Parasitology Final
Parasitology Final
Parasitology Final
Introduction :
What is the definition and description of parasitology ?
• Study of parasites
• An animal can be a parasite when lives with different kind of
animal/plant/host.
• Must have some kind of benefit also harmful to the host.
• None animal can not be a parasite alone
• Is animal association / individual cooperation with different
species, herds, flocks etc
• The animal association also belongs to different zoological
species (parasitism, commensalism, symbiosis etc).
• Our interest is parasitism association (always some harm done to
the host and vise versa).
• The parasitic association depends on the characteristic of the
parasite ie temporary and permanent (external & internal).
•Have many means of transmission depending on their
nature/species, type of host etc and how?
This is through major openings .
1.Mouth – with feed or water
2. Anus – eg. Oxyuris ( pin worm)
3. Excretory and reproductive – eg Equiperdium (Dourine), 4.Skin –
eg. Schistosoma, hook worm, bunostomum
5. Insects/arthropod blood feeders– eg. Trypanosomes by biting flies,
tsetse; piroplasmosis by ticks
6.Transplacental – eg. In dog Toxocara,in women toxoplasmosis by
cat.
7. Trans ovarian– eg. in the vector itself babesia
Chapter 2. Classissification, taxonomy &
terminologies of parasitology
2.1 Top general are medical major to human, veterinary to
domesticated and wild animals, soil and plant.
Anterior
esophagus
part of
Nematode
Intestine
paired
Remember that the alae can exist also around tail called as
caudal alae that help for differentiations of generas/spp 5.
Bursa(streoscopic) – helps to hold the F during copulation. Is
found only on 3 super families ( Trichostrongloidea,
Streongloidea & Metastrongloidea) which use as additional M
differenciation. This is developed from the much extended
caudal alae and have papillae called as rays at different
positioning which are help full for spp differenciation. The rays
are bounded by dorsal lobe. As paired form (left & right
sides) & from anterior to posterior the rays are called ventral,
lateral, externodorsal ( caudal boundry) & dorsal ray usually
caudal middle. All rays can be paired or single in left or right
depending on spp. The bursa also holds also spicule &
gubernaculum.
Reminder:- refer schematic drawings of all the above
anatomical structures & in practical activity for better
2. Simple classifications of Nemathehelminthes
Super family Anatomy Lifecycle type Infective stage
3rd stage
larva of
Nematudurus
spp
5.2 Strongloidea (direct L/Cy & L3 infective stage):
∑26 of which 3 oesophgostomum spp ,giageria
agriostomum are less important
Generally most are with large buccal capsule, with
cutting teeth/plates & in some prominent leaf
crown,
Except Syngamus & Mammomonogamus generas
in lung others are in SI & are grouped as
strongyles found in LI like Strongylus, Chabertia ,
Oesphgostomum, Trichonema (small strongyle,
<1.5cm,
Large buccal capsule & external, internal leaf
crowns in cecum & colon)) & hook worms in SI
like Ancylostoma, Bunostomum & Unicinaria.
A. Strongylus :
are large strongyles ; H= equine : site = cecum &
colon ;are 3 species
the spp are vulgaris of 1.5- 2.5 cm two ear
shaped rounded teeth , edentatus of 2.5-4.5 cm
without teeth & equinus 2.5-5 cm with 3 conical
teeth where one dorsally located , is larger than
the others & bifid, all eggs similar with
ostertagia,
in general in cooler areas PPP(prepatent period)
is 3 weeks & hot shorter.egg is like oestriotagia
Life cycle :-
1) vulgaris
L3 after entering mucosa moult to L4→ through
small arteries goes to final site to cranial mesentric
arteries to moult in several months to L5 being
returned to SI mucosa, forms nodule, rupture &
release the young worm in to lumen (PPP 6-7 months)
is migratory spp.
2) Edentatus : L3 after mucosa travel via portal vein to
liver parenchyma ;then
moults to L4 & migrates & located in hepatorenal
ligament.
Again migrates to predilection site to flanks & hepatic
ligament to occur L5 continued forming nodule in the
wall of LI to be released as vulgaris (PPP 10-12
months) .is migratory.
3) Equinus :
least is known its larval migration (PPP 8-9
months).its life cycle unknown.
In general the pathology (clinical sigh) is seen in
their specific sites which include
anuerusim(blocking of blood vessel by parasite) in
vessels that cause colic ቁርፀት ; inappetence &
sometimes colic for vulgaris which is major among
the two ; endentatus having nodular formation but
little known on equinus.
Single No
All 3
Teeth teeth
tooth
dorsa
l Two Two
tooth tooth
B.Triodontopharus
• are none migratory large strongyle affecting equine
& placed in colon & caecum.
• Produce disease when there is mixed infection with
other strongyles & WW distribution.
• Their size is 1-2.5cm & there are 3 spp affecting all
equine & lifecycle like Trichonema
C.Trichonema
have over 40 spp, WW found & are called as
cyathostomes or small strongyles,
affect equine, site on colon & cecum having length
of < 1.5 cm,
large buccal capsule with external & internal leaf
crown.
Lifecycle infective L3 enter with grass into LI tissue
& insheathed which moult to L4 & later in lumen
to L5 & young adult
D.Chabertia ovina only :
• Mainly affects shoats; very large buccal capsule
bell shaped; 1.5-2 cm;
• double row papillae around rim;
• no t.eeth & egg as ostertagia.
• Lifecycle is similar to trichostronglidae,Only
afects shoats not cattle
E. Oesophagostomum :
colombianum & venulosum hosts are shoats ;
radiatum cattle & bufallo; for pigs dentatum &
quadrispinulatum ( in general there are 8 spp) ;
site colon & caecum ;
small buccal capsule sarrounded by leaf crown ;
tepered head grossly ;
has cephalic & servical vesicle; 1-2 cm & egg as
ostertagia.
F. Syngamus trachea
only : H= domestic & game fowl ;
site trachea ; 0.5-2 cm ;
shallow buccal with 10 teeth at base;
Male and Famale copula as “Y” & egg elipsoidal
with operculum at both ends.
Rx(tretment) thiabendazole & fenbendazole ( in
feed for 3- 14 days); also use niroxynil &
levamizole in water.
G. Stephanurus dentatus only : H= pig ;
• site = kidney & perirenal tissue ;
• large stout form ; up to 4.5 cm ;
• transparent cuticle ( internal organs seen);
diagnosis check egg in urine ( but difficult to
find) & cerehotic liver in pork inspectio ;
• Rx benzimidazole, levamisole & ivermectin.
H. Dog & cat hook worms :
are hook posture anteriorly & blood sucking.
A. Ancylostoma. Is important parasite
• 1: caninum (3 pairs theeth) in dogs & fox ;
• 2:tubaeforme (3 pairs teeth) in cat ;
• 3: braziliens ( 2 pairs teeth) dog & cat ;
• 4:duodnale man ; site = SI ; 1-2 cm & smaller
than ascaris parasite that found similarly ;
hooked head ; large buccal with marginal teeth ;
egg as ostertagia; infestation by skin& oral.
Lifecycle :5 life cycle
1. if skin larva migrans through blood to lung & L3 moult L4
, following passes to bronchi & trachea ,then coughed up and
swollew & to SI to have L5.
2. Ingestion either penetrate buccal mucosa & then
pulmonary migration to travel similarly to SIor
3. if directly ingested all development takes place in SI;
4.the female has high egg fecundity ; but caninum proportion
of the L3 have a feature in susceptible bitches(female dog)
when reach in lung migrate to skeletal muscle to become
dormant(keep quite) until the bitch gets pregnancy.
Then at birth/whelping the dormant L3 stimulated to pass
through milk for 3 weeks & infect pupies/ transmammary
transmission for at least 3 births.
5. Additionally the dormant L3 in bitch, dogs & in muscle
can migrate develop in SI at stress. So the parasite found in
PPP is 14-21 days.
In acute cases anemia is majorly seen on
pupies & respiratory signs & diagnosis high
EPG & haematology but may not be for
dormant & pupies.cause coughing ,
Rx mebendazole, fenbendazole.
Control : regular therapy ( for pregnant dog
at least once & nursing pupies twice at 1-2
weeks age & 2 weeks later); hygiene
( bedding & kennel floors); avoid stress.
B. Unicinaria stenocephala: only affect dog, cat fox
in SI ;less than 1 cm found in temperate.
C
a
u
d
al
al
a
e
Microflarae
of D.immitus
from lysis
blood
Species of recondium with blunt head & hooked
tail.
Rx & control : the dog need to be tested for function
of heart, kidney & liver; IV thiacetarsamide twice /day
for 3 days. Following to treat larva after 6 weeks
levamisole is given 10-14 days. As mosquito difficult
to control medication to host is necessary.
E. Onchocerca: on cattle 4 spp & affect also
equine mainly sp of reticulata; IHs Culicoides &
Simulinium; site ligaments & intermuscular
connective tissue ;2-6 cm cylender & tightly coiled
in tissue nodule;
lifecycle:- is like dirofilaria but microfilaria is not in
blood but in tissues , occur in Ethiopia &
rx:- using ivermectin.
Diagnosis:- depth skin scraping in warm water &
incubate for 6 hours later centrifuge & coiled
movement in solution.
Genus Setaria is harmless.
5.9 Trichuroidea : direct or indirect in aquatic &
L1 infective
A. Trichuris (4spp) : H= ovis for shoats,
globulosa for cattle, suis for pig & vulpis for
dog; LI/ caecum;4-6 cm long; thicker posteriorly
& filament nous anteriorly/thinner called as
whip worm; male tail is coiled & single specule;
female tail is merely curved; egg lemon shape
plug at both ends .
Lifecycle : infective is L1 with in egg, ingested egg
unplugged its end & released L1 penetrate glands of
cecal mucosa that develop up to L5. PPP 6-12 weeks.
Clinical signs occur sporadically when high & more on
dog & pigs with watery diarrhea.
Epidemiology:- survival of egg in animal houses for 3-4
years.
Diagnosis:- fecal egg count. Rx : benzimidazole
compounds, ivermectin, levamisole for dogs
mebendazole & dichlorophos can be choice.
In control:- more attention prophylactic rx to dogs &
pigs. For man T.trichiura is similar in morphology with
suis but are host specific.
B.Capilaria spp in birds & mammals ; 1-5 cm
filamentos; egg bipolar like trichuris
C.Trichnella spiralis: is zoonosis; ww; H= most
mammals ( mainly pig & man) ; adult in SI
larvae in striated muscle ( massater, intercostal
& diaphragm); WW; because of life span adult
is rarely found; adult 1-3mm;
life cycle:- adult & larvae in one host as adult on villi
of SI after fertilization male dies & female goes deeper
producing L1 that travels from lymphatic to blood
vessels to be in skeletal muscle forming encapsulated
as coiled position as nurse cell which later can be
infective stage reaming for years. After this if larvae
swallowed by another host L1 liberated in SI & molts
L1-L5 to continue;
Diagnosis:- in meat inspection occasionally seen but
good take suspected sample muscle crush & look the
larvae. ELISA also is used.
Rx:- with group benzimidazole (for adult & larvae)
Additional & general information on morphology &
life cycle grouping on nematodes as my part.
1.Morphology
-Bursate & none bursate anatomy at the tail part of
nematode adult parasites
-This anatomical feature is important for males
which have bursate but not females. Its physiology is
anatomy that support copulation of male and
female. It contains one bursal lobe/ cover that have
ventral, lateral, externo-dorsal & dorsal rays ( 2-3
rays) if freshly and well formalized during collection
of adult parasites.
-The bursate are trichostrongloidea, strongloidea,
Metastrongloidea but the rest none bursate.
2. Types of life cycle the direct are families of
Trichostrongloidea, Strongyloidea, Rhabitoidea,
Ascaridoidea, Oxyuroidea & Trichuroidea ( 6). The remaining
Metastrongloidea, Filaroidea, Spiruroidea &
Dictophymatoidea have indirect life cycle but only
Trichuroidea direct or indirect.
Regarding infectivity stage of larva L2 in egg is infective for
Ascaridoidea, L1 Trichuroidea & the rest L3 where by
Spiruroidea & Filaroidea from insect and Metastrongloidea
from other intermediate hosts but others not.
3. Other means for identification of M , F general
morphology:
Other than bursa for male testis difficult to see in none
stained mounted adult parasite , spicule mostly paired can be
seen through unstained & appreciated length to shape and
finally cloaca depression can be seen similarly. Female has
ovary un distinct towards anterior in none stained, uterus
with egg visible,vulva/ovijector posterior some times visible
with flap & anus not well seen. Generally any observant has
first to define which is anterior mouth part and tail/posterior
part of any stage of nematode to easily go for identification.
Additionally for identification & generally females are longer
in size than male and there are 6 types of esophagus that are
help full for identification called as Rhabiditi form and Double
bulb can confuse for identification which need experience but
others are easy for differentiation which are Filariform, Bulb,
Muscular glandular and Trichuroid.
Further more Trichostronglodea have small buccal
capsule; Stronglodea have well developed buccal
capsule and usually with leaf teeth crown;
Metastronglodea small buccal capsule;
Rhabditoidea small worms with small buccal
capsule; Ascaridoidea large white worms;
Oxyuroidea female has pointed tail; Spiruroidea
female has spiral tail; Filariodea long thin worm;
Trichuroidea whip like or hair like worm.
In relation to egg morphology differences:
- In Trichostrolidea F. Nematodirus genus has large ovoid
with distict morula cells; In Strogloidea - Syngamus has egg
of both end operculated; Metastrongloidea -
Metastrogylus has rough oval thick shell, larvated
In Rhibtoidea - Strongloides egg has thin shell oval
shape & very large two morula cells; in Ascaridoidea
Ascaris genus irregular thick shell round; Toxocara,
Paraascaris (Toxocara & Neoascaris other names)
rounded brown pitted outer shell but T.leonia &
T.canis sps. have smooth outer but all still thick;
differently thick oval shape in generas of Ascaridia &
Hetarakis ; In Oxyuroidea -Oxyuris has yellow ovoid
with mucoid plug at one end; In Spiruroidea-
Spirocerca has elongated with parallel sides egg,
Habronema genus has elongated thin shell larvated
egg, In Filaroidea – Parafilaria has rounded thick small egg
and finally in Trichuroidea – Trchuris has lemon shape egg.
The rest unmentioned unless they vary in length & diameter
are more or less oval thin & smooth shell, have none
distinct morula cells & can be larvated depending on their
type of family and/or group and/or species. So for genus
and/or species identification is better to do larva culture for
further identification regardless areas of distribution, type
of host, location of the parasite in the host & their virulent
to animals. In fact remember that the criteria mentioned
are also help full for identification for those listed above
nematodes that have different shapes of egg. To
summarized nearly 16 genera out of nearly 30 have
different egg that help to identify the parasite or infection
together with the other criteria including egg load per
gram, age, condition of nutrition and/ or management
stress and clinical signs.
Foundations for control in Helminthosis
1. The role of veterinary officer in the control of
helminth diseases in the tropics
Is the merit of treatment or control in light of local
conditions.
Giving recommendation to the owner regarding
optimal methods for treatment or control.
Providing the owner means of treatment or carry out
minimum procedures to facilitate healing.
When the disease is hazard to human health or to
livestock take all necessary actions.
Have records on the pattern of the disease specific to
the local area.
2. Economic importance
2.1 Observed losses : deaths, wasting & condemnation of animal
product but of human food
2.2 Hidden losses : reduced live weight, poor feed conversion
efficiency, decreasing at decreasing rate of milk production, poor
fleece production so on. In aggregate these losses are probably
more serious than obvious losses. However often are noticed
due to :
Are ubiquitous (ever- present, every where)
Its process is insidious/dangerous, chronic & enzootic
Most losses occurs when poor condition is regarded as normal.
E.g: on young ages, growing animals & those under physiological
stress
2.3 Control costs : drug, wages, fence, inefficient use of land,
transport so on
3.General considerations of control
3.1 Aims of control :
Eliminate or reduce prevalence of zoonotic parasites
Improve profitability of animal industry if then is essential that cost of
control is less than cost of the disease
Increase aesthetic acceptability of pet animals
3.2 Types of control :
3.2.1 Reduction of parasites prevalence may be achieved by reducing the
chance of survival or development as example : introducing poison
(anthelminthic, larvicidal so on) & as
Selecting or developing resistant hosts
Disturbing the larva microclimate
Introducing predator for hosts or parasite
Keeping apart the host & the parasite
3.2.2 To increase the ability of the host to tackle the parasite as:
Better nutrition
Special protection to young & under stress
Supportive therapy
3.3 Limitations of control
1. Financial
2. Knowledge : is a contribution of research &
education. The essential data includes:
Species of parasite & host involved
Lifecycle of the parasite
Bionomics of the free living stage in lifecycle
Details of host parasite relationship
Local climatic, agricultural, sociological &
economic factors
3. Fecundity of most helminths
4. Pre-existing efficient natural checks
5. Danger of breakdown
4.Classifications of anthelminthics & Preparations
This classification is mainly dependent on their chemical
structure:
4.1 Benzimidazoles & probenzimidazloes
Currently most antheminthics belong to this groups.
Historically:
Thiabendazole introduced 1961
Parbendazole 1967
Cambendazole 1970
Mebendazole 1971
Oxibendazole 1973
Fenbendazole 1974
Oxfendazole 1975
Albendazole 1976
Triclabendazole 1981
Thiophanate & Febantel are probenzimidazole which are
metabolize in the body to active benzimidazole.
Benzimidazoles are highly effective against most stomach
and intestinal nematodes. The more recently introduced
may also are active against lungworms, tape worms & liver
flukes.
Triclabendazole is exceptional & effective only against liver
fluke.
4.2. Imidazothiazoles : Levamisole & are highly effective a
wide range of stomach & intestinal nematodes. It is also
immuno-potentiator.
4.3. Tetrahydropyramidines : are like Morantel & Pyrantel
& highly effective against stomach & intestinal nematodes
4.4. Avermectins: Ivermectin is active on a wide range of
stomach & intestinal nematode plus lungworms at very
low dose rates. Is also effective on a number of
4.5.Salicylanilides & substituted phenols :
These are Oxyclozanide, Rafoxanide, Nitroxynil, Bithionol & Brothianide
are effctive against adult liver fluke. Some of these are also active against
other trematodes & blood sucking nematodes. But Resorantel is
particularly effective on paramphistomum. Disophenol has prolonged
residual action on Haemonchus contortus.
Niclosamide is highly effective against tape worm and some trematodes.
4.6.Diphenoxyalkyl ethers : Diamphenethide is marketed only for
treatment of Fasciola in sheep (is effective to all above one week old
stages.
4.7.Organophasphates: Dichlorvos, Haloxon & Metriphonate are
effective on stomach & intestinal nematodes of horses
4.8.Chlorinated hydrocarbons : Carbon tetrachloride, hexachlorophene
& Hexachloroethane are used for Fasciola in ruminants. Now have been
superseded by modern flukicides.
4.9. Piperazines: Diethylcarbamazine is used for lungworms & different
salts of piperazine are active on Ascarids & Oxyurids.
4.10.Others : Nitroscanate, Praziquintel, Bunamidine & Arecoline are
active against tape worms. Praziquintel is very effective on Schistosomes
and some intestinal trematodes.
Regarding anthelminthic preparations as an example the following formulations exist
based on the company , type of drug & cost effectiveness without changing its potency.
Moreover the manufacturer instruction/leaflet/prescription has to be consider on :
1. Drench & paste forms: If suspension shake well containers to ensure adequate
dispersion of the chemical in the solvent. Although most modern anthelminthes
are safe assess body weight to avoid under dose. Ensure drenching gun is well
calibrated and in good working order.
2. Injectable preparations : Levamisole, Ivermectin, Diethylcarbamazine,
Rafoxanide, Nitroxynil, & Paraziquintale are mostly in injectable forms.
Abcessation is problem if not sterile needle is used & inject on area where there
is low quality meat cuts.
3. Pour-on : this contain lemisole or ivermectin
4. In feed : appears more convenient but allow little control on the amount
consumed by individual animal unless are fed separately or in small supervised
groups. For this reason is less satisfactory method. Thus the following points are
important for assurance :-
i. Note either the drug to be given in single feed or over period of several days
ii. Ensure through mixed
iii. Avoid using powdered formulations in pelleted rations as the powder will sift through pelletes to
the bottom of feed trough
iv. Allow adequate feed trough space for each animal
v. If possible watch reluctant feeding animals and give separately
vi. Only use on animals accustomed type of concentrate/ration
5. Medicated blocks: This has similar disadvantage as feed preparation and problem of ensuring
each animal continues to receive an adequate dose over a period of time. However the
necessary precautions are:
vii. Only use on animals that are accustomed to ordinary blocks & remove other feed blocks when
medicated are made available
viii. Ensure adequate number of blocks are available for the number and weights of animals being
treated
ix. Identify reluctants and treat separately
6. Slow- release device : Presently about two are available designed to be lodge in the
recticulum/rumen of cattle over 100Kg in weight. Neither should be used in lactating dairy
cattle or in those with in 6 months calving. These are :
Paratec ( Pfizer product): is metal cylinder having Morantel tartrate in slowly dissolving vehicle
& releases the drug for about 90 days
Autoworm (Coopers product) : is pulse release device relying on corrosion of a central metal core
to subsequently expose 5 doses of Oxfenbendazole at 3 weeks interval the first being released 3
weeks after administration
• Anthelminthic Drug Resistance:
• Although when chemicals are on use resistance is inevitable
through proper dosing, scaling of weight and not frequently use of
the same drug it can be minimized. At present is becoming common
problem in the world which are using the same drug for so many years.
• Historically it was first detected the resistant for anthelminthics
commonly in Australia and to a lesser extent in other countries of
strains of H.contortus to Benzimidazole, Levamisole & Morantel
indicating for the need alternate drug with different mode of action.
Here side resistance within a single group & multiple is common.
However true cross resistance in which multiple resistance is
conferred by a single gene does not occur except in so far as
resistance to Levamisole also confers resistance to Morantel group
since both have similar mode of action.
• The greater the efficacy of anthelminthic the more is frequently
used the more likely is the onset of resistance.
• The common & usually advantageous practice is moving treated
grazing animals on to clean pasture tends to increase the rate at
which drug resistance will develop.
5. Diagnosis
The advent/ start use of broad spectrum anthelminthic is no
substitute for diagnosis. However the blanket application is
excluded due to economic grounds even to short term. For long
term the indiscriminate use of drugs will be discourage for
ecological reasons but enlighten application of specific agents may
always be crucial in the long and short program of applications and
clinical outbreaks. So this indicate the demand of clear
understanding of the organism evolved.
Relevant diagnostics include:
CLINICAL : usually the presented signs. Occasionally are fairly
specific but most in helminth diseases are not specific such as loss of
wt, anorexia, anemia, diarrhea/diarrhoea specially in light infections.
HISTORY: often the greatest diagnostic significance. Which are
as example--- Was there outbreak of helminth disease in the past?
Was the animal exposed to environment which makes infection
high? And others use of irrigation water & pasture, history of
pasture or its source , age of the animal, whether given anthelminth
POST-MORTEM EXAMINATION: gives specific spot check at
one time. Is morphological identification and direct count of the
worms but consider number can be lower because of self cure or
anthelminthic treatment before death.
Here the host site parasite lists given in text book together with an
idea of the approximate size of the different spp are useful in
making a tentative diagnosis which again can be confirmed by
microscopic examination. There is little merit to memorizing & such
lists as names can come when readily with use.
The ability to use microscope correctly & hence to see the features
present in the specimen is the most important factors in the
identification of helminths & especially of nematodes.
FECAL EXAMINATION: rapid & fairly specific. Quantitatively
unreliable due to concentration of eggs or larvae in the feces may
vary with several factors inaddtion to the number of worms present.
Example: variation in host resistance, fecal consistency,species, age
of the heliminth present , uneven distribution in feces so on
OTHER METHODS : example serum enzyme assay, histology,
pasture larva studies, eosinophilia, serological tests etc
6.Epidemilogy:
Remember that a very small proportion of the
individuals of any helminth species complete the
life cycle
Unsuitble host host Ejected by host
sp Adult Anthelminthics
Resistant host worm in Infertile
Abnormal migration host
in host
Host parasite
relationship Egg in
Infective
form Infection CORE Contamination excreta
Microclimate
Not on pasture
Free living fails to develop
Fails to develop population and dies
& dies