated surgical by identifying the rickettsial organisms in smears of placental
instruments. secretions. The organism has been found in the placentas of
clinically normal animals. The organism stains red with modi-
Necropsyfindings. Necropsy findings include splenic enlarge- fied Ziehl-Neelsen and Macchiavello stains and purple with
ment and tissue icterus. Giemsa stain.

Pathogenesis. The organism invades and destroys red blood

Differential diagnosis. Because of the organisms' similarity
cells. It is believed that intravascular hemolysis and erythro-
to Chlamydia, confirmation must be made by culture tech-
phagocytosis contribute to the macrocytic anemia. As with
niques, immunofluorescent procedures, ELISA, and comple-
other red blood cell parasites, splenectomy aggravates the
ment fixation tests.
disease.
Treatment. Coxiella can be treated with oxytetracyclines. A
Differential diagnosis. Clontridium novyi type D, babesiosis,
vaccine is not commercially available.
and leptospirosis are the primary differentials.

Prevention and control. Following strict sanitation practices Prevention and control. Any aborting animals should be seg-
for surgical procedures and controlling external parasites pre- regated from other animals, and other pregnant animals should
vent the disease. be treated prophylactically with tetracycline. Serologic screen-
ing of ruminant sources should be performed routinely. Barrier
Treatment. Treatment is not usually recommended, but oxy- housing, a review of ventilation exhaust, and defined handling
tetracycline has been used. Sheep will develop immunity if sup- procedures are often required. All placentas and all aborted tis-
ported nutritionally during the disease. sues should be handled and disposed of carefully. Q fever has
been reported in many mammalian species, including cats.
Research complications. Splenectomized animals are the ex-
perimental models used to study these diseases. Research complications. Coxiella burnetii-free animals are
particularly important in studies involving fetuses and placen-
ii. Q fever, or query fever (Coxiella burnetii) tation. Because of its zoonotic potential, C. burnetii presents a
Etiology. Coxiella burnetii is a small, gram-negative, obligate unique problem in the animal research facility environment. A
intracellular rickettsial organism that causes query fever and is single organism has been shown to cause disease. Some of the
regarded as a major cause of late abortion in sheep. greatest concerns are the risk to immunocompromised individ-
uals, pregnant women, and other animals, and the presence of
Clinical signs. Infection of ruminants with C. burnetii is usu- carrier animals or those that may shed the organism in placen-
ally asymptomatic. Experimental inoculation in other mammals tas, for example.
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 565

2. Viral Diseases If animals are pregnant, the virus crosses the placenta and
causes central nervous system lesions. Abortions may occur at
a. Adenovirus Infections any stage of gestation in cattle. Prolonged gestation may result
Etiology. The ruminant adenoviruses are DNA viruses that from cerebellar hypoplasia and lack of normal sequence to in-
cause respiratory and reproductive tract diseases. Nine anti- duce parturition. Cerebellar hypoplasia will also be present in
genic types of the bovine adenovirus have been identified, with young born of the infected dams, as well as hydrocephalus,
type 3 associated with respiratory disease. Two of the ovine and cataracts, gingival hyperplasia, or arthrogryposis.
two of the caprine antigenic types have been identified. Diagnosis is suspected with the characteristic clinical signs
and exposure to viral vectors. Virus isolation is the best diag-
Clinical Signs. Signs of infection range from subclinical to nostic approach if blood is collected during the febrile stage
severe, including pneumonia, enteritis, conjunctivitis, kerato- of the disease or brains from aborted fetuses. Fluorescent anti-
conjunctivitis, weak calf syndrome, and abortion. Respiratory body tests, ELISA, virus neutralization tests, PCR, and agar gel
tract and intestinal tract diseases may be concurrent. Infections immunodiffusion (AGID) tests are also used to confirm the
caused by this virus are often found associated with other viral diagnosis.
and bacterial infections.
Epizootiology and transmission. Severe outbreaks have oc-
Epizootiology and transmission. The virus is believed to be curred in other countries during this century. Screening for this
widespread, but prevalence and characteristics of infection have disease has limited the strains present in the United States. The
not been characterized. Transmission of adenoviruses in other disease is most common in outdoor-housed animals primarily
species (e.g., canine) is by aerosols or fecal-oral routes. in the western United States. The virus is primarily transmitted
by biting midges, Culicoides. Culicoides variipennis is the most
Necropsy findings. Lesions found after experimental infec- common vector in the United States. A combination of factors
tions include atelectasis, edema, and consolidation of the lungs. associated with viral strain, available and susceptible hosts, en-
vironmental conditions (such as damp areas where flies breed),
and vector presence are factors in the severity of outbreaks. The
b. Bluetongue Virus Infection (Reoviridae)
disease is rarely transmitted by animal-to-animal contact or by
Etiology. The bluetongue virus is an RNA virus in the Or- infected animal products. Virus-contaminated semen, transpla-
bivirus genus and Reoviridae family. Five serotypes (2, 10, 11, cental transfer, and carriage on transferred embyros are other
13, and 17) have been identified in the United States, where it is possible means of transmission.
seen mostly in western states. Bluetongue is an acute arthropod-
borne viral disease of ruminants, characterized by stomatitis, Necropsy findings. At necropsy, erosive lesions may be ob-
depression, coronary band lesions, and congenital abnormali- served around the mouth, tongue, palate, esophagus, and pillars
ties (Bulgin, 1986). of the rumen. Ulceration or hyperemia of the coronary bands
may also be seen. Many of the internal organs will contain pe-
Clinical signs and diagnosis. Sheep are the most likely to techial and ecchymotic hemorrhages of the surfaces, and hem-
show clinical signs. Clinical disease is less common in goats orrhage may be seen at the base of the pulmonary artery.
and cattle. Early in the infection, animals will spike a fever and
will develop hyperemia and congestion of tissues of the mouth, Pathogenesis. The virus multiplies in the hemocoel and sali-
lips, and ears. The virus name, bluetongue, is associated with vary glands of the fly and is excreted in transmissible form in
the typical cyanotic membranes. The fever may subside, but tis- the insect's saliva. After entering the host, the virus causes pro-
sue lesions erode, causing ulcers. Increased salivary discharges longed viremia. The incubation period is 6 - 1 4 days. The virus
and anorexia are often related to ulcers of the dental pad, lips, migrates to and attacks the vascular endothelium. The resulting
gums, and tongue, although salivation and lacrimation may pre- vasculitis accounts for the lesions of the skin, mouth, tongue,
cede apparent ulceration. Chorioretinitis and conjunctivitis are esophagus, and rumen and the edema often found in many tis-
also common signs in cattle and sheep. Lameness may be ob- sues. Ballooning degeneration of affected tissues, followed by
served associated with coronitis and is evident in the rear legs. necrosis and ulceration, occurs. The effects on fetuses appear to
Skin lesions such as drying and cracking of the nose, alopecia, be due to generalized infections of developing organs.
and mammary glands are also observed. Secondary bacterial
pneumonia may also occur. Animals may also develop severe Differential diagnosis. Differentials include other infectious
diarrhea and become recumbent. Sudden deaths due to car- vesicular diseases such as foot-and-mouth disease, contagious
diomyopathy may occur at any time during the disease. Hema- ecthyma, bovine viral diarrhea virus-mucosal disease, infec-
tologically, animals will be leukopenic. The course of the dis- tious bovine rhinotracheitis, bovine papular stomatitis, and ma-
ease is about 2 weeks, and mortality may reach 80%. lignant catarrhal fever. Rinderpest is a differential in countries
566 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

where it is endemic. Photosensitization should be considered. effects of the masses are loss of condition, dysphagia, rumen
Foot rot is a differential for the lameness and coronitis. Differ- tympany, and fatal bloat. The cutaneous presentation has a
entials for the manifestations such as arthrogryposis include longer course and may wax and wane. The masses are found at
border disease virus and genetic predispositions of some breeds the anus, vulva, escutcheon, shoulder, and flank; they are
such as Charolais cattle and Merino sheep. painful when palpated, raised, and often ulcerated. The animals
are anemic, and neoplastic involvement may affect cardiac
Prevention and control. Cellular and humoral immunity are function. Generalized or limited lymphadenopathy may be
necessary for protection from infection. The bluetongue virus is apparent.
insidious because the genome is capable of reassortment, and Only the adult, or enzootic, form of bovine lymphosarcoma is
some vaccines will not have the antigenic components repre- associated with BLV infection. Many animals do not develop
sented in the local infection. In addition, there is little to no any malignancies or clinical signs of infection and simply re-
cross protection between strains. Modified live vaccines are main permanently infected. Some cows manifest disease only
available in some parts of the United States but should not be during the periparturient period. Malignant lymphoma is the
used in pregnant animals. Vaccinating lambs and rams in an more common, whereas leukosis, due to B-lymphocyte prolif-
outbreak is worthwhile, for example, but vaccinating late- eration, is rare. Clinical signs are loss of condition and a drop in
gestation ewes may cause birth defects or abortions. Congenital production of dairy cattle, anorexia, diarrhea, ataxia, paresis,
defects are more common from vaccine use than from naturally and other signs dependent on the location of the neoplastic tis-
occurring infection. Minimizing exposure to the vector in en- sue. Tumors are associated with lymphoid tissues. Common
demic areas will decrease the incidence of the disease. sites also include the abomasum, spinal canal, and uterus. Car-
diac tumors develop at the right atrial or left ventricular my-
Treatment. Supportive care and nursing care are helpful, in- ocardium, and associated beat and rate abnormalities may be
cluding gruels or softer feeds, easily accessed water, and shaded auscultated. The common ocular manifestation of the disease is
resting places. Nonsteroidal anti-inflammatory drugs are often exophthalmos due to retrobulbar masses. Many internal organs
administered. For the cases of secondary bacterial pneumonia may be involved, and tumors may be palpable per rectum. Sec-
and some cases of bluetongue conjunctivitis, antibiotics may be ondary infections will be due to immunosuppression and the
administered. weakened state of the animal.
Sheep have acquired BLV infection naturally and have been
Research complications. This is a reportable disease because used as experimental models; in both situations, this species is
clinical signs resemble foot-and-mouth disease and other exotic susceptible to tumor and leukemia development. Goats sero-
vesicular diseases. convert but do not develop the clinical syndromes.
Diagnosis is based on the animal's age, clinical signs, serol-
ogy, hematology findings according to the form, aspirates or
Bovine Lymphosarcoma (Bovine Leukemia Virus
biopsies of masses, and necropsy findings. Kits are available for
Infection, Bovine Leukosis)
running AGID, for which the BLV antigens gp-51 and gp-24 are
Etiology. Bovine lymphosarcoma refers to lymphoprolifera- used; antibodies may be detected within weeks after exposure
tive diseases in young cattle that are not associated with bovine and may also help in predicting disease in clinically normal cat-
leukemia virus (BLV) infection, and those in older cattle that are tle. ELISA and PCR diagnostic aids will also be helpful.
associated with B LV. B LV is a B lymphocyte-associated retro-
virus (Johnson and Kaneene, 1993a,b,c). Epizootiology and transmission. This disease is present
worldwide. It is estimated that at least 50% of the cattle in the
Clinical signs. Forms of bovine lymphosarcoma that are not United States are infected with BLV. As few as 1% of these an-
associated with BLV infection are calf, or juvenile; thymic, or imals develop lymphosarcoma, but the adult form of the disease
adolescent (animals 6 months to 2 years old); and cutaneous described here is the most common bovine neoplastic disease in
(any age). The calf form is rare and characterized by general- the United States. Larger herds tend to have higher rates. Ge-
ized lymphadenopathy. Onset may be sudden, and the disease is netic predisposition may be involved; in addition to the pres-
usually fatal within a few weeks. Signs include lymphadenopa- ence of BLV, the type of bovine lymphocyte antigen (BoLA)
thy, anemia, weight loss, and weakness. Some animals may be may be correlated to resistance or susceptibility and to the
paralyzed because of spinal cord compression from subpe- course of the disease. Transmission is believed to be by in-
riosteal infiltration of neoplastic cells. The adolescent form is halation of BLV in secretions; in colostrum; horizontally by
also rare, the course rapid, and the prognosis poor. The disease contaminated equipment not sanitized between cattle; and by
is seen most often in beef breeds such as Hereford cattle and is rectum (e.g., mucosal irritation during per-rectum exams or
characterized by space-occupying masses in the neck or thorax. procedures). Natural-service bulls may transmit the infection
These masses are also often present in the brisket. Secondary to cows. Cows infected with BLV may transmit the infection to
14. BIOLOGYAND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 567

their calves in utero. Tabanid and other flies also serve as vec- Epizootiology and transmission. The virus is reported to be
tors, but these represent a minor means of transmission. widespread. Occurrence is often seasonal, and biting insects
may be vectors. Transmission with successful infection requires
Necropsy findings. Neoplastic infiltration of many organs deep penetration of the skin. Transmission may be by con-
and tissues are found in the calf form and the cutaneous forms. taminated milkers' hands, contaminated equipment, and other
Tumors may be local or widely distributed in the enzootic fomites.
form. Definitive diagnosis of neoplastic tissue specimens is by
histology. Differential diagnosis. Differential diagnoses include other
diseases that cause lesions on teats such as pseudocowpox, pa-
Pathogenesis. As with other retroviruses, the BLV integrates pillomatosis, and vesicular stomatitis. Other vesicular diseases
viral DNA into host target cell DNA by means of the reverse may be considered, but other more severe clinical signs might
transcriptase enzyme, creating a provirus. be associated with those.

Prevention and control. There is no vaccine for this disease. Prevention and control. Established milking hygiene prac-
Development and maintenance of a BLV-free herd, or control- tices are important control measures: having milkers wash their
ling infection within a herd, requires financial and program- hands with germicidal solutions or wear gloves, cleaning equip-
matic commitments: BLV-positive and BLV-negative animals ment between animals, and separating affected animals.
maintained separately; serologic testing (such as at least every
Treatment. There is no treatment, and affected animals should
6 months) and separating positive animals; and washing and
be separated from the herd and milked last. Lesions can be
then disinfecting instruments, needles (or using sterile single-
cleaned and treated with topical antibacterials.
use products), and equipment for ear tagging and dehorning and
other such equipment between animals. A fresh rectal exam
sleeve and lubricant should be used for each animal examined. e. Bovine Viral Diarrhea Virus
Otherwise serologically positive cows may have undetectable Etiology. The bovine viral diarrhea virus (BVDV) is a pes-
antibodies during the periparturient period. Embryo transfer re- tivirus of the Flaviviridae family. The Flaviviridae include hog
cipients should be negative, and the virus will not be transferred cholera virus and border disease virus of sheep. The virus con-
by the embryonic stage. Calves should be fed colostrum from tains a single strand of positive-sense RNA. A broad range of
serologically negative cows. disease and immune effects is produced by B VDV only in
cattle. In addition, this virus is important in the etiology of
Treatment. Treatment regimens of corticosteroids and cancer bovine pneumonias. Bovine viral diarrhea/mucosal disease
chemotherapeutic agents provide only short-term improvement. (BVD/MD) is one of the most important viral diseases and one
In cases where ova, embryos, or semen need to be collected, of the most complex diseases of cattle. Strains of BVDV are
supportive care for the affected animals is essential. characterized as cytopathic (CP) and noncytopathic (NCP),
based on cell-culture growth characteristics. The virus has
Research complications. The United States and several coun- also been categorized as type 1 and type 2 isolates. Heterolo-
tries, some in Europe, have official programs for eradication of gous strains exist that may confound even sound vaccination
enzootic bovine leukosis. programs.

Clinical signs and diagnosis. Signs of BVDV infections may

Bovine Herpes Mammillitis (Bovine Herpesvirus 2
be subclinical but also include abortions, congenital abnormal-
Bovine Ulcerative Mammillitis)
ities, reduced fertility, persistent infection (PI) with gradual de-
Etiology. Bovine herpesvirus 2 causes bovine herpes mam- bilitation, and acute and fatal disease. The presence of antibod-
millitis, a widespread disease characterized by teat and udder ies, whether from passive transfer or immunizations, does not
lesions, as well as oral and skin lesions. necessarily guarantee protection from the various forms of the
disease.
Clinical signs and diagnosis. Lesions begin suddenly with An acute form of the disease, caused by type 2 BVDV, occurs
teat swelling; the tissue will be edematous and tender when in cattle without sufficient immunity. After an incubation period
touched. The udder lesions may extend to the perineum. The of 5 - 7 days, clinical signs include fever, anorexia, oculonasal
lesions progress to vesicles, then to ulcers; these may take discharge, oral erosions (including on the hard palate), diarrhea,
10 weeks to heal. Lesions rarely may also develop focally and decreased milk production. The disease course may be
around the mouth and generally on the skin of the udder. Sec- shorter with hemorrhagic syndrome and death within 2 days.
ondary mastitis may occur, because of bacteria associated with Clinical signs of B VDV in calves also include severe enteritis
the scabs. Diagnosis is by clinical signs and serologically. and pneumonia.
568 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

When susceptible cows are infected in utero from gestational be found extending throughout the gastrointestinal tract to the
days 50-100, or gestational cows are vaccinated with a modi- cecum. The respiratory tract lesions will often be complicated
fled live vaccine, abortion or stillbirth result. Congenital defects by secondary bacterial pneumonia. When the hemorrhagic syn-
caused by BVDV during gestational days 90-170 include drome develops, petechiation and mucosal bleeding will be
impaired immunity (thymic atrophy), cerebellar hypoplasia, oc- present.
ular defects, alopecia or hypotrichosis, dysmyelinogenesis, hy-
dranencephaly, hydrocephalus, and intrauterine growth retarda- Pathogenesis. The CP and NCP strains are thought to be re-
tion. Typical signs of cerebellar dysfunction will be evident in lated mutations of the BVDV; the CP short-lived isolates are be-
calves, such as wide-based stance, weakness, opisthotonus, hy- lieved to arise from the NCP strains. The NCP strains are those
perflexion, hypermetria, nystagmus, or strabismus. Some se- present in the PI animals, and the strains are maintained in cat-
verely affected calves will not be able to stand. Ophthalmic ef- tle populations. CP and NCP isolates vary in virulence, and
fects include retinal degeneration and microphthalmia. classification of these types is based on viral surface proteins.
Fetuses can also be infected in utero, normal at birth, im- Considerable antigenic variation also exists between strains and
munotolerant to the virus, and persistently infected (PI). The types. Other viral infections, such as bovine respiratory syncy-
term mucosal disease is commonly associated with this form of tial virus and infectious bovine rhinotracheitis, may also be
the infection. Many PI animals do not survive to maturity, how- present in the same animals.
ever, and many have weakened immune systems. The PI ani- The pathology caused by B VDV is due to its ability to infect
mals are important because they shed virus and will probably epithelial cells and impair the functioning of immune cell pop-
show the clinical signs of mucosal disease (MD) caused by a CP ulations through out the bovine system. In type 2 BVDV hem-
B VDV strain derived from an NCP B VDV strain. These MD orrhagic syndrome, death results from viral-induced thrombo-
clinical signs include fever, anorexia, and profuse diarrhea that cytopenia. In fetuses, the virus infects developing germinal cells
may include blood and fibrin casts, and oral and pharyngeal ero- of the cerebellum. The Purkinje's cells in the granular layer are
sions, as well as erosion at the interdigital spaces and on the killed, and necrosis and inflammation follow. The immune ef-
teats and vulva. Many other associated clinical signs include fects are the result of the virus's interfering with neutrophil and
anemia, bloat, lameness, or corneal opacities and discharges. macrophage functions and of lymphocyte blastogenesis. All
Secondary effects of hemorrhage and dehydration also con- of these predispose the affected animals to bacterial infections
tribute to the morbidity and mortality. Animals that do not suc- with Pasteurella haemolytica. B VDV damages dividing cells
cumb to the disease will be chronically unthrifty, debilitated, in fetal organ systems, resulting in abortions and congenital
and infection-prone. effects.
Diagnosis in affected calves is based on herd health history,
clinical signs, and antibodies to B VDV in precolostral serum. Differential diagnosis. Many differentials must be considered
Viral culturing from blood may be useful. In older animals, oral for the clinical manifestations of B VDV infections. Differen-
lesions, serology, detection of viral antigen, and virus isolation tials for enteritis of calves include viral infections, Crypto-
contribute to the diagnosis. Leukopenia, and especially lym- sporidia, Escherichia coli, Salmonella, and Coccidia. Salmo-
phopenia, are seen. Serology must be interpreted with the nella, winter dysentery, Johne's disease, intestinal parasites,
awareness of the possibility of PI immunotolerant animals. malignant catarrhal fever (MCF), and copper deficiency are dif-
Vaccination against the disease carries its own set of side ef- ferentials for the diarrhea seen in the disease in adult animals.
fects and potential problems, especially when using modified Respiratory tract pathogens such as bovine respiratory syncytial
live vaccines, whether against CP or NCP strains. The condition virus, Pasteurella, Haemophilus, and Mycoplasma must be
of the animals is also a variable. considered for the respiratory tract manifestations. Oral lesions
are also produced by MCF, vesicular stomatitis, bluetongue,
Epizootiology and transmission. BVDV is present throughout and papular stomatitis. Infectious bovine herpesvirus 1, lep-
the world. Transmission occurs easily by direct contact between tospirosis, brucellosis, trichomoniasis, and mycosis should be
cattle, from feed contaminated with secretions or feces, and by considered in cases of abortion.
aborted fetuses and placentas. PI females transmit the virus to
their fetuses. Semen also is a source of virus. Prevention and control. Combined with sound management
in a typical cattle herd, vaccination is the best way to prevent
Necropsy findings. In affected calves, histopathologic find- B VDV and should be integrated into the herd health program,
ings include necrosis of external germinal cells, focal hemor- timed appropriately preceding breeding, gestation, or stressful
rhages, and folial edema. Later in the disease, large cavities de- events. Vaccine preparations for B VDV are modified live virus
velop in the cerebellum, and atrophy of the cerebellar folia and (MLV) or killed virus. Each has advantages and disadvantages.
thin neuropil are evident. Older calves may have areas of intes- The former induces rapid immunity (within 1 week) after a
tinal necrosis. In cases where oral erosions occur, erosions will single dose, provides longer duration of immunity against sev-
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 569

eral strains, and induces serum neutralizing antibodies. MLV and antibodies found in white-tailed deer. Transmission is by
vaccines are not recommended for use in pregnant cattle, may arthropods during the first trimester of pregnancy.
induce mucosal disease, and may be immunosuppressive at the
time of vaccination. The immunosuppression is detrimental if
g. Caprine Arthritis Encephalitis Virus
cattle are concurrently exposed to field-strain virus because it
will facilitate infection and possible clinical disease. The MLV Etiology. Caprine arthritis encephalitis virus (CAEV) occurs
strains may cross the placenta, resulting in fetal infections. The worldwide, with a high prevalence in the United States. Caprine
killed vaccines are safer in pregnant animals but require booster arthritis encephalitis (CAE) is considered the most important
doses after the initial immunization, may need to be given 2 - viral disease of goats. The CAEV is in the Lentivirus genus of
3 times per year, and do not induce cell-mediated immunity. the Retroviridae family. It causes chronic arthritis in adults and
Passive immunity may protect most calves for up to 6 - encephalitis in young. CAEV is in the same viral genus as the
8 months of age. Subsequent vaccination with MLV may pro- ovine progressive pneumonia virus (OPPV).
vide lifelong immunity, but this is not guaranteed. Annual
boosters are recommended to protect against vaccine breaks. Clinical signs and diagnosis. The most common presentation
The virus persists in the environment for 2 weeks and is sus- in goats is an insidious, progressive arthritis in animals 6 months
ceptible to the disfectants chlorhexidine, hypochlorite, iodo- of age and older. Animals become stiff, have difficulty getting
phors, and aldehydes. up, and may be clinically lame in one or both forelimbs. Carpal
Maintenance of a closed herd to prevent any possibility of the joints are so swollen and painful that the animal prefers to eat,
introduction of the virus is difficult. Isolation of new animals, drink, and walk on its "knees." In dairy goats, milk production
avoidance of the purchase of pregnant cows, scrutiny of records decreases, and udders may become firmer.
from source farms, use of semen tested bulls, minimization of This retrovirus also causes neurological clinical signs in
stress, testing of embryo-recipient cows, and maintainenance of young kids 2 - 6 months old. Kids may be bright and alert,
populations of ruminants (smaller or wild species) separately on afebrile, and able to eat normally even when recumbent. Some
the premises will minimize viral exposure. Other management kids may initially show unilateral weakness in a rear limb,
strategies may require a program for testing and culling PI which progresses to hemiplegia or tetraplegia. Mild to severe
cattle. This can be expensive but may be a worthwhile invest- lower motor neuron deficits may be noted, but spinal reflexes
ment to remove the virus shedders from a herd. are intact. Clinical signs may also include head tilt, blindness,
ataxia, and facial nerve paralysis.
Treatment. No specific treatment is available. Supportive care Older animals in the group may experience interstitial pneu-
and treatment with antibiotics to prevent secondary infection monia or chronic arthritis. The pneumonia is similar to the
are recommended. Animals that survive the infection should be pneumonia in sheep caused by OPPV; the course is gradual but
evaluated a month after recovery to determine their status as PI progressive, and animals will eventually lose weight and have
or virus-free. respiratory distress. Some animals in a herd may not develop
any clinical signs.
Diagnosis is based on clinical signs, postmortem lesions, and
f. Cache Valley Virus
positive serology for viral antibodies to CAEV. An agar gel im-
Etiology. Cache Valley virus (CVV), of the arbovirus genus munodiffusion (AGID) test identifies antibodies to the virus and
of the Bunyaviridae family, is a cause of congenital defects in is used for diagnosis. Kids acquire an anti-CAEV antibody in
lambs. colostrum, and this passive immunity may be interpreted as in-
dicative of infection with the virus. The antibody does not pre-
Clinical signs and diagnosis. Teratogenic effects of in utero vent viral transmission.
CVV infection in fetal and newborn lambs include arthrogry-
posis, microencephaly, hydranencephaly, porencephaly, cere- Ep&ootiology and transmission. The virus is prevalent in
bellar hypoplasia, and micromyelia. Stillbirths and mummi- most industrialized countries. The common means of transmis-
fied fetuses are seen. Lambs will be born weak and will act sion, from adults to kids, is in the colostrum and milk in spite of
abnormally. the presence of anti-CAEV antibody in the colostrum. Trans-
Diagnosis is by evidence of seroconversion in precolostral mission may occur among adult goats by contact. Intrauterine
blood samples or fetal fluids, as the result of in utero infection. transmission is believed to be rare. Transmission to sheep has
occurred only experimentally; there is no documented case of
Epizootiology and transmission. The virus is present in the natural transmission.
western United States, although it has been isolated in a few
Midwestern states. Although considered a disease of sheep, Necropsy findings. Necropsy and histopathology reveal a
virus has been isolated from cattle and from wild ruminants striking synovial hyperplasia of the joints with infiltrates of
570 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

lymphocytes, macrophages, and plasma cells. Other histologic Clinical signs and diagnosis. Diseases caused by the virus in-
lesions include demyelination in the brain and spinal cord, with clude conjunctivitis, rhinotracheitis, pustular vulvovaginitis,
multifocal invasion of lymphocytes, macrophages, and plasma balanoposthitis, abortion, encephalomyelitis, and mastitis. The
cells. In severe cases of mastitis, the udder may appear to be respiratory form is known as infectious bovine rhinotracheitis,
composed of lymphoid tissue. and clinical signs may range from mild to severe, the latter par-
ticularly when there are additional respiratory viral infections
Pathogenesis. The virus infects cells of the mononuclear sys- or secondary bacterial infections. The mortality rate in more
tem, resulting in the formation of non-neutralizing antibody to mature cattle is low, however, unless there is secondary bacte-
viral core proteins and envelope proteins. Immune complex for- rial pneumonia. Fever, anorexia, restlessness, hyperemia of the
mation in synovial, mammary gland, and neurological tissue is muzzle, gray pustules on the muzzle (that later form plaques),
thought to result in the clinical changes observed. Most com- nasal discharge (that may progress from serous to mucopuru-
monly, the carpal joint is affected, followed by the stifle, hock, lent), hyperpnea, coughing, salivation, conjunctivitis with ex-
and hip. The infection is lifelong. cessive epiphora, and decreased production in dairy animals are
typical signs. Open-mouth breathing may be seen if the larynx
Differential diagnosis. The differential diagnosis for the neu- or nasopharygneal areas are blocked by mucopurulent dis-
rologic form of CAEV should include copper deficiency, en- charges. Neonatal calves may develop respiratory as well as
zootic pneumonia, white muscle disease, listeriosis, and spinal general systemic disease. In these cases, in addition to the
cord disease or injury. The differential diagnosis for CAEV symptoms already noted, the soft palate may become necrotic,
arthritis should include chlamydia and mycoplasma. and gastrointestinal tract ulceration occurs. Young calves are
most susceptible to the encephalitic form; signs include dull at-
Prevention and control. Herds can be screened for CAE by titude, head pressing, vocalizations, nystagmus, head tilt, blind-
testing serologically, using an AGID or an enzyme-linked im- ness, convulsions, and coma, as well as some signs, such as dis-
munosorbent assay (ELISA) test. The ELISA is purported to be charges, seen with respiratory tract presentations. This form is
more sensitive, whereas the AGID is more specific. Individual usually fatal within 5 days. Abortion may occur simultaneously
animals show great variation in development of antibody. Be- with the conjunctival or respiratory tract diseases, when the res-
cause CAE is highly prevalent in the United States, and because piratory infection appears to be mild, or may be delayed by as
seronegative animals can shed organisms in the milk, retesting much as 3 months after the respiratory tract disease signs. In-
herds at least annually may be necessary. Recently, an immuno- fectious pustular vulvovaginitis is most commonly seen in dairy
precipitation test for CAE has been developed that has high sen- cows, and clinical signs may be mild and not noticed. Other-
sitivity and specificity. wise, signs are fever, depression, anorexia, swelling of the vul-
Control measures include management practices such as test var labia, vulvar discharge, and vestibular mucosa reddened by
and cull, prevention of milk transmission, and isolation of af- pustules. The cow will often carry her tail elevated away from
fected animals. Parturition must be monitored, and kids must be these lesions. These soon coalesce, and a fibrous membrane
removed immediately and fed heat-treated colostrum (56~ for covers the ulcerated area. If uncomplicated, the infection lasts
1 hr). CAEV-negative goats should be separated from CAEV- about 4 - 5 days, and lesions heal in 2 weeks. Younger infected
positive goats. bulls may develop balanoposthitis with edema, swelling, and
pain such that the animals will not service cows.
Treatment. There is no treatment for CAEV.
Epizootiology and transmission. IBRV is widely distributed
throughout the world, and adult animals are the reservoirs of in-
h. Infectious Bovine Rhinotracheitis Virus (Infectious
fection. The disease is more common in intensive calf-rearing
Bovine Rhinotracheitis-Infectious Pustular
situations and in grouped or stressed cattle. Transmission is pri-
Vulvovaginitis)
marily by secretions, such as nasal, during and after clinical
Etiology. The infectious bovine rhinotracheitis virus (IBRV) signs of disease. Modified live vaccines are capable of causing
is also referred to as bovine herpesvirus 1 (BHV-1) and is an al- latent infections.
phaherpesvirus. IBRV causes or contributes to several bovine
syndromes, including respiratory and reproductive tract dis- Necropsy findings. Fibrinonecrotic rhinotracheitis is consid-
eases. It is one of the primary pathogens in the bovine respira- ered pathognomic for IBRV respiratory tract infections. There
tory disease complex. Strains include BHV-I.1 (associated with will be adherent necrotic lesions in the respiratory, ocular, and
respiratory disease), BHV 1.2 (associated with respiratory and reproductive mucosa. When there are secondary bacterial infec-
genital diseases), and BHV 1.4 (associated with neurological tions, such as Pasteurella bronchopneumonia, findings will in-
diseases), which has been reclassified as bovine herpesvirus 5. clude congested tracheal mucosa and petechial and ecchymotic
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 571

hemorrhages in that tissue. Lesions from the encephalitic form Clinical signs and diagnosis. Infections ranging from asymp-
include lymphocytic meningoencephalitis and will be found tomatic to mild signs of upper respiratory tract disease are as-
throughout the gray matter (neuronal degeneration, perivascular sociated with this virus by itself; infections are almost never fa-
cuffing) and white matter (myelitis, demyelination). Intra- tal. Clinical signs include ocular and nasal discharges, cough,
nuclear inclusion bodies are not a common finding with this fever, and increased respiratory rate and breath sounds. In preg-
herpesvirus. nant animals, exposure to PI-3 can result in abortions. Clinical
signs become apparent or more severe when additional viral
Pathogenesis. In the encephalitic form, the virus first grows pathogens are present, such as bovine viral diarrhea virus, or a
in nasal mucosa and produces plaques. These resolve within secondary bacterial infection, such as Pasteurella haemolytica
11 days, and the encephalitis develops after the virus spreads infection, is involved. Greater morbidity and mortality will be
centripetally to the brain stem by the trigeminal nerve dendrites. sequelae of the bacterial infections. Viral isolation or direct im-
Latent infections are also established in neural tissue. munofluorescence antibody (IFA) from nasal swabs can be used
for definitive diagnosis.
Differential diagnosis. The severe oral erosions seen with
BVDV infections are rare with infectious bovine rhinotra- Epizootiology and transmission. The virus is considered
cheitis-infectious pustular vulvovaginitis (IBR-IPV). The con- ubiquitous in cattle and is a common infection in sheep.
junctivitis of IBR may initially be mistaken for that of a Presently it is assumed that the virus is widespread in goats, but
Moraxella bovis (pinkeye) infection; the IBR will be peripheral, firm evidence is lacking.
and there will not be corneal ulceration. Bovine viral diarrhea
virus and IBRV are the most common viral causes of bovine Necropsy findings. For an infection of PI-3 only, findings will
abortion. Differentials for balanoposthitis include trauma from be negligible. Some congestion of respiratory mucosa, swelling
service. of respiratory tract-associated lymph nodes, and mild pneu-
monitis may be noted grossly and histologically. Intranuclear
Prevention and control. Vaccination options include inacti- and intracytoplasmic inclusion bodies may be present in the
vated, attenuated, modified live, and genetically altered prepa- mucosal epithelial cells. Findings will be similar but not as se-
rations. Some are in combination with parainfluenza 3 (PI-3) vere as those caused by bovine respiratory syncytial virus. Im-
virus. The MLV preparations are administered intranasally; munohistochemistry may also be used.
these are advantageous in calves for inducing mucosal immu-
nity even when serologic passive immunity is already present Pathogenesis. PI-3 infects the epithelial mucosa of the respi-
and adequate. Some newer vaccines, with gene deletion, allow ratory tract; however, the disease is often asymptomatic when
for serologic differentiation between antibody responses from uncomplicated.
infection or immunization. Bulls with the venereal form of the
infection will transmit the virus in semen; intranasal vaccine Differential diagnosis. Differentials, particularly in cattle, in-
may be used to provide some immunity. clude infections with other respiratory tract viruses of rumi-
nants: IBRV, BVDV, bovine respiratory syncytial virus, and
Treatment. Uncomplicated mild infections will resolve over a type 3 bovine adenovirus.
few weeks; palliative treatments, such as cleaning ocular dis-
charges and supplying softened food, are helpful in recovery. Prevention and control. Immunization, management, and nu-
Antibiotics are usually administered because of the high likeli- trition are important for this respiratory pathogen, as for others.
hood of secondary bacterial pneumonia. The encephalitic ani- In cattle, modified live vaccines for intramuscular (IM), sub-
mals may need to be treated with anticonvulsants. cutaneous (SC), or intranasal (IN) administration are available.
The IM and SC routes provide immune protection within
1 week after administration but will not provide protection
i. Parainfluenza 3 (PI-3)
in the presence of passively acquired antibodies. It is con-
Etiology. Parainfluenza 3, an RNA virus of the family Para- traindicated for pregnant animals because it will cause abortion.
myxoviridae, causes mild respiratory disease of ruminants The IN route immunizes in the presence of passively acquired
when it is the sole pathogen. The viral infection often predis- antibodies, provides immunity within 3 days of administra-
poses the respiratory system to severe disease associated with tion, and stimulates the production of interferon. Other vaccine
concurrent viral or bacterial pathogens. Viral strains are re- formulations, about which less information is reported, include
ported to vary in virulence. Serotypes seen in the smaller rumi- inactivated or chemically altered live-virus preparations; both
nants are distinct from those isolated from cattle. are administered IM, and followup immunizations are needed
572 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

within 4 weeks. Booster vaccinations are recommended for all Differential diagnosis. Differentials should include other ru-
preparations within 2 - 6 months after the initial immunization. minant respiratory tract viruses.
All presently marketed vaccine products come in combination
with other bovine respiratory viruses as multivaccine products. Prevention and control. Vaccination should be part of the
The humoral immunity protects against PI-3 abortions. standard health program, and all animals should be vaccinated
There is no approved PI-3 vaccine for sheep and goats. The regularly. Vaccinations should be administered within 1-2
use of the cattle formulation in these smaller ruminants is not months of stressful events, such as weaning, shipping, and in-
recommended. troduction to new surroundings. Currently available vaccines
Sound management of housing, sanitation, nutrition, and pre- include an inactivated preparation and a modified live virus
ventive medicine programs are all equally important compo- preparation administered intramuscularly or subcutaneously;
nents in prevention and control. immunity develops well in yearling animals, and colostral anti-
bodies develop when cows are vaccinated during late gestation.
Treatment. Uncomplicated disease is not treated. Passive immunity from colostrum provides at least partial pro-
tection to calves in herds where disease is prevalent. But this
j. Respiratory Syncytial Viruses of Ruminants immunity suppresses the mucosal IgA response and serum an-
tibody responses. The basis for successful immune protection is
Etiology. The respiratory syncytial viruses are pneumoviruses the mucosal memory IgA, but this is difficult to achieve with
of the Paramyxoviridae family and are common causes of se- present vaccine formulations. The virus is easily inactivated in
vere disease in ruminants, especially calves and yearling cattle. the environment.
Two serotypes of the bovine respiratory syncytial virus (BRSV) Preventive measures in preweaning animals should include
have been described for cattle; these may be similar or identical preconditioning to minimize weaning stress.
to the virus seen in sheep and goats.
Treatment. Recovery can be spontaneous; however, antibi-
Clinicalfindings and diagnosis. Infections may be subclinical
otics and supportive therapy are useful to prevent or control sec-
or develop into severe illness. Clinical signs include fever, hy-
ondary bacterial pneumonia. In severe cases, antihistamines
perpnea, spontaneous or easily induced cough, nasal discharge,
and corticosteriods may also be necessary. Use of vaccine dur-
and conjunctivitis. Interstitial pneumonia usually develops, and
ing natural infection is not productive and may result in severe
harsh respiratory sounds are evident on auscultation. Develop-
disease.
ment of emphysema indicates a poor prognosis, and death may
occur in the severe cases of the viral infection. Secondary bac-
terial pneumonia, especially with Pasteurella haemolytica, with Ulcerative Dermatosis (Ovine Venereal Disease,
morbidity and mortality, is also a common sequela. Abortions Balanoposthitis )
have been assciated with BRSV outbreaks.
Diagnosis is based on virus isolation and serology (acute
Etiology. Ulcerative dermatosis is a contagious disease of
sheep only. It is caused by a poxvirus similar to but distinct from
and convalescent). Nasal swabs for virus isolation should be
the causative agent of contagious ecthyma ("Current Veterinary
taken when animals have fever and before onset of respiratory
Therapy," 1993).
disease.

Epizootiology and transmission. These viruses are considered Clinical signs and diagnosis. Lesions include ulcers and
ubiquitous in domestic cattle and are transmitted by aerosols. crusts associated with the skin and mucous membranes of the
genitalia, face, and feet (Bulgin, 1986). Genital lesions are
Necropsy findings. Gross lesions include consolidation of an- much more common than the facial or coronal lesions. Discom-
teroventral lung lobes. Edema and emphysema are present. As fort may be associated with the lesions. Paraphimosis occasion-
the name indicates, syncytia, which may have inclusions, form ally occurs. These lesions are painful; during breeding season,
in areas of the lungs infected with the virus. Necrotizing bron- animals will avoid coitus. Morbidity is low to moderate, and
chiolitis, bronchiolitis obliterans, and hyaline membrane for- mortality negligible if the flock is otherwise healthy. Diagnosis
mation will be evident microscopically. is based on clinical signs.

Pathogenesis. The severe form of the disease, which often Epizootiology and transmission. Endemic to the western
follows a mild preliminary infection, is thought to be caused by United States, ulcerative dermatosis is transmitted through
immune-mediated factors during the process of infection in the direct contact with abraded skin of the prepuce, vulva, face,
lung. Virulence may vary greatly among viral strains. and feet.
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 573

Necropsy findings. Necropsy would rarely be necessary to di- when no contact with cattle has occurred. Persistently infected
agnose an outbreak in a healthy flock. Findings will be similar animals, such as lambs, are shedding reservoirs of the virus in
to those described for contagious ecthyma. urine, feces, and saliva throughout their lives.

Pathogenesis. Following an incubation period of 2 - 5 days, Necropsy findings. Lesions include placentitis, and character-
the virus replicates in the epidermal cells and leads to necrosis istic joint and hair-coat changes in the fetus. Histologically, ax-
and pustule formation. Pustules rapidly break, forming weeping onal swelling, neuronal vacuolation, dysmyelination, and focal
ulcers. The ulcers scab over and eventually form a fibrotic scar. microgliosis are observed in central nervous system structures.
The disease usually resolves in 2 - 6 weeks. Rarely, the disease
will persist for many months to more than a year. Pathogenesis. The virus entering the ewe via the gastroin-
testinal or respiratory tracts penetrates the mucous membranes
Differential diagnosis. The main differential is contagious and causes maternal and fetal viremia. Infection during the first
ecthyma, which is grossly and histopathologically associated 45 days of gestation causes embryonic death. In lambs infected
with epithelial hyperplasia. This is also a feature of ulcerative between 45 and 80 days, the virus activates follicular develop-
dermatosis. ment, diminishes the myelination of neurons, and causes dys-
function of the thyroid gland. Infection after 80 days of gesta-
Prevention and control. No vaccine is available. Affected an- tion results in lambs that are born persistently infected. Infected
imals, especially males, should not be used for breeding. lambs have high perinatal mortality; survivors have diminished
signs over time but, as noted, continue to shed the virus.
Treatment. Affected animals should be separated from the rest
of the flock. Treatment is supportive, including antiseptic oint-
Prevention and control. Border disease can be prevented by
ments and astringents.
vaccinating breeding ewes with killed-BVDV vaccine. Congen-
Research complications. Breeding and maintenance of the itally affected lambs should be maintained separately and dis-
flocks' condition, because of the pain associated with eating, posed of as soon as humanely possible. New animals to the
will be compromised during an outbreak. flock should be screened serologically. If cattle are housed
nearby, vaccination programs for BVDV should be maintained.
I. Border Disease Treatment. There is no treatment other than supportive care
Etiology. Border disease, also known as hairy shaker disease for affected animals.
(or "fuzzies" in the southwestern United States), is a disease of
sheep caused by a virus closely related to the bovine viral diar- m. Contagious Ecthyma (Contagious Pustular Dermatitis,
rhea virus (BVDV), a pestivirus of the Togaviridae family. Sore Mouth, Orf)
Goats are also affected. The virus causes few pathogenic effects
in cattle. Etiology. Contagious ecthyma, also known as contagious pus-
tular dermatitis, sore mouth, or off, is an acute dermatitis of
Clinical signs and diagnosis. Border disease in ewes causes sheep and goats caused by a parapoxvirus. This disease occurs
early embryonic death, abortion of macerated or mummified fe- worldwide and is zoonotic. Naturally occurring disease has also
tuses, or birth of lambs with developmental abnormalities. been reported in other species such as musk ox and reindeer.
Lambs infected in utero that survive until parturition may be Other parapoxviruses infect the mucous membranes and skin of
born weak and often exhibit a number of congenital defects cattle, causing the diseases bovine pustular dermatitis and
such as tremor, hirsutism (sometimes darkly pigmented over pseudocowpox.
the shoulders and head), hypothyroidism, central nervous sys-
tem defects, and joint abnormalities, including arthrogryposis. Clinical signs and diagnosis. The disease is characterized by
Later, survivors may be more susceptible to diseases and may the presence of papules, vesicles, or pustules and subsequently
develop persistent, sometimes fatal, diarrhea. The virus infec- scabs of the skin of the face, genitals of both sexes, and coro-
tion produces similar clinical manifestations in goats, except nary bands of the feet. Lesions develop most frequently at mu-
that the hair changes are not seen. cocutaneous junctions and are found most commonly at the
Diagnosis includes the typical signs described above, as well commissures of the mouth. Off is usually found in young ani-
as serological evidence of viral infection. Virus isolation con- mals less than 1 year of age. Younger lambs and kids will have
firms the diagnosis. difficulty nursing and become weak. Lesions may also develop
on udders of nursing dams, which may resist suckling by off-
Epizootiology and transmission. The virus is present world- spring to nurse, leading to secondary mastitis. The scabs may
wide, and reports of disease are sporadic. Disease has occurred appear nodular and raised above the surface of the surrounding
574 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

skin. Morbidity in a susceptible group of animals may exceed animals in flocks already free of the disease. Affected dairy
90%. Mortality is low, but the course of the disease may last up goats should be milked last, using disposable towels for clean-
to 6 weeks. ing teat ends.
Diagnosis is based on characteristic lesions. Biopsies may
reveal eosinophilic cytoplasmic inclusions and proliferative le- Treatment. Affected animals should be isolated and provided
sions under the skin. Electron microscopy will reveal the virus supportive care, especially tube feeding for young animals
itself. Disease is confirmed by virus isolation. whose mouths are too sore to nurse. Treatment should also
address secondary bacterial infections of the orf lesions, in-
Epizootiology and transmission. All ages of sheep and goats cluding systemic antibiotics for more severe infections. Treat-
are susceptible. Seasonal occurrences immediately after lamb- ment for myiasis may also be necessary. The viral infection is
ing and after entry into a feedlot are common; stress likely plays self-limiting, with recovery in about 4 weeks.
a role in susceptibility to this viral disease. Older animals de-
velop immunity that usually prevents reinfection for at least 1 or Research complications. Carrier animals may be a factor in
more years. Resistant animals may be present in some flocks or flock or herd outbreaks. Contagious ecthyma is a zoonotic dis-
herds. The virus is very resistant to environmental conditions ease, and human-to-human transmission can also occur. The
and may contaminate small-ruminant facilities, pens, feedlots, virus typically enters through abrasions on the hands and results
and the like for many years as the result of scabs that have been in a large (several centimeters) nodule that is described as being
shed from infected animals. Transmission occurs through su- extremely painful and lasting for as many as 6 weeks. Lesions
perficial lesions such as punctures from grass awns, scrapes, heal without scarring.
shearing, and other common injuries.
n. Foot-and-Mouth Disease
Necropsy findings. Necropsy findings include ballooning de-
generation of epidermal and dermal layers, edema, granuloma- Etiology. Foot-and-mouth disease (FMD) is caused by the
tous inflammation, vesiculation, and cellular hyperplasia. Sec- foot-and-mouth disease virus, a picornavirus in the Aphthovirus
ondary bacterial infection may also be evident. genus. The disease is also referred to as aftosa or aphthous fever.
Seven immunologically distinct types of the virus have been
Pathogenesis. The virus is typical of the Poxviridae, resem- identified, with 60 subtypes within those 7. Epidemics of the
bling sheep poxvirus (not found in the United States) and vac- disease have occurred worldwide. North and Central America
cinia virus and replicating in the cytoplasm of epithelial cells. have been free of the virus since the mid-1950s. This is a re-
Following an incubation period of 2-14 days, papules and portable disease in the United States; clinical signs are very sim-
vesicles develop around the margins of the lips, nostrils, eye- ilar to other vesicular diseases. Cattle (and swine) are primarily
lids, gums, tongue, or teats; skin of the genitalia; or coronary affected, but disease can occur in sheep and is usually subclini-
band of the feet. The vesicles form pustules that rupture and cal in goats.
finally scab over.
Clinical signs and diagnosis. In addition to vesicle formation
Differential diagnosis. Ulcerative dermatosis and bluetongue around and in the mouth, hooves, and teats, fever, anorexia,
virus should be considered in both sheep and goats. An impor- weakness, and salivation occur. Vesicles may be as large as
tant differential in goats is staphylococcal dermatitis. 10 cm, rupture after 2 days, and subsequently erode. Secondary
bacterial infections often occur at the erosions. Anorexia is
Prevention and control. Individuals handling infected ani- likely due to the pain associated with the oral lesions. High mor-
mals should be advised of precautions beforehand, should wear bidity and low mortality, except for the high mortality in young
gloves, and should separate work clothing and other personal cattle, are typical.
protective equipment. Clippers, ear tagging devices, and other Diagnosis must be based on ELISA, virus neutralization,
similar equipment should always be cleaned and disinfected af- fluorescent antibody tests, and complement fixation.
ter each use. Colostral antibodies may not be protective. Vacci-
nating lambs and kids with commercial vaccine best prevents Epizootiology and transmission. Domestic and wild rumi-
the disease. Dried scabs from previous outbreaks may also be nants and several other species, such as swine, rats, bears, and
used by rubbing the material into scarified skin on the inner llamas are hosts. Asymptomatic goats can serve as virus reser-
thigh or axilla. Animals newly introduced to infected premises voirs for more susceptible cohoused species such as cattle.
should be vaccinated upon arrival. Precautions must be taken Greater mortality occurs in younger animals. The United States,
when vaccinating animals, because the vaccine may induce Great Britain, Canada, Japan, New Zealand, and Australia are
orf in the animal handlers; it is not recommended to vaccinate FMD-free, whereas the disease is endemic in most of South
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 575

America, parts of Europe, and throughout Asia and Africa. The o. Malignant Catarrhal Fever
virus is very contagious and is spread primarily by the inhalation
Etiology. Malignant catarrhal fever (MCF) is a severe disease
of aerosols, which can be carried over long distances. Transmis-
primarily of cattle. The agents of MCF are viruses of the
sion may also occur by fomites, such as shoes, clothing, and
Gammaherpesvirinae subfamily. Alcelaphine herpesvirus 1 and
equipment. Human hands, soiled bedding, and animal products
2 and ovine herpesvirus 2 are known strains. The alcelaphine
such as frozen or partially cooked meat and meat products,
strains are seen in Africa. The ovine strain is seen in North
hides, semen, and pasteurized milk also serve as sources of virus.
America. The alcelaphine and ovine strains differ in incubation
times and duration of illness. Disease may occur sporadically or
Necropsy findings. Vesicles, erosions, and ulcers are present
in the oral cavity as well as on the rumen pillars and mammary as outbreaks.
alveolar epithelium. Myocardial and skeletal muscle degenera-
tion (Zenker's) is most common (and accounts for the greater Clinical signs and diagnosis. Signs range from subclinical to
mortality) in younger animals. Histological findings include recrudescing latent infections to the lethal disease seen in sus-
lack of inclusion bodies. Vesicular lesions include intracellular ceptible species, such as cattle. Sudden death may also occur in
and extracellular edema, cellular degeneration, and separation cattle. Presentations of the disease may be categorized as ali-
of the basal epithelium. mentary, encephalitis, or skin forms; all three may occur in an
animal. Corneal edema starting at the limbus and progressing
Pathogenesis. The incubation period is 2 - 8 days. The virus centripetally is a nearly pathognomonic sign; photophobia, se-
replicates in the pharynx and digestive tract in the cells of the vere keratoconjunctivitis, and ocular involvement may follow.
stratum spinosum, and viremia and spread of virus to many tis- Other signs include prolonged fever, oral mucosal erosions,
sues occur before clinical signs develop. Virus shedding begins salivation, lacrimation, purulent nasal discharge, encephalitis,
about 24 hr before clinical signs are apparent. Vesicles result and pronounced lymphadenopathy. As the disease progresses,
from the separation of the superficial epithelium from the basal cattle may shed horns and hooves. In North America, cattle will
epithelium. Fluid fills the basal epithelium, and erosions de- also have severe diarrhea. The course of the disease may extend
velop when the epithelium sloughs. Persistent infection also oc- to 1 week. Recovery is usually prolonged, and some permanent
curs, and virus can be found for months or years in the pharnyx; debilitation may occur. The disease is fatal in severely affected
the mechanisms for the persistence are not known. individuals.
History of exposure, as well as the clinical signs and lesions,
Differential diagnosis. Vesicular stomatitis is the principal contributes to the diagnosis. Serology, PCR-based assays, viral
differential. Other differentials include contagious ecthyma isolation, and cell-culture assays, such as cytopathic effects on
(orf), rinderpest, bluetongue, malignant catarrhal fever, bovine thyroid cell cultures, are also used. Because of the susceptibil-
papular stomatitis, bovine herpes mammillitis, and infectious ity of rabbits, inoculation of this species may be used. In less se-
bovine rhinotracheitis virus infection. vere outbreaks or individual animal disease, definitive diagnosis
may never be made.
Prevention and control. Movement of animals and animal
products from endemic areas is regulated. Quarantine and
Epizootiology and transmission. Most ruminant species are
slaughter are practiced in outbreaks in endemic areas. Quaran-
susceptible to MCE Sheep are sources of infection for cattle,
tine and vaccination are also used in endemic areas, but vac-
which are dead-end hosts. Other ruminants, including goats,
cines must be type-specific and repeated 2 or 3 times per year to
may harbor the virus. Both the African and North American
be effective and will provide only partial protection. Autoge-
strains are transmissible to rabbits; these animals develop a fa-
nous vaccines are best in an outbreak. Passive immunity pro-
tal lymphoproliferative disease. The virus is shed from the na-
tects calves for up to 5 months after birth. The virus is inacti-
sopharynx. Infection of lambs is horizontal from direct contact.
vated by extremes of pH, sunlight, high temperatures, sodium
Other sources of the virus include water troughs, placental tis-
hydroxide, sodium carbonate, and acetic acid.
sues, contaminated fomites, aerosols, birds, and caretakers.
Treatment. Nursing care and antibiotic therapy to minimize
secondary reactions help with recovery. Humoral immunity is Necropsy. Gross findings at necropsy include necrotic and
considered the more important immune mechanism, with cell- ulcerated nasal and oral mucosa; thickened, edematous, ulcer-
mediated immunity of less importance. ated, and hemorrhagic areas of the intestinal tract; swollen,
friable, and hemorrhagic lymph nodes and other lymphatic tis-
Research complications. Rare cases in humans have been re- sues; and erosion of affected mucosal surfaces. Lymph nodes
ported. Importation into the United States of animal products should be submitted for histological examination. Histological
from endemic areas is prohibited. findings include nonsuppurative vasculitis and encephalitis;
576 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

large numbers of lymphocytes and lymphoblasts will be present lobes; and hematological findings indicate anemia and leuko-
without evidence of virus. cytosis. The rare neurological signs include flexion of fetlock
and pastern joints, tremors of facial muscles, progressive pare-
Pathogenesis. The incubation period may be up to 3 months. sis and paralysis, depression, and prostration. Death occurs in
Vascular endothelium and all epithelial surfaces will be af- weeks to months.
fected. The virus is believed to cause proliferation of cytotoxic The disease can be serologically diagnosed with agar gel im-
T lymphocytes with natural killer cell activities, and the result- munodiffusion (AGID) tests, virus isolation, serum neutraliza-
ing lesions are due to an autoimmune type of phenomenon. tion, complement fixation, and enzyme-linked immunosorbent
assay (ELISA) tests.
Differential diagnoses. The differentials for this disease are
bovine viral diarrhea/mucosal disease, bovine respiratory dis- Epizootiology and transmission. Sixty-eight percent of sheep
ease complex, infectious bovine rhinotracheitis, bluetongue, in some states have been infected with the virus (Radostits
vesicular stomatitis, and foot-and-mouth disease. Causes of en- et al., 1994). It is transmitted horizontally via inhalation of
cephalitis, such as bovine spongiform encephalopathy and ra- aerosolized virus particles and vertically between the infected
bies, should be considered. In Africa, rinderpest is also a differ- dam and fetus. In addition, transmission through the milk or
ential. Other differentials are arsenic toxicity and chlorinated colostrum is considered common (Knowles, 1997).
naphthalene toxicity.
Necropsy findings. Lesions are observed in lungs, mammary
Prevention and control. No vaccine is available at this time. glands, joints, and the brain. Pulmonary adhesions, ventral lung
In North America, sheep, as well as cattle that have been either lobe consolidation, bronchial lymph node enlargement, masti-
exposed or that have survived the disease, are reservoirs for out- tis, and degenerative arthritis are visualized grossly. Meningeal
breaks in other cattle. If there is concern regarding presence of edema, thickening of the choroid plexus, and foci of leukoen-
the virus, animals should be screened serologically; once an an- cephalomalacia are seen in the central nervous system (CNS).
imal has been infected, it remains infected indefinitely. Lambs Histologically, interalveolar septal thickening, lymphoid hyper-
can be free of the infection if removed from the flock at wean- plasia, histiocyte and fibrocyte proliferation, and squamous ep-
ing. The virus is very fragile outside of host's cells and will not ithelial changes are seen in the lungs. Meningitis, lymphoid hy-
survive in the environment for more than a few hours. perplasia, demyelination, and glial fibrosis are seen in the CNS.

Treatment. Affected and any exposed animals should be iso- Pathogenesis. The virus has a predilection for the lungs, me-
lated from healthy animals. There is no specific treatment for diastinal lymph nodes, udder, spleen, joints, and rarely the
MCF; supportive treatment may improve recovery rates. Corti- brain. After initial infection, the virus integrates into the DNA
costeroids may be useful. of mature monocytes and persists as a provirus. Later in the an-
imal's life, infected monocytes mature as lung (and other tissue)
macrophages and establish active infection. The virus induces
p. Ovine Progressive Pneumonia (Maedi/Visna) lymphoproliferative disease, histiocyte and fibrocyte prolifera-
tion in the alveolar septa, and squamous metaplasia. Pulmonary
Etiology. An RNA virus in the lentivirus group of the Retro-
alveolar and vascular changes impinge on oxygen and carbon
viridae family causes ovine progressive pneumonia (OPP), or
dioxide exchange and lead to serious hypoxia and pulmonary
maedi/visna. Maedi refers to the progressive pneumonia pres-
hypertension. Secondary bacterial pneumonia may contribute
entation of the disease; visna refers to the central nervous sys-
to the animal's death.
tem disease, which is reported predominantly in Iceland. Visna
has been reported in goats but may have been due to caprine
Differential diagnosis. Pulmonary adenomatosis is the differ-
arthritis encephalitis infection.
ential diagnosis.
Clinical signs and diagnosis. OPP is a viral disease of adult
Prevention and control. Isolating or removing infected ani-
sheep characterized by weakness, unthriftiness, weight loss,
mals can prevent the disease. Facilities and equipment should
and pneumonia (Pepin et al., 1998; de la Concha Bermejillo,
also be disinfected.
1997). Clinically, animals exhibit signs of progressive pul-
monary disease after an extremely long incubation period of up
Treatment. Treatment is unsuccessful.
to 2 years. Respiratory rate and dyspnea gradually increase as
the disease progresses. The animal continues to eat throughout
q. Poxviruses of Ruminants
the disease; however, animals progressively lose weight and be-
come weak. Additionally, mastitis is a common clinical feature. i. Ovine viral dermatosis. Ovine viral dermatosis is a vene-
Thoracic auscultation reveals consolidation of ventral lung real disease of sheep caused by a parapoxvirus distinct from
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 577

contagious ecthyma. The disease resolves within 2 weeks in Prevention and control. There is no vaccine available for
healthy animals, but lesions are painful and resemble those bovine papular stomatitis. Because of the similarity of this virus
of Corynebacterium renale posthitis/vulvovaginitis. Sympto- to the parapoxvirus of contagious ecthyma, it is important to be
matic treatment may be necessary in some cases. There is no aware of the persistence in the environment and susceptibility
vaccine. Animals should not be used for breeding while clinical of younger cattle. Vaccination using the local strain, and the
signs are present. skin scarification technique for off, have been protective. Han-
dlers should wear gloves and protective clothing.
ii. Proliferative stomatitis (bovine papular stomatitis)
Etiology. A parapoxvirus is the causative agent of bovine Treatment. Cattle usually will not require extensive nursing
papular stomatitis. This virus is considered to be closely related care, but lesions with secondary bacterial infections should be
to the parapoxvirus that causes contagious ecthyma and treated with antibiotics.
pseudocowpox. It is also a zoonotic disease. The disease is not
considered of major consequence, but high morbidity and mor- Research complications. Handlers may develop lesions on
tality may be seen in severe outbreaks. In addition, lesions are their hands at sites of contact with lesions of cattle.
comparable in appearance to those seen with vesicular stomati-
tis, bovine viral diarrhea virus, and foot-and-mouth disease. iii. Pseudocowpox
The disease occurs worldwide. Etiology. Pseudocowpox is a worldwide cattle disease caused
by a parapoxvirus related to the causative agents of contagious
Clinical signs and diagnosis. Raised red papules or erosions ecthyma and bovine papular stomatitis (see Sections III,A,2,m
or shallow ulcers on the muzzle, nose, oral mucosa (including and III,A,2,q,ii). Lesions are confined to the teats. This is also a
the hard palate), esophagus, and rumen of younger cattle are the zoonotic disease.
most common findings. In some outbreaks, the papules will be
associated with ulcerative esophagitis, salivation, diarrhea, and Clinical signs and diagnosis. Minor lesions are usually con-
subsequent weight loss. Lesions persist or may come and go fined to the teats. These are distinctive because of the ring- or
over a span of several months. Morbidity among herds may be horseshoe-shaped scab that develops after 10 days. Additional
100%. Mortalities are rare. Bovine papular stomatitis is associ- lesions sometimes develop on the udder, the medial aspect of
ated with "rat tail" in feedlot cattle. Animals continue to eat and the thighs, and the scrotum. The teat lesions may predispose to
usually do not show a fever. No lesion is seen on the feet. The mastitis.
infection may also be asymptomatic.
Diagnosis is based on clinical signs, histological findings, and Pathogenesis. The virus is spread by contaminated hands,
viral isolation. equipment, and fomites.

Epizootiology and transmission. Cattle less than 1 year of age Differential diagnosis. Differentials include bovine herpes
are most commonly affected, and disease is rare in older cattle. mammillitis and papillomatosis.
Transmission is by animal-to-animal contact.
Prevention and control. Milking hygiene is helpful in control.
Necropsy findings. Raised papules may be found around the
muzzle and mouth and involve the mucosa of the esophagus and Treatment. Lesions should be treated symptomatically, and
rumen. Histologically, epithelial cells will show hydropic de- affected animals milked last.
generation and hyperplasia of the lamina propria. Eosinophilic
inclusions will be in the cytoplasm of infected epithelial cells. Research complications. Like other related poxviruses, this
virus causes nodular lesions on humans.
Pathogenesis. Following exposure to the virus, erythematous
macules most commonly appear on the nares, followed by the
r. Pulmonary Adenomatosis (Jaagsiekte)
mouth. These become raised papules within a day, regressing
after days to weeks; the lesions that remain will be persistent Etiology. Pulmonary adenomatosis is a rare but progressive
yellow, red, or brown spots. Some infections may recur or per- wasting disease of sheep, with worldwide distribution. Pul-
sist, with animals showing lesions intermittently or continu- monary adenomatosis is caused by a type D retrovirus antigeni-
ously over several months. cally related to the Mason-Pfizer monkey virus. Jaagsiekte was
the designation when the disease was described originally in
Differential diagnosis. Pseudocowpox, vesicular stomatitis, South Africa.
foot-and-mouth disease, and bovine viral diarrhea virus infec-
tion are the differentials for this disease. The differential for the Clinical signs and diagnosis. Typical clinical signs include
"rat tail" clinical sign is Sarcocystis infection. progressive respiratory signs such as dyspnea, rapid respiration,
578 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

and wasting. The disease is diagnosed by these chronic clinical comfort or incapacitation such as between the digits, on the lips,
signs and histology. or over the joints. In adult sheep, warts may transform to squa-
mous cell carcinoma. In goats, the disease is rare, and the warts
Epizootiology and transmission. The disease is transmitted by are also of the verrucous type and occasionally may develop
aerosols. Body fluids of viremic animals, such as milk, blood, into squamous cell carcinoma. Warts on goat udders tend to be
saliva, tears, semen, and bronchial secretions, will contain the persistent.
virus or cells carrying the virus. Diagnosis is made by observing the typical proliferative
lesions.
Necropsy. The adenomas and adenocarcinomas will be small
firm lesions distributed throughout the lungs. The adenocarci- Epizootiology and transmission. Older animals are less sensi-
nomas metastasize to regional lymph nodes. tive to papillomatosis than young animals, although immunosu-
pressed animals of any age may develop warts as the result of
Pathogenesis. As with ovine progressive pneumonia (OPP), harbored latent infections. The virus is transmitted by direct and
the incubation period is up to 2 years long. Adenocarcinoma- indirect (fomite) contact, entering through surface wounds and
tous lesions arising from type II alveolar epithelial cells may be sites such as tattoos.
discrete or confluent and involve all lung lobes.
Pathogenesis. The incubation period ranges from 1 to 6
Differential diagnosis. This disease occurs coincidentally months. The virus induces epidermal and fibrous tissue prolif-
with or is a differential diagnosis for OPP. eration, often described as cauliflower-like skin tumors. The
disease is generally self-limiting.
Treatment. No treatment is effective.
Differential diagnosis. In sheep and goats, differentials in-
clude contagious ecthyma, ulcerative dermatosis, strawberry
s. Papillomatosis (Warts, Verrucae) foot rot, and sheep and goat pox.
Etiology. Cutaneous papillomatosis is a very common disease Prevention and control. Commercial vaccines (available only
in cattle and is much less common among sheep and goats. The for cattle) or autogenous vaccines must be used with a recogni-
disease is a viral-induced proliferation of the epithelium of the tion that papovavirus strains are host-specific and that immunity
neck, face, back, and legs. These tumors are caused by a papil- from infection or vaccination is viral-type-specific. Autoge-
lomavirus (DNA virus) of the Papovaviridae family, and the nous vaccines are generally considered more effective. Some
viruses are host-specific and often body site-specific. Most are vaccine preparations are effective at prevention but not treat-
benign, although some forms in cattle and one form in goats can ment of outbreaks. Viricidal products are recommended for dis-
become malignant. In cattle, the site specificity of the papillo- infection of contaminated environments. Minimizing cutaneous
mavirus strains are particularly well recognized. Designations injuries and sanitizing equipment (tattoo devices, dehorners, ear
of the currently recognized bovine papillomavirus (BPV) types taggers, etc.) in a virucidal solution between uses are also rec-
are BPV-1 through BPV-5. ommended preventive and control measures. Halters, brushes,
and other items may also be sources of virus.
Clinical signs and diagnosis. The papillomas may last up to
12 months and are seen more frequently in younger animals. Treatment. Warts will often spontaneously resolve as immu-
Lesions have typical wart appearances and may be single or nity develops. In severe cases or with flockwide or herdwide
multiple, small (1 mm) or very large (500 mm). The infections problems, affected animals should be isolated from nonaffected
will generally be benign, but pain will be evident when warts animals, and premises disinfected. Warts can be surgically ex-
develop on occlusal surfaces or within the gastrointestinal tract. cised and autogenous vaccines can be made and administered to
In addition, when infections are severe, weight loss may occur. help prevent disease spread. Cryosurgery with liquid nitrogen
When warts occur on teats, secondary mastitis may develop. or dry ice has also proven to be successful for wart removal.
In cattle, BPV-1 and BPV-2 cause fibropapillomas on teats Topical agents such as podophyllin (various formulations) and
and penises or on head, neck, and dewlap, respectively. BPV-3 dimethyl sulfoxide may be applied to individual lesions once
causes flat warts that occur in all body locations, B PV-4 causes daily until regression.
warts in the gastrointestinal tract, and B PV-5 causes small
white warts (called rice-grain warts) on teats. Warts caused by
t. Pseudorabies (Mad Itch, Aujeszky's Disease)
BPV-3 and BPV-5 do not regress spontaneously. Prognosis in
cattle is poor only when papillomatosis involves more than 20% Etiology. Pseudorabies is an acute encephalitic disease caused
of the body surface. by a neurotropic alphaherpesvirus, the porcine herpesvirus 1.
In sheep, warts are the verrucous type. The disease is of little One serotype is recognized, but strain differences exist. The dis-
consequence unless the warts develop in an area that causes dis- ease has worldwide distribution. It is a primarily a clinical dis-
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 579

ease of cattle, with less frequent reports (but no less severe clini- Differential diagnoses. Differentials for the neurologic signs
cal manifestations) in sheep and goats. of pseudorabies infection include rabies, polioencephalomala-
cia, salt poisoning, meningitis, lead poisoning, hypomagne-
Clinical signs and diagnosis. A range of clinical signs is seen semia, and enterotoxemia. Those for the intense pruritus in-
during the rapid course of this usually fatal disease. At the site clude psoroptic mange and scrapie in sheep, sarcoptic mange,
of virus inoculation or in other locations, abrasions, swelling, and pediculosis.
intense pruritus, and alopecia are seen. Pruritus will not be
asymmetric. Animals will also become hyperthermic and will Prevention and control. Pseudorabies is a reportable disease
vocalize frantically. Other neurological signs range from hoof in the United States, where a nationwide eradication program
stamping, kicking at the pruritic area, salivation, tongue chew- exists; states are rated regarding status. Effective disinfectants
ing, head pressing and circling, to paresthesia or hyperesthesia, include sodium hypochlorite (10% solution), formalin, per-
ataxia, and conscious proprioceptive deficits. Nystagmus and acetic acid, tamed iodines, and quaternary ammonium com-
strabismus are also seen. Animals will be fearful or depressed, pounds. Five minutes of contact time is required, and then
and aggression is sometimes seen. Recumbency and coma pre- surfaces must be rinsed. Other disinfectant methods for viral
cede death. killing include 6 hr of formaldehyde fumigation, or 360 min of
Diagnostic evidence includes clinical findings; virus isolation ultraviolet light. Transport vehicles should be cleaned and dis-
from nasal or pharyngeal secretions or postmortem tissues; and infected between species. Serological screening for pseudora-
histological findings at necropsy. Serology of affected animals bies of swine housed near ruminants is essential.
is not productive, because of the rapid course. If swine are
housed nearby, or if swine were transported in the same vehicles Treatment. There is no treatment, and most affected ani-
as affected animals, serological evaluations are worthwhile mals die.
from those animals.
Research complications. Swine housed close to research ru-
Epizootiology and transmission. Swine are the primary hosts minants should be serologically screened prior to purchase, and
for pseudorabies virus, but they are usually asymptomatic and all transport vehicles should be cleaned and disinfected between
serve as reservoirs for the virus. The infection can remain latent loads of large animals. Humans have been reported to serocon-
in the trigeminal ganglion of pigs and recrudesce during stress- vert. The porcine herpesvirus 1 shares antigens with the infec-
ful conditions. Other animals are dead-end hosts. The unpro- tious bovine rhinotracheitis virus.
tected virus will survive only a few weeks in the environment
but may remain viable in meat (including carcasses) or saliva
u. Rabies (Hydrophobia)
and will survive outside the host, in favorable conditions, in the
summer for several weeks and the winter for several months. Etiology. Rabies is a sporadic but fatal, acute viral disease af-
Transmission is by oral, intranasal, intradermal, or subcuta- fecting the central nervous system. The rabies virus is a neu-
neous introduction of the virus. When the virus is inhaled, the rotropic RNA virus of the Lyssavirus genus and the Rhab-
clinical signs of pruritus are less likely to be seen. Transmission doviridae family. Sheep, goats, and cattle are susceptible. The
can also be by inadvertent exposure (e.g., contaminated sy- zoonotic potential of this virus must be kept in mind at all times
ringes) of ruminants to the modified live vaccines developed for when handling moribund animals with neurological signs char-
use in swine. Spread between infected ruminants is a less likely acteristic of the disease. Rabies is endemic in many areas of the
means of transmission, because of the relatively short period of world and within areas of the Unites States. This is a reportable
virus shedding. Transport vehicles used for swine may also be disease in North America.
sources of the virus. Raccoons are believed to be vectors of the
virus. Horses are resistant to infection. Clinical findings and diagnosis. Animals generally progress
through three phases: prodromal, excitatory, and paralytic.
Necropsy findings. There is no pathognomonic gross lesion. Many signs in the different species during these stages are non-
Definitive histologic findings include severe, focal, nonsuppu- specific, and forms of the disease are also referred to as dumb
rative encephalitis and myelitis. Eosinophilic intranuclear in- or furious. During the short prodromal phase, animals are hy-
clusion bodies (Cowdry type A) may be present in some af- perthermic and apprehensive. Animals progress to the excita-
fected neurons. Methods such as immunofluorescence and tory phase, during which they refuse to eat or drink and are ac-
immunoperoxidase staining can be used to show presence of the tive and aggressive. Repeated vocalizations, tenesmus, sexual
porcine herpesvirus 1. excitement, and salivation occur during this phase. The final
paralytic stage, with recumbency and death, occurs over several
Pathogenesis. The incubation period is 90-156 hr and dura- hours to days. This paralytic stage is common in cattle, and an-
tion of the illness is 8 - 7 2 hr. The longest duration is seen in an- imals may simply be found dead. The clinical course is usually
imals with pruritus around the head. 1 - 4 days.
580 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

Diagnosis is based on clinical signs, with a progressive and fa- v. Transmissible Spongiform Encephalopathies
tal course. Confirmation presently is made with the fluorescent
antibody technique on brain tissue. i. Bovine spongiform encephalopathy (mad cow disease).
Bovine spongiform encephalopathy, a transmissible spongi-
Epizootiology and transmission. The rabies virus is transmit- form encephalopathy (TSE), is not known to occur in the United
ted via a bite wound inflicted by a rabid animal. Cats, dogs, rac- States, where since 1989 it has been listed as a reportable dis-
coons, skunks, foxes, wild canids, and bats are the common dis- ease. The profound impact of this disease on the cattle industry
in Great Britain during the past two decades is well known. The
ease vectors in North America. Virus is also transmitted in milk
and aerosols. disease may be caused by a scrapielike (prion) agent. It is be-
lieved that the source of infection for cattle was feedstuff de-
rived from sheep meat and bonemeal that had been inadequately
Necropsy findings. Few lesions are seen at necropsy. Many
secondary lesions from manic behaviors during the course of treated during processing. The incubation period of years, the
lack of detectable host immune response, the debilitating and
disease may be evident. Histological findings will include non-
progressive neurological illness, and the pathology localized to
suppurative encephalitis. Negri bodies in the cytoplasm of neu-
rons of the hippocampus and in Purkinje's cells are pathogno- the central nervous system are characteristics of the disease, and
monic histologic findings. are is comparable to the characteristics of other TSE diseases
such as scrapie, which affects sheep and goats. In addition, the
infectious agent is extremely resistant to dessication and disin-
Pathogenesis. After exposure, the incubation period is vari-
fectants. Confirmation of disease is by histological examination
able, from 2 weeks to several months, depending on the distance
of brain tissue collected at necropsy; the vacuolation that occurs
that the virus has to travel to reach the central nervous system.
during the disease will be symmetrical and in the gray matter of
The rabies virus proliferates locally, gains access to neurons by
the brain stem. Molecular biology techniques, such as Western
attaching to acetylcholine receptors, via a viral surface glyco-
blots and immunohistochemistry, may also be used to identify
protein, migrates along sensory nerves to the spinal cord and
the presence of the prion protein. Differentials include many in-
brain, and then descends via cranial nerves (trigeminal, facial,
fectious or toxic agents that affect the bovine nervous and mus-
olfactory, glossopharyngeal) to oral and nasal cavity structures
culoskeletal systems, such as rabies, listeriosis, and lead poi-
(i.e., salivary glands). The fatal outcome is currently believed to
soning. Metabolic disorders such as ketosis, milk fever, and
be multifactorial, related to anorexia, respiratory paralysis, and
effects on the pituitary. grass tetany are also differentials. There is no vaccine or treat-
ment. Prevention focuses on import regulations and not feeding
ruminant protein to ruminants; recent USDA regulations pro-
Differential diagnosis. Rabies should be included on the
hibit feeding any mammalian proteins to ruminants.
differential list when clinical signs of neurologic disease are
evident. Other differentials for ruminants include herpesvirus
encephalitis, thromboemobolic meningoencephalitis, nervous ii. Scrapie
ketosis, grass tetany, and nervous cocciodiosis. Etiology. Scrapie is a sporadic, slow, neurodegenerative dis-
ease caused by a prion. Scrapie is a reportable disease. It is much
Prevention and control. Vaccines approved for use cattle and more common in sheep than in goats. The disease is similar
sheep are commercially available and contain inactivated virus; to transmissible mink encephalopathy, kuru, Creutzfeldt-Jakob
there is not one available in the United States for goats. Rumi- disease, and bovine spongiform encephalopathy (mad cow dis-
nants in endemic areas, such as the East Coast of the United ease). Prions are nonantigenic, replicating protein agents.
States, should be routinely vaccinated. Any animals housed
outside that may be exposed to rabid animals should be vacci- Clinical signs and diagnosis. During early clinical stages, an-
nated. Vaccination programs generally begin at 3 months of imals are excitable and hard to control. Tremors of head and
age, with a booster at 1 year of age and then annual or triennial neck muscles, as well as uncoordinated movements and unusual
boosters. Awareness of the current rabies case reports for the re- "bunny-hopping" gaits are observed. In advanced stages of the
gion and wildlife reservoirs, however, is important. Monitoring disease, animals experience severe pruritus and will self-muti-
for and exclusion of wildlife from large-animal facilities are late while rubbing on fences, trees, and other objects. Blindness
worthwhile preventive measures. The virus is fragile and unsta- and abortion may also be seen. Morbidity may reach 50%
ble outside of a host animal. within a flock. Most animals invariably die within 4 - 6 weeks;
some animals may survive 6 months. In goats, the disease is also
Research complications. Aerosolized virus is infective. Per- fatal. Pruritus is generally less severe but may be localized.
sonal protective equipment, including gloves, face mask, and A wide range of clinical signs have also been noted in goats,
eye shields, must be worn by individuals handling animals that including listlessness, stiffness or restlessness, or behavioral
are manifesting neurological disease signs. changes such as irritability, hunched posture, twitching, and
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 581

erect tail and ears. As with sheep, the disease gradually pro- Research complications. As noted, this is a reportable dis-
gresses to anorexia and debilitation. ease. Stringent regulations exist in the United States regarding
Diagnosis can be made by clinical signs and histopathologi- importation of small ruminants from scrapie-infected countries.
cal lesions. A newer diagnostic test in live animals is based on
sampling from the third eyelid. Tests for genetic resistance or
w. Vesicular Stomatitis Virus
susceptibility require a tube of EDTA blood and are reasonably
priced. Etiology. Vesicular stomatitis (VS) is caused by the vesicular
stomatitis virus (VSV), a member of the Rhabdoviridae. Three
Epizootiology and transmission. The Suffolk breed of sheep serotypes are recognized: New Jersey, Indiana, and Isfahan. The
tends to be especially susceptible. Scrapie has also been re- New Jersey and Indiana strains cause sporadic disease in cattle
ported in several other breeds, including Cheviot, Dorset, in the United States. The disease is rare in sheep.
Hampshire, Corriedale, Shropshire, Merino, and Rambouillet.
It is believed that there is hereditary susceptibility in these Clinical signs and diagnosis. Adult cattle are most likely to de-
breeds. Targhees tend to be resistant. Genomic research indi- velop VS. Fever and development of vesicles on the oral mucous
cates there are two chromosomsal sites governing this trait; these membranes are the initial clinical signs. Lesions on the teats and
sites are referred to codons 171 (Q, R, or H genes can be pres- interdigital spaces also develop. The vesicles progress quickly to
ent) and 136 (A or V genes can be present). Of the five genes, R ulcers and erosions. The animal's tongue may be severely in-
genes appear to confer immunity to clinical scrapie in Suffolks volved. Anorexia and salivation are common. Weight loss and
in the United States. Affected Suffolks in the United States that decreased milk production are noticeable. Morbidity will be
have been tested have been AA QQ. The disease is also enzootic high in an outbreak, but mortality will be low to nonexistent.
is many other countries. The disease tends to affect newborns Diagnostic work should be initiated as soon as possible to dis-
and young animals; however, because the incubation period tinguish this from foot-and-mouth disease. Diagnosis is based
tends to range from 2 to 5 years, adult animals display signs of on analysis of fluid, serum, or membranes associated with the
the disease. Scrapie is transmitted horizontally by direct or in- vesicles. Virus isolation, enzyme-linked immunosorbent assay
direct contact; nasal secretions or placentas serve as sources of (ELISA), competitive ELISA (CELISA), complement fixation,
the infectious agent. Vertical transmission is questioned, and and serum neutralization are used for diagnosis.
transplacental transmission is considered unlikely.
Epizootiology and transmission. This disease occurs in sev-
Necropsy findings. At necropsy, no gross lesion is observed. eral other mammalian species, including swine, horses, and
Histopathologically, neuronal vacuolization, astrogliosis, and wild ruminants. VSV is an enveloped virus and survives well in
spongiform degeneration are visualized in the brain stem, the different environmental conditions, including in soil, extremes
spinal cord, and especially the thalamus. Inflammatory lesions of pH, and low temperatures. Outbreaks of VS occur sporadi-
are not seen. cally in the United States, but it is not understood how or in what
species the virus survives between these outbreaks. Incidence of
disease decreases during colder seasons. Equipment, such as
Pathogenesis. Replication of the prions probably occurs first
milking machines, contaminated by secretions is a mechanical
in lymphoid tissues throughout the host's body and then pro-
vector, as are human hands. Transmission may also be from
gresses to neural tissue.
contaminated water and feed. Transmission is also believed to
occur by insects (blackflies, sand flies, and Culicoides) that may
Differential diagnosis. In sheep and goats, depending on the simply be mechanical vectors. It is believed that carrier animals
speed of onset, differentials for the pruritus include ectopara- do not occur in this disease.
sites, pseudorabies, and photosensitization.
Necropsy. It is rare for animals to be necropsied as the result
Prevention and control. If the disease diagnosed in a flock, of this disease. Typical vesicular lesion histology is seen, with
quarantine and slaughter, followed by strict sanitation, are usu- ballooning degeneration and edema. There is no inclusion body
ally required. The U.S. Department of Agriculture has approved formation.
the use of 2% sodium hydroxide as the only disinfectant for san-
itation of scrapie-infected premises. Prions are highly resistant Pathogenesis. Lesions often begin within 24 hr after expo-
to physicochemical means of disinfection. Artificial insemina- sure. The virus invades oral epithelium. Injuries or trauma in
tion or embryo transfer has been shown to decrease the spread any area typically affected, such as mouth, teats, or interdigital
of scrapie (Linnabary et al., 1991). areas, will increase the likelihood of lesions developing there.
Animals will develop a long-term immunity; this immunity can
Treatment. No vaccine or treatment is available. be overwhelmed, however, by a large dose of the virus.
582 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

Differential diagnosis. Foot-and-mouth disease lesions are Coronavirus, of the family Coronaviridae, produces a more
identical to VS lesions. Other differentials in cattle include severe, long-lasting disease when compared with rotavirus.
bovine viral diarrhea, malignant catarrhal fever, contagious ec- Clinical signs are similar to above, although the incubation pe-
thyma, photosensitization, trauma, and caustic agents. riod tends to be shorter (20-36 hr), and animals exhibit less an-
orexia than those with rotavirus. Additionally, mild respiratory
Prevention and control. Quarantine and restrictions on ship- disease may be noted (Janke, 1989). Like rotavirus, coronavirus
ping infected animals or animals from the premises housing af- also destroys enterocytes of the villus tips. The virus can be vi-
fected animals are required in an outbreak. Vaccines are avail- sualized with electron microscopy. Treatment is supportive;
able for use in outbreaks and have decreased the severity of close consideration of hydration and acid-base status is essen-
lesions. Phenolics, quaternaries, and halogens are effective for tial. Bovine vaccines are available.
inactivating and disinfecting equipment and facilities.
ii. Caprine. Rotavirus, coronavirus, and adenoviruses af-
Treatment. Affected animals should be segregated from the fect neonatal goats; however, little has been documented on the
rest of the herd and provided with separate water and softened pathology and significance of these agents in this age group. It
feed. These animals should be cared for after unaffected ani- appears that bacteria play a more important role in neonatal kid
mals. Any feed or water contaminated by these animals should diarrheal diseases then in neonatal calf diarrheas.
not be used for other animals; contaminated equipment should
be disinfected. Topical or systemic antibiotics control second- iii. Bovine. Rotaviruses, coronaviruses, parvoviruses, and
ary bacterial infections. Cases of mastitis secondary to teat le- bovine viral diarrhea virus (BVDV) are associated with diar-
sions must be treated as necessary. Any abrasive materials that rheal disease in calves. Each pathogen multiplies within and de-
could cause further trauma to the animals should be removed. stroys the intestinal epithelial cells, resulting in villous atrophy
and clinical signs of diarrhea (soft to watery feces), dehydra-
Research complications. Animals developing vesicular le- tion, and abdominal pain. These viral infections may be com-
sions must be reported promptly to eliminate the possibility of plicated by parasitic infections (e.g., Cryptosporidium, Eime-
an outbreak of foot-and-mouth disease. Personal protective ria) or bacterial infections (e.g., Escherichia coli, Salmonella,
equipment, especially gloves, should be worn when handling Campylobacter). Treatment is aimed at correcting dehydration,
any animals with vesicular lesions. VSV causes a flulike illness electrolyte imbalances, and acidosis; cessation of milk replac-
in humans. ers and administration of fluid therapy intravenously and by
stomach tube may be necessary, depending on the presence of
suckle reflex and the condition of the animals. Diagnosis is by
x. Viral Diarrhea Diseases
immunoassays available for some viruses, viral culture, exclu-
i. Ovine. Rotavirus, of the family Reoviridae, induces an sion or identification of presence of other pathogens (by culture
acute, transient diarrhea in lambs within the first few weeks of or fecal exams), and microscopic examination of necropsy
life. Four antigenic groups (A-D) have been identified by dif- specimens. Prevention focuses on calves suckling good-quality
ferences in capsid antigens VP3 and VP7. Primarily group A, colostrum; other recommendations for calf care are in Sec-
but also groups B and C, have been isolated from sheep. The tion II,B,5. Combination vaccine products are available for im-
disease is characterized by yellow, semifluid to watery diarrhea munizing dams against rotavirus, coronavirus, and enterotoxi-
occurring 1-4 days after infection. The disease can progress to genic E. coli. Additional supportive care for calves includes
dehydration, anorexia and weight loss, acidosis, depression, and providing calves with sufficient energy and vitamins until milk
occasionally death. The virus is ingested with contaminated intake can resume.
feed and water and selectively infects and destroys the entero- Rotaviruses of serogroup A are the most common type in
cytes at the tips of the small intestinal villi. The villi are re- neonatal calves; 4- to 14-day old calves are typically affected,
placed with immature cells that lack sufficient digestive en- but younger and older animals may also be affected. The small
zymes; osmotic diarrhea results. Virus may remain in the intestine is the site of infection. Antirotavirus antibody is pres-
environment for several months. The disease is diagnosed by ent in colostrum, and onset of rotavirus diarrhea coincides with
virus isolation, electron microscopy of feces, fecal fluorescent the decline of this local protection. Transmission is likely from
antibody, fecal ELISA tests (marketed tests generally detect other affected calves and asymptomatic adult carriers. The diar-
group A rotavirus), and fecal latex agglutination tests. Rotavirus rhea is typically a distinctive yellow. Colitis with tenesmus, mu-
diarrhea is treated by supportive therapy, including maintaining cus, and blood may be seen. This virus may be zoonotic.
hydration, electrolyte, and acid-base balance. A rotavirus vac- Coronaviruses are commonly associated with disease in
cine is available for cattle; because of cross-species immunity, calves during the first month of life, and they infect small- and
oral administration of high-quality bovine colostrum from vac- large-intestinal epithelial cells. The virus infection may extend
cinated cows to infected sheep may be helpful ("Current Veteri- to mild pneumonia. Transmission is by infected calves and also
nary Therapy," 1993). by asymptomatic adult cattle, including dams excreting virus at
14. BIOLOGYAND DISEASESOF RUMINANTS:SHEEP, GOATS,AND CATTLE 583

the time of parturition. Calves that appear to have recovered antigen is common among all Chlamydia; the specific antigen
continue to shed virus for several weeks. is common to related subgroups. Two subgroups are recog-
Parvovirus infections are usually associated with neonatal nized, one that causes EAE and one that causes polyarthritis and
calves. B VDV infections also are seen in neonates and also af- conjunctivitis. The disease is transmitted by direct contact with
fect many systems and produce other clinical signs and syn- infectious secretions such as placental, fetal, and uterine fluids
dromes that are described in Section III,A,2,e. or by indirect contact with contaminated feed and water.

iv. Winter Dysentery. Winter dysentery is an acute, winter- Necropsy. Placental lesions include intercotyledonary plaques
seasonal, epizootic diarrheal disease of adult cattle, although it and necrosis and cotyledonary hemorrhages. Histopathological
has been reported in 4-month-old calves. The etiology has not evidence of leukocytic infiltration, edema, and necrosis is found
yet been defined, but a viral pathogen is suspected. Corona- throughout the placentome. Fetal lesions include giant-cell ac-
virus-like viral particles have been isolated from cattle feces, ei- cumulation in mesenteric lymph nodes and lymphohistiocytic
ther the same as or similar to the coronavirus of calf diarrhea. proliferations around the blood vessels within the liver. Diagno-
Outbreaks typically last a few weeks, and first-lactation or sis is based on clinical signs and laboratory (serological or
younger cattle are affected first, with waves of illness moving histopathological) identification of the organism. Impression
through a herd. Individual cows are ill for only a few days. The smears in placental tissues stained with Giemsa, Gimenez, or
incubation period is estimated at 2 - 8 days. The outbreaks of modified Ziehl-Neelsen can provide preliminary indications of
disease are often seen in herds throughout the local area. Clini- the causative agent. Immunofluorescence, enzyme-linked im-
cal signs include explosive diarrhea, anorexia, depression, and munosorbent assay (ELISA), and polymerase chain reaction
decreased production. The diarrhea has a distinctive musty, (PCR) methods also aid in diagnosis.
sweet odor and is light brown and bubbly, but some blood
streaks or clots may be mixed in with the feces. Animals will Differential diagnosis. Q fever will be the major differential
become dehydrated quickly but are thirsty. Respiratory symp- for late-term abortion and necrotizing placentitis. Campylo-
toms such as nasolacrimal discharges and coughing may de- bacter and Toxoplasma should also be considered for late-term
velop. Recovery is generally spontaneous. Mortalities are rare. abortion.
Diagnosis is based on characteristic patterns of clinical signs,
and elimination of diarrheas caused by parasites such as coc-
Treatment. Animals may respond to treatment with oxytetra-
cycline. Abortions are prevented through administration of a
cidia, bacterial organisms such as Salmonella or Mycobac-
commercial vaccine, but the vaccine will not eliminate infec-
terium paratuberculosis, and viruses such as B VDV. Pathology
tions. This is a sheep vaccine and should be administered before
is present in the colonic mucosa, and necrosis is present in the
breeding and annually to at least the young females entering the
crypts.
breeding herd or flock.
3. Chlamydial Diseases
Research complications. In addition to losses or compromise
a. Enzootic Abortion of Ewes (Chlamydial Abortion) of research animals, pregnant women should not handle aborted
tissues.
Etiology. Chlamydia psittaci is a nonmotile, obligate, intracy-
toplasmic, gram-negative bacterium.
b. Chlamydial Polyarthritis of Sheep
Clinical signs. Enzootic abortion in sheep and goats is a con- Etiology. Chlamydia psittaci is a nonmotile, obligate intracel-
tagious disease characterized by hyperthermia and late abortion lular, gram-negative bacterium. Chlamydial polyarthritis is an
or by birth of stillborn or weak lambs or kids (Rodolakis et al., acute, contagious disease characterized by fever, lameness
1998). The only presenting clinical sign may be serosan- (Bulgin, 1986), and conjunctivitis (see Section III,A,3,c) in
guineous vulvar discharges. Other animals may present with growing and nursing lambs.
arthritis or pneumonia. Infection of animals prior to about 120
days of gestation results in abortion, stillbirths, or birth of weak Clinical signs. Clinically, animals will appear lame on one or
lambs. Infection after 120 days results in potentially normal all legs and in major joints, including the scapulohumeral,
births, but the dams or offspring may be latently infected. humeroradioulnar, coxofemoral, femorotibial, and tibiotarsal
Latently infected animals that were infected during their dry pe- joints. Lambs may be anorexic and febrile. Animals frequently
riod may abort during the next pregnancy. Ewes or does gener- also exhibit concurrent conjunctivitis. The disease usually re-
ally only abort once, and thus recovered animals will be im- solves in approximately 4 weeks. Joint inflammation usually
mune to future infections. resolves without causing chronic articular changes.

Epizootiology and transmission. Chlamydia possess group Epizootiology and transmission. The disease is transmitted to
and specific antigens associated with the cell surface. The group susceptible animals by direct contact as well as by contaminated
584 SCOTT A. MISCHLER,WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

feed and water. The organism penetrates the gastrointestinal The chlamydial organism may penetrate the bloodstream and
tract and migrates to joints and synovial membranes as well as migrate to the opposite eye or joints, leading to arthritis. Diag-
to the conjunctiva. The organism causes acute inflammation and nosis is suggested by the clinical signs. Cytoplasmic inclusions
associated fibrinopurulent exudates. observed on conjunctival scrapings and immunofluorescent
techniques help confirm the diagnosis.
Necropsy findings. Lesions are found in joints, tendon
sheaths, conjunctiva, and lungs. Pathological sites will be ede- Differential diagnosis. Nonchlamydial keratoconjunctivitis
matous and hyperemic, with fibrinous exudates but without ar- also occurs in sheep and goats. The primary agents involved in-
ticular changes. Lesions will be infiltrated with mononuclear clude Mycoplasma conjunctiva, M. agalactiae in goats, and
cells. Lung lesions include atelectasis and alveolar inspissation. Branhamella (Neisseria) ovis. A less common differential for
Diagnosis is based on clinical signs. Synovial taps and subse- sheep and cattle is Listeria monocytogenes. Other differentials
quent smears may allow the identification of chlamydial inclu- include eye worms, trauma, and foreign bodies such as wind-
sion bodies. blown materials (pollen, dust) and poor-quality hay; these latter
irritants and stress may predispose the animals' eyes to the in-
Treatment. Animals respond to treatment with parenteral fectious agents.
oxytetracycline.
Prevention and control. Source of mechanical irritation
should be minimized whenever possible. Quarantine of new an-
Chlamydial Conjunctivitis (Infectious
imals and treatment, if necessary, before introduction into the
Keratoconjunctivitis, Pinkeye)
flock or herd are important measures. Shade should be provided
Etiology. Chlamydia psittaci, a nonmotile, obligate intracel- for all animals.
lular, gram-negative bacterium, is the most common cause of
infectious keratoconjunctivitis in sheep. Chlamydia and My- Treatment. The infections can be self-limiting in 2 - 3 weeks
coplasma are considered to be the most common causes of this without treatment. Treatment consists of topical application of
disease in goats. Chlamydial conjunctivitis is not a disease of tetracycline ophthalmic ointments. Systemic or oral oxytetracy-
cattle. cline treatments have been used with the topical treatment. At-
ropine may be added to the treatment regimen when uveitis is
Clinical signs. Infectious keratoconjunctivitis is an acute, present. Shade should be provided.
contagious disease characterized in earlier stages by conjuncti-
val hyperemia, epiphora, and edema and in later stages by, 4. Parasitic Diseases
corneal edema, ulceration, and opacity. Perforation may result
a. Protozoa
from the ulceration. Animals will be photophobic. In less severe
cases, corneal healing associated with fibrosis and neovascular- i. Anaplasmosis
ization occurs in 3 - 4 days. Lymphoid tissues associated with Etiology. Anaplasmosis is an infectious, hemolytic, noncon-
the conjunctiva and nictitating membrane may enlarge and pro- tagious, transmissible disease of cattle caused by the protozoan
lapse the eyelids. Morbidity may reach 80-90%. Bilateral and Anaplasma marginale. Anaplasma is a member of the Anaplas-
symmetrical infections characterize most outbreaks. Relapses matacae family within the order Rickettsiales. In sheep and
may occur. Other concurrent systemic infections may be seen, goats, the disease is caused by A. ovis and is an uncommon
such as polyarthritis or abortion in sheep and polyarthritis, mas- cause of hemolytic disease. Anaplasmosis has not been re-
titis, and uterine infections in goats. ported in goats in the United States. Some controversy exists re-
garding the classification. Most recently it is classified as a pro-
Epizootiology and transmission. Direct contact, and mechan- tozoal disease because of similarities to babesiosis. It has also
ical vectors such as flies easily spread the organism. been classified as a rickettsial pathogen. This summary ad-
dresses the disease in cattle with limited reference to A. ovis in-
Necropsy. If the chlamydial or mycoplasmal agents are sus- fections, but there are many similarities to the disease in cattle.
pected, diagnostic laboratories should be contacted for recom-
mendations regarding sampling. Conjunctival smears are also Clinical signs and diagnosis. Acute anemia is the predomi-
useful. nant sign in anaplasmosis, and fever coincides with parasitemia.
Weakness, pallor, lethargy, dehydration, and anorexia are the
Pathogenesis. The pathogen penetrates the conjunctival ep- result of the anemia. Four disease stagesnincubation, develop-
ithelium and replicates in the cytoplasm by forming initial and mental, convalescent, and carriermare recognized. The incu-
elementary bodies. The infection moves from cell to cell and bation stage may be long, 3 - 8 weeks, and is characterized by a
causes an acute inflammation and resultant purulent exudate. rise in body temperature as the infection moves to the next
 14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 585

stage. Most clinical signs occur during the 4- to 9-day develop- whole organism) programs are not entirely effective, and vac-
mental stage, with hemolytic anemia being common. Death is cine should not be administered to pregnant cows. Neonatal iso-
most likely to occur at this stage or at the beginning of the con- erythrolysis may occur because of the antierythrocyte antibod-
valescent stage. Death may also occur from anoxia, because of ies stimulated by one vaccine product. Vaccinated animals can
the animal's inability to handle any exertion or stress, especially still become infected and become carriers. The cattle vaccine
if treatment is initiated when severe anemia exists. Reticulocy- has shown no efficacy in smaller ruminants, and there is no A.
tosis characterizes the convalescent stage, which may continue ovis vaccine. Identifying carriers serologically and treating with
for many weeks. Morbidity is high, and mortality is low. The tetracycline during and/or after vector seasons may be an op-
carrier stage is defined as the time in the convalescent stage tion. Removing carriers to a separate herd is also an approach.
when the animal host becomes a reservoir of the disease, and Interstate movement of infected animals is regulated.
Anaplasma organisms and any parasitemia are not discernible.
Common serologic tests are the complement fixation test and Treatment. Oxytetracycline, administered once, helps reduce
the rapid card test. These become positive after the incubation the severity of the infection during the developmental stage.
phase and do not distinguish between the later three stages of Other tetracycline treatment programs have been described to
disease. Definitive diagnosis is made by clinical and necropsy help control carriers.
findings. Staining of thin blood smears with Wright's or Giemsa
stain allows detection of basophilic, spherical A. marginale ii. Babesiosis (red water, Texas cattle fever, cattle tick fever)
bodies near the red blood cell peripheries. Evidence will most Etiology. Babesia bovis and Ba. bigemina are protozoa that
likely be found before a hemolytic episode. A negative finding cause subclinical infections or disease in cattle. These are in-
should not eliminate the pathogen from consideration. traerythrocytic parasites. Babesia bovis is regarded as the more
virulent of the two organisms. This disease is not seen in the
Epizootiology and transmission. The disease is common in smaller ruminants in the United States.
cattle in the southern and western United States. Anaplasma or-
ganisms are spread biologically or mechanically. Mechanical Clinical signs and diagnosis. The more common presentation
transmission occurs when infected red blood cells are passed is liver and kidney failure due to hemolysis with icterus, hemo-
from one host to another on the mouthparts of seasonal biting globinuria, and fever. Hemoglobinuria indicates a poor progno-
flies. Sometimes mosquitoes or instruments such as dehorners sis. Acute encephalitis is a less common presentation and be-
or hypodermic needles may facilitate transfer of infected red gins acutely with fever, ataxia, depression, deficits in conscious
cells from one animal to another. Biological transmission oc- proprioception, mania, convulsions, and coma. The encepha-
curs when the tick stage of the organism is passed by Derma- litic form generally also has a poor prognosis. Sudden death
centor andersoni and D. occidentalis ticks. The carrier stage may occur.
covers the time when discernible Anaplasma organisms can be Thin blood smears stained with Giemsa will show Babesia
found on host blood smears. Recovered animals serve as im- trophozoites at some stages of the disease, but lack of these can-
mune carriers and disease reservoirs. not be interpreted as a negative. The trophozoites occur in a va-
riety of shapes, such as piriform, round, or rod. Complement
Necropsy. Pale tissues and watery, thin blood are typical find- fixation, immunofluorescent antibody, and enzyme immunoas-
ings. Splenomegaly, hepatomegaly, and gallbladder distension say are the most favored of the available serologic tests.
are common findings.
Epizootiology and transmission. Babesiosis is present on sev-
Pathogenesis. The parasites infect the host's red blood cells, eral continents, including the Americas. In addition to domes-
and acute hemolysis occurs during the parasites' developmental tic cattle, some wild ruminants, such as white-tailed deer and
stage. The four stages of the parasite's life cycle are described American buffalo, are also susceptible. Bos indicus breeds have
above because these are closely linked to the clinical stages. resistance to the disease and the tick vectors. Innate resistance
factors have been found in all calves. If infected, these animals
Differential diagnosis. The clinical disease closely resembles will not show many signs of disease during the first year of life
the protozoal disease babesiosis. and will become carriers. Stress can cause disease development.

Prevention and control. Offspring of immune carriers resist Necropsy findings. Signs of acute hemolytic crisis are the
infection up to 6 months of age because of passive immunity. most common findings, including hepatomegaly, splenomegaly,
Vector control and attention to hygiene are essential, such as dark and distended gallbladder, pale tissues, thin blood, scat-
between-animal rinsing in disinfectant of mechanical vectors tered hemorrhages, and petechiation. Animals dying after a
such as dehorners. There is no entirely effective means, how- longer course of disease will be emaciated and icteric, with thin
ever, to prevent and control the disease. Vaccination (killed blood, pale kidneys, and enlarged liver.
586 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

Pathogenesis. The protozoon is transmitted by the cattle fever least 9 species of Eimeria have been recognized in the goat
ticks Boophilus annulatus, B. microplus, and B. decoloratus; (Foreyt, 1990). Eimeria ninakohlyakimovae, E. arloingi, and E.
these one-host ticks acquire the protozoon from infected ani- christenseni are regarded as the most pathogenic. Eimeria bovis
mals. It is passed transovarially, and both nymph and adult ticks and E. zuernii (highly pathogenic), and E. auburnensis and E.
may transmit to other cattle. Only B. ovis is transmitted by the alabamensis (moderately pathogenic), are among the 13 species
larval stage. Clinical signs develop about 2 weeks after tick in- known to infect cattle. Eimeria zuernii is more commonly seen
festations or mechanical transmission but may develop sooner in older cattle and is the agent of "winter coccidiosis."
with the mechanical transmission. Hemolysis is due to intracel-
lular reproduction of the parasites and occurs intra- and ex- Clinical signs and diagnosis. Hemorrhagic diarrhea develops
travascularly. In addition to the release of merozoites, prote- 10 days to 3 weeks after infection. Fecal staining of the tail
olytic enzymes are also released, and these contribute to the and perineum will be present. Animals will frequently display
clinical metabolic acidosis and anoxia. The development of the tenesmus; rectal prolapses may also develop. Anorexia, weight
encephalitis form is believed to be the result of direct invasion loss, dehydration, anemia, fever (infrequently), depression, and
of the central nervous system, disseminated intravascular co- weakness may also be seen in all ruminants. The diarrhea is wa-
agulation, capillary thrombosis by the parasites and infarction, tery and malodorous and will contain variable amounts of blood
and/or tissue anoxia. and fibrinous, necrotic tissues. The intestinal hemorrhage may
subsequently lead to anemia and hypoproteinemia. Depending
Differential diagnosis. In addition to anaplasmosis, other dif- on the predilection of the coccidial species for small and/or
ferentials for the hemolytic form of the disease are leptospiro- large intestines, malabsorption of nutrients or water may occur,
sis, chronic copper toxicity, and bacillary hemoglobinuria. and electrolyte imbalances may be severe. Concurrent disease
Several differentials in the United States for the encephalitic with other enteropathogens may also be part of the clinical
presentation include rabies, nervous system coccidiosis, po- picture.
lioencephalomalacia, lead poisoning, infectious bovine rhino- In sheep, secondary bacterial infection with organisms such
tracheitis, salt poisoning, and chlorinated hydrocarbon toxicity. as Fusobacterium necrophorum may ensue. Young goats may
die peracutely or suffer severe anemia from blood loss into the
Prevention and control. Control or eradication of ticks and bowel. Older goats may lose the pelleted form of feces. Cattle
cleaning of equipment to prevent mechanical transmission, as may have explosive diarrhea and develop anal paralysis.
noted in Section III,A,3,a,i, are important preventive measures. The disease is usually diagnosed by history and clinical signs.
Some vaccination approaches have been effective, but a com- Numerous oocysts will frequently be observed in fresh fecal
mercial product is not available. flotation (salt or sugar solution) samples as the diarrhea begins.
Laboratory results are usually reported as number of oocysts
Treatment. Supportive care is indicated, including blood per gram of feces. Coccidia seen on routine fecal evaluations
transfusions, fluids, and antibiotics. Medications such as dimi- reflect shedding, possibly of nonpathogenic species, without
nazene diaceturate, phenamidine diisethionate, imidocarb dipri- necessarily being indicative of impending or resolving mild
onate, or amicarbalide diisethionate are most commonly used. disease.
Treatment outcomes will be either elimination of the parasite
or development of a chronic carrier state immune to further
disease. Epkzootiology and transmission. As noted, coccidiosis is a
common disease in young ruminants. In goats, young animals
Research complications. This is a reportable disease in the aged 3 weeks to 5 months are primarily affected, but isolated
United States. outbreaks in adults may occur after stressful conditions such as
transportation or diet changes. Coccidia are host-specific and
iii. Coccidiosis also host cell-specific. The disease is transmitted via ingestion
Etiology. Coccidiosis is an important acute and chronic proto- of sporulated oocysts. Coccidial oocysts remain viable for long
zoal disease of ruminants. In young ruminants, it is character- periods of time when in moist, shady conditions.
ized primarily by hemorrhagic diarrhea. Adult ruminants may
carry and shed the protozoa, but they rarely display clinical Necropsy. Necropsies provide information on specific loca-
signs. Intensive rearing and housing conditions and stress in- tions and severity of lesions that correlate with the species
crease the severity of the disease in all age groups. involved. Ileitis, typhlitis, and colitis with associated necrosis
Coccidia are protozoal organisms of the phylum Apicom- and hemorrhage will be observed. Mucosal scrapings will fre-
plexa, members of which are obligatory intracellular parasites. quently yield oocysts. Various coccidial stages associated with
There are at least 11 reported species of coccidia in sheep, of schizogony or gametogony may be observed in histopathologi-
which several are considered pathogenic: Eimeria ashata, E. cal sections of the intestines. Fibrin and cellular infiltrates will
crandallis, and E. ovinoidalis (Schillhorn van Veen, 1986). At be found in the lamina propria.
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 587

Pathogenesis. This parasite has a complex life cycle in which iv. Cryptosporidiosis
sexual and asexual reproduction occurs in gastrointestinal ente- Etiology. Cryptosporidium organisms are a very common
rocytes (Speer, 1996). The severity of the disease is correlated cause of diarrhea in young ruminants. Four Cryptosporidium
primarily with the number of ingested oocysts. Specifics of life species have been described in vertebrates: C. baileyi and C.
cycles vary with the species, and those characteristics con- meleagridis in birds and C. parvum and C. muris in mammals.
tribute to the pathogenicity. In most cases, the disease is well es- Cryptosporidium parvum is the species affecting sheep (Rings
tablished by the time clinical signs are seen. Oocysts must un- and Rings, 1996). Debate continues regarding whether there are
dergo sporulation over a 3- to 10-day period in the environment. definite host-specific variants.
After ingestion of the sporulated oocysts, sporozoites are re-
leased and penetrate the intestinal mucosa and form schizonts. Clinical signs and diagnosis. Cryptosporidiosis is character-
Schizonts initially undergo replication by fission to form mero- ized by protracted, watery diarrhea and debilitation. The diar-
zoites and eventually undergo sexual reproduction, forming rhea may last only 6 - 1 0 days or may be persistent and fatal. The
new oocysts. The organisms cause edema and hyperemia; pene- diarrhea is watery and yellow, and blood, mucus, bile, and undi-
tration into the lamina propria may lead to necrosis of capillar- gested milk may also be present. Infected animals will display
ies and hemorrhage. tenesmus, anorexia and weight loss, dehydration, and depres-
sion. In relapsing cases, animals become cachectic. Overall,
Differential diagnosis. Differential diagnoses include the morbidity will be high, and mortality variable.
many enteropathogens associated with acute diarrhea in young Mucosal scrapings or fixed stained tissue sections may be
ruminants: cryptosporidia, colibacilli, salmonella, enterotox- useful in diagnosis. The disease is also diagnosed by detecting
ins, Yersinia, viruses, and other intestinal parasites such as the oocysts in iodine-stained feces or in tissues stained with pe-
helminths. In cattle, for example, bovine viral diarrhea virus riodic acid-Schiff stain or methenamine silver. Cryptosporid-
and helminthiasis caused by Ostergia must be considered. ium also stains red on acid-fast stains such as Kinyoun or Ziehl-
Management factors, such as dietary-induced diarrheas, are Neelsen. Fecal flotations should be performed without sugar
also differentials. In older animals, differentials in addition to solutions or with sugar solutions at specific gravity of 1.27
stress are malnutrition, grain engorgement, and other intestinal (Foryet, 1990). Fecal immunofluorescent antibody (IFA) tech-
parasitisms. niques have also been described.
Prevention and control. Good management practices will
help prevent the disease. Oocysts are resistant to disinfectants Epizootiology and transmission. Younger ruminants are com-
but are susceptible to dry or freezing conditions. Proper sanita- monly affected: lambs, kids (especially kids between the ages of
tion of animal housing and minimizing overcrowding are es- 5 and 10 days old), and calves less than 30 days old. Like other
sential. Coccidiostats added to the feed and water are helpful in coccidians, Cryptosporidium is transmitted via the fecal-oral
preventing the disease in areas of high exposure. route. In addition to local contamination, water supplies have
also been sources of the infecting oocysts. The oocysts are ex-
Treatment. Affected animals should be isolated. On an indi- tremely resistant to desiccation in the environment and may sur-
vidual basis, treatment should also include provision of a dry, vive in the soil and manure for many months.
warm environment, fluids, electrolytes (orally or intravenously),
antibiotics (to prevent bacterial invasion and septicemia), and Necropsy findings. The lesions caused by Cryptosporidium
administration of coccidiostats. Coccidiostats are preferred to are nonspecific. Animals will be emaciated. Moderate enteritis
coccidiocidals because the former allow immunity to develop. and hyperplasia of the crypt epithelial cells with villous atrophy
Although many coccidial infections tend to be self-limiting, as well as villous fusion, primarily in the lower small intestines,
sulfonamides and amprolium may be used to aid in the treat- will be present. Cecal and colonic mucosae may sometimes be
ment of disease. Other anticoccidial drugs include decoquinate, involved. Gastrointestinal smears may be made at necropsy and
lasalocid, and monensin; labels should be checked for specific stained as described above.
approval in a species or specific indications. Animals treated
with amprolium should be monitored for development of sec- Pathogenesis. Although Cryptosporidium infections are clin-
ondary polioencephalomalacia. Pen mates of affected animals ically similar to Eimeria infections (Moore, 1989), Crypto-
should be considered exposed and should be treated to control sporidium, in contrast to Eimeria, invades just under the surface
early stages of infection. but does not invade the cytoplasm of enterocytes. There is no in-
Mechanisms of immunity have not been well defined but ap- termediate host. The oocysts are half the size of Eimeria oocysts
pear to be correlated with the particular coccidial species and and are shed sporulated; they are, therefore, immediately infec-
their characteristics (for example, the extent of intracellular tive. Within 2 - 7 days of exposure, diarrhea and oocyst shed-
penetration). Immunity may result when low numbers are in- ding occur. The diarrhea is the result of malabsorption and, in
gested and there is only mild disease. Immunity also may de- younger animals, intraluminal milk fermentation. Autoinfec-
velop after more severe infections. tion within the lumen of the intestines may also occur and result
588 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

in persistent infections. In addition, several other pathogens blood. Animals exhibit fever, dehydration, and depression.
may be involved, such as concurrent coronavirus and rota- Chronic cases may result in a "poor doer" syndrome with
virus infections in calves. Environmental stressors such as cold weight loss and unthriftiness.
weather increase mortality. Intensive housing arrangements in- Giardia can be diagnosed by identifying the motile piriform
crease morbidity and mortality. trophozoites in fresh fecal mounts. Oval cysts can be floated
with zinc sulfate solution (33%). Standard solutions tend to be
Differential diagnosis. Other causes of diarrhea in younger too hyperosmotic and to distort the cysts. Newer enzyme-linked
ruminants include rotavirus, coronavirus, and other enteric viral immunosorbent assay (ELISA) and IFA tests are sensitive and
infections; enterotoxigenic Escherichia coli; Clostridium; other specific.
coccidial pathogens; and dietary causes (inappropriate use of
milk replacers). In addition, these other agents may also be Epizootiology and transmission. Giardia infection may occur
causing illness in the affected animals and may complicate the at any age, but young animals are predisposed. Chronic oocyst
diagnosis and the treatment picture. Eimeria is more likely shedding is common. Transmission of the cyst stage is fecal-
to cause diarrhea in calves and lambs at 3 - 4 weeks of age. oral. Wild animals may serve as reservoirs.
Giardia organisms may be seen in fecal preparations from
young ruminants but are not considered to play a significant role Necropsy findings. Gross lesions may not be evident. Villous
in enteric disease. atrophy and cuboidal enterocytes may be evident histologically.

Prevention and control. Precautions should be taken when

Pathogenesis. Following ingestion, each Giardia cyst re-
leases four trophozoites, which attach to the enterocytes of the
handling infected animals. Affected animals must be removed
duodenum and proximal jejunum and subsequently divide by
and isolated as soon as possible. Animal housing areas should
binary fission or encyst. The organism causes little intestinal
be disinfected with undiluted commercial bleach or 5% ammo-
pathology, and the cause of diarrhea is unknown but is thought
nia. Formalin (10%) fumigation has proven successful (Foryet,
to be related to disruption of digestive enzyme function, leading
1990). After being cleaned, areas should be allowed to dry thor-
to malabsorption. Disturbances in intestinal motility may also
oughly and should remain unpopulated for a period of time. Be-
occur (Rings and Rings, 1996).
cause enteric disease often is multifactorial, other pathogens
should also be considered, and management and husbandry
Prevention and control. Intensive housing and warm environ-
should be examined.
ments should be minimized. Cysts can survive in the environ-
ment for long periods of time but are susceptible to desiccation.
Treatment. No known drug treatment is available. The disease
Effective disinfectants include quaternary ammonium com-
is generally self-limiting, so symptomatic, supportive therapy
pounds, bleach-water solution (1:16 or 1:32), steam, or boil-
aimed at rehydrating, correcting electrolyte and acid-base bal-
ing water. After cleaning, areas should be left empty and al-
ance, and providing energy is often effective. Supplementation
lowed to dry completely.
with vitamin A may be helpful. Age resistance begins to de-
velop when the animals are about 1 month old. Treatment. Giardia has been successfully treated with oral
metronidazole. Benzimidazole anthelmintics are also effective,
Research complications. Cryptosporidiosis is a zoonotic dis- but these are not approved for use in animals for this purpose.
ease. It is easily spread from calves to humans, for example,
even as the result of simply handling clothing soiled by calf Research complications. Giardia is zoonotic. Precautions
diarrhea. Adult immunocompetent humans are reported to ex- should be taken when handling infected animals.
perience watery diarrhea, cramping, flatulence, and headache.
The disease can be life-threatening in immunocompromised vi. Neosporosis
individuals. Etiology. Neosporosis is a common, worldwide cause of
bovine abortion caused by the protozoal species Neospora cani-
v. Giardiasis num. Abortions have also been reported in sheep and goats.
Etiology. Giardia lamblia (also called G. intestinalis and G. Neonatal disease is seen in lambs, kids, and calves. Until 1988,
duodenalis) is a flagellate protozoon. Giardiasis is a worldwide these infections were misdiagnosed as caused by Toxoplasma
protozoal-induced diarrheal disease of mammals and some birds gondii. Some similarities exist between the life cycles and
(Kirkpatrick, 1989), but it not considered to be a significant pathogeneses of both organisms.
pathogen in ruminants.
Clinical signs and diagnosis. Abortion is the only clinical
Clinical signs and diagnosis. Diarrhea may be continuous or sign seen in adult cattle and occurs sporadically, endemically, or
intermittent, is pasty to watery, is yellow, and may contain as abortion storms. Bovine abortions occur between the third
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 589

and seventh month of gestation; fetal age at abortion correlates undergoes sexual replication in the dog's intestinal tract, and
with the parity of the dam as well as with pattern of abortion oocysts are shed in the feces. The intermediate hosts develop
in the herd. Although cows that abort tend to be culled after nonclinical systemic infections, with tachyzoites in several or-
the first or second abortion, repeated N. caninum-caused abor- gans, and parasites then localize and become encysted in par-
tions will occur progressively later in gestation (up to about ticular tissues, especially the brain. Infections of this type are
6 months) and within a shorter time frame in the same cow latent and lifelong. Except when immunocompromised, most
(Thurmond and Hietala, 1997). Although infections in adults cattle do not usually develop clinical signs and do not have
are asymptomatic other than the abortions, decreased milk pro- fetal loss. Fetuses become infected, leading to fetal death,
duction has been noted in congenitally infected cows. mid-gestation abortions, or live calves with latent infections or
Many Neospora-infected calves will be born asymptomatic. congenital brain disease. It usually takes 2 - 4 weeks for a fetus
Weakness will be evident in some infected calves, but this re- to die and to be expelled. Many aspects of the role of the ma-
solves. Rare clinical signs include exophthalmos or asymmetric ternal immune response and pregnancy-associated immuno-
eyes, weight loss, ataxia, hyperflexion or hyperextension of all deficiency in the patterns of Neospora abortions remain to be
limbs, decreased patellar reflexes, and loss of conscious propri- elucidated.
oception. Some fetal deaths will occur, and resorption, mummi-
fication, autolysis, or stillbirth will follow. Differential diagnosis. Even when there is a herd history of
Immunohistochemistry and histopathology of fetal tissue are confirmed Neospora abortions, leptospirosis, bovine viral di-
the most efficient and reliable means of establishing a post- arrhea virus (BVDV), infectious bovine rhinotracheitis virus
mortem diagnosis. Serology (IFA and ELISA) is useful, includ- (IBRV), salmonellosis, and campylobacteriosis should be con-
ing precolostral levels in weak neonates, but this indicates only sidered. BVDV in particular should be considered for abortion
exposure. Titers of dams will not be elevated at the time of abor- storms. Differentials for weak calves are B VDV, perinatal hy-
tion; fetal serology is influenced by the stage of gestation and poxia following dystocia (immediate postpartum time), blue-
course of infection. Earlier and rapid infections are less likely to tongue virus, Toxoplasma, exposure to teratogens, or congeni-
yield antibodies against Neospora. None of the currently avail- tal defects.
able tests is predictive of disease.
Prevention and control. The primary preventive measure is
Epizootiology and transmission. The parasite is now ac- preventing contact with contaminated feces. Oocysts will not
knowledged to be widespread in dairy and cattle herds. The life survive dry environments or extremes of temperature. Dog
cycle of N. caninum is complex, and many aspects remain to be populations should be controlled, and dogs and other canids
clarified. The definitive host is the dog (McAllister et al., 1998). should not have access to placentas or aborted fetuses. Dogs
Placental or aborted tissues are the most likely sources of infec- should also be restricted from feed bunks and other feed storage
tion for the definitive host and play a minor role in transmission areas. Preventive culling is not economically practical for most
to the intermediate hosts. The many intermediate hosts include producers. A vaccine recently became available. If embryo
ruminants, deer, and horses. Transplacental transmission is the transfer is practiced, recipients should be screened serologically
major mode of transmission in dairy cattle and is the means by before use.
which a herd's infection is perpetuated. A less significant mode
of transmission is by ingestion of oocysts, which sporulate in Treatment. There is no known treatment or immunoprophy-
the environment or in the intermediate host's body. Reactivation laxis.
in a chronically infected animal's body is the result of rupture
of tissue cysts in neural tissue. Seropositive immunity does vii. Sarcocystosis
not protect a cow from future abortions. Many seropositive Etiology. Sarcocystosis is the disease caused by the cyst-
cows and calves will never abort or show clinical signs, respec- forming sporozoon Sarcocystis. Sarcocystis capricanus, S. ovi-
tively. Some immunological cross-reactivity may exist among canus, and S. tenella are the species that infect sheep and goats.
Neospora, Cryptosporidia, and Coccidium. Sarcocystis cruzi, S. hirsuta, and S. hominis are the species that
Necropsy findings. Aborted fetuses will usually be autolysed. infect cattle. Definitive hosts are carnivores, and all ruminant
In those from which tissue can be recovered, tissue cysts are species are intermediate hosts.
most commonly found in the brain. Spinal cord is also useful.
Histological lesions include mild to moderate gliosis, non- Clinical signs and diagnosis. Clinical signs of sarcocystosis
suppurative encephalitis, and perivascular infiltration by mixed infection are seen in cattle during the stage when the parasite
mononuclear cells. encysts in soft tissues. Often the infections are asymptomatic.
Fever, anemia, ataxia, symmetric lameness, tremors, tail-switch
Pathogenesis. As with Toxoplasma, cell death is the result of hair loss, excessive salivation, diarrhea, and weight loss are
intracellular multiplication of Neospora tachyzoites. Neospora clinical signs. Abortions in cattle occur during the second
590 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

trimester and in smaller ruminants 28 days after ingestion of the Clinical signs and diagnosis. Clinical signs depend on the or-
sporulated oocysts. gan or tissue parasitized. Toxoplasmosis is typically associated
Definitive diagnosis is based on finding merozoites and with placentitis, abortion, stillbirths, or birth of weak young
meronts in neural tissue lesions. Clinical hematology results in- (Underwood and Rook, 1992; Buxton, 1998). It has also been
clude decreased hematocrit, decreased serum protein, and pro- shown to cause pneumonia and nonsuppurative encephalitis.
longed prothrombin times. Sarcocystis-specific IgG will in- The enteritis at the early stage of infection may be fatal in some
crease dramatically by 5 - 6 weeks after infection. There is no hosts. Hydrocephalus does not occur in animals as it does in hu-
cross-reaction between Sarcocystis and Toxoplasma. man fetal Toxoplasma infections. Rare clinical presentations in
ruminants include retinitis and chorioretinitis; these are usually
Epizootiology and transmission. Infection rates among cattle asymptomatic.
in the United States are estimated to be very high. Transmission Infection of the ewe during the first trimester usually leads to
is by ingestion of feed and water contaminated by feces of the fetal resorption, during the second trimester leads to abortion,
definitive hosts. Dogs are the definitive hosts for the species that and during the third trimester leads to birth of weak to normal
infect the smaller ruminants. Cats, dogs, and primates (includ- lambs with subsequent high perinatal mortality. Congenitally
ing humans when S. hominis is involved) are the definitive hosts infected lambs may display encephalitic signs of circling, inco-
for the species that infect cattle. ordination, muscular paresis, and prostration. In sheep, weak
young will develop normally if they survive the first week after
Necropsy. Aborted fetuses may be autolysed. Lesions in neu- birth. Infected adult sheep show no systemic illness. Infected
ral tissues, including meningoencephalomyelitis, focal malacia, adult goats, however, may die.
perivascular cuffing, neuronal degeneration, and gliosis, are Diagnosis may be difficult, and biological, serological, and
most marked in the cerebellum and midbrain. Lesions may be histological methods are helpful. Serological tests are the most
found in other tissues, such as lymphadenopathy, and hemor- readily available. Complement fixation and the Sabin-Feldman
rhages may be found in muscles and on serous surfaces. Cysts antibody test may assist in diagnosis. Antibodies found in fe-
in cardiac and skeletal muscles are common incidental findings tuses are indicative of congenital infection and are typically de-
during necropsies. tectable 35 days after infection; fetal thoracic fluid is especially
useful in demonstrating serological evidence of exposure. Bio-
Pathogenesis. Ingestion of muscle flesh from an infected ru- logical methods, such as tissue culture or inoculation of mice
minant results in Sarcocystis cysts' being broken down in the with maternal body fluids, or with postmortem or necropsy tis-
carnivore's digestive system, release of bradyzoites, infection of sues, are more time-consuming and expensive.
intestinal mucosal cells by the bradyzoites, differentiation into
sexual stages, fusion of the male and female gametes to form Epizootiology and transmission. This protozoon is considered
oocysts, and shedding as sporocysts by the definitive hosts. The ubiquitous. Fifty percent (50%) of adult western sheep and 20%
sporocysts are eaten by the ruminant and penetrate the bowel of feedlot lambs have positive hemagglutination titers (1:64
walls; several stages of development occur in endothelial cells or higher) (Jensen and Swift, 1982). Transmission among the
of arteries. Merozoites are the form that enters soft tissues, such definitive host is by ingestion of tissue cysts.
as muscle, and subsequently encysts.
Necropsy findings. At necropsy, placental cotyledons contain
Prevention and control. Feed supplies of ruminants must be multiple small white areas that are sites of necrosis, edema,
protected from fecal contamination by domestic and wild car- and calcification. Fetal brains may show nonspecific lesions
nivores. These animals should be controlled and must also not such as coagulative necrosis, nonsuppurative encephalomy-
have access to carcasses. In larger production situations, mon- elitis, pneumonia, myocarditis, and hepatitis. Histologically,
ensin may be fed as a prophylactic measure. granulomas with Toxoplasma organisms may be seen in the
retina, myocardium, liver, kidney, brain, and other tissues. Im-
Treatment. Monensin fed during incubation is prophylactic, pression smears of these tissues, stained appropriately (e.g.,
but the efficacy in clinically affected cattle is not known. with Giemsa), provide a rapid means of diagnosis. Identifi-
cation of the organism in tissue sections (especially of the heart
viii. Toxoplasmosis and the brain) also confirms the findings. Toxoplasma gondii is
Etiology. Toxoplasmosis is caused by the obligate intracellu- crescent-shaped, with a clearly visible nuclei, and will be found
lar protozoon Toxoplasma gondii, a coccidial parasite of the within macrophages.
family Eimeridae. Cats are the only definitive hosts, and several
warm-blooded animals, including ruminants, have been shown Pathogenesis. The protozoon has three infectious stages: the
to be intermediate hosts. The disease is a major cause of abor- tachyzoite, the bradyzoite, and the sporozoite within the oocyst.
tion in sheep and goats and less common in cattle. The definitive hosts, felids, become infected by ingesting cyst
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 591

stages in mammalian tissues, by ingesting oocysts in feces, and ometras and abortions during the first half of gestation. Often
by transplacental transfer. Ingested zoites invade epithelial cells the problem is not recognized until herd pregnancy checks
and eventually undergo sexual reproduction, resulting in new indicate many "open," delayed-estrus, late-bred cows, or cows
oocysts, which the cats will shed in the feces. Cats rarely show with postcoital pyometras. The abortion rate varies from 5% to
clinical signs of infection. One cat can shed millions of oocysts 30%, and placentas will be expelled or retained. Tritrichomonas
in 1 gm of feces, but the asymptomatic shedding takes place for fetus also causes mild salpingitis but this does not result in per-
only a few weeks in its life. Oocysts sporulate in cat feces after manent damage. Other than these manifestations, infection with
1 day. Ruminants are intermediate hosts of toxoplasmosis and T. fetus causes no systemic signs.
become infected by ingesting sporulated oocyst-contaminated Diagnosis is based on patterns of infertility and pyometras.
water or feed. As in the definitive host, the ingested sporozoite For example, pyometras in postcoital heifers or cows are sug-
invades epithelial cells within the intestine but also further in- gestive of this pathogen. Diagnostic methods include identify-
vades the bloodstream and is transported throughout the host. ing or culturing the trichomonads from preputial smegma,
The organism migrates to tissues such as the brain, liver, cervicovaginal mucus, uterine exudates, placental fluids, or
muscles, and placenta. Placental infection develops about abomasal contents of aborted fetuses. Other nonpathogenic pro-
14 days after ingestion of the oocysts. The damage caused by an tozoa from fecal contamination may be present in the sample.
infection is due to multiplication within cells. Toxoplasma does The trichomonad has three anterior flagellae, one posterior
not produce any toxin. flagella, and an undulating membrane; it travels in fluids with
a characteristic jerky movement. Culturing must be done on
Differential diagnosis. Differentials for abortion include Cam- specific media, such as Diamond's or modified Pastridge.
pylobacter, Chlamydia, and Q fever.
Epizootiology and transmission. All transmission is by vene-
Prevention and control. Feline populations on source farms real exposure from breeding bulls or cows or, in some cases,
should be controlled. Eliminating contamination of feed and contaminated breeding equipment.
water with cat feces is the best preventive measure. Sporulated
oocysts can survive in soil and other places for long periods of Necropsy findings. Nonspecific lesions, such as pyogranulo-
time and are resistant to desiccation and freezing. Vaccines for matous bronchopneumonia of fetuses and placentitis, may be
abortion prevention in sheep are available in New Zealand and seen in aborted material; some cases will have no gross lesions.
Europe. Histologically, trichomonads may be visible in the fetal lung le-
sions and the placenta; those tissues are also the most useful for
Treatment. Toxoplasmosis treatment is ineffective, although culturing.
feeding monensin during pregnancy may be helpful (Under-
wood and Rook, 1992). (Monensin is not approved for this use Pathogenesis. Tritrichomonas fetus colonizes the female re-
in the Unites States.) Weak lambs that survive the first week af- productive tract, and subsequent clinical manifestations may be
ter birth will mature normally and will not deliver Toxoplasma- related to the size of the initial infecting dose. Tritrichomonas
infected young. fetus does not interfere with conception. Embryonic death oc-
curs within the first 2 months of infection. Affected cows will
Research complications. Because toxoplasmosis is zoonotic, clear the infection over a span of months and maintain immu-
precautions must be taken when handling tissues from any nity for about 6 months. Infections in younger bulls are tran-
abortions or neurological cases. Infections in immunocompro- sient; apparently organisms are cleared by the bulls' immune
mised humans have been fatal. systems and are dependent on exposure to infected females.
Older bulls become chronic carriers, probably because of the
ix. Trichomoniasis ability of T.fetus to colonize deeper epithelial crypts of the pre-
Etiology. Trichomoniasis is an insidious venereal disease puce and penis.
of cattle caused by Tritrichomonas (also referred to as Tri-
chomonas) fetus, a large, pear-shaped, flagellated protozoon. Differential diagnosis. Campylobacteriosis is the other pri-
The organism is an obligate parasite of the reproductive tract, mary differential for reduced reproductive efficiency of a herd.
and it requires a microaerophilic environment to establish Other venereal diseases should be considered when infertility
chronic infections. In the United States, it is now primarily a problems are noted in a herd: brucellosis, mycoplasmosis, urea-
disease seen in western beef herds. There are many similarities plasmosis, and infectious pustular vulvovaginitis. In addition,
between trichomoniasis and campylobacteriosis; both diseases management factors such as nutrition and age of heifers at in-
cause herd infertility problems. troduction to the herd should be considered.

Clinical signs and diagnosis. Clinical signs include infertility Prevention and control. A bacterin vaccine is available.
manifested by high nonpregnancy rates as well as periodic py- Heifers, cows, and breeding bulls are vaccinated subcutaneously
592 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

twice at 2 to 4 week intervals, with the booster dose adminis- younger cattle and are similar to the disease in sheep. Hae-
tered 4 weeks before breeding season starts. Similar timing is monchus is extremely pathogenic, and the adults feed by suck-
recommended for administration of the annual booster; a long, ing blood from the mucosa of the abomasum. Severe anemia
anamnestic response does not occur. Bulls used for artificial in- may lead to death. Weight loss, decreased milk production, poor
semination (AI) are screened routinely for T.fetus (and Campy- wool growth, and intermandibular and cervical edema due to
lobacter). AI reduces but does not eliminate the disease. The hypoproteinemia ("bottle jaw") are also common clinical signs.
use of younger, vaccinated bulls is recommcmded in all circum- Diarrhea is not seen in all cases but may sometimes be severe or
stances. New animals should be tested before introduction to chronic. The life cycle is direct. Under optimal conditions, a
the herd. Control measures also include culling affected cows or complete life cycle, from ingestion of larvae to eggs passed in
else removing them from the breeding herd for 3 months to rest the feces, occurs in 3 weeks. Embryonated eggs may develop
and clear the infection. Culling chronically infected bulls is into infective larvae within a week. Hypobiotic (arrested) larvae
strongly recommended. may exist for several months in animal tissues, serving as a
reservoir for future pasture contamination. Periparturient in-
Treatment. Imidazole compounds have been effective, but the creases in egg shedding by ewes contribute to large numbers of
use of these is not permitted in food animals in the United eggs spread on spring pastures ("spring rise"). Resistance to
States. Therapeutic immunizations are worthwhile when a pos- common anthelmintics has developed; currently ivermectin or
itive diagnosis has been made. These will not curtail fetal losses benzimidazole products are used, with a minimum of 2 dosings
but will shorten the convalescence of the affected cows and im- given 2 - 3 weeks apart. Levamisole is also used. In severe cases,
prove immunity of breeding bulls. animals may benefit from blood transfusions and iron supple-
mentation. Because animals may easily acquire infective larvae
Research complications. Trichomoniasis should be consid- from ingestion of contaminated feed and from contaminated
ered whenever natural service is used and fertility problems are pastures, general facility sanitation and pasture management
encountered. and rotation are important preventive and control measures.
Haemonchus contortus is susceptible to destruction by freezing
temperatures and dry conditions.
b. Nematodes
Nematodes are important ruminant pathogens that cause ii. Ostertagia (Teladorsagia) circumcincta (medium stomach
acute, chronic, subclinical, and clinical disease in adults and worm). Ostertagia circumcincta is also highly pathogenic for
adolescents. The major helminths may cause gastroenteritis as- sheep and goats and, like Haemonchus, attaches to the abomasal
sociated with intestinal hemorrhage and malnutrition. Nemato- mucosa and ingests blood. The life cycle is comparable to that
diasis is associated with grazing exposure to infective larvae; of Haemonchus, including the phenomenon of hypobiosis. Lar-
animals procured for research may have had exposure to these vae are especially resistant to cool temperatures, however, and
helminths. Mixed infections of these parasites are common. will overwinter on pastures. Larvae-induced hyperplasia of abo-
Generally, older animals develop resistance to some of the spe- masal epithelial glands results in a change of gastric pH from
cies; thus, animals between about 2 months and 2 years of age about 2.0 to near 7.0, leading to decreased digestive enzyme ac-
are most susceptible to infection. Because of the parasites' ef- tivity and malnutrition. Clinical syndromes are categorized as
fects on the animals' physiology, infection in these younger an- type 1 or type 2. The former type is associated with infections
imals is a major contributor to a cycle of poor nutrition and di- acquired in fall or spring and is seen in younger animals. The
gestion, compromised immune responses, and impaired growth latter type is associated with emergence of the arrested larvae
and development. Diagnosis is primarily based on fecal flota- during spring or fall. Clinical signs include anemia, weight loss,
tion techniques; however, because many of these nematodes decreased milk production, and unthriftiness. Diarrhea is usu-
have similar-appearing ova, hatching the ova and identifying ally seen in type 1 only; the symptoms of type 2 are comparable
the larvae are often required (Baermann technique). A number to those of Haemonchus infections. Anthelmintic drug therapy
of anthelmintics can be used to interrupt nematode life cycles. is comparable to that for Haemonchus, and drug resistance is
See Zajac and Moore (1993) and Pugh et al. (1998) for com- also a problem with Ostertagia.
prehensive reviews of treatment and control of nematodiasis.
iii. Ostertagia ostertagi (cattle stomach worm). Ostertagia
i. Haemonchus contortus, H. placei (barber's pole worm, ostertagi is the most pathogenic and most costly of the cattle ne-
large stomach worm). Haemonchus contortus is the most im- matodes. Ostertagia leptospicularis and O. bisonis also cause
portant internal parasite of sheep and goats, and the brief de- disease. The life cycle is direct, and egg shedding by the cattle
scription here focuses on the disease in the smaller ruminants. may occur within 3 - 4 weeks of ingestion of infective larvae.
Haemonchus contortus and H. placei infections do occur in Hypobiosis is also a characteristic of O. ostertagi. In the initial
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 593

steps of infection, the normal processes of the abomasum are vii. Strongyloides papillosus. Strongyloides papillosus is a
profoundly disrupted and cells are destroyed as the larvae de- small-intestinal parasite of sheep and cattle. Strongyloides has a
velop within and emerge from the glands. Moroccan leather ap- different life cycle from that of many nematodes. The eggs, ex-
pearance is the term to describe the result of cellular hyperpla- pelled in the feces, are larvated, and when they hatch, they form
sia and loss of cell differentiation. Cycles of infection and both free-living males and females or parasitic females only.
morbidity depend on geographic location, climate, and produc- The parasitic females may enter the gastrointestinal tract
tion cycles. Type 1 cattle ostertagiasis is associated with inges- through oral ingestion, such as in milk during nursing, or
tion of large numbers of infective larvae, occurs in animals less through direct penetration of the skin. Penetrating larvae enter
than 2 years old, and causes diarrhea and anorexia. Type 2 the bloodstream and are transported to the lungs, where they
ostertagiasis occurs in cattle 2 - 4 years old and older adults, is penetrate the alveoli, are coughed up, and then swallowed to ul-
the result of the emergence and development of hypobiotic lar- timately enter the gastrointestinal tract. Adult females may re-
vae, and in addition to signs seen with type 1, hypoproteinemia produce in the small intestines by parthenogenesis. Clinical
with development of submandibular edema, fever, and anemia signs associated with Strongyloides include weight loss, diar-
is a clinical sign. Treatment options include ivermectin, fenben- rhea, unthriftiness, and dermatitis in cases where large numbers
dazole, and levamisole; all are effective against the arrested migrate through the skin. The current broad-spectrum an-
larvae. Ostertagia is susceptible to desiccation but is resistant to thelmintics are effective against Strongyloides.
freezing.
viii. Bunostomum trigonocephalum (hookworm). Bunosto-
iv. Trichostrongylus vitrinus, T. axei, T. colubriformis (hair mum trigonocephalum is a hookworm that occasionally infects
worms). Trichostrongylus species favor cooler conditions, sheep in locales in the southwestern United States. Like
and some larvae may overwinter. Although the different species Strongyloides, Bunostomum infection may involve oral inges-
may affect different segments of the gastrointestinal tract, the tion or direct penetration of the skin (followed by tracheal mi-
nematode attaches to the mucosa and affects secretion and/or gration and swallowing). The larvae mature in the small intes-
absorption. Trichostrongylus vitrinus and T. colubriformis in- tines and suck blood. Larvae are susceptible to desiccation and
fect the small intestine of sheep and goats. Trichostrongylus freezing. Heavy infection with Bunostomum may result in ane-
axei infects the abomasum of cattle, sheep, and goats and causes mia, diarrhea, intestinal hemorrhage, edema, and weight loss.
increases in abomasal pH similar to those seen with Ostertagia.
Mucosal hyperplasia is not seen. The prepatent period is about ix. Oesophagostomum columbianum, O. venulosum (nodule
3 weeks. Affected animals display unthriftiness, anorexia, de- worms). Oesophagostomum spp. primarily infect the large
creased milk production, weight loss, diarrhea, and dehydra- intestine and occasionally the distal small intestine, causing
tion. These worms show intermediate resistance to freezing nodule worm disease, or simply gut. Oesophagostomum colum-
temperatures and dry conditions. bianum and O. venulosum infect sheep and cattle. These nema-
v. Nematodirus spathiger, N. battus (thread-necked worms). todes may affect sheep from 3 months to 2 years of age, and the
Nematodirus has lower pathogenicity compared with other prepatent period is about 6 weeks. Larvae are highly sensitive to
gastrointestinal nematodes. The larvae cause small-intestinal freezing and desiccation and rarely overwinter. Larvae pene-
necrosis and inflammation. The larvae are especially resistant trate the large-intestinal mucosa but occasionally move into the
to desiccation and freezing. Clinical signs include depression, deeper areas of the intestinal wall near the serosa. The resultant
weight loss, anorexia, and diarrhea. inflammatory reaction may lead to the formation of a caseous
nodule that may mineralize over time. Intestinal lesions may ac-
vi. Cooperia (small intestinal worms). Cooperia primarily celerate peristalsis, leading to diarrhea, or may inhibit peristal-
affects younger animals less than 1 year of age. Cooperia cur- sis (later stages), resulting in constipation. Clinical signs in-
ticei infects the small intestine of sheep and goats; C. punctata clude weakness, unthriftiness, alternating episodes of diarrhea
and C. oncophora infect the small intestines of cattle, sheep, and constipation, and severe weight loss. Nodular lesions are
and goats. Cooperia pectinata infects the stomach of cattle. typical at necropsy.
Large numbers lead to clinical infection, and the prepatent pe-
riod is about 3 weeks. Cooperia and Osteragia infections, like x. Chabertia ovis (large-mouth bowel worm). Chabertia
infections of some other nematode species, may act synergisti- ovis is a minor colon parasite of sheep, goats, and cattle and is
cally. Because these nematodes suck blood, clinical signs in- seen primarily in sheep. Signs of infection are not usually seen
clude anemia, gastrointestinal hemorrhage, and malnutrition. in cattle. Prepatent periods are up to 50 days. Heavy infection,
Animals exhibit weight loss, diarrhea, and depression. Coope- which may result from as few as 100 worms located at the prox-
ria species are intermediate to resistant to the effects of cold imal end of the colon, may lead to hemorrhagic mucoid diar-
temperatures. rhea, weight loss, weakness, colitis, and mild anemia.
594 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

xi. Trichuris (whipworms). Trichuris spp. are mildly patho- be silent carriers, showing no clinical signs and serving as a
genic nematodes and are usually attached to the cecal mucosa. means for the infection to survive over winter or a dry season.
Trichuris has a rather long prepatent period, extending from 1 Pastures can be heavily contaminated during the next grazing
to 3 months. The oval eggs are double-operculated and survive season.
well in pasture environmental extremes. The adult worms also Necropsy lesions include bronchiolitis and bronchitis, atelec-
have a characterisitic morphology, with one thicker end appear- tasis, and hyperplasia of peribronchiolar lymphoid tissue. Ne-
ing as a whip handle. The nematodes cause a minor cecitis and matodes frequently reside in the bronchi of the diaphragmatic
will feed on blood. Clinical infection is rare and results in diar- lung lobes and are frequently enmeshed with frothy exudate.
rhea with mucus and blood. Treatment and prevention methods Prevention and control of the disease involve appropriate pas-
are similar to those for other nematodes. ture management. Elimination of intermediate hosts is impor-
tant in sheep and goat pastures. In a laboratory setting, animals
xii. Dictyocaulus (lungworms). Dictyocaulus spp., or lung- may be procured that are already harboring the disease. Infected
worms, are nematodes that cause varying clinical signs in rumi- animals can be treated with anthelmintics such as ivermectin or
nants. In sheep, Dictyocaulus filaria, Protostrongylus rufes- levamisole. Muellerius tends to be resistant to levamisole. There
cens, and Muellerius capillaris cause disease; Dictyocaulus is is no anthelmintic currently approved for goats, but fenbenda-
the most pathogenic. Goats are infected by the same species as zole, administered 2 weeks apart, has been effective for all three
sheep, but infections are uncommon. Dictyocaulus viviparus is nematodes. Treating D. viviparus depends on the type and stage
the only lungworm found in cattle, causing "fog fever." Infec- of life of the cattle; label directions must be followed. There is
tions with these parasites in the United States tend to be associ- no vaccine for D. viviparus in the United States. Even if infec-
ated with cooler, moister climates. Lungworms induce a severe tions are not severe and do resolve with treatment, permanent
parasitic bronchitis (known as husk, or verminous pneumonia) lesions may be inflicted on the lung tissue.
in sheep between approximately 2 and 18 months of age. Sheep
infected with any of the lungworm species may display cough-
c. Cestodes (Tapeworms)
ing, dyspnea, nasal discharge, weight loss, unthriftiness, and
occasionally fever. Coughing and dyspnea are symptoms in i. Moniezia expansa and Thysanosoma actinoides infections.
goats. Diagnosis is suggested by persistent coughing and nasal Tapeworms are rarely of clinical or economic importance. In
discharge and is confirmed by identifying larvae in the feces or younger animals, heavy infections result in potbellies, constipa-
adults in pathological samples. The Baermann technique, in- tion or mild diarrhea, poor growth, rough coat, and anemia.
volving prompt examination of room-temperature feces, is usu- Moniezia expansa, and less commonly Moniezia benedini, in-
ally used; zinc sulfate flotation is also used. habit the small intestines of grazing ruminants. Moniezia ex-
Dictyocaulus has a direct life cycle. The adult worms reside pansa has the widest distribution of the tapeworm species in
in the large bronchi. Dictyocaulus produces embryonated eggs North America. Soil mites (Galumna spp. and Oribatula spp.)
that are coughed up and swallowed; the eggs then hatch in the contribute to the life cycle as intermediate hosts, a period that
intestines, and larvae are expelled in the feces. The expelled lar- lasts up to 16 weeks. Cysticercoids released from the mites are
vae are infectious in about 7-10 days and, after ingestion, pen- grazed, pass into the small intestines, and mature. No clinical or
etrate the intestinal mucosa and move through the lymphatics pathological sign is usually observed with Moniezia infection;
and blood into the lungs, where they develop into adults in about diagnosis is made by observing the characteristic triangular-
5 weeks. Dictyocaulus filaria causes an especially severe bron- shaped eggs in fecal flotation examinations. Infection is treated
chitis in sheep. Protostrongylus inhabits smaller bronchioles. with cestocides.
Muellerius is of minor pathogenicity. Protostrongylus and Thysanosoma actinoides, or the fringed tapeworm, is a ces-
Muellerius require the snail or slug as an intermediate host. In- tode that resides in the duodenum, bile duct, and pancreatic duct
fection occurs through ingestion of infected snails; infections of sheep and cattle raised primarily west of the Mississippi
are less likely than those caused by the direct ingestion of Dic- River in the United States. Thysanosoma is of the family
tyocaulus larvae. Immunity wanes over a year. Viral and bacte- Anoplocephalidae. The life cycle is indirect, and the inter-
rial respiratory tract infections may be associated with the par- mediate host is the psocid louse. Larval forms, or cysticercoids,
asitic infection. are ingested by grazing animals, and the prepatent period is sev-
Dictyocaulus viviparus causes the obvious signs in cattle. eral months. Typically, no clinical signs are observed with
More severe illness is seen after infections with Cooperia and Thysanosoma infection; nonetheless, liver damage, resulting in
Ostertagia, because of a synergism between the nematodes liver condemnation at slaughter, occurs. Necropsy lesions in-
even if the cattle are not currently infected with those parasites. clude bile and/or ductal hyperplasia and fibrosis. Thysanosoma
Hypobiosis (arrested development of immature worms in lung is diagnosed premortem by identifying the gravid segments in
tissue) is associated with Dictyocaulus infections; cattle will the feces.
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 595

ii. Abdominal or visceral cysticercosis. Abdominal or vis- and convulsions are observed. Diagnosis is usually made at
ceral cysticercosis is an occasional finding at slaughter. The so- necropsy. Eliminating transfer from the canid hosts prevents the
called bladder worms typically affect the liver or peritoneal cav- disease.
ity and are the larval form of Taenia hydatigena, the common
tapeworm of the dog family. Taenia hydatigena resides in the
d. Trematodes
small intestines of canids, and its gravid segments, oncospheres,
contaminate feed and water sources. After ingestion, the larvae i. Fascioliasis (liver fluke disease). Liver flukes are an im-
penetrate the intestinal mucosa, are transported via the blood- portant cause of acute and chronic disease in grazing sheep and
stream to the liver, and cause migration tracts throughout the cattle. There are three common species of flukes in ruminants of
liver parenchyma. The larvae may leave the liver and migrate the continental United States: Fasciola hepatica, Fascioloides
into the peritoneal cavity, where they attach and develop over magna, and Dicrocoelium dendriticum. Fasciola hepatica in-
the next 1-9 months into small fluid-filled bladders. The life fections are primarily seen in Gulf Coast and western states.
cycle is completed only after these bladders are ingested by a Fascioloides magna infections are typically seen in Gulf, Great
carnivore, thus completing the maturation of the adult tape- Lake, and northwestern states, where ruminants share pasture
worms. Although larval migration may cause nonspecific signs with deer, elk, and moose. Dicrocoelium dendriticum infections
such as anorexia, hyperthermia, and weight loss, affected ani- occur only in New York State. Liver fluke eggs are passed in
mals are usually asymptomatic. At necropsy, the bladder worms the bile and feces and hatch in 2 - 3 weeks to form the free-
will be observed attached to the peritoneal or organ surfaces. swimming miracidia. It is important to note that each fluke egg
Migration tracts may result in fibrosis and inflammation. Diag- represents the source of eventually thousands of cercariae or
nosis is usually made at necropsy. Because of the migration metacercariae. The miracidia penetrate the body of an interme-
through the liver, Fasciola hepatica is a differential diagnosis. diate host (usually freshwater snails) and develop through
Minimizing exposure to canine feces-contaminated feeds and sporocyst and redia stages, finally forming cercariae. (Dicro-
water effectively interrupts the life cycle. Research animals may coelium is unique because it utilizes a land snail that expels
have been exposed prior to purchase. slime balls, each containing several hundred cercariae. These
are eaten by a second intermediate host, the ant Formica fusca.)
iii. Echinococcosis (hydatidosis, hydatid cyst disease). The cercariae leave the intermediate host, swim to grassy vege-
Echinococcosis, like cysticercosis, is an occasional finding at tation, lose their tail, and become a cystlike metacercaria. The
slaughter or necropsy. The hydatid cyst is the larval intermedi- metacercariae may remain in a dormant stage on the grass for
ate of the adult tapeworm Echinococcus granulosus, which re- 6 months or longer until ingested by a ruminant. The ingested
sides in the small intestines of dogs and wild canids. Embry- metacercariae penetrate the small-intestinal wall and migrate
onated ova are expelled in the feces of the primary host and are through the abdominal cavity to the liver. There they locate in a
ingested by herbivores, swine, and potentially humans. The bile duct, mature, and remain for up to 4 years.
eggs hatch in the gastrointestinal tract, and the oncospheres Acute liver fluke disease is related to the damage caused by
penetrate the mucosal lining, enter the bloodstream, and are the migration of immature flukes. Migratory flukes may lead to
transported to various organs such as the liver and lungs. The liver inflammation, hemorrhage, necrosis, and fibrosis. Fasci-
cystic structure develops and potentially ruptures, forming new oloides magna infections in sheep and goats can be fatal as the
cystic structures. Clinically, echinococcosis presents minimal result of just one fluke tunneling through hepatic tissue. In cat-
clinical signs; unthriftiness or pneumonic lesions may be asso- tle, infections are often asymptomatic because of the host's en-
ciated with infected organs. Cysts are typically observed at capsulation of the parasite. Liver fluke damage may predispose
necropsy. Prevention should be aimed at decreasing fecal con- to invasion by anaerobic Clostridium species such as C. novyi
tamination of feed and water by canids. Additionally, tape- that could lead to fatal black disease or bacillary hemoglobin-
worm-infected dogs can be treated with standard tapeworm uria. Chronic disease may result from fluke-induced physical
therapies. Treatment of infected ruminants is uncommon. damage to the bile ducts and cholangiohepatitis. Blood loss into
the bile may lead to anemia and hypoproteinemia. Liver damage
iv. Gid. Coenuris cerebralis, the larval form of the canid also is evidenced by increases in liver enzymes such as y-glu-
tapeworm Taenia (Multiceps) multiceps, is the causative agent tamyl transpeptidase (GGT). Persistent eosinophilia is also seen
of the rare condition called gid. The disease occurs in ruminants with liver fluke disease. Other clinical signs of liver fluke dis-
as well as many other mammalian species. The larval parasite, ease include anorexia, weight loss, unthriftiness, edema, and as-
ingested from fecal-contaminated food and water, invades the cites. At necropsy, livers will be pale and friable and may have
brain and spinal cord and develops as a bladder worm that distinct migration tunnels along the serosal surfaces. Bile ducts
causes pressure necrosis of the nervous tissues. The resultant will be enlarged, and areas of fibrosis will be evident.
signs of hyperesthesia, meningitis, paresis, paralysis, ataxia, Diagnosis can be made from clinical signs and postmortem
596 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

analyses. Blood chemistries suggestive of liver disease and tus. The psoroptic mite Psoroptes cuniculi commonly occurs in
eosinophilia support the diagnosis. Liver fluke control involves the ear canal and causes head shaking and scratching. Repeated
removal of the intermediate hosts. In a laboratory setting, liver treatments of lime sulfur, amitraz, or ivermectin may be effec-
fluke infection is unlikely. Nonetheless, incoming animals from tive (Smith and Sherman, 1994). Goats are also susceptible to
pasture environments may be infected. Liver flukes can be demodectic mange caused by Demodex caprae. Adult mites in-
treated by using the anthelmintic albendazole. vade hair follicles and sebaceous glands. Pustules may develop
with secondary bacterial infection.
ii. Rumen fluke infections (paramphistomosis). Paramphis- Psoroptes bovis continues to be present in cattle in the United
tomosis is an uncommon disease found in sheep and cattle in States, although it has been eradicated from sheep. Chorioptes
southern states. Paramphistomum microbothrioides and P. cervi bovis typically infects lower hindlimbs, perineum, tail, and
inhabit the duodenum and rumen of affected sheep. Eggs are scrotum but can become generalized. The sarcoptic mange mite
passed in the feces and hatch in approximately 1 month, and the S. scabei can survive off the host, so fomite transmission is a
miracidia penetrate the intermediate snail hosts. Cercariae de- factor. The mange usually begins around the head but then
velop in the snail over the next month, emerge, and encyst on spreads. This parasite can be transmitted to humans. Demodex
grasses as metacercariae. When eaten, the metacercariae de- bovis infects cattle; nodules on the face and neck are typical.
velop into adult flukes and attach to the mucosal lining. The life Demodex bovis infections may resolve without treatment. Lin-
cycle is complete in approximately 100 days. The flukes cause dane, coumaphos, malathion, and lime sulfur are used to treat
localized injury to the mucosa and, by interfering with digestive Psoroptes and Psorergates. Ivermectin is effective against Sar-
processes, cause diarrhea and protein loss. Clinically, animals coptes and is approved for use in cattle.
may experience anorexia, dehydration, weight loss, and diar-
rhea with or without blood. Mortality may reach 25%. Diagno-
sis is based on clinical findings as well as the identification of f. Lice (Pediculosis)
flukes or eggs in the feces. Animals can be treated with fluki-
Lice that infect ruminants are of the orders Mallophaga, bit-
cides. Eliminating the intermediate host prevents the disease.
ing or chewing lice, and Anoplura, sucking lice. These are
wingless insects. Members of the Mallophaga are colored yel-
low to red; members of the Anoplura are blue gray. Lice pro-
e. Mites (Mange)
duce a seasonal (winter-to-spring), chronic dermatitis. In sheep,
Mites cause a chronic dermatitis. The principal symptom of biting lice include Damalinia (Bovicola) ovis (sheep body
these infections is intense pruritus. In addition, papules, crusts, louse). Sucking lice that infect sheep include Linognathus ovil-
alopecia, and secondary dermatitis are seen. Anemia, disrup- lus (blue body louse) and L. pedalis (sheep foot louse). In goats,
tion of reproductive cycles, and increased susceptibility to other biting lice infection are caused by D. caprae (goat biting louse),
diseases may also occur. Mites are rare in ruminants in the D. limbatus (Angora goat biting louse), and D. crassipes. Suck-
United States, but infections of Sarcoptes and Psorergates ir/g louse infections in goats are caused by L. stenopis and L.
mange must be reported to animal health officials. Ruminants africanus. Damalinia bovis is the cattle biting louse. Sucking
in poorly managed facilities are generally the most susceptible lice include L. vituli, Solenopotes capillatus, Haematopinus eu-
to infection, and infections are more frequent during winter rysternus, and H. quadripertusus.
months. Diagnosis is based on signs, examination of skin scrap- Pruritus is the most common sign and often results in alope-
ings, and response to therapy. No effective treatment for de- cia and excoriation. The host's rubbing and grooming may not
modectic mange in large animals has been found. The differen- correlate with the extent of infestation. Hairballs can result from
tial for mite infestations is pediculosis. overgrooming in cattle. In severe cases, the organisms can lead
Several genera of mites may affect sheep. These have been to anemia, weight loss, and damaged wool in sheep and dam-
eradicated from flocks in the United States or are very rare and aged pelts in other ruminants. Young animals with severe infes-
include Psoroptes ovis (common scabies), Sarcoptes scabiei tations of sucking lice may become anemic or even die. Preg-
(head scabies, barn itch), Psorergates ovis (sheep itch mite), nant animals with heavy infestations may abort. In sheep
Chorioptes ovis (foot scabies, tail mange), and Demodex ovis infected with the foot louse, lameness may result.
(follicular mange). Lice are generally species-specific. Those infecting ruminants
Goats can also be infected by sarcoptic, chorioptic, and are usually smaller than 5 mm. Goats may serve as a source of
psoroptic mange. The scabies mite Sarcoptes rupicaprae in- infection for sheep by harboring Damalinia ovis. Transmission
vades epidermal tissue and causes focal pruritic areas around is primarily by direct contact between animals. Transmission
the head and neck. The chorioptic mite, either Chorioptes bovis can also occur by attachment to flies or by fomites. Some ani-
or C. caprae, does not invade epidermal tissue but rather feeds mals are identified as carriers and seem to be particularly sus-
on dead skin tissue. The chorioptic mite prefers distal limbs, the ceptible to infestations.
udder, and the scrotum and can be a significant cause of pruri- Biting or chewing lice inhabit the host's face, lower legs, and
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 597

flanks and feed on epidermal debris and sebaceous secretions. transmission. Removal of the ticks reverses the syndrome un-
Sucking lice inhabit the host's neck, back, and body region and less paralysis has migrated anteriorly to the respiratory centers
feed on blood. Lice eggs or nits are attached to hairs near the of the medulla. In these cases, death due to respiratory failure
skin. Three nymphal stages, or instars, occur between egg and occurs.
adult, and the growth cycle takes about 1 month for all species.
Lice cannot survive for more than a few days off the host. All Treatment. Ticks can be treated using systemic or topical
ruminant mite infestations are differentials for the clinical signs insecticides.
seen with pediculosis.
Animals that are carriers should be culled, because these in- h. Other Parasites
dividuals may perpetuate the infection in the group. Lice are
i. Nasal bots (nasal myiasis, head grubs). Nasal myiasis
effectively treated with a variety of insecticides, including cou-
causes a chronic rhinitis and sinusitis. The disease is caused by
maphos, dichlorvos, crotoxyphos, avermectin, and pyrethroids.
the larval forms of the botfly Oestrus ovis. The botfly deposits
Label directions should be read and adhered to, including with-
eggs around the nostrils of sheep. The ova hatch, and the larvae
drawal times. Products should not be used on female dairy ani-
migrate throughout the nasal cavity and sinuses, feeding on mu-
mals. Treatments must be repeated at least twice at intervals ap-
cus and debris. In 2-10 months, the larvae complete their grow-
propriate for nit hatches (about every 16 days) because nits will
ing phase, migrate back to the nasal cavity, and are sneezed
not be killed. Fall treatments are useful in managing the infec-
out. The mature larvae penetrate the soil and pupate for 1-1.5
tions. Systemic treatments in cattle are contraindicated when
months and emerge as botflies. Clinically, early in the disease
there may be concurrent larvae of cattle grubs (Hypoderma line-
course, animals display unique behaviors such as stamping,
atum and H. bovis). Back rubbers with insecticides, capitaliz-
snorting, sneezing, and rubbing their noses against each other or
ing on self-treatment, are useful for cattle. Sustained-release
objects. Hypersensitivity to the larvae occurs (Dorchies et al.,
insecticide-containing ear tags are approved for use in cattle.
1998). Later, mucopurulent nasal discharges associated with the
larval-induced inflammation of mucosal linings will be ob-
served. At necropsy, larvae will be observed in the nasal cavity
g. Ticks
or sinuses. Mild inflammatory reactions, mucosal thickening,
Etiology. Ruminants are susceptible to many species of Ixo- and exudates will accompany the larvae. The disease is diag-
didae (hard-shell ticks) and Argasidae (softshell ticks). Many nosed by observing the behaviors or identifying organisms at
diseases, including anaplasmosis, babesiosis, and Q fever are necropsy. Up to 80% of a flock will potentially be infected;
transmitted by ticks. treatment should be employed on the rest of the flock. Iver-
mectins and other insecticides will eliminate the larvae; but
Clinical signs and diagnosis. Tick infestations are associated treatment should be done in the early fall, when larvae are
with decreased productivity, loss of blood and blood proteins, small. Fly repellents may be helpful at preventing additional
transmission of diseases, debilitation, and even death. Feeding infections.
sites on the host vary with the tick species. Ticks are associated
with an acute paralytic syndrome called tick paralysis. This dis- ii. Screwworm flies. Cochliomyia hominivorax (Callitroga
ease is characterized by ascending paralysis and may lead to americana) is the the screwworm that causes occasional disease
death if the tick is not removed before the paralysis reaches the in the southwestern United States along the Mexico border.
respiratory muscles. Diagnosis is based on identification of the Eradication programs have been pursued, and the disease is re-
species. portable. Large greenish flies lay large numbers of white eggs
as shinglelike layers at the edges of open wounds (including
docking and castration sites), soiled skin, or abrasions. Eggs
Epizootiology and transmission. Ticks are not as host-specific
hatch within 24 hr. Larvae are obligate parasites of living tissue,
as lice. Ticks are classified as one-host, two-host, or three-host;
and the cycle is perpetuated because the increasingly large
this refers to whether they drop off the host between larval and
wound continues to be attractive to the next generation of
nymphal stages to molt.
flies. Larvae eventually drop off, pupate best in hot climates,
and hatch in 3 weeks. Large cavities in parasitized tissue are
Pathogenesis of tick infestations. Patterns of feeding on the formed, and lesions are characterized by malodor, large vol-
host differ between Argasidae and Ixodidae. The former feed umes of brown exudate, and necrosis. Single animals or entire
repeatedly, whereas the latter feed once during each life stage. herds may be affected. Treatment is intensive, with dressings
and larvicidal applications. If there is no intervention, the host
Pathogenesis of tick paralysis. Following a tick-feeding pe- succumbs to secondary infections and fluid loss. Effective cur-
riod of 4 - 6 days, the tick salivary toxin travels hematogenously rent control regimens include subcutaneous injection of iver-
to the myoneural junctions and spinal cord and inhibits nerve mectin and programs that release sterile male flies.
598 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

iii. Sheep keds ("sheep ticks"). In sheep and goats, sheep portant, other immune mechanisms are not well understood.
keds produce a chronic irritation and dermatitis with associated Immunity may not be of long duration. Recovery is enhanced
pruritus. The disease is caused by Melophagus ovinus, which by correcting nutritional deficiencies and improving housing
is a fiat, brown, blood-sucking, wingless fly; the term sheep tick and ventilation problems. A number of topical treatments, such
is incorrectly used. The adult fly lives entirely on the skin of as 2 - 5 % lime-sulfur solution, 3% captan, iodophors, thiaben-
sheep. Females mate and produce 10-15 larvae following a dazole, and 0.5% sodium hypochlorite, can be used. In severe
gestation of about 10-12 days. The larvae attach to the wool cases, systemic therapy with griseofulvin may be successful.
or hair and then pupate for about 3 weeks. The adult female
feeds on blood and lives for 4 - 5 months; the life cycle is com- Prevention and control. The animals' environment and over-
pleted in about 5 - 6 weeks. Infection is highest in fall and win- all physical condition should be reassessed with particular at-
ter. Pruritus develops around the neck, sides, abdomen, and tention to ventilation, crowding, sanitation, and nutrition. Pens
rump. In severe cases, anemia may occur. Keds can transmit should be thoroughly cleaned and disinfected.
bluetongue virus. Keds are diagnosed by gross or microscopic
identification. Ivermectin or other insecticides are useful treat- Research complications. Ringworm is a zoonotic disease.
ment agents.

5. Fungal Disease: Dermatophytes (Ringworm) B. Genetic, Metabolic, Nutritional,

and Management-Related Diseases
Etiology. Dermatophytosis, or infection of the keratinized
layers of skin, is caused mostly by species of the genera Tri-
1. Genetic Diseases
chophyton and Microsporum. The primary causes in sheep are
T. mentagrophytes and T. verrucosum. In goats, the agents are a. Entropion
T. mentagrophytes, M. canis, M. gypseum, T. verrucosum, T.
schoenleinii, and Epidermophyton floccosum. In cattle, T. ver- Inverted eyelids are a common inherited disorder of lambs
rucosum is the primary causative agent. Dermatophytosis is a and kids of most breeds. Generally, the lower eyelid is affected
common fungal infection of the epidermis of cattle and is less and turns inward, causing various degrees of trauma to the
common in sheep and goats. conjunctiva and cornea. Young animals will display tearing,
blepharospasm, and photophobia initially. If the disorder is left
Clinical signs and diagnosis. Multiple, gray, crusty, circum- uncorrected, corneal ulcers, perforating ulcers, uveitis, and
scribed, hyperkeratotic lesions are characteristic of infection. blindness may occur. Placing a suture or a surgical staple in the
Lesions will vary in size. In all ruminants, lesions will be lower eyelid and the cheek, effectively anchoring the lid in an
around the head, neck, and ears. In goats and cattle, lesions will everted position, successfully treats the condition. The proce-
extend down the neck, and in cattle, lesions develop particularly dure likely results in the formation of some degree of scar tis-
around the eyes and on the thorax. Cattle lesions are unique in sue within the lower lid, because when the suture eventually is
the marked crustiness, which progressively appears wartlike. removed, the condition rarely returns. Other treatments include
Hair shafts become brittle and break off. Intense pruritus is of- the injection of a "bleb" of penicillin in the lid, regular manual
ten associated with the alopecic lesions. correction over a 2-day period early in the animal's life, and ap-
The disease can be diagnosed by microscopic identification of plication of ophthalmic ointments, powders, and solutions.
hyphae and conidia on the hairs following skin scraping and Boric acid or 10% Argyrol solutions have been used as treat-
20% potassium hydroxide digestion. Dermatophyte test media ments. Because of the genetic predisposition, prevention of the
(DTM) cultures are the most reliable means to diagnose the fun- condition requires removal of maternal or paternal carriers.
gus. Broken hairs from the periphery of the lesion are the best
sources of the fungus.
b. ~-Mannosidosis of Goats
Epizootiology and transmission. Younger animals are more
[3-Mannosidosis is an autosomal recessive lysosomal storage
susceptible, and factors such as crowding, indoor housing,
disease of goats. The disease affects kids of the Nubian breed
warm and humid conditions, and poor nutrition are also impor-
and is identified by intention tremors and difficulty or inability
tant. Transmission is by direct contact or by contact with con-
of newborns to stand. Cells of affected animals are vacuolated
taminated fomites, such as equipment, fencing, or feed bunks.
because of a lack of lysosomal hydroxylase, which results in ac-
Pathogenesis. Incubation can be as long as 6 weeks. The or- cumulation of oligosaccharides. Newborn kids are unable to
ganisms invade and multiply in hair shafts. rise, and they have characteristic flexion of the carpal joint and
hyperextension of the pastern joint. Kids are born deaf and with
Treatment. Spontaneous recovery occurs in all species in 1- musculoskeletal deformities such as domed skull, small narrow
4 months. Although cell-mediated immunity is considered im- muzzle, small palpebral fissures, enophthalmos, and depressed
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 599

nasal bridge (Smith and Sherman, 1994). Carrier adults can be Some bovine genetic defects are also regarded as models of ge-
identified by plasma measurements of [3-mannosidase activity. netic disease, such as leukocyte adhesion deficiency of Holstein
cattle. Some of the more commonly reported defects include
syndactyly in Holsteins and other breeds and polydactyly in
c. Congenital Myotonia of Goats
Simmentals; lysosomal storage diseases such as a-mannosido-
Caprine congenital myotonia is an inherited autosomal dom- sis in some beef breeds; enzyme deficiencies such as citrulline-
inant disease that affects voluntary striated skeletal muscles. mia in Holsteins; and progressive degenerative myeloencepha-
Goats with this disease are commonly known as fainting goats. lopathy ("weaver") in Brown Swiss.
"Fainting" is actually transient spasms of skeletal musculature
brought about by visual, tactile, or auditory stimuli (Smith and ii. Goiter of sheep. A defect in the synthesis of thyroid hor-
Sherman, 1994). Muscle fiber membranes appear to have fewer mone has been identified in Merino sheep (Radostits et al.,
chloride channels than normal, resulting in decreased chloride 1994). Lambs born with the defect have enlargement of the thy-
conduction across the membrane, with subsequent increased roid gland, a silky appearance to the wool, and a high degree of
membrane excitability and repetitive firing (Smith and Sher- mortality. Edema, bowing of the legs, and facial abnormalities
man, 1994). Contractions of skeletal muscle are sustained for have also been noted in animals with this disorder. Immaturity
up to 1 min. Kids exhibit the condition by 6 weeks of age, and of the lungs at birth causes neonatal respiratory distress and re-
males appear to exhibit more severe clinical signs than females suits in dyspnea and respiratory failure.
(Smith and Sherman, 1994). Electromyographic studies pro-
duce an audible "dive-bomber" sound characteristic of hyper- iii. Spider lamb syndrome (hereditary chondrodysplasia).
excitable cell membranes (Smith and Sherman, 1994). Spider lamb syndrome is an inherited, often lethal, musculo-
skeletal disorder primarily occurring in Suffolk and Hampshire
breeds. Severely affected lambs die shortly after birth. Animals
d. Inherited Conditions of Cattle
that survive the perinatal period develop angular limb deformi-
i. Congenital erythropoietic porphyria. Congenital eryth- ties, scoliosis, and facial deformities. With time, affected ani-
ropoietic porphyria (CEP) is an autosomal recessive disease of mals become debilitated, exhibit joint pain, and develop neu-
cattle seen primarily in Holsteins, Herefords, and Shorthorns. rological problems associated with the spinal abnormalities.
The disease also occurs in Limousin cattle, humans, and some Radiologically, secondary ossification centers--especially the
other species. In the homozygous recessive animal, symptoms physis, subchondral areas, and cuboidal bonesmare affected.
of the disease may vary from mild to severe and occur at differ- Abnormal endochondral ossification leads to excess cartilage
ent times of the year and in different ages of animals. A reddish formation, notably apparent in the elbows. Lambs will typically
brown discoloration of teeth and bones is a characteristic of the display abnormally long limbs, medial deviation of the carpus
disease, as is discolored urine, general weakness and failure to and tarsus, flattening of the sternum, scoliosis/kyphosis of the
thrive, photosensitization, and photophobia. Bones are more vertebrae, and a rounded nose. Muscle atrophy is common. Di-
fragile compared with bones of normal animals. A regenerative agnosis can be based on typical clinical signs, which are similar
anemia occurs as the result of the shortened life span of ery- to those seen with Marfan syndrome in humans (Rook et al.,
throcytes, due to accumulations of porphyrins. The genetic de- 1986). Long-term survival is rare; treatment is unsuccessful.
fect is associated with low activity of an essential enzyme, uro-
porphyrinogen III synthase, in the porphyrin-heme synthesis 2. Metabolic Diseases
pathway in erythrocytic tissue. The ranges in the presentation of
a. Abomasal Disorders
the disease are believed to be related to varying cycles of por-
phyrin synthesis. Porphyrins are excreted in varying amounts in i. Abomasal and duodenal ulcers. Abomasal and duodenal
the urine and the discoloration fluoresces under a Wood's lamp. ulcers occur more frequently in calves and adult cattle than in
Diagnosis is based on these clinical and visible signs of por- sheep and goats. Like rumenitis, abomasal and duodenal ulcers
phyria; skin biopsy provides definitive diagnosis. Heterozy- may be associated with lactic acidosis. Concurrent disease, such
gotes may have milder symptoms. as salmonellosis, bluetongue, or overuse of anti-inflammatory
Many other genetic defects, in all major organ systems, have drugs, or recent shipping or environmental stresses may also
been described in numerous breeds of cattle and are described lead to ulcer formation. Copper deficiency, dietary changes,
in detail elsewhere ("Large Animal Internal Medicine," 1996). mycotic infections, Clostridium perfringens abomasitis, and
In many cases, the genetic basis has been clarified, and associ- abomasal bezoars are associated with this disease in calves. In
ated defects also noted. Many defects are reported in particular older adult cattle, abomasal lymphosarcoma may be the under-
breeds, but as crossbreeding increases and new breeds are de- lying condition. Gastric acid hypersecretion in conjunction with
veloped, these traits are appearing in these animals. The bovine insufficient gastric mucous secretion will physically destroy the
genome continues to be further characterized, and more linkage gastric epithelium. Deep ulceration may cause serious hemor-
maps and gene locations are forthcoming (Womack, 1998). rhage and/or perforation with peritonitis. Chronic hemorrhage
600 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

may lead to anemia. Although ulcers are often asymptomatic in manent correction. Emergency surgery is necessary for RTA;
calves, perforation with peritonitis is more common than hem- the disorder is fatal within 72 hr. Recurrence is rare after surgi-
orrhage. Dark feces or melena and abdominal pain may be cal correction. Electrolyte and acid-base imbalances are likely
observed. Arched back, restlessness, kicking at the abdomen, in severe cases and especially with RTA. Prevention includes
bruxism, and anorexia are common signs of abdominal pain. reducing stress, taking greater care in the introduction and feed-
Fecal occult blood is as an easy diagnostic test. Treatment in- ing of concentrates, and reducing incidence of predisposing dis-
cludes gastrointestinal protectants and histamine antagonists. eases noted above (Rohrbach et al., 1999).
Anemia may be symptomatically treated with parenteral iron
injections and anabolic steroids. Preventive measures in cattle b. Fat Cow Syndrome, Hepatic Lipidosis
herds include ensuring optimal passive immunity for calves,
Fat cow syndrome is seen in peri- or postparturient overcon-
minimizing stress to calves, and striving for a herd free of
ditioned or obese multiparous dairy cows. Factors in the devel-
bovine leukosis virus.
opment of the condition include negative energy balance related
to the normal decreased dry matter intake as parturition ap-
ii. Abomasal emptying defect. Abomasal emptying defect
proaches; hormonal changes associated with parturition; and
of sheep is a sporadic syndrome associated with abomasal dis-
concurrent diseases of parturition that decrease feed intake
tension and weight loss. Suffolks tend to be especially predis-
and increase energy needs. The possible concurrent diseases in-
posed, although the disease has been diagnosed in Hampshires,
clude metritis, retained fetal membranes, mastitis, parturient
Columbias, and Corriedales. The mechanism of the disease is
paresis, and displaced abomasum. Signs are nonspecific and in-
unknown. Affected animals will exhibit a gradual weight loss
clude depression, anorexia, and weakness. Prognosis is usually
with a history of normal appetites. Feces will continue to be
guarded. Diagnosis is based on herd management, the animal's
normal. Ventral abdominal distension associated with abomasal
condition, ketonuria, and clinical signs. In prepartum cattle and
accumulation of feedstuffs will be apparent in many of the ani-
in lactating cows, blood levels of nonesterified fatty acids
mals. Diagnosis is primarily based on history and clinical signs.
(NEFA) greater than 1000 ~tEq/liter and 325-400 ~tEq/liter, re-
Elevations in rumen chloride concentrations (> 15 mEq/liter)
spectively, are abnormal (Gerloff and Herdt, 1999). Triglyc-
are commonly found. Radiography or ultrasonography may be
eride analysis of liver biposy specimens are useful. In affected
helpful at identifying the distended abomasum. Abomasal emp-
cows, body fat is mobilized, in the form of NEFA in response to
tying defect is usually eventually fatal. Medical treatment with
the energy demands. Hepatic lipidosis occurs rapidly as the
metoclopramide and mineral oil may be helpful in early disease.
NEFA are converted into hepatic triglycerides. The ability of
the liver to extract the albumin-bound NEFA from the blood is
iii. Abomasal displacement. Displaced abomasum (DA) is
better than that of other tissues that need and can also use NEFA
a sporadic disorder usually associated with multiparous 4- to 7-
as an energy source. Treatment for any concurrent diseases
year-old dairy cows in early lactation, but the condition can oc-
must be pursued aggressively, as well as measures to increase
cur even in young calves. Displacement to the right (RDA) may
and stabilize blood glucose, decrease NEFA production, and in-
be further complicated by torsion (RTA), a surgical emergency.
crease forestomach digestion to improve production of nor-
Left displacement (LDA) is more common than RDA. Clini-
mally metabolized volatile fatty acids. Therapeutic measures
cal signs include anorexia, lack of cud chewing, decreased fre-
include intravenous glucose drips, insulin (NPH or Lente) in-
quency of ruminal contractions, shallow respirations, increased
jections every 12 hr, and transfaunation of ruminal fluid from
heart rate, treading, and decreased milk production. Diagnosis
a normal cow. Prevention includes minimizing stress to late-
is based on characteristic areas of tympanic resonance during
gestation cows. Dry and lactating cows should be maintained
auscultation-percussion of the lateral to lateral-ventral abdo-
separately; their energy, protein, and dry matter requirements
men ("pings"), ruminal displacement palpated per rectum, and
are very different. Cows with prolonged lactation or delayed
clinical signs. Cow-side clinical chemistry findings include hy-
breeding should be managed to prevent weight gain.
poglycemia and ketonuria; more extensive evaluations will of-
ten indicate moderate to severe electrolyte and acid-base ab-
c. Rumen and Reticulum Disorders
normalities. DA occurs because of gas accumulation within the
viscus, and the abomasum "floats" up from its normal ventral i. Bloat. Bloat or tympanites refers to an excessive accu-
location to the lateral abdominal wall. No exact cause of DA has mulation of gas in the rumen. The condition most frequently
been identified, but it is commonly associated with stress; high occurs in animals that have been recently fed abundant quanti-
levels of concentrate in the diet, leading to forestomach atony; ties of succulent forages or grains. Bloat is classified into two
and many disorders, including lack of regular exercise, mastitis, broad categories: frothy bloat and free-gas bloat. Frothy bloat is
hypocalcemia, retained placenta, metritis, or twins. Factors such associated with ingestion of feeds that produce a stable froth
as body size and conformation indicate the possibility of ge- that is not easily expelled from the rumen. Fermentation gases
netic predisposition. Treatments include surgical and nonsurgi- such as CO2, CH4, and minor gases such as N2, 02, H2, and H2S
cal techniques for LDA; the former has a better chance of per- incorporate into the froth, overdistend the rumen, and eventu-
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 601

ally compromise respiration by limiting diaphragm movement. will become anorexic, depressed, and weak within 1-3 days af-
The froth is often derived from a combination of salivary muco- ter the initial insult. Incoordination, ataxia, dehydration, hemo-
proteins, protozoal or bacterial proteins, and proteins, pectins, concentration, rapid pulse and respiration, diarrhea, abdominal
saponins, or hemicellulose associated with ingested leaves or pain, and lameness will also be noted 9Rumen distension and an
grain. Typical foodstuffs that cause frothy bloat include green acetone-like odor to the breath, milk, or urine may also be ob-
legumes, leguminous hay (alfalfa, clover), or grain (especially served. Diagnosis is based on history and clinical signs. Blood,
barley, corn, and soybean meal). Free-gas bloat is less related to urine, or milk ketones can be detected (Moore and Ishler, 1997).
feeds ingested; rather, it is caused by rumen atony or by physi- Additionally, rumen pH, which is normally above 6.0, will drop
cal or pathological problems that prevent normal gas eructation. to less than 5.0 and in severe cases may achieve levels as low as
Some examples of causes of free-gas bloat are esophageal ob- 3.8. Similarly, urine pH will become acidic, blood pH will drop
structions (foreign bodies, tumors, abscesses, and enlarged cer- below 7.4, and hematocrit will appear to increase due to the rel-
vical or thoracic lymph nodes), vagal nerve paralysis or injury, ative hemoconcentration. Necropsy findings will be determined
and central nervous system conditions that affect eructation by secondary conditions. The primary lactic acidosis will cause
reflexes. Clinically, the animal will exhibit rumen distension, swelling and necrosis of rumen papillae and abomasal hemor-
and tympany will be observed in the left paralumbar fossa. Ad- rhages and ulcers. Treatment must be applied early in the syn-
ditional signs may include colic-like pain of the abdomen and drome. In early hours of severe carbohydrate engorgement, ru-
dyspnea. Passage of a stomach tube helps to differentiate be- menotomy and evacuation of the contents are appropriate. The
9 t 9

tween free-gas bloat and frothy bloat; and with free-gas bloat, patient should be given mineral oil and antlfermentatlves to pre-
expulsion of gas through the stomach tube aids in treatment of vent the continued conversion of starches to acids and the ab-
the disorder. Once rumen distension is alleviated with free-gas sorption of metabolic products. Bicarbonate or other antacids
bloat, the underlying cause must be investigated to prevent re- like magnesium carbonate or magnesium hydroxide introduced
currence. Frothy bloat is more difficult to treat, because the into the rumen will aid in adjusting rumen pH. Furthermore, an-
foam blocks the stomach tube. Addition of mineral oil, house- imals can be given oral tetracycline or penicillin, which will de-
hold detergents, or antifermentative compounds via the tube crease the gram-positive bacterial population.
may help break down the surface tension, allowing the gas to be
expelled. In acute, life-threatening cases of bloat, treatment iii. Rumen parakeratosis. Parakeratosis is a degenerative
should be aimed at alleviating rumen distension by placing a condition of the rumen mucosa that leads to keratinization of
trocar or surgical rumenotomy into the rumen via the paralum- the papillary epithelium 9 Excessive and continuous feeding of
bar fossa. Limiting the consumption of feedstuffs prone to in- diets low in roughage causes the mucosal changes 9 Generally,
duce bloat can prevent the disease. Additionally, poloxalene or this condition is seen in feedlot lambs and steers that are fed an
monensin will decrease the incidence of frothy bloat. all-grain diet. Clinically, animals may exhibit only poor rates of
gain, due to changes in the absorptive capacity of the injured
ii. Lactic acidosis. Lactic acidosis, or rumen acidosis, is an mucosa. At necropsy, papillae will be thickened and rough.
acute metabolic disease caused by engorgement of grains or They will frequently be dark in color, and multiple papillae will
other highly fermentable carbohydrate sources. The disease is clump together. Abscessation may be observed. Histopatholog-
most frequently related to a rapid change in diet from one con- ically, papilla surfaces will have hyperkeratinization of the
taining high roughage to one containing excessive carbohy- squamous epithelium. Chronic laminitis may be observed.
drates. Diet components that predispose to acidosis include However, diagnosis of parakeratosis is generally made at nec-
common feed grains; feedstuffs such as sugar beets, molasses, ropsy. Feeding adequate roughage, such as stemmy hay, will
and potatoes; by-products such as brewer's grains; and bakery prevent the disease. Antibiotics may be administered to prevent
products. Biochemically, ingestion of large amounts of the car- secondary liver abscess formation.
bohydrate-rich diet causes the normally gram-negative rumen
bacterial populations to shift to gram-positive Streptococcus iv. Rumenitis. Rumenitis is an acute or chronic inflamma-
and Lactobacillus species. The gram-positive organisms effi- tion of the rumen, which occurs most commonly as a sequela to
ciently convert the starches to lactic acid. The lactic acid lactic acidosis 9 In addition to concentrate feeding, inadequate
acidifies the rumen contents, leading to rumen mucosal inflam- roughage in the diet is also associated with this disorder 9 Ru-
mation, and increases the osmolality of rumen fluids, leading to menitis may occur with contagious ecthyma infection or fol-
sequestration of fluids and osmotic attraction of plasma and tis- lowing ingestion of poisons or other irritants. Because rumeni-
sue fluid to the rumen. Lactic acid-induced rumenitis predis- tis is often associated with lactic acidosis, it tends to occur in
poses the animal to ulcers, to liver abscesses from "absorbed" feedlot animals. The inflamed ruminal epithelium becomes
bacterial pathogens, to laminitis from absorbed toxins, and to necrotic and sloughs, creating ulcers. Endogenous rumen bac-
polioencephalomalacia from the inability of the new rumen bac- teria such as Fusobacterium necrophorum may invade the
terial populations to produce sufficient thiamine needed to ulcers, penetrate the circulatory system, and induce abscesses
maintain normal nervous system function. Clinically, animals of the liver. Clinically, the animals will appear depressed and
602 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

anorexic. Rumen motility will be decreased, and animals will Differential diagnosis. Differentials include abomasal ulcers,
lose weight. The disease may resolve in a week to 10 days; mor- hepatic ulcers, neoplasia (such as lymphosarcoma, usually in
tality may reach 20%. Necropsy lesions include rumen inflam- older animals, or intestinal carcinoma), laminitis, and cor pul-
mation and ulcers in the anteroventral sac. Granulation tissue monale. Infectious diseases that are differentials include sys-
and scarring may be observed following healing. Rumenitis is temic leptospirosis and internal parasitism. Diseases causing
not typically diagnosed clinically; thus, specific treatment is not sudden death may need to be considered.
commonly done. The disease can be prevented by minimizing
the incidence of lactic acidosis. Prevention and control. This problem can be prevented en-
tirely by elimination of sharp objects in cattle feed and in the
housing and pasture environments. Adequately sized magnets
Traumatic Reticulitis-Reticuloperitonitis placed in feed handling equipment and forestomach magnets
(Hardware Disease) (placed per os with a bailing gun in young stock at 6 - 8 months
Etiology. Traumatic reticulitis-reticuloperitonitis is a disease of age) are also significant prevention measures.
of cattle related to their exploratory tendencies and ingestion of
many different, nonvegetative materials. The disease is rarely Treatment. Provision of a forestomach magnet, confinement,
seen in smaller ruminants. and nursing care, including antibiotics, are the initial treat-
ments. In severe cases, rumenotomy may be considered.
Clinical signs. Clinical signs range from asymptomatic to se-
vere, depending on the penetration and damage by the foreign Pregnancy Toxemia (Ketosis),
object after settling in the animal's forestomach. Many signs Protein Energy Malnutrition
during the early, acute stages will be nonspecific, ranging from
arched back, listlessness, anorexia, fever, decrease in produc-
Etiology. Pregnancy toxemia is a primary metabolic disease
of ewes and does in advanced pregnancy. Beef heifers are sus-
tion, ketosis, regurgitation, decrease or cessation of ruminal
ceptible to protein energy malnutrition (PEM) syndrome, which
contractions, bloat, tachypnea, tachycardia, and grunts when
urinating, defecating, or being forced to move. The prognosis is is also referred to as pregnancy toxemia.
poor when peritonitis becomes diffuse. Sudden death can occur
if the heart, coronary vessels, or other large vessels are punc-
Clinical signs. In sheep, this disease is characterized by hypo-
glycemia, ketonemia, ketonuria, weakness, and blindness. Hy-
tured by the migrating object.
poglycemic and ketotic ewes begin to wander aimlessly and to
move away from the flock. They become anorexic and act un-
Epizootiology and transmission. This is a noncontagious dis- coordinated, frequently leaning against objects. Advanced signs
ease. The occurrence is directly related to sharp or metallic in-
may include blindness, muscle tremors, teeth grinding, convul-
digestible items in the feed or environment that the cattle mouth sions, and coma. Body temperature, heart rate, respiratory rate,
and swallow. and rumen motility continue normally. Up to 80% of infected
ewes may die from the disease. The course of the disease may
Necropsy findings. In severe cases, necropsy findings include last up to a week.
extensive inflammation throughout the cranial abdomen, mal- In goats, the disease usually occurs in the last 6 weeks of ges-
odorous peritoneal fluid accumulations, and lesions at the retic- tation, especially in does carrying triplets. Pregnancy toxemia
ular sites of migration of the foreign objects. Cardiac puncture should be considered with any goat showing signs of illness in
will be present in those animals succumbing to sudden death. late gestation. The doe may separate herself from the herd,
stagger, or circle and may appear blind. Appetite is poor, and
Pathogenesis. Consumed objects initially settle in the rumen tremors may be evident. A rapid metabolic acidosis results in
but are dumped into the reticulum during the digestive process, subsequent recumbency. Urinalysis will readily reveal keto-
and normal contraction may eventually lead to puncture of the nuria. If fetal death occurs, acute toxemia and death of the doe
reticular wall. This sets off a localized inflammation or a local- may result.
ized or more generalized peritonitis. The inflammation may In beef heifers, weight loss and thin body condition, weakness
also temporarily or permanently affect innervation of local tis- and inability to stand, and depression are clinical signs. Some
sues and organs. Further damage may result from migration and cows develop diarrhea. Because the catabolic state is often so
penetration of the diaphragm, pericardium, and heart. Diagno- advanced, most affected heifers die even if treated.
sis is based on clinical signs, knowledge of herd management Pregnancy toxemia is diagnosed by evidence of typical clini-
techniques in terms of placement of forestomach magnets, and cal signs. Sodium nitroprusside tablets or ketosis dipsticks may
reflection of acute or chronic infection on the hemogram. Radi- be used to identify ketones in the urine or plasma of ewes and
ographs and abdominocentesis may be useful. does. Blood glucose levels found to be below 25 mg/dl and
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 603

ketonuria are good diagnostic indicators. In cattle, ketonuria is dividual. Treating the individual is usually unsuccessful. Oral
not a typical finding; hypocalcemia and anemia may be present. administration of 200 ml of propylene glycol or 50% glucose
twice a day, anabolic steroids, and high doses of adrenocorti-
Epizootiology. Pregnancy toxemia occurs primarily in ewes costeroids may be helpful. If ewes are still responsive and not
that are obese or bearing twins or triplets. The disease develops severely acidotic or in renal failure, cesarean section may be
during the last 6 weeks of pregnancy. PEM most frequently oc- successful by rapidly removing the fetus, which is the dietary
curs in heifers during the final trimester of pregnancy. drain for the ewe. In goats, pregnancy toxemia is best treated by
removal of the fetuses either by cesarean section or induction of
Necropsy findings. At necropsy, affected ewes will often have parturition. Parturition can be induced in does by either dexam-
multiple fetuses, which may have died and decomposed. The ethasone (10 mg) or PGF2a (10 ~tg). In addition, goats may be
liver will be enlarged, yellow, and friable, with fatty degenera- treated with 10% dextrose (100 to 200 ml iv) or propylene gly-
tion. The adrenal gland may also be enlarged. In cattle, heifers col (60 ml per os 2 or 3 times a day). Adjunctive therapy in-
will be very thin, and in addition to a fatty liver, signs of con- cludes normalizing acid base and hydration status, administra-
current diseases may be present. tion of vitamin B 12and transfaunation. Heifers may be force-fed
alfalfa gruels, given propylene glycol per os, placed on IV 50%
Pathogenesis. Rapid fetal growth, a decline in maternal nutri-
glucose drips, and treated for concurrent disease.
tion, and a voluntary decrease in food intake in overfat ewes re-
sult in an inadequate supply of glucose needed for both mater-
nal and fetal tissues. The ewe develops a severe hypoglycemia Research complications. In research requiring pregnant ewes
in early stages of the disease. The ruminant absorbs little dietary in late stages of gestation, for example, this disease should be
glucose; rather, it produces and absorbs volatile fatty acids considered if the animals are likely to bear twins and will be
(acetic, propionic, and butyric acids) from consumed feedstuffs. transported or stressed in other ways during that time.
Propionic acid is absorbed and selectively converted to glucose
through gluconeogenesis. When the animal is in a state of neg-
ative energy balance, it hydrolyzes fats to glycerol and fatty f Hypocalcemia (Parturient Paresis, Milk Fever)
acids. Glycerol is converted to glucose while the fatty acids are Etiology. Hypocalcemia is an acute metabolic disease of ru-
metabolized for energy. The oxidation of fatty acids in the face minants that requires emergency treatment; the presentation is
of declining oxaloacetate levels (required for normal Krebs slightly different in ewes, does, and cows.
cycle function) results in the formation of ketone bodies (ace-
tone, acetoacetic acid, and [3-hydroxybutyric acid), thus causing
Clinical signs and diagnosis. In sheep, the disease is seen in
the condition ketoacidosis.
ewes during the last 6 weeks of pregnancy and is characterized
Heifer cattle have high energy requirements for completing
by muscle tetany, incoordination, paralysis, and finally coma.
normal body growth and supporting a pregnancy. Additional
As calcium levels drop, ewes begin to show early signs such as
energy requirements are needed during pregnancy for winter
stiffness and incoordination of movements, especially in the
conditions and during concurrent diseases. Marginal diets
hindlimbs. Later, muscular tremors, muscular weakness, and re-
and poor-quality forage will place the cows in a negative energy
cumbency will ensue. Animals will frequently be found breath-
balance.
ing rapidly despite a normal body temperature. Morbidity may
Differential diagnosis. Hypocalcemia is a common differen- approach 30%, and mortality may reach as high as 90% in un-
tial diagnosis. In cattle, differentials include chronic or un- treated animals. Affected does become bloated, weak, unsteady,
treated diseases such as Johne's disease, lymphosarcoma, para- and eventually recumbent. Cows are affected within 2 4 - 4 8 hr
sitism, and chronic respiratory diseases. before or after parturition. Cows initially are weak and show
evidence of muscle tremors, then deteriorate to sternal recum-
Prevention and control. Pregnancy toxemia can be prevented bency, with the head usually tucked to the abdomen, and an
by providing adequate nutrition during late gestation and by inability to stand. Tachycardia, dilated pupils, anorexia, hypo-
maintaining animals in appropriate nonfat condition during thermia, depression, ruminal stasis, bloat, uterine inertia, and
pregnancy. In late pregnancy, the dietary energy and protein loss of anal tone are also seen at this stage. The terminal stage
should be increased 1.5-2 times the maintenance level. PEM of disease is a rapid progression from coma to death. Heart rates
can be prevented by maintaining appropriate body condition will be high, but pulse may not be detectable.
earlier in pregnancy and supplying good-quality forage for the Hypocalcemia is diagnosed based on the pregnancy stage of
last trimester. the female and on clinical signs. It is later confirmed by labora-
tory findings of low serum calcium. With hypocalcemia in
Treatment. In sheep, because the morbidity may be as high as ewes, the plasma concentrations of calcium drop from normal
20%, treatment should be directed at the flock rather than the in- values of 8-12 mg/dl to values of 3 - 6 mg/dl. In cattle, plasma
604 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

levels below 7.5 mg/dl are hypocalcemic; at the terminal stages animal is treated early in the disease, but the prognosis will
levels may be 2 mg/dl. often be poor when treatment is initiated in later stages of the
disease.
Epizootiology. Hypocalcemia occurs primarily in overweight
ewes during the last 6 weeks of pregnancy or during the first few
g. Urinary Calculi (Obstructive Urolithiasis, Water Belly)
weeks of lactation. The disease is not as common in the dairy
goat as in the dairy cow. High-producing, older, multiparous Etiology. Urolithiasis is a metabolic disease of intact and cas-
dairy cows are the most susceptible, and the Jersey breed is con- trated male sheep, goats, and cattle that is characterized by the
sidered susceptible. Cows that have survived one episode are formation of bladder and urethral crystals, urethral blockage,
prone to recurrence. In addition, dry cows must be managed and anuria (Murray, 1985). The disease occurs rarely in female
carefully regarding limiting dietary calcium. The disease is not ruminants.
common in beef cattle unless there is an overall poor nutrition
program. Clinical signs and diagnosis. Affected animals will vocalize
and begin to show signs of uneasiness, such as treading, strain-
Necropsy findings. There is no pathognomonic or typical find- ing postures, arched backs, raised tails, and squatting while
ing at necropsy. attempting to urinate. These postures may be mistaken for
tenesmus. Male cattle may develop swelling along the ventral
Pathogenesis. During the periparturient period, calcium re- perineal area. Affected animals will not stay with the herd or
quirements for fetal skeletal growth exceed calcium absorbed flock. Small amounts of urine may be discharged, and crystal
from the diet and from bone metabolism. Additionally, dietary deposits may be visible attached to the preputial hairs.
calcium intake is thought to be compromised because, in ad- Additionally, in smaller ruminants, the filiform urethral ap-
vanced pregnancy, animals may not be able to eat enough to sus- pendage (pizzle) often becomes dark purple to black in color.
tain adequate nutrient levels, and intestinal absorption capabil- The pulsing pelvic urethra may be detected by manual or digi-
ities do not respond as quickly as needed. After parturition, tal rectal palpation, and bladder distention may be noticeable in
calcium needs increase dramatically because of calcium levels cattle by the same means. As the disease progresses to complete
in colostrum and milk. Recent information suggests that legume urethral blockage, the animal will become anorexic and show
and grass forages, high in potassium and low in magnesium, signs of abdominal pain, such as kicking at the belly. The abdo-
create a slight physiological alkalosis (at least in cattle), which men will swell as the bladder enlarges, and rupture can occur
antagonizes normal calcium regulation (Rings et al., 1997). within 36 hr after development of clinical signs. Bladder or ure-
Thus, bone resorption, renal resorption, and gastrointestinal ab- thral rupture may cause a short-lived period of apparent pain re-
sorption of calcium are less than maximal. lief; subsequent development of uremia will eventually lead to
death. The disease may progress over a period of 1-2 weeks,
Prevention and control. Maintaining appropriate nutrition and the mortality is high unless the blockages are reversed.
during the last trimester is helpful in preventing the disease. In Diagnosis is made by the typical clinical signs. Abdominal
cows and does, for example, limiting calcium intake by remov- taps may yield urine. Calculi are usually composed of calcium
ing alfalfa from the diet is helpful. phosphate or ammonium phosphate matrices.

Treatment. Hypocalcemia must be treated quickly based on Epizootiology and transmission. Clinical disease is usually
clinical signs; pretreatment blood samples can be saved for later seen in growing intact or castrated males. The disease may be
confirmation. Twenty percent calcium borogluconate solution sporadic or there may be clusters of cases in the flock or herd.
should be administered by slow intravenous infusion. Response
will often be rapid, with the resolution of the animal's dull men- Necropsy findings. Necropsy findings include urine in the ab-
tation. Less severely affected animals will often try to stand in a domen with or without bladder or urethral rupture. Renal hy-
short time. Relapses are common, however, in sheep and cattle. dronephrosis may be evident. Calculi or struvite crystal sedi-
Hypermagnesemia and hypophosphatemia often coincide with ment will be observed in the bladder and urethra. Histologically,
hypocalcemia. These imbalances should be considered when trauma to the urethra and ureters will be present.
animals appear to be unresponsive to treatment. Hypocalcemia
in the goat can be treated with 50-100 ml of calcium boroglu- Pathogenesis. Urolithiasis is multifactorial and involves di-
conate. Heart rate should be monitored closely throughout etary, anatomical, hormonal, and environmental factors. Male
calcium administration. If an irregular or rapid heart rate is de- sheep and goats have a urethral process that predisposes them to
tected, then calcium treatment should be slowed or discon- entrapment of calculi. In cattle, the urethra narrows at the sig-
tinued. Calcium gels and boluses are also available for treat- moid flexure, and calculi lodge there most frequently. Addition-
ment (Rings et aL, 1997). Prognosis is generally good if the ally, the removal of testosterone by early castration is thought to
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 605

result in hypoplasia of the urethra and penis. This physical re- junctions, narrow chests, painful joints, and reluctance to move.
duction in the size of the excretory tube may predispose to the Spontaneous fractures of long bones may occur. Animals will
precipitation of and blockage by the struvite minerals. Grains recover when dietary phosphorus is provided and if joint dam-
fed to growing animals tend to be high in phosphorus and age is not severe.
magnesium content. These calculogenic diets lead to the for-
mation of struvite (magnesium ammonium phosphate) crystals.
Other minerals associated with urolithiasis include silica (range 3. Nutritional Diseases
grasses), carbonates (some grasses and clover pastures), cal-
cium (exclusively alfalfa hay), and oxalates (fescue grasses). a. Copper Deficiency (Enzootic Ataxia, Swayback)
Etiology. Chronic copper deficiency in pregnant ewes and
Differential diagnosis. Grain engorgement colic, gastroin- does may produce a metabolic disorder in their lambs and kids
testinal blockage, and causes of tenemus, such as enteritis called enzootic ataxia. In goats, this deficiency also causes
or trauma, are differentials. Trauma to the urethral process swayback in the fetuses.
should be considered. Urinary tract infections are uncommon in
ruminants.
Clinical signs and diagnosis. This disease results in a pro-
gressive hindlimb ataxia and apparent blindness in lambs up to
Prevention and control. One case often is indicative of a po-
about 3 months of age. Additionally, because copper is essential
tential problem in the group. Urolithiasis can be minimized by
for osteogenesis, hematopoiesis, myelination, and pigmentation
monitoring the calcium:phosphorus ratio in the diet. The nor-
of wool and hair, ewes may appear unthrifty, may be anemic,
mal ratio should be 2:1. Additionally, increasing the amount of
and may have poor, depigmented wool with a decrease in wool
dietary roughage will help balance the mineral intake. Increas-
crimp. Affected kids are born weak, tremble, and have a char-
ing the amount of salt (sodium chloride, 2 - 4 % ) in the diet to in-
acteristic concavity to the spinal cord, leading to the name
crease water consumption, or adding ammonium chloride to the
swayback. When the deficiency occurs later during gestation,
diet, at 10 gm/head/day or 2% of the ration, to acidify the urine,
demyelination is limited to the spinal cord and brain stem. Kids
will aid in the prevention of this disease. Palatability of and ac-
are born normally but develop a progressive ataxia, leading to
cessibility to water should be assessed as well as functioning of
paralysis, muscle atrophy, and depressed spinal reflexes with
automatic watering equipment.
lower motor neuron signs. Diagnosis is based on low copper
levels found in feedstuffs and tissues at necropsy. Diagnosis is
Treatment. Treatment is primarily surgical (Van Metre et al.
based on clinical signs, feed analysis, and pathological findings.
1996). Initially, amputation of the filiform urethral appendage
may alleviate the disease since urethral blockage often begins
here. As the disease progresses, urethral blockage in the sig- Epizootiology and transmission. Enzootic ataxia is rarely
moid flexure as well as throughout the urethra may occur. In seen in western states; most North American diets have suffi-
more advanced stages, perineal urethrostomy may yield good cient copper levels to prevent this disease. Copper antagonists
results. The prognosis is poor when the condition becomes in the feed or forage at sufficient levels, such as molybdenum,
chronic, reoccurs, or surgery is required. sulfate, and cadmium, however, may predispose to copper
deficiencies.
Research complications. Young castrated and intact male ru-
minants used in the laboratory setting will be the susceptible Pathogenesis. The maternal copper deficiency leads to a dis-
age group for this disorder. turbance early in the embryonic development of myelination in
the central nervous system and the spinal cord. Copper is part of
the cytochrome oxidase system and other enzyme complexes
h. Rickets and is important in myelination, osteogenesis, hematopoiesis
Rickets is a disease of young, growing animals but rarely oc- (iron absorption and hemoglobin formation), immune system
curs in goats. It is a metabolic disease characterized by a failure development, and maintenance and normal growth (Smith and
of bone matrix mineralization at the epiphysis of long bones Sherman, 1994).
due to lack of phosphorus. The condition can occur as an ab-
solute deficiency in vitamin D2, an inadequate dietary supply Differential diagnosis. The differential diagnosis for new-
of phosphorus, or a long-term dietary imbalance of calcium borns includes [3-mannosidosis, hypoglycemia, and hypother-
and phosphorus. The syndrome must be differentiated from mia. For older animals the differential should include caprine
epiphisitis (unequal growth of the epiphyses of long bones in arthritis encephalitis (goats), enzootic muscular dystrophy,
young, rapidly growing kids fed diets with excess calcium). listeriosis, spinal trauma or abscessation, and cerebrospinal
Clinical signs include poor growth, enlarged costochondral nematodiasis.
606 SCOTT A. MISCHLER, WENDY J. UNDERWOOD, AND MARGARET L. DELANO

Prevention and control. Copper deficiency can be prevented Necropsy findings. Common findings at necropsy include
by providing balanced nutrition for pregnant animals. icterus; a soft, dark, friable, enlarged spleen; an enlarged,
yellow-brown friable liver; and "gun-barrel" black kidneys.
Necropsy findings. Gross encephalomalacia has been noted. Hemoglobin-stained urine will be visible in the bladder. Copper
Histopathologically, white matter of the brain and spinal cord accumulations in the liver reaching 1000-3000 ppm are toxic.
displays gelatinization and cavitation. Extensive nerve demyeli-
nation and necrosis are evident. Postmortem lesions include ex- Pathogenesis. Hemolysis occurs when sufficient amounts of
tensive demyelination and neuronal degeneration. copper are ingested or released suddenly from the liver and is
believed to be due direct interaction of the copper with red-cell
Treatment. Because the condition is developmental, supple- surface molecules. Stresses such as transportation, lactation,
mental copper may improve clinical signs but not elimi- and poor nutrition or exercise may precipitate the hemolysis.
nate them.
Differential diagnosis. Other causes of hemolytic disease in-
b. Copper Toxicosis clude babesiosis, trypanosomiasis, and plant poisonings such as
kale. Arsenic ingestion, organophosphate toxicity, and cyanide
Etiology: Acute or chronic copper ingestion or liver injury of- or nitrate poisoning should also be considered as the source of
ten causes a severe, acute hemolytic anemia in weanling to adult poisoning. Urethral obstruction and gastrointestinal emergen-
sheep and in calves and adult dairy cattle. Growing lambs may cies should be considered for the abdominal pain.
be the most susceptible. Copper toxicosis is rare in goats.

Control and prevention. The disease is prevented by carefully

Clinical signs and diagnosis. The clinical course in sheep can
monitoring copper access in sheep and copper supplementation
be as short as 1 - 4 days, and mortality may reach 75%. Hemo-
in cattle. Sheep and goats should not be fed feedstuffs formu-
lysis, anemia, hemoglobinuria, and icterus characterize the acute
lated for cattle, and dairy calf milk replacer should not be used
hemolytic crisis, associated with copper released from the over-
for lambs and kids. Molybdenum may be administered to ani-
loaded liver. Some clinical signs are related to direct irritation to
mals considered at high risk. Molybdenum-deficient pastures
the gastrointestinal tract mucosa. Weakness, vomiting, abdom-
may be treated with molybdenum superphosphate. Herd copper
inal pain, bruxism, diarrhea, respiratory difficulty, and circula-
supplementation should be undertaken with the knowledge of
tory collapse are followed by recumbency and death.
existing hepatic copper levels, and existing copper and molyb-
Hepatic biopsy is currently considered the best diagnostic ap-
denum levels, in the feedstuffs.
proach; serum or plasma levels of copper and hepatic enzymes
such as aspartate aminotransferase (AST) and y-glutamyltrans-
ferase (GGT) may provide some information, but it is generally Treatment. Oral treatment for sheep consists of ammonium
believed that these will not accurately reflect total copper load or sodium molybdenate (50-100 mg/day), and sodium thiosul-
or hepatic damage. fate (0.5-1.0 mg/day) for 3 weeks aids in excretion of copper.
Oral D-penicillamine daily for 6 days (50 mg/kg) has also been
Epizootiology and transmission. A single toxic dose for sheep shown to increase copper excretion in sheep. Ammonium
and goats is the range of 20-100 mg/kg, and for cattle it is molybdenate has been administered intravenously to goats at
220-880 mg/kg. Chronic poisoning in sheep may occur when 1.7 mg/kg for 3 treatments on alternate days. Cattle have been
3.5 mg/kg is ingested. Copper-containing pesticides, soil addi- treated orally with sodium molybdenate (3 gm/day) or sodium
tives, therapeutics, and improperly formulated feeds may po- thiosulfate (5 gm/day). Treatment for anemia and nephrosis
tentially lead to copper toxicity. Phytogenous sources include may be necessary in severe cases.
certain pastures such as subterranean clover. Feed low in
molybdenum, zinc, or calcium may lead to increased uptake of Research complications. Some breeds of sheep, such as
copper from properly balanced rations. A common cause of the Merino crosses and the British breeds, may be more susceptible
disease in sheep is feeding concentrates balanced for cattle; to copper toxicosis caused by phytogenous sources.
cattle feeds and mineral blocks contain much higher quantities
of copper than are required for sheep. Chronic ingestion of these
feedstuffs leads to copper accumulation and toxicity. Copper
Selenium~Vitamin E Deficiency (Nutritional Muscular
toxicosis has been reported in calves given regular oral or
Dystrophy, Nutritional Myodegeneration, White Muscle
parenteral copper supplements, and in adult dairy cattle given
Disease, Stiff Lamb Disease)
copper supplements to compensate for copper-deficient pasture.
Pregnant dairy cattle may be more susceptible to copper toxic- Etiology. White muscle disease, also known as stiff lamb dis-
ity. Rare sources of copper ingestion may include copper sulfate ease, is a nutritional muscular dystrophy caused by a deficiency
footbaths. of selenium or vitamin E.
14. BIOLOGYAND DISEASESOF RUMINANTS: SHEEP, GOATS,AND CATTLE 607

Clinical signs and diagnosis. Clinically two forms of the dis- quality roughage, vitamin E and selenium supplementation, and
ease have been identified: cardiac and skeletal. The cardiac parenteral injections prior to parturition and weaning.
form occurs most commonly in neonates. In these, respiratory
difficulty will be a manifestation of damage to cardiac, di- Treatment. Affected animals may be treated by administering
aphragmatic, and intercostal muscles. Young will be able to vitamin E or selenium injections. Administering vitamin E or
nurse when assisted. In slightly older animals, the disease is selenium to ewes in late pregnancy can prevent white muscle
characterized by locomotor disturbances and/or circulatory fail- disease (Kott et al., 1998). The label dose for selenium is 2.5-
ure. Clinically, animals may display paresis, stiffness or inabil- 3 mg/45 kg of body weight. Combination products are available
ity to stand, rapid but weak pulse, and acute death. Mortality and can be used in goats at the sheep dose (Smith and Sherman,
may reach 70% (Jensen and Swift, 1982). Paresis and sudden 1994). Proper mineral balance in the diet is critical.
death in neonates with associated pathological signs are fre-
quently diagnostic. With the skeletal form, affected animals are d. Selenium Toxicity
stiff and reluctant to move, and muscles of affected animals are
Selenium toxicity occurs most frequently as the result of ex-
painful. Young will be reluctant to get up but will readily nurse
cessive dosing to prevent or correct selenium deficiency or as
when assisted. Peracute to acute myocardial degeneration may
the result of ingestion of selenium-converting plants. The main
occur in the cardiac form, and animals may simply be found
preventive measure for the former is the use of the appropriate
dead. Serum selenium levels are usually below 50 ppb (normal
product for the species. Secondarily, the concentration of the
is 158-160 ppb) (Nelson, 1983).
available product should be double-checked. In the United
Diagnosis may also include determination of antemortem
States, ruminants in the Midwest and western areas may be sub-
whole blood levels of selenium and plasma levels of vitamin E.
ject to selenium toxicity when pastured in areas containing
Glutathione peroxidase levels in red blood cells can be meas-
selenium-converting plants. Signs of overdosing include weak-
ured as an indirect test. Clinical biochemistry findings of
ness, dyspnea, bloating, and diarrhea. Shock, paresis, and death
significant elevations of aspartate aminotransferase (AST) in
may occur. Initial clinical signs of excessive selenium intake
creatinine kinase (CK) are also supportive of the diagnosis.
from plants are observed in the distal limb, with cracked hoof
walls and subsequent infection and irregular hoof growth.
Epizootiology and transmission. Selenium deficiency has
been associated with formulated diets deficient in selenium, for-
e. Thiamin Deficiency (Polioencephalomalacia)
ages grown on selenium-deficient soils in certain geographic re-
gions, and forages such as alfalfa and clover that have an in- Etiology. Polioencephalomalacia (PEM) is a noninfectious,
ability to efficiently extract available selenium from the soils. noncontagious disease characterized by neurological signs.
Rumen bacterial reduction of selenium compounds to unavail- Growing and adult ruminants on high-concentrate diets are typ-
able elemental selenium may also contribute to the disease. ically affected. Animals exposed to toxic plants or moldy feed
containing thiaminases, feed high in sulfates, or unusually high
Necropsy findings. Necropsy lesions include petechial hemor- doses of some medications are also at risk.
rhages and muscle edema. Hallmarks are pale white streaking
of affected skeletal and cardiac muscle. These are due to coag- Clinical signs and diagnosis. An early sign may be mild diar-
ulation necrosis. Pale striated muscles of the limb, diaphragm, rhea. Acute clinical signs include bruxism, hyperesthesia, in-
and tongue are also seen. voluntary muscle contractions, depression, partial or complete
opisthotonus, nystagmus, dorsomedial strabismus, seizures, and
Pathogenesis. Selenium and vitamin E function together as death. In subacute cases of the disease, animals may appear to
antioxidants that protect lipid membranes from oxidative de- walk aimlessly as if blind or may display head-pressing pos-
struction. Selenium is a cofactor for glutathione peroxidase, tures. Hypersalivation may be present, but body temperatures
which converts hydrogen peroxide to water and other nontoxic and ocular reflexes are normal. Morbidity and mortality may
compounds. Lack of one or both results in loss of membrane be high, especially in younger animals. Diagnosis is suggestive
integrity. from clinical signs and from response to intensive parental thi-
amine hydrochloride.
Differential diagnosis. In neonatal ruminants presenting with
respiratory and cardiac dysfunction, differentials include con- Epizootiology and transmission. PEM is caused by a thiamin
genital cardiac anomalies. Differentials generally for weak neo- deficiency. The disease tends to be seen more frequently in
nates or sudden or peracute neonatal deaths should include sep- cattle and sheep feedlots where the concentrates fed are high in
ticemia, pneumonia, toxicity, diarrhea, and dehydration. fermentable carbohydrates. Pastured animals are also vulner-
able if grain is feed. Thiaminase-containing plants, such as
Prevention and control. Awareness of regional selenium bracken fern, are often unpalatable so will less likely be a con-
deficiencies is important. Control involves providing good- tributing factor. Recent studies have also indicated that high
608 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARET L. DELANO

levels of sulfate in the diet, such as in the fermentable, low-fiber Sherman, 1994). Vitamin A deficiencies associated with hyper-
concentrates, may play an important role. Medications such keratosis have been reported, as well as vitamin E-responsive
as as amprolium, levamisole, and thiabendazole have thiamin- and selenium-responsive dermatitis.
antagonizing activity when given in excessive doses.

Necropsy signs. Cerebral lesions characterized by softening 4. Management-Related Diseases

and discoloration are grossly observed in the gray matter. Mi-
croscopically, neurons will exhibit edema, chromatolysis, and a. Failure of Passive Transfer
shrinkage. Gliosis and cerebral capillary proliferation may be
Neonatal ruminants are born without immunoglobulins and
observed.
must receive colostrum by 24 hr after birth. The morbidity and
mortality associated with failure of or inadequate passive trans-
Pathogenesis. A lack of thiamin results in inappropriate
fer, such as enteric and respiratory illnesses, can be severe.
carbohydrate metabolism and accumulation of pyruvate and
Measures to assure passive immunity for neonatal ruminants are
other intermediaries that lead to cerebral edema and neuronal
covered in Section II,B,5, and clinical signs of illness associated
degeneration.
with lack of immunity are addressed in the discussions of bac-
terial diseases (e.g., Escherichia coli infections) and, of viral
Differential diagnosis. Several important differentials include
diseases (e.g., diarrheas) in Section III,A,1 and III,A,2. Gener-
acute lead poisoning, nitrofuran toxicity, hypomagnesemia, vi-
ally, transfer of less than 600 mg/dl of immunoglobulins in the
tamin A deficiency, listeriosis, pregnancy toxemia, infectious
serum is classified as failure of transfer, 600-1600 mg/dl is
thromboembolic meningoencephalitis, and type D clostridial
partial, and above 1600 mg/dl is complete transfer. Methods
enterotoxemia.
to determine success of transfer should be performed within a
week of birth and include single radial immunodiffusion (quan-
Prevention and control. The disease can be prevented by
titates immunogloblin classes); zinc sulfate turbidity (semi-
monitoring the diet and by providing adequate roughage neces-
quantitative); sodium sulfite precipitation (semiquantitative);
sary to prevent overgrowth of thiaminase-producing ruminal
glutaraldehyde coagulation (coagulates above specific level);
flora and to maximize ruminal production of B vitamins. If ex-
and, y-glutamyltransferase (assays enzyme in high concentra-
cess sulfur is the primary factor, immediate removal of the
tion in colostrum and absorbed simultaneously with colostrum).
source is critical.

Treatment. Early aggressive treatment is essential to save an- b. Laminitis

imals. The disease is treated by frequent parenteral administra-
Laminitis is common in ruminants and can be caused by sud-
tion of thiamine hydrochloride, the first dose being adminis-
den changes in diet, excess dietary energy, and grain overload
tered intravenously. Dexamethasone, B vitamins, and diazepam
(or overeating). Laminitis is also associated with mastitis and
may also be required. Treatment is less successful when sulfur
metritis. Facility conditions, such as concrete flooring, poor
plays a prominent role in the etiology.
manure management, and inadequate resting areas may also
contribute to the pathogenesis of the disease. The complete
Research complications. This disease is preventable. Al-
pathogenesis of laminitis is poorly understood; however, it is
though the disease is less likely to occur in smaller groups of
thought that changes in the diet cause changes in rumen micro-
confined ruminants, the risks of feeding concentrates or moldy
bial populations, resulting in acidosis and endotoxemia. Dra-
feed, for example, with minimal good-quality roughage, should
matic changes in the vascular endothelium result in chronic
be kept in mind.
inflammation of the sensitive laminae of the hoof, separation of
corium and hoof wall, and rotation of the third phalanx. Af-
f Vitamin D Toxicity fected animals may be reluctant to get up or walk, will shift their
weight frequently, and will grind teeth or walk on carpi. Chron-
Vitamin D toxicity can result either from iatrogenic overad-
ically, the hoof wall takes on a "slipper" appearance. Treatment
ministration or ingestion of the plant Trisetum flavescens.
consists of identifying the underlying cause, administering anti-
Serum calcium levels may be high enough that blood in EDTA
inflammatories (phenylbutazone, flunixin meglumin), feeding
tubes will clot.
good-quality forages only, and regular foot trimming.

g. Nutritional Deficiencies c. Nutritional Diarrhea

In goats, nutritional deficiencies often manifest as a gen- Otherwise normal, well-managed lambs, kids, and calves can
eralized poor coat that is dry, scaly, thin, and erectile. Zinc- develop loose, pasty feces due to a nutritional imbalance caused
responsive dermatitis has been reported in goats (Smith and by overfeeding and/or improper mixing of milk replacers. Only
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS,AND CATTLE 609

milk replacer formulated for the particular species should be from excessive straining associated with dysuria from the
used. Once nutritional imbalances are corrected, the feces read- pressure of the fetuses and/or abdominal contents on the blad-
ily return to normal. Sudden changes in diet can also result in der. If the prolapse obstructs subsequent urination, rupture
loose feces. of the bladder may occur. The vaginal prolapse can be reduced
and repaired if discovered early, and techniques in small and
large ruminants are comparable. The animal should be re-
d. Photosensitization(Bighead)
strained, and the prolapsed tissue should be cleansed with dis-
Photosensitization is an acute dermatitis associated with an infectants. Best done under epidural anesthesia, the vagina is
interaction between photosensitive chemicals and sunlight. The replaced into the pelvic canal and the vulvar or vestibular open-
photosensitive chemicals are usually ingested, but in some cases ing is sutured closed (Buhner suture). Alternatively, a commer-
exposure may be by contact. Animals with a lack of pigment are cial device called a bearing retainer (or truss) can be placed into
more susceptible to the disease. Three types of photosensitiza- the reduced vagina and tied to the wool, thereby holding the
tion occur: primary; secondary, or hepatogenous; and aberrant. vagina in proper orientation without interfering with subse-
Primary photosensitization is related to uncommon plant pig- quent lambing.
ments or to drugs such as phenothiazine, sulfonamides, or tetra- Vaginal prolapses may have a hereditary basis in ewes and
cyclines. Secondary photosensitization is more common in cows and may prolapse the following year. These animals
large animals and is specifically related to the plant pigment should be culled. Vaginal prolapses may occur in nonpregnant
phylloerythrin. Phylloerythrin, a porphyrin compound, is a animals that graze estrogenic plants or as a sequela to docking
degradation product of chlorophyll released by rumen micro- the tail too close to the body (Ross, 1989).
bial digestion. Liver disease or injury, which prevents normal Uterine prolapses occur sporadically in postpartum ewes and
conjugation of phylloerythrin and excretion through the biliary cattle. The gravid horn invaginates after delivery and protrudes
system, predisposes to photosensitization. The only example of from the vulva. The cause is unknown, but excessive traction
aberrant photosensitization is congenital porphyria of cattle utilized to correct dystocia or retained placenta, uterine atony,
(see Section III,B,1). Pathologically, the photosensitive chemi- hypocalcemia, and overconditioning or lack of exercise have
cal is deposited in the skin and is activated by absorbed sunlight. been implicated. In cattle, the uterine prolapses usually develop
The activated pigments transfer their energy to local proteins within 1 week of calving, are more common in dairy cows than
and amino acids, which, in the presence of oxygen, are con- in beef cows, and are often associated with dystocia or hypocal-
verted to vasoactive substances. The vasoactive substances in- cemia. Cows may also have concurrent parturient paresis. Ini-
crease the permeability of capillaries, leading to fluid and tially, the tissue will appear normal, but edema and environ-
plasma protein losses and eventually to local tissue necrosis. mental contamination or injuries of the tissue develop quickly.
Photosensitization can occur within hours to days after sun ex- Clinical signs will include increased pulse and respiratory rates,
posure and produces lesions of the face, vulva, and coronary straining, restlessness, and anorexia. If identified early, the
bands; lesions are most likely to occur on white-haired areas. uterus can be replaced as for vaginal prolapses. Electrolyte im-
Initially, edema of the lips, corneas, eyelids, nasal planum, face, balances should be corrected if present. Additional supportive
vulva, or coronary bands occurs. The facial edema, nostril therapy, including the use of antibiotics should always be
constriction, and swollen lips potentially lead to difficulty in considered. Tetanus prophylaxis should be included. Oxytocin
breathing. With secondary photosensitization, icterus is also should be administered to induce uterine reduction. Vaginal
common. Necrosis and gangrene may occur. Diagnosis is closures are less successful at retaining uterine prolapses.
based on clinical lesions and exposure to the photosensitive Preventive and control measures include regular exercise for
chemi-cals and sunlight. Treatment is symptomatic. The prog- breeding animals, and management of prepartum nutrition and
nosis for hepatogenous type may be guarded if hepatic disease body condition.
is severe.

f Rectal Prolapse
e. ReproductiveProlapses (Vaginal Uterine)
Rectal prolapse is common in growing, weaned lambs and
Vaginal and uterine prolapses occur in ewes, does, and cows. in cattle from 6 months to 2 years old. The physical eversion of
The conditions are not common in does. Vaginal prolapses usu- the rectum through the anal sphincter is usually secondary to
ally occur during late gestation and may be related to relaxation other diseases or management-related circumstances. Rectal
of the pelvic ligaments in response to hormone levels. In sheep, prolapses may occur secondary to gastrointestinal infection or
these are most common in overconditioned ewes that are also inflammation, especially when the colon is involved. Diseases
carrying twins or triplets. Overconsumption of roughages, that cause tenesmus, such as coccidiosis, salmonellosis, and in-
which distends the rumen, and lack of exercise leading to intra- testinal worms, may result in prolapse. Urolithiasis may result
abdominal fat may predispose an animal to vaginal prolapse by in prolapses as the animal strains to urinate. Any form of cysti-
increasing intra-abdominal pressure. The condition may result tis or urethritis, vaginal irritation, or vaginal prolapse and some
610 SCOTT A. MISCHLER, WENDYJ. UNDERWOOD,AND MARGARETL. DELANO

forms of hepatic disease may lead to rectal prolapse. Abdomi- ally be sources of bite wounds. Standard veterinary wound as-
nal enlargement related to advanced stages of pregnancy, ex- sessment and care are essential for wounds or bites. Tetanus an-
cessive rumen filling or bloat, and overconditioning may cause titoxin may be indicated. Use of approved antibiotics may be
prolapse. Finally, excessive coughing during respiratory tract appropriate. The lesion should be cleaned with disinfectants
infections, improper tail docking (too short), growth implants, and repaired with primary closure if it is clean and uncontami-
prolonged recumbency, or overcrowded housing with animal nated. Thorough cleaning, regular monitoring, and healing by
piling may lead to prolapses. second intention are recommended for older wounds. Ab-
Diagnosis is based on clinical signs. Early prolapses may be scesses may also occur in the soft tissues of the hooves (sole ab-
corrected by holding the animal with the head down, while a scesses; see Section III,C,3) because of entrapped foreign bod-
colleague places a pursestring suture around the anus. The mu- ies or hoof cracks that fill with dirt. Preventive measures include
cosa and underlying tissue of prolapses that have been present improvement of housing facilities, pens, and pastures; monitor-
for longer periods of time will often become necrotic, dry, fri- ing hierarchies among animals penned together; and imple-
able, and devitalized and will require surgical amputation or the menting predator control measures, such as sound fencing, flock
placement of prolapse rings to remove the tissue. Rectal pro- guard dogs, or donkeys, in pasture situations.
lapse may also be accompanied by intestinal intussusceptions
that will further complicate the treatment and increase mortal-
ity. Occasionally, acute rectal prolapse with evisceration will re- D. Iatrogenic Diseases
sult in shock and prompt death of the animal. Prognosis depends
on the cause and extent of the prolapse as well as the timeliness 1. Anaphylactic Reactions
of intervention. In all cases of treatment, determination and
elimination of the underlying cause are essential. Acute anaphylatic reactions in sheep, goats, and cattle are of-
ten clinically referable to the respiratory system. Anaphylactic
g. Trichobezoars vaccine reactions cause acute lung edema; lungs are the primary
site of lesions if collapse and death are sequelae. The animals
Gastrointestinal accumulations or obstructions of hair (and/ will also be anxious and shivering and will become hyperther-
or sometimes very coarse roughage, forming bezoars) occur in mic. Salivation, diarrhea, and bloat also occur. Immediate ther-
cattle and sheep. Cattle that are maintained on a low-roughage apy must include epinephrine by intravenous infusion at (1 ml
diet, that lick their coats frequently, that have long hair coats of 1:1000 per 50 kg of body weight for goats and 1:10,000 (0.1
from outdoor housing, or that have heavy lice or mite infesta- mg/ml) or 0.01 mg/kg (about 5 ml) for adult cows.) Furosemide
tions and associated pruritus will often develop bezoars. In ad- (5 mg/kg) may be beneficial to reduce edema. Prognosis is usu-
dition, younger calves with abomasal ulcers have been found to ally guarded. Recovery can occur within 2 hr.
be more likely to have abomasal tric.hobezoars as well. Clinical
signs may be mild or severe according to size, number, and lo-
cation. Ruminal trichobezoars rarely result in clinical signs. 2. Catheter Sites and Experimental Surgeries
Obstruction will be accompanied by signs of pain, development
In a research environment, catheter sites or experimental sur-
of bloat, and decreased fecal production. Serum profiles will
geries may be sources of iatrogenic infection. Traumatic in-
show hypochloridemia; other imbalances depend on the dura-
juries to peripheral nerves can cause acute lameness. Improper
tion of the problem. Diagnosis is also based on abdominal aus-
administration of therapeutics can easily cause this type of
cultation, rectal palpation, and ultrasound (useful in calves and
lameness. Injections given in gluteals or between the semimem-
smaller ruminants). Treatment is surgical, such as paracostal la-
branosus and semitendinosus can cause irritation to the sciatic
parotomy (for abomasal), paralumbar celiotomy with manual
nerve and subsequent lameness. Contraction of the quadriceps
breakdown, or enterotomy. Supportive care should be adminis-
results in the limb being pulled forward. Injections in the caudal
tered as necessary to correct electrolyte imbalances and to pre-
thigh can damage the peroneal nerve and cause knuckling at the
vent inflammation and sepsis. Prognosis is generally good if the
fetlock. Traumatic injury to the radial nerve can result in a
condition is diagnosed and treated before dehydration and im-
"dropped elbow" (Nelson, 1983). Husbandry procedures such
balances become severe and peritonitis develops. Prevention in-
as tail docking, castration, dehorning, dosing with a bailing gun,
cludes providing good-quality roughage and treating lice and
and shearing may result in superficial lesions, dermal infec-
mange infestations.
tions, or cases of tetanus. Bailing-gun injuries to the pharynx
may lead to cellulitis with coughing, decreased appetite, and
Co Traumatic Disorders (Wounds, Bites, sensitivity to palpation.
and Entrapped Foreign Bodies) Standard veterinary assessment and care are essential for
these cases. Local and systemic antibiotics with supportive care
Wounds may be sustained from poorly constructed pens or may be indicated. Swelling around peripheral nerves caused by
fences, or from skirmishes among animals. Predators will usu- inoculations may be reduced by diuretics and anti-inflammato-
14. BIOLOGY AND DISEASES OF RUMINANTS: SHEEP, GOATS, AND CATTLE 611

ries. Mild cases of peripheral nerve damage may recover in 7- albumin values and foaming urine. The proteinuria also distin-
14 days. Personnel training, including review of relevant anat- guishes amyloidosis (and glomerulonephritis) from other causes
omy, preprocedure preparation, appropriate technique, careful of weight loss and diarrhea in cattle such as Johne's disease,
surgical site preparation, rigorous instrument sanitation, and parasitism, copper deficiency, salmonellosis, and bovine viral
sterile technique will minimize the incidence of potential com- diarrhea virus infection. Prognosis is poor, and no treatment is
plications from surgical procedures. reported.

2. Dental Wear
E. Neoplastic Diseases
Dental wear is seen most commonly in sheep. As sheep age,
excessive dental wear may lead to an inability to properly mas-
Neoplasia and tumors are relatively rare in ruminants.
ticate feed, manifesting as weight loss and unthriftiness. Several
Lymphosarcoma/leukemia in sheep has been shown to result
factors predisposing to dental wear should be considered. The
from infection by a virus related (or identical) to the bovine
diet should be properly balanced for minerals, especially cal-
leukemia virus. Pulmonary carcinoma (pulmonary adenomato-
cium and phosphorus, because primary or secondary calcium
sis) and hepatic tumors are found in sheep. Virus-induced pa-
deficiency during teeth development results in softening of the
pillomatosis (warts), discussed in Section III,A,2,s, and squa-
enamel and dentin. Dietary contamination with silica (i.e., hays
mous cell carcinomas have also been reported in sheep.
In goats, thymoma is one of the two most common neoplasias and grains harvested in sandy regions) will lead to mechanical
reported, although no distinct clinical syndrome has been de- wear on the teeth. Likewise, animals grazing or being fed in
scribed. Cutaneous papillomas are the most common skin and sandy environments will have excessive tooth wear. Sheep older
udder tumor of goats, and although outbreaks involve multiple than about 5 years of age are especially prone to tooth wear and
animals, no wart virus has been identified. Persistent udder pa- should be checked frequently, especially if signs of weight loss
pillomas may progress to squamous cell carcinoma. Lym- or malnutrition are evident. Managing the content and consis-
phosarcoma is reported rarely in goats. Although adrenocortical tency of the diets can best prevent the disease.
adenomas have been reported frequently and almost exclusively
in older wethers, no clinical condition has been described. 3. Sole abscesses
Lymphosarcoma of various organ systems and "cancer eye" Of the ruminants, cows are the most frequently affected by
(bovine ocular squamous cell carcinoma, or OSCC) are the subsolar absesses. Dirt becomes packed into cracks in the
most commonly reported cancers in cattle. Lymphosarcoma is horny layer of the sole of the hoof, and contamination eventu-
described in Section III,A,2,c. Lack of periocular pigmentation ally extends into the sensitive areas of the hoof, with lameness
and the amount and intensity of exposure to solar ultraviolet and infection resulting. Animals maintained in very soiled or
light are considered important factors in OSCC. Genetic factors muddy conditions, combined with poor hoof care, are more
may also play a role. Many cases occur in Herefords. This is a likely affected. Fusobacterium necrophorum is often the patho-
disease of older cattle; no case has been reported in animals less gen involved. Separation of the animal, supportive care, surgi-
than 4 years of age. The cancer metastasizes through the lymph cal drainage, and antibiotic treatment are indicated.
system to major organs. Treatment in either lymphosarcoma or
OSCC is recommended only as a palliative measure. The extent
of ocular neoplastic involvement is a significant criterion for
carcass condemnation. Papillomatosis (warts) are common in REFERENCES
cattle (see Section III,A,2,s).

Major References Cited Addressing Husbandry,

F. Miscellaneous Management, and Clinical Medicine

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The loss of protein in the urine contributes to abnormal plasma Howard, ed.). Saunders, Philadelphia.
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"Current Veterinary Therapy: Food Animal Practice" (1999). Vol. 4 (J. L. Auza, N. J., Olson, W. G., Murphy, M. J., and Linn, J. G. (1999). Diagnosis and
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Iowa State Univ. Press, Ames. "Bibliography of Naturally Occurring Models of Human Disease" (1981a).
Houpt, K. A. (1998). "Domestic Animal Behavior for Veterinarians and Animal Edited by G. Hegreberg, and C. Leathers. Washington State Univ., Pullman.
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