General Veterinary

Parasitology and
Helminthology VPA-211
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COURSE OVERVIEW

 Outline on types of helminths, its life cycle, pathogenesis and clinical signs.
 Zoonotic significance of helminths and its control.
 Diagnosis, treatment and control of helminths.
 Economic loss due to helminths.

MODULE-1: PARASITES AND PARASITISM

Learning objectives

 The module, parasites and parasitism will enlighten the students on the need to study veterinary
parasitology, their importance in the field of medicine and veterinary sciences, the relationship
between various organisms and the the types of parasitism.

INTRODUCTION

WHAT IS VETERINARY PARASITOLOGY ?

 In simple terms, Veterinary Parasitology is the study of parasites of domestic animals. On a

broader platform, Veterinary Parasitology is the science that explores the relationship between
various animal hosts and their parasites. Precisely, Veterinary Parasitology is the science that
dwells on the anatomy and physiology of parasites, their host(s), transmission, development,
impact and their detection and control.

IMPORTANCE OF PARASITES

 Parasitic diseases are known since time immemorial and yet many of the parasitic diseases have
not been controlled and continue to evade and plaque mankind.. Helminthic infections have been
found in ancient Egyptian mummies ( 1210 – 1000 BC ). According to the famous ebers papyrus
of 1550 BC at least four worm infections were recognized in ancient Egypt including Ascaris
lumbricoides, Taenia saginata, Dracunculus medinesis (guinea worm) and Schistosoma
haematobium . The papyrus also provides information on arthropods such as fleas, flies, and lice.
More recently, evidence was obtained from examining tissue sections of ancient Egyptian
mummies that Trichinella spiralis existed as an infection during that period. Helminths were also
were mentioned by Assyrian, Babylonian, and Greek physicians. Therefore, all of you should
appreciate the fact that parasites have existed in this world for a long time and have become very
successful in forging a good relationship with the host and discreetly utilize the relationship to
their advantage and finally depriving the host of their nutrients.

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 Parasitic diseases have their place in the history of the world and many wars were influenced by
parasitic diseases. Alexander the Great could not continue his conquest of the world owing to
malaria that killed many of his soldiers. Kingdoms in Northern Africa could not invade the
Southern Africa owing to trypanosomosis. In many parts of the world, livestock could not be
raised owing to parasitic diseases. Parasitic diseases continue to be the single most cause of
mortality and morbidity in livestock resulting in immense economic loss to farmers. In India
gastrointestinal nematodiosis in sheep and goats is so common and continue cause havoc to the
small ruminant industry. Calves and lambs if infected with great numbers of parasites such as
liver flukes or Haemonchus or coccidia may succumb to the infection. Diseases such as
theileriosis continue to cause mortality in cross bred cattle. Cattle, pigs, sheep and goats infected
with parasites fail to gain weight and may not reproduce there by affecting the economy of the
livestock enterprise. In our country, coccidiosis is so common in broiler poultry farms, if the farm
management is poor, the farm can be easily destroyed by coccidiosis.
 In the case of pet animals, toxocariosis and ancylostomosis are so common that is rare to come
across a dog that is free of these worms. Puppies infected with hookworms and Ascarids die of the
infection and heart worm infection in dogs continues to be a great challenge to veterinarians in
certain parts of the world. Of course, heart worm infection is a problem only in North East India
but it poses a great challenge to veterinarians in the United States. Cats infected with Toxoplasma
gondii are a threat to other livestock and humans. If you take arthropods, mankind is yet to
conquer so many of them. Mosquitoes continue to pose a big challenge to scientists. Only in the
near past, the genome of mosquitoes and Plasmodium was sequenced.
o During the course of evolution, living forms came together and associated as groups to
ensure their survival in the environment. This association is referred to as symbiosis or
symbiotic relationships.

 When the association is between members of the same genotype, it is known as homogenetic
association , for example, a flock of sheep or a pack of dogs.

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 When the association is between members of different genotype as between a cattle and an insect,
it is referred to as heterogenetic association.

SYMBIOSIS, COMMENSALISM AND PREDATORISM

 Symbiosis may be of different kinds viz., mutualism, commensalism, phoresis, parasitism or

predatorism.

 Symbiosis is association between two different organisms living in close physical association
usually to the advantage of both as opposed to free living organisms or simply, living together.
 Any organism that is intimately associated with another organism of a different species is
considered to be a Symbiont.

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 Phoresis is a relationship between two symbionts which are merely traveling together and
without physiological or biochemical dependence on each other.
 One will be larger than the other and the smaller phoront will be mechanically carried by the
larger phoront, for example, mites carried by beetles or bacteria on the legs of a fly.

 Mutualism is relationship involving symbionts that are mutually dependant on each for food
and shelter. This relationship is usually obligatory and one symbiont cannot survive without the
other, e.g., intestinal protozoa in termites.
 Termites feed on food that they do not digest but protozoa living in their intestine digest the food.
 Termites do not have the enzyme cellulase, but still feed on food that is rich in cellulose.
 Protozoa living in the intestine of termites synthesize the enzyme cellulase and help in digesting
the food ingested by the termite.
 Commensalism is a type of relationship, in which one symbiont derives benefit from the other
symbiont (host) but the host is neither benefited nor harmed. The term commensalism refers to
eating at the same table. Commensalism may be either facultative or obligatory.
 It is obligatory when the host is required for their survival and facultative when the host is not
required for their survival.
 The amoeba, Entamoeba gingivalis, is an obligatory commensal that is present in the mouth of
humans where it feeds on bacteria, food and dead epithelial cells but never harms the healthy
tissue in the mouth.
 On the other hand, the ciliate, Vorticella, a facultative commensal, may associate with small
crustaceans in a pond but are not dependant on them for their survival.

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 Predatorism is the relationship between predators and prey where the predators kill the prey
for food.
 Predators are animals or invertebrates that prey on other animals or invertebrates for food. Both
Parasites and Predators live at the expense of the host or prey .
 Parasites seldom kill their host and are small in relation to the size of the host whereas predators
kill the prey. Parasites have a higher reproductive potential than their hosts and are more
numerous while predators have a lower reproductive potential than their prey, and are less
numerous .
 Parasitoids are those, whose immature stages develop on other parasites and emerge by killing
the parasite. E.g. Hymenopteran flies on dipteran flies

PARASITES AND PARASITISM

 Parasitism may be defined as association between two-species, in which one species, the parasite,
lives in or on a second species, the host, for a significant period of its life and is metabolically
dependant on the host for its survival.
 The organism that derives benefit from the association is called as the parasite while the other
that is harmed is called as the Host.
 The word ‘parasite’ is derived from the Greek word and means ‘besides food” (Para-beside, sitos -
food).
 The parasite lives at the expense of the host without endangering the host.
 It does not kill the goose that lays the golden eggs.
 A predator kills the prey to feed upon the flesh but a parasite takes advantage of the host without
killing it.

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TYPES OF PARASITISM

 Ectoparasite is a parasite that lives on the surface of a host e.g. Fleas, ticks, lice, flies etc.

 Endoparasites are parasites that live inside the body of the host e.g. Flukes, tapeworms,
roundworms etc.

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 Obligate parasites are parasites that cannot complete their life cycle without spending a part of
their life cycle on the host e.g. trematodes.

 Facultative parasites are not normally parasitic but become parasitic when they accidentally find
a host, E.g. Naegleria fowleri in humans causing primary amoebic meningitis and Chrysomyia
sp. larva in wound

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 Accidental parasites are free living organisms that enter or attaches to the host by accident and
leads a short parasitic existence. E.g. Larva of Musca domestica in hosts
 Incidental parasite is a parasite found in a host that is not its original host e.g. Toxocara
vitulorum in goats
 Permanent parasites are those that spend their entire life cycle in or on the body of the host e.g.
lice

 Temporary parasites are those whose life cycles are not spent entirely on the host and are seen
only for certain periods of time (short or long duration) E.g. mosquitoes and bugs.

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 Erratic or aberrant or ectopic parasites are present in locations that are not their usual site e.g.
liver fluke in lungs.

 Hyperparasites are those that parasitize other parasites e.g. Plasmodium on mosquitoes.
 Spurious parasites are parasites found transiently in the excretions of the host in view of the host
having consumed a parasite of another host E.g. Eggs of Moniezia in dog faeces after ingestion of
Moniezia infected sheep, goat and cattle intestines by the dog.
 Pseudoparasites or artifacts are parasites that resemble a parasite and which are present in the
clinical specimens e.g. plant fibres, yeast, pollen grains etc .

Pseudoparasites Eg. Yeast

 A monogenetic parasite is one where there is no alternation of generation (e.g. Ascarids, amoeba,
trichomonads, etc.) while a digenetic parasite is one in which there is alternation of generation
(Coccidia, Plasmodium, piroplasmids, trematodes of higher vertebrates where asexual generation
alternates with the sexual generation, for e.g. in piroplasmids, the asexual stages are present in
vertebrate host and the sexual stages in invertebrate host).
 Parasites that require more than one host to complete its life cycle, are termed Heteroxenous e.g.
Theileria annulata – Cattle and ticks while parasites that require only one host to complete its life
cycle are said to be Homoxenous/Monoxenous e.g. amoeba, coccidia etc.

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 Parasites with a narrow host range are referred to as Stenoxenous e.g. Haematopinus suis in pigs
and coccidia whereas parasites with a wide host range are known as Euryxenous parasites e.g.
Toxoplasma gondi.

Stenoxenous parasite, Eg.

Louse Euryxenous parasite, Eg. Toxoplasma gondii

 Synanthropic parasites are parasites that are present or frequent human dwellings e.g. houseflies,
cockroaches etc.

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MODULE-2: TYPES OF PARASITES

On the basis of activity in a day, parasites are further divided into

 Diurnal parasites
 Nocturnal parasites
 Crepuscular parasites
 Diurnal parasites are those that are active in the day, e.g. Musca domestica, Tabanus sp. of flies

 Nocturnal parasites are those that are active at night, e.g. Anopheline mosquitoes

 Crepuscular refers to parasites that are active at twilight (dawn or dusk), e.g. the biting midge,
Culicoides sp.

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TYPES OF PARASITISM

 Infections refer to parasitism of host by internal parasites (e.g. amphistomes in livestock)

 Infestations refer to parasitism of host by external parasites (fleas, lice, ticks, flies etc.).

Infestation with ectoparasites

 Autoinfection refers to a condition where the juvenile infective form of a parasite, without
escaping from the host infects the same host e.g. Enterobius vermicularis
 Hyperinfection refers to a condition where the juvenile form of a parasite without exiting the host
penetrates in an area adjacent to the site of predilection and establishes in the same host e.g.
Strongyloides sp.
 Congenital (Transuterine or Transplacental) infection is transmission of parasites from the dam
to the foetus across placental membranes e.g. Toxocara canis in dogs
 Transmammary (Transcolostral) is transmission of parasites from the dam to the young one
through the milk of the infected dam e.g . (Toxocara cati in cats)

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 Transovariantransmission is transmission of parasite from the female parent to the progeny
through the ova. E.g. Babesia bigemina in ticks

 Transtadial (stage to stage) is transmission of parasite from one stage to another stage of the
vector as in Theleria annulata in Hyalomma spp. of ticks
 Zoonoses are diseases common to humans and animals (Singular – Zoonosis). According to WHO
(1959), zoonoses are diseases transmissible between vertebrate animals and man.

 Anthropozoonoses is a disease of animals transmitted to humans e.g., Cystic echinococcosis from

animals to humans

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 Zooanthroponoses is a disease of humans transmitted to animals e.g. Taenia solium from humans
to pigs

TYPES OF HOST

 Definitive hosts are hosts that harbour the adult (sexual) form of the parasite. e.g. Sheep for
Fasciola gigantica, Dog for Echinoccocus granulosus, and Horse for Habronema muscae.
 Intermediate hosts are those that harbour the asexual form of the parasite (only when there is
an obligatory passage through the host).
o Intermediate hosts may be divided into passive intermediate hosts (snails for
trematodes) and active intermediate hosts (Tabanus sp. for Trypanosoma evansi))

Passive intermediate hosts (Snails) Active intermediate host (eg. Tabanus)

 Reservoir hosts are hosts that harbour a parasite of another host without itself getting affected,
but act a source of infection for the original host e.g. Game animals for the protozoan parasite
Trypanosoma gambiense.
 Carrier hosts are hosts that have a residual population of the parasite and acts as a source of
infection for the same type of host.
 Transport hosts are those that harbour the immature/infective stage of a parasite of another
host and help in disseminating the parasite without any development in itself. E.g. Earthworms
for Egg/larvae of Ascaridia galli

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 Paratenic hosts are those that harbour the immature/infective stage of a parasite in an
encapsulated form and helps in dissemination of the parasite to the definitive host e.g. Calotes for
Spirocerca lupi.

 Intercalary host is a host that liberates the infective stages of a parasite of another trapped in
the body of the original host E.g. Cats by eating mice liberate the eggs of Capillaria hepatica
which are trapped in the liver parenchyma.

VECTOR

 A Vector is a latin word which means bearer. In the broad sense any agent that carries infectious
organisms between animals. A vector is an arthropod that carries the parasite between two
vertebrate hosts. E.g. Ticks and mosquitoes for various blood protozoans.
 Vector may be divided into mechanical vector and cyclical vector.
 A mechanical vector is an arthropod that carries the infectious agent from, one vertebrate host to
another without any development in its body. E.g. Tabanus transmitting T.evansi by interrupted
feeding or house flies transmitting cysts of Entamoeba histolytica while a cyclical vector is a
vector in which the parasite undergoes development/multiplication before being transmitted to
the next host (Ticks transmitting haemoprotozoan parasites)

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TERMINOLOGIES USED IN PARASITIC DISEASES

 Epidemiology is the study of a disease in relation to the population, aspects of disease such as
incidence, prevalence and transmission in a population
 Endemic disease refers to a disease that occurs with a predictable frequency with minor
fluctuations in a population
 Epidemic disease refers to diseases that occur at a higher level in a place at a time than expected
for the disease in the place at that particular time
 Sporadic diseases are those diseases that occurs irregularly with widely dispersed incidence or a
disease that occurs infrequently
 Pandemic is an epidemic occurring in a wide/larger area.
 Incubation period is the time lapse between the entry of the parasite and the first appearance or
onset of clinical signs.
 Prepatent Period is the period in which the form of the parasite is demonstrated in the clinical
material of the host.
 Hypobiosis refers to temporary cessation in the development of immature stages of some
nematode parasites in the host due to adverse environmental conditions, for example, Ostertagia
ostertagi in cattle

 Hibernation(Winter Sleep) refers to low activity of parasites in winter.

 Aestivation (summer sleep) is the period of low activity in summer
 Diapause is aperiod of low activity in arthropods.

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 Parthenogenesis is a(Virgin birth) refers to formation of progeny without fertilization e.g.
Haemaphysalis ticks and Strongyloides sp. of nematodes.

 Paedogenesis (Juvenile multiplication) refers to multiplication of juvenile/immature stages of

parasite in intermediate hostS. E.g. Multiplication of immature stages of trematodes in snail

 Metagenesis (Alternation of generation) refers to sexual multiplication alternating with asexual

multiplication, E.g. Trematodes, Sexual multiplication in definitive host alternating with
paedogenesis in intermediate hosts

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 Schizogony is a type of asexual division/multiplication in protozoa where a parasite multiplies

into numerous individuals by multiple fission. The nucleus of the parasites undergoes repeated
division without cytokinesis. e.g. apicomplexan parasites

 Gametogony is the differentiation of gamonts in to male and female gametes

 Syngamy is the union of the male and female gametes to form the zygote e.g. apicomplexan
parasites

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 Sporogony is the differentiation of zygote to oocyst, sporocyst and sporozoites e.g. all
apicomplexan parasites.

HOST PARASITE RELATIONSHIP

 Host parasite relationship as the term implies is the relationship between two organisms namely
the host and the parasite where the parasites invariably succeed in forging a relationship to its
advantage.
 Parasites upon entering their hosts through various routes may survive or die in the host. If
parasites survive they develop and multiply causing infection or disease in the host.
 In evolution, there is always a tendency towards mutual adjustment between two organisms and
therefore both parasite and the host forge a relationship that may either limit the infection so that
parasite control is achieved without any pathological changes. Therefore, successful parasites
tend to become harmless to the host.
 Majority of the parasites that survive in their hosts do not endanger their hosts, since they do not
want to lose their shelter and food. However, the host tries to expel or kill the parasite by immune
responses. When the host attempts to kill the parasite by immune mediated mechanisms,
immunopathological lesions develop leading to disease in the animal.
 Host-Parasite relationship is a dynamic process where the host employs innate and acquired
immune mechanisms to destroy the parasite.
 The nutrition status of the host and the energy resources of the host, at the start of an infection
play a role in determining the ultimate outcome of the host parasite relationship. Malnutrition
will impede the animal's ability to respond immunologically to the parasite.
 As parasites are large and complex, the host finds it difficult to counter the parasites by immune
mediated mechanisms, resulting in responses that are not always protective.
 In addition, parasites also evade the immune responses of the host by various ways to ensure
their survival and propagation. Therefore, host parasite relationship is an intricate relationship
where the host attempts to destroy the parasite but the parasite does not endanger their host lest
that they so lose their shelter and food.
 Host parasite relationship occurrs in a complex ecological setting where in vivo and external
environments change continuously.

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MODULE-3: MODES OF TRANSMISSION OF PARASITES

Learning objectives

 This module will focus on the various routes of transmission of parasites between hosts. In other
words, how parasites are transmitted between hosts will be dealt in this chapter. Parasites are
commonly transmitted through ingestion of parasite contaminated food and water besides other
routes such as skin penetration, intra nasal transmission, coitus and congenital transmission.
Each mode of transmission will be dealt in detail with suitable examples.

INTRODUCTION

 Parasites have distinct routes of entering a host.

 Endoparasites enter the hosts in general through natural openings on the exterior of the body or
through the skin.
 Parasites are transmitted from one animal to another by
o Ingestion
o Skin penetration
o Contact
o Predation
o Coitus
o Transplacental/Tranmammary transmission

THROUGH INGESTION

 The most common mode of transmission of parasites is through ingestion. The host may become
infected by direct ingestion of an infective stage through contamination of food and water or by
ingestion of an intermediate host or transport host containing infective stages.

Mode of infection through ingestion of parasite

contaminated food

 For parasites with direct life cycles, the infective stages viz., egg containing the second larval stage
(ascarids), cysts (Entamoeba and Giardia) and oocysts (coccidia) find their way into the feed and
water of the host thereby gaining access to the host or the infective stages (third larval stage) may
climb up the vegetations and wait for the host to ingest.

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 For parasites with indirect life cycle, the host becomes infected by ingestion of an intermediate
host or transport host containing infective stages.

 In certain parasites, the definitive hosts are infected through ingestion of infective stages (larval
stages) in intermediate hosts (fish for Diphyllobothrium latum and crabs for Paragonimus sp)
and through ingestion of raw or undercooked meat/organs/milk of intermediate hosts (Taenia
solium, Echinococcus granulosus).

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THROUGH SKIN PENETRATION

 After mouth, skin is the most common route of entry for many parasites.
 The infective stages of the parasite may actively penetrate the skin and in this process, the
secretions of the parasite help to digest the host tissue (cercariae in schistosomes).

 Penetration of the host’s skin is the predominant route by which the infective larvae of
hookworms enter their hosts, although they also enter through the mouth.

 Certain parasites enter the hosts via the bite of an intermediate host serving as a vector. These
parasites develop in blood sucking insects and ticks and when these vectors feed to obtain the
blood and tissue fluids from hosts, the infective stages of the parasites are introduced into the
host.

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CONTACT AND PREDATION

 Parasites are transmitted between animals by contact especially when they are confined in
sheds or houses. Eg. Lice infestation and mange is chiefly transmitted between animals by
contact.

Transmission by direct contact (eg. lice, mites, etc.)

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 Parasites are also transmitted during predation by a host. For example, when cats predate on rats,
cats may acquire an infection with parasites.

Transmission through
predation (eg. Toxocara cati,
Toxoplasma gondii)

ENTRY THROUGH NOSTRILS

 Oestrus ovis, the nasal bot fly, deposit its young larvae around the nostrils of the host, where
upon they crawl upward and enter the nasal sinuses.

 Naegleria fowleri, a fresh water amoebae present in surface water of polluted pools gains
access to the hosts through the intranasal route.

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ENTRY THROUGH EXTERNAL GENITALIA

 Tritrichomonas foetus, the protozoan parasite that causes abortion in cattle and Trypanosoma
equiperdum, the protozoa that causes dourine in horses are transmitted during coitus.

TRANSPLACENTAL/TRANSMAMMARY TRANSMISSION

 Transplacental or prenatal infection refers to transmission from mother to foetus across the
placenta as in Toxocara canis and transcolostral or transmammary transmission refers to
transmission from infected dams to nursing offspring via colostrum or milk as in Toxocara
vitulorum or Toxocara cati.

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MODULE-4: METHODS OF DISSEMINATION OF THE INFECTIVE STAGES OF
PARASITES

Introduction

 Most of the parasites leave the host passively through excretions of the host.
 Many exit from the hosts through faeces as eggs (ascarids, strongyles, flukes etc.), cysts
(Entamoeba, Giardia) and oocysts (coccidia).

 Few exit through urine (Eg. Schistosoma haematobium, Stephanurus dentatus) and some leave
through genital discharges (Eg. Tritrichomonas foetus).
 Some parasites are imbibed by arthropods inadvertently when they feed on a host (eg. Malarial
parasites transmitted by mosquitoes) while the extraintestinal stages of parasites may be removed
from the host during predation and the parasite subsequently infects the predator and leaves it
passively through their faeces (eg. Cyst forming coccidia).

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DISSEMINATION OF PARASITES

 Permanent ectoparasites such as louse and flea exit the hosts actively by either crawling or
jumping on to another host during moments of contact between hosts.

 Few parasites exit actively from the hosts (mother) to their foetuses through placenta
(transuterine route) eg. Toxocara canis, Toxoplasma gondii

 Some parasites leave the host through the medium of milk to infect the young ones
(transmammary route), eg. Toxocara vitulorum, Toxocara cati.

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METHODS OF DISSEMINATION OF INFECTIVE STAGES OF PARASITES

 Once parasites are outside the hosts, they have to survive in the environment until they find a
suitable host. As the environmental conditions are generally adverse to their survival, the
infective stages of parasites are endowed with resilience. These resistant stages have the capability
to survive the adverse conditions and remain infective to find a host. Temperature and moisture
are two important factors that facilitate or deter parasite survival and development.
 Parasites generally do not develop below 10oC or above 40oC. When climatic conditions are
hostile (freezing temperatures), parasites cease development in hosts (arrested development) and
wait for the conditions to improve before they resume development and discharge their eggs in
faeces.

Dispersal of parasites

 Parasites are disseminated in the environment mechanically through the agency of water and
fomites beside human interventions.
 Water is an important agent for dissemination of parasites especially for those that require an
aquatic habitat for development (eggs of many trematodes, larvae of Dracunculus etc).
 Trematodes whose intermediate hosts are aquatic snails are carried by the surface water into
water bodies where they develop in aquatic snails. Similarly, larvae of Dracunculus require water
bodies for gaining access to cyclops.
 Parasites that require aquatic habitats for developments such as mosquitoes and black flies are
carried to long distances by streams and rivers.

 Human interventions such as construction of irrigation canals directly facilitate breeding of

snails’ thereby aiding dissemination of trematode parasites besides aiding breeding of insects.

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 The use of sewage and sludge to fertilize pasture is another potential method of dissemination of
parasites.
 Fomites such as insects mechanically disseminate the parasites from one place to another.
 The fungus Pilobolus aids in the dispersal of the lungworm infective larvae from faecal pats to the
pasture thereby facilitating infection of cattle hosts.
 Wild animal hosts may serve as a reservoir of infection for domesticated livestock.

 Wild reservoir hosts are important factor in the epidemiology of Fasciolosis. Overcrowding of
hosts also facilitates dispersal of parasites.

Parasite induced host behavioural changes

 Metacercariae of Dicrocoelium enters the brain of ants and paralyse them thereby aiding
dissemination of parasite infected ants for herbivores during grazing.
 Grasshoppers infected with tetramers and beetles infected with cysticercoids of tapeworms
become sluggish thereby facilitating ingestion of definitive hosts.
 Ruminants heavily infected with hydatid cysts become debilitated, making them easier prey for
carnivores.

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Strategies adopted by parasites to infect hosts

 Some parasites employ certain strategies to augment their chances of finding a host. Liver fluke
encysts on green parts of plants and on higher parts of the plants to facilitate ingestion by
herbivore hosts.

 As cattle are reluctant to feed on herbages near faeces, the motile gravid segments of Taenia
saginata leave the faeces to contaminate the herbage and increase its chances of being eaten by
an herbivore as against the non motile gravid segments of Taenia solium which does not have to
leave the faeces because pigs being coprophagic consume the faeces and pick up the infection.

 Some parasites are endowed with sensory organs to locate hosts. Warmth, CO 2, fatty acids, amines etc.,
serve as stimuli for parasites especially arthropods to locate hosts.

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MODULE-5: PARASITE SPECIFICITY IN RELATION TO SPECIES, BREED, SEX AND
LOCATION

Learning objectives

This module will focus on

 parasite specificity in relation to host species, breed, sex, location within the host and the
geographapical location of parasites.
 Parasite specificity determines the host range of parasites.

PARASITE SPECIFICITY IN RELATION TO SPECIES, BREED, SEX AND LOCATION

INTRODUCTION

 Parasite specificity or Host Specificity is the natural adaptability of a species or groups of parasite
to certain species or groups of host and is dependent upon the compatibility of a host to a
parasite.
 In natural host parasite relationships, the parasite must be precisely adapted to the structural and
physiological conditions that characterize the host species. This adaptation, which develops over
long periods of evolutionary change, is the basis for the phenomenon of host specificity or
parasite specificity.
 Parasite specificity is usually defined in terms or establishment or failure to establish in a host.
However, a range of parameters, such as establishment, number, size, developmental stage of
worms, duration, level of egg production and duration of infection can give indication of the
degree of adaptation to a particular host. For example, the eggs of the human ascarid, Ascaris
lumbricoides can hatch in a variety of mammalian hosts but can develop into adults in humans
alone. However, in some cases, the restriction is absolute or total as occurring in Eimeria species
or the restriction may be very loose and parasite can undergo development in and be transmitted
between, a wide variety of hosts as occurring in the nematode Trichinella spiralis.
 Parasite specificity may be supra specific where, groups of parasites are associated with groups of
hosts or infra specific where a specific parasite is associated with a specific species of host.
 Parasite specificity determines the host range of a parasite and accordingly, the parasite may have
a narrow or wider host range. Certain parasites such as Haematopinus suis infest only pigs
(narrow host range), while some such as Trypanosoma evansi, have a wider host range and infect
many hosts.

Trypanosoma evansi, the

Haematopinus suis, a parasite with a wider host
parasite with narrow host range
range

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 Specificity may also vary between larval and adult stages of the same parasite to hosts.
 In some, the larval stages have strong host specificity to intermediate hosts (snails) and less for
definitive hosts as in trematodes while in some such as Toxoplasma gondii, the asexual stages
have a wider host range and infect a wide variety of intermediate hosts while the sexual stages
infect only one host.
 In some parasites, as in Eimeria, the host specificity is less at the generic level where they infect a
wide variety of hosts but very strong at the individual species level with very high niche specificity
in hosts.

FACTORS INFLUENCING PARASITE SPECIFICITY

 Parasite specificity is also governed by anatomical, physiological and nutritional, beside ecological
factors.
 The anatomy of the host animal may prevent the establishment of a parasite.
 The intestinal villi or crypts may be too short or intestinal movements too rapid to prevent the
establishment of a parasite.
 Physiological factors such as composition of the bile, dissolved carbon dioxide in hosts, pO2,
redox potential and the normal temperature of a host may also regulate host specificity.
 In unnatural hosts, the unsuitable body temperature may fail to provide the right stimulus for the
parasite to establish in hosts.

PARASITE SPECIFICITY IN RELATION TO HOST SPECIES

 Host animals are susceptible to some parasites and resistant to others. For example, majority of
the helminths of cattle are incapable of infecting sheep and goats. Th normal resistance of various
species of animals to various pathogens is due to the presence of antibodies on their erythrocytes
called isohaemagglutinins.
 Many parasites do not develop in hosts other than their natural hosts. A good example for host
specificity is Eimeria sp.
 The red worms (Strongylus sp) of horses are specific to equine hosts and cannot infect cattle,
buffalo, sheep and goat.

 The nematode Ancylostoma caninum is a parasite of both dogs and cats. However, the strain
adapted to dog survives better and produces more eggs in dog, as compared to the strain found in
cat. Similarly, the cat adapted strain develops better and produces more eggs in the cat as
compared to dogs.

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 Limited degree of development of parasite occurs in unnatural host in some cases as in the case of
larvae of Ostertagia ostertagi (cattle parasite) in sheep where only few reach to adult stage or the
dog parasite, Toxocara canis which undergoes limited development in children causing the
condition visceral larval migrans.

PARASITE SPECIFICITY IN RELATION TO SEX

 Some parasites affect only the females and not the males as in the case of the trematode,
Prosthogonimus species which is mostly found in the oviduct of female gallinaceous birds. The
influence of sex on helminth burden appears to be largely hormonal. In animals whose oestrus
cycle is seasonal, parasites tend to synchronize their development with that of the host. For
example, ewes show a spring rise in faecal egg counts after lambing and onset of lactation.
Similarly, in the case of bitches above six months old, development of Toxocara canis is
influenced by hormonal changes. When bitches become pregnant, the dormant larvae are
activated and transported to the foetus and so puppies are born with Toxocara canis infection.
However in the case of male dogs older than 6 months, dormant larvae are not activated but
become calcified. Therefore, older male dogs serve as dead end hosts for Toxocara canis.

The oviduct fluke, Prosthogonimus

species affects only the female of the
host species

PARASITE SPECIFICITY IN RELATION TO BREEDS

 Different parasites have varied susceptibility to different breeds.

 Indigenous breeds of cattle suffer less from tick infestation and tick borne diseases in comparison
to cross breds and exotic breeds.
 N’Dama & Mutura breeds of cattle in Africa and their crosses are tolerant to trypanosomes.

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N'Dama and Mutura breeds of cattle in

Africa are resistant to trypanosomes

PARASITE SPECIFICITY IN RELATION TO LOCATION IN HOSTS

 Each parasite has a specific predilection site or a location in hosts. The best example for site
specificity is Eimeria species which parasitize only certain areas of the intestine.

 Other examples include the nematode Dictyocaulus species which affect only the lungs in
ruminants and the trematode, Paragonimus species in lungs of dogs.

Example for location specific parasite -

Dictyocaulus species

PARASITES IN RELATION TO LOCALITY

 When parasites are limited to certain ecological or geographical areas as in the case of African
animal trypanosomes and human trypanosomes that are restricted to Western, Central and
Eastern Africa, it is referred to as ecological or geographical restriction.

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MODULE-6: TISSUE REACTIONS CAUSED BY PARASITES TO THE HOST

Learning objectives

 This module will inform the students about the effects of parasites on hosts or in other words the
injury and lesions inflicted by parasite during its invasion, estabishment and development in the
host.

TISSUE REACTIONS CAUSED BY PARASITES TO THE HOST

INTRODUCTION

 Parasites affect the host by two major ways. They may cause direct injuries during the process of
entry, establishment, feeding and multiplication in the host and indirectly by transmitting
pathogens that may kill or affect the well being of the host.

EFFECTS OF PARASITES ON HOST

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INJURIES DURING ENTRY OF PARASITES

 Certain parasites cause direct injuries to the host, during the process of entering the host.
 The hookworms (Anclystoma sp., Bunostomum sp.) cause injuries to the cells and underlying
connective tissue when they penetrate the skin of the host.

Injuries caused during penetration of

host skin

 Cercaria of certain schistosomes causes dermatitis while penetrating the host’s skin.

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LOSS OF BLOOD AND THE ASSOCIATED ANAEMIA

 Some parasites suck blood (hookworms, barbers pole worm, mosquitoes, tick etc) from the hosts
resulting in anaemia.
 The quantum of blood imbibed by insects and ticks and the resultant blood loss may not impair
the health of the host, but the quantum of blood imbibed by some species of helminths, such as
barber’s pole worm, hookworms and red worms of equines is immense and may prove fatal to the
hosts.
 Haemonchus contortus, in large numbers may bleed the animals causing severe anaemia and
mortality in lambs.

Suck blood causing anaemia in hosts

 Heavy infestations with ticks can lead to severe anaemia in animals. A single adult female tick is
reported to such around 0.5 to 2.0 ml of blood and therefore if an animal is heavily infested with
ticks, substantial blood loss may occur.

Heavy tick infestation can lead to anaemia in

animals

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Development of oedema in hosts

 Loss of plasma proteins especially albumin (hypoalbuminaemia) results in oedema where fluid
accumulates in the submandibular space, between the mandibles which is commonly known as
bottle jaw or in the peritoneal cavity (ascites) and thoracic cavity (hydrothorax).
 Exchange of fluid between blood and interstitial spaces is controlled by Hydrostatic Pressure (HP)
and Plasma Colloid Osmotic Pressure (COP). If the hydrostatic pressure is high, fluid will leave
the blood vessels and seep into the interstitial spaces. On the contrary, if Colloid Osmotic
Pressure is high, then fluid will be drawn into the blood vessels.
 The plasma protein, albumin balances these two forces. Loss of blood results in
hypoalbuminaemia and as a sequel Colloid Osmotic Pressure is reduced and Hydrostatic Pressure
is increased. This results in seepage of fluid from the blood vessels into interstitial spaces
resulting in oedema. Oedema is commonly seen in parasitic diseases where loss of blood occurs as
in Haemonchosis, Fascioliosis, Amphistomosis etc.

CHANGES IN PROTEIN METABOLISM AND MINERAL LEVELS

 Changes in protein metabolism and mineral levels commonly occur in parasitic infections
especially in helminthic infections.
 Reduced level of aminoacid incorporation in muscle protein results in reduced weight gain and
weight loss.
 Reduced incorporation of aminoacids into protein by wool follicles affects the wool quality.
 The wool of helminths affected sheep become brittle and wither away.
 Mineral deficiences affects the growth rates since skeletal size (bone size) ultimately determines
the capacity of growing animal to accumulate muscle.
 All these results in reduced weight gain, reduced wool growth and reduced milk production in
infected animals.

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DESTRUCTION OF TISSUES

 Many parasites during their course of development undergo migration in the tissues of hosts.
 Examples include, immature stages of liver flukes that migrate in the liver of cattle, sheep and
goats causing traumatic hepatitis.

 Larvae of Toxocara canis, T. cati, T. vitulorum and Ascaris suum migrate through liver and lungs
inflicting physical damage, especially to lungs.

 Trichinella spiralis larvae cause severe myositis as they migrate through the muscles of their
hosts.

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MODULE-7: TISSUE REACTIONS CAUSED BY PARASITES TO THE HOST

Learning objectives

 This module will continue to inform about the effects of parasite on hosts.
 The tissue reactions caused by different parasites during establishment and feeding on hosts,
mechanical interference, pathological changes, effect of secretions or excretions and the
immunological reactions of the host to parasites resulting in immunopathological lesions will be
taken up in this chapter.

INJURIES DURING ESTABLISHMENT AND FEEDING

 Flukes, tapeworms and acanthocephalans armed with suckers, hooks and spines cause irritation
to the mucosal surfaces of intestines.

 Immature stages of amphistomes ingest plugs of mucosal tissues as they feed.

Immature amphistomes plug out mucosal

tissues as they feed

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 Biting lice such as Bovicola bovis browse on the epidermis and cause intense irritation,
inflammation and leakage of serum from damaged skin.
 Ticks also cause inflammation and leakage of serum from damaged skin in sensitized animals.

 Sarcoptes mites pierce and burrow into the skin of animals leading to irritation, itching, and
inflammation of the skin characterized by keratinization, thickening and wrinkling of skin.

Sarcoptes mites pierce and burrow into the

skin causing the condition Sarcoptic mange

MECHANICAL INTERFERENCE

Occlusion

 Death due to intestinal obstruction by parasites is common, eg. ascarids and tapeworms.
 Occlusions of bile ducts by liver flukes obstruct the flow of bile resulting in icteri.

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 Adult filarids lodged in lymphatic ducts cause aggregation of connective tissue that results in
blockage of lymph flow and oedema in hosts.
 Gapeworms block the air passages causing dyspnoea and asphyxia in fowls.
 Lungworms such as Dicytocaulus viviparous cause blockage of bronchi leading to atelectasis and
emphysema in lungs of cattle.

Lungworms blocking the bronchi in

sheep

 Occlusion of blood vessels with thrombus as in the case of Strongylus vulgaris in horse may
prove fatal if the coronary artery or brachiocephalic trunk is involved.
 In haemoprotozoan diseases, such as babesiosis and malaria, protozoa infected erythrocytes get
trapped in the microcirculation of organs, impeding blood flow resulting in hypoxia and necrosis
of tissues.

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Pressure atropy

 Pressure upon organs by larval stages of parasites, especially those of tapeworms result in atropy
or distortion of the organ involved.
 Coenurus cerebralis, the larval stage of the tapeworm Taenia multiceps exert pressure on the
brain of sheep causing the condition known as Gid or Staggers.

Coenurus cerebralis, the larval

tapeworm of Taenia multiceps
causes pressure atrophy in brain

 Similarly, the larval stages of Echinococcus granulosus, form hydatid cysts in various organs,
especially in liver and lungs of animals and man that causes severe problems in intermediate
hosts, especially humans.

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PATHOLOGICAL CHANGES

 One of the effects of parasites on hosts includes changes in tissues that are affected by the
parasite.
 Some parasites cause chronic inflammatory reactions resulting in fibrosis and formation of
nodules in the inflamed tissues.
 In Ascaris suum infections, spots of white fibrous tissue (Milkspots) are formed in the liver of
affected piglets.

 In sensitized sheep, larvae of Oesophagostomum columbianum are encapsulated within nodules

owing to inflammation and infiltration of eosionophils and foreign body giant cells to cause the
condition known as pimply gut.

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 Larvae of warble flies form cysts in the back of cattle and develop within it until ready to leave the
hosts for pupation on the ground.

Hypertrophy

 Hypertrophy commonly occurs in all intracellular parasites, for example, in coccidiosis, the
intestinal epithelial cells are markedly enlarged.

Intestinal cells are hypertrophied

(eg. coccidiosis)

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Hyperplasia

 Hyperplasia is associated with some parasites as in liver flukes that cause increased division of
cells lining the bile ducts resulting in thickening of the bile duct.

Neoplasia

 Another tissue change is neoplasia which is associated with Spirocerca lupi, the gullet worm of
dogs. Oesophageal nodules, transformed into a granuloma and later into sarcoma are common in
S. lupi infections.

Metaplasia

 In infections caused by the lung fluke, Paragonimus westermani, the parasite is surrounded by
epithelial cells and fibroblast cells in lungs. This is a classical example of metaplasia where one
type of tissue transforms into another without the intervention of embryonic tissue.

EFFECTS OF SECRETIONS AND EXCRETIONS

 Ticks secrete a toxin that causes the condition known as tick paralysis in mammals. Eleven hard
ticks and one soft tick is associated with tick paralysis. Tick paralysis is characerized by aacute
ascending flaccid motor paralysis.

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 Release of parasite internal antigens results in anaphylactic shock in some cases.
 Metabolic products released during erythrocyte destruction in malaria causes febrile responses in
hosts and toxins/metabolic products secreted by trypanasomes cause injuries to the hot.

IMMUNOLOGICAL REACTIONS

 Host immune response to eggs of Schistosoma nasale cause nasal granuloma in cattle.

 The nodular worm of sheep and goats, Oesophagostomum columbianum, may cause calcified
nodules in sensitized hosts impairing digestion and absorption of nutrients in their hosts.

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MODULE-8: RESISTANCE OF HOSTS TO PARASITIC INFECTIONS/INFESTATION

Learning objectives

 This module will introduce the students to parasitic immunity, factors that influence the host
immunity, natural and acquired resistance to parasitic infection, types of parasitic immunity etc.

INTRODUCTION

What is Resistance?

 Resistance is the defense mechanism exhibited by the host against a foreign body or a pathogen.
 The host’s defense mechanism, which is directed against the parasites either kills or retards their
establishment and limits their multiplication.
 A host is said to be susceptible if it is capable of being infected by a specific parasite. This implies
that the physiological state of the host is such that a parasite is capable of establishing itself in the
host.
 A host is said to be resistant if its physiological state prevents the establishment and survival of a
parasite.

FACTORS THAT INFLUENCE HOST RESISTANCE

Species resistance

 Host animals are susceptible to some parasites and resistant to others.

 For example, majority of the helminths of cattle are incapable of infecting sheep and goats.
 The normal resistance of various species to various pathogens is due to presence of antibodies on
their erythrocytes called isohemagglutinins.

Breed Resistance

 Certain breeds of animals show natural / innate resistance to some parasitic infections, e.g., West
African hump less cattle (NDama and Mutura) are resistant to trypanosomiosis and they are
called as trypanotolerant breeds.

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 Similarly, Red masai sheep of East Africa is more resistant to Haemonchus contortus. Zebu (Bos
indicus) shows high resistance to Boophilus ticks than exotic cattle (Bos taurus).
 This is probably a result of selection of the most resistant animals over many years.

Age of the host

 Young animals are generally more susceptible than adults to parasitic infections, eg. pigs less than
4 months old are more susceptible to Ascaris suum.
 Similarly, lambs are more susceptible to Moniezia spp (tapeworm) and Trichostrongyles (round
worms).
 Conversely, young animals are more resistant to babesiosis than older cattle and this
phenomenon is known as inverse/reverse age registance.

Nutritional status of the host

 Poorly fed animals are more susceptible to parasitic infections, e.g., Vitamin (A, D & B Complex)
and iron deficiency may interfere with establishment and maintenance of host resistance to blood
sucking parasites.

Genetic constitution of host

 The best analyzed example of genetically determined resistance is sickle cell anaemia and its role
in resistance to malaria in humans. Humans who inherit the sicke cell anaemia trait possess
haemoglobin S (HbS) which confers resistance on humans to malaria.
 Sheep with Haemoglobin A show superior resistance to infections with Haemonchus contortus
and Ostertagia circumcincta as compared to sheep with Haemoglobin B. Sheep with
Haemoglobin A mount an effective self cure phenomenon than sheep without Haemoglobin A.

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TYPES OF PARASITIC RESISTANCE

 Innate resistance or natural resistance to parasites is the resistance or immunity

possessed by the host animal from birth. In other words, innate resistance is physiological
incompatibility between certain parasites and the host that prevents the entry and establishment
of the parasite in the host. Eg. Helminths such as hookworms and schistosomes may not be able
to penetrate the skin and gain entry into the host, Trypanosomes upon reaching the blood stream
may be destroyed by substances present in serum. Intracellular parasites such as Theileria
annulata of cattle may be unable to enter other hosts because of defeciency of essential surface
molecules in the host cells of unnatural hosts.
 Innate resistance or immunity can be complete / absolute or incomplete / Relative.
 A host is said to possess complete innate resistance or immunity when a parasite is not able to
infect a host under any circumstance, eg. sheep cannot be infected with ascarids.
 When a host innately resistant to a species of parasite becomes infected owing to lowered health,
it is incomplete innate resistance .
 Acquired resistance or immunity is resistance acquired by the host during its life time as a
result of exposure to a particular parasite or through inoculation of parasite antigen.
 Acquired resistance may be either active or passive. Active acquired resistance is
resistance acquired in response to the introduction of live or killed parasites. This may be either
natural or artificial.
 Natural active resistance or immunity is derived following repeated exposure to an
infection while artificial active immunity is derived by inoculation of parasites or their stages. It is
stronger, longer lasting, and diverse and takes time to fully develop.
 An immunity that is developed in host following natural exposure to parasites is actively
acquired natural resistance or immunity .

TYPES OF NATURAL RESISTANCE

 Different types of natural resistance or immunity viz., premunity, concomitant immunity and
sterile/ solid immunity are seen in parasitic infections.
 Premunity is a term used to describe resistance that is established after the primary infection
has become chronic and is only effective only if the parasite persists in the host or in other words
Premunity is immunity developed due to presence of residual parasites in the host.
 It is also known as incomplete immunity or infection immunity (Coinfectious immunity).
 Premunity is commonly associated with haemoprotozoan diseases such as theileriosis and
babesiosis.

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 Concomitant immunity: It is one type of premunity developed as a result of stimulation of the

host’s immune system by existing adult parasites. This immunity does not interfere with the
survival of existing adult parasites but prevents the entry and establishment of newly invading
larvae. This type of immunity is seen in schistosomiosis and cystic echinococcosis (hydatidosis).

 Sterile immunity: Immunity maintained by the host even after the parasite is eliminated. The
immune system remains sensitized for many years e.g. Theileria annulata infection in cattle,
Plasmodium cynomolgi infection in monkeys, etc.

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 Self cure is a phenomenon where adult worm populations are expelled following larval
challenge.
 It is a natural remedial mechanism by which the host gains a temporary respite from persistent
blood loss while aging parasite population is eventually replaced by robust young generation.
 The expulsion of adult worm population is considered to be a sequel to immediate type
hypersensitivity reaction (mediated by Ig E) to antigens derived from developing larvae. Self cure
will not protect the animal since larval challenge often develops to maturity.
 Self cure phenomenon is commonly associated with Haemonchus contortus infection in small
ruminants and cattle.

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PASSIVE IMMUNITY

 Passive immunity refers to transfer of antibodies or lymphocytes from immune to non immune
animals.
 It is only temporary and does not last long. It could be either natural or artificial.
 Natural passive immunity refers to transfer of immunity naturally from mother to offspring by
placenta or through colostrum and these antibodies protect the young for a certain period.

 Artificial passive immunity is immunity transferred to a non immune animal through injections
of sera produced in another animal by repeated injections of particular antigens.
 The process of producing excess antibodies against pathogens is termed as hyperimmunisation.

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MODULE-9: IMMUNITY AGAINST PARASITIC INFECTIONS

Learning objectives

 The objective of this module is to elucidate the types of immune response against parasitic
diseases and how the immune response prevents the establishment and development of the
parasite in the host besides immunopathological lesions or effects that occur following an
immune response to the parasite. The kinds of parasite antigens is also dealt in this chapter.

TYPES OF IMMUNE RESPONSE IN PARASITIC DISEASES

 If the parasite successively overcomes the animal's innate defence mechanisms, it will elicit an
immune response specific to the parasite and these immune responses may be humoral mediated
or cell mediated. Humoral immunity is mediated through antibodies which are large
glycoproteins released by B cells. These antibodies are present in blood, lymph and cerebrospinal
fluid. There are five classes of antibodies, each of which is distinguished from the other by their
heavy chains.
o Immunoglobulin G (IgG): Major antibody in serum. Long half life
o Immunoglobulin M (IgM): Largest and the first antibody to be produced in an immune
response. Presence denotes acute infection. These antibodies are able to neutralize, fix
complement, agglutinate and immobilize parasitic antigens.
o Immunoglobulin A (IgA) : Predominantly found in secretions (mucous, saliva, tears) and
colostrums and hence called secretory Ab. It is also known as mucosal antibody.
o Immunoglobulin E (IgE): Also called as reaginic antibody. This Ab binds to the surface of
mast cells and causes degranulation of the cell and release of histamine into circulation.
This Ab is associated with helminthic infections or allergies.
o Immunoglobulin D (IgD): The function of this Ab with respect to parasitic infections is
not known.
 Parasites are not composed of a single antigen but a mosaic of antigens. Animal hosts therefore
will recognize a number of these different antigens resulting in a polyclonal antibody response. In
addition, the host will produce different immunoglobulin classes having the same antigen
specificity.
 In general, humoral immune response (antibodies) controls extracellular parasites in the
intestine, blood stream and tissue fluids. Humoral immune response is predominant in
helminthic infections involving IgE, IgA and IgG antibodies. Many helminth infections are
associated with characteristic type I hypersensitivity, including eosinophilia, oedema, asthma and
urticarial dermatitis where IgE levels and eosinophil levels are increased. One of the major tasks
of eosinophils is the destruction of helminths.
 Complement is the name given to a complex of proteins that are present in the serum and
which are capable of being activated to become enzymatically active. When complement is
attached to an antigen antibody complex, a series of reactions occur with each component acting
enzymatically to activate subsequence components in a cascade fashion. Activation of
complement can also occur in the absence of immune complexes by molecules present on the
surface of parasites.

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HOW ANTIBODIES PREVENT THE ESTABLISHMENT OF PARASITES ?

 Opsonins are antibodies that render the antigens more sensitive for phagocytosis by leukocytes.
The presence of complement is essential for opsonisation.
 Ablastins are antibodies that inhibit the reproduction of parasites. These antibodies have been
demonstrated in trypanosome infections. They can be transferred from mother to offspring
through the milk.

 Neutralisation: Antibodies that bind to parasites and neutralize their toxins and inactivate the
enzymes. Antibodies neutralize the proteases used by larvae to penetrate tissues, antibodies also
bind with the excretory and secretory products of helminths and prevent moulting, antibodies
also act against exsheathing antigens and inhibit larval development. Antibodies also block the
enzyme pathways of helminths resulting in cessation of egg production and development of
adults.
 Immobilization: Antibodies bind to flagella and prevent these parasites from phagocytosis
 Lysis of bound parasites with the help of complement.
 Presence of IgA in secretions will prevent the attachment of parasites in the mucosal surfaces.
 Masking of certain target cells by antibodies so that parasites are not able to attach to them
 The openings and orifices of parasites are blocked by the antigen antibodies complexes causing
lysis/death.

CELL MEDIATED IMMUNITY

 Cellular immunity is mediated by T cells and like the antibody response, there is involvement of
macrophages and the presentation of antigens in combination with specific macrophage surface
molecules to the T cells. Specific cytotoxic cells can directly kill parasite infected cells. Some
parasites preferentially stimulate T helper cells (subsets Th-1 or Th-2) and each helper T cell
subset secretes a characteristic set of cytokines, referred to as a T cell cytokine profile. For
example, in Leishmania infections, there will be Th-1 response with a characteristic cytokine
profile of interleukins (IL2, IL3, IL-12 and Interferon). Cellular immunity is often directed against
intracellular parasites (e.g. Theileria, Toxoplasma etc).

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IMMUNOPATHOLOGICAL EFFECTS

Immunopathological effects due to immunological reactions against parasitic diseases

 Immune response evoked by the host against parasitic antigens, causing variety of harmful
pathological effects to the host.
 Pimply gut in oesophagostomiosis

 Oesophageal nodules in Spirocerca lupi infections

 Avascular granuloma in hepatic schistosomiosis

 Hypersensitivity reactions.

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HYPERSENSITIVITY REACTIONS

 During the process of destruction and removal of parasites by the host immune system,
surrounding body tissues may be damaged. These harmful effects are called as hypersensitivity
reaction.
 The different types of hypersensitivity include.
o Type –I (Anaphylactic shock) immediate reaction due to binding of antigen with IgE
fixed to mast cells and basophils leading to release of vasoactive, amines (histamine &
serotonin) e.g., anaphylactic shock following rupture of hydatid cyst and release of
hydatid fluid into the system.

 Type I hypersensitivity is a feature of trichomoniosis and causes local irritation and inflammation
in the genital tract.
 Type-II (Cytotoxic) is associated with development of anaemia in malaria and haemoglobinuria
in babesiosis.

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 Type-III (Immune Complex disease): Circulating antigen antibody complexes coupled with
complement are deposited in tissue space causing damage to the tissues, e.g., glomerulonephritis
in babesiosis, malaria, and schistosomiosis.

 Type-IV (Delayed): Biting fleas secrete saliva into the skin wound and some low molecular weight
components present in the flea saliva act as haptens by binding to dermal collagen resulting in
local type IV hypersensitivity reaction characterized by mononuclear cell infiltration. This is
commonly known as flea bite dermatitis. However, in some sensitized animals, after some
months, type I reaction takes over resulting in eosiniphil infiltration.

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KINDS OF PARASITIC ANTIGENS

 ES antigens: Antigens from the excretions (E) and secretions (s) of the parasite are called ES
antigens.
 Somatic antigens: Antigens elaborated by the entire body of the parasite is called somatic
antigen.
 Internal antigens: Antigens obtained after the disruption of the parasites.
 External antigens : Antigens manifested by intact parasites.
 Released antigens: Metabolic products of parasites are released antigens and these are
comparable to external antigens.
 Concealed or Hidden antigens: Antigens present on the intestinal surfaces of helminths and
arthropods which are not recognized by the host. However, these concealed antigens are excellent
targets for artificially induced responses.

EFFECT OF RESISTANCE ON PARASITES

 Prevention or reduction in the rate of establishment

 Structural or metabolic alterations in the parasites
 Retardation or inhibition of development, for example adult female Ostertagia ostertagi
recovered from immunized calves show absence of vulvar flaps as compared to those recovered
from non immunized calves, Simiarly, Cooperia males derived from immunized animals showed
altered morphology of spicules.
 Inhibition of reproduction, for example in ticks that fed on immunized animals there will be
extended oviposition, reduced egg laying and diminished hatchability of eggs.
 Destruction of parasites in situ
 Elimination of existing infection

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MODULE-10: STANDARDIZED NOMENCLATURE OF ANIMAL PARASITIC DISEASES
(SNOAPAD)

Learning objectives

 This module will deal about classification of parasites on the basis of relationships and naming of
parasites in accordance with the Standardized Nomenclature of Animal and Parasitic
Diseases (SNOAPAD)

STANDARDIZED NOMENCLATURE OF ANIMAL PARASITIC DISEASES (SNOAPAD)

 The standard and uniform nomenclature formulated by the World Association for Advancement
of Veterinary Parasitology (WAAVP) is Standardized Nomenclature of Animal Parasitic Diseases
(SNOAPAD).
 Nomenclature is the process of naming the parasites.
 Members belonging to the animal kingdom are classified into phyla, classes, orders, families,
genus and species. Later, additional categories such as super or sub were created to accommodate
the increasing number of species discovered over the years. Super/Sub was prefixed to the
existing categories (Superfamily/ Suborder). The family group includes taxa ranked as at the
family and tribe levels (including super and subfamilies). The genus group includes taxa below
subtribe and above species. The species group includes taxa ranked as species or subspecies.
 The names of parasites must be from Latin or Greek and not in the local language. The genus
name should be a noun and the species names should be either noun or adjective.
 The name of the order ends in ‘ida’, e.g. Strongylida, superfamily ends in ‘oidea’, e.g.
Ancylostomatoidea, family ends in ‘idae', e.g. Ancylostomatidae and subfamily ends in ‘inae’, e.g.
Ancylostominae.
 The first letter of the genus should always be in capital letter while the first letter of the species
should be in small letter excepting for those whose names have been derived from persons, where,
it shall be either in small letter or in capital letter, e.g., Trypanosoma evansi or Trypanosoma
Evansi, Cotugnia bhaleraoi or Cotugnia Bhaleraoi. In printed formats, the names of the genus
and species should be italicized while in written text, the names of the genus and species should
be underlined. The genus and species are also named after morphological characteristics, host,
anatomical location, geographical location, scientists etc.
 The law of giving importance to the scientist who first named the parasite is known as Law of
Priority. If the genus and species names are after scientists, the name of the scientists and the
year should follow the scientific name. While writing, a comma should be used after the scientists
and not anywhere, e.g. Schistosoma nasale, Rao, 1932. If the name of the original author is
changed subsequently for valid reasons, his name and the year have to be written within brackets
after the new classified name for e.g. Ancylostoma caninum (Ercolani, 1859) Hall, 1913. If a
parasite name is changed subsequently for valid reasons, the earlier name is considered as the
synonym e.g. Neoascaris vitulorum is the synonym for Toxocara vitulorum.

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Recommendations of SNOAPAD include

 The practice of using the suffix ‘osis’ to denote parasitic disease with apparent clinical signs and
the suffix ‘iasis’ for subclinical infections are to be discontinued.
 The suffix ‘osis’ should be added to the full generic name or the stem of an appropriate higher
taxon name or from the genitive name of the parasite by deleting the last one or two letters.
 In some, the suffix ‘osis’ is added to the full generic name of the parasite, eg., Hepatozoon -
Hepatozoonosis, Leucocytozoon - Leucocytozoonosis
 For certain parasites, the ‘osis’ is added to the appropriate higher taxon name as in the case of
Schistosoma eg. Schistosom+osis = Schistosomosis, Ancylostoma -Ancylostom+osis =
Ancylostomosis, Babesia - Babesi+osis = Babesiosis
 When the taxa, ends in ‘x’ as in Demodex, the stem is formed from the genitive as in the given
example Demodex, Demodicis - Demodic+osis=Demodicosis
 Use of nomenclature such as Malaria, Surra, Myiasis, Mange etc., to be continued in addition to
the new names as these are well established names and have been in use for a long period.

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