HELMINTHOLOGY NOTES

Contents
Sr. TOPICS
1 Raillietina tetragona, Davainea proglottina
2 Spirometra mansoni, Diphyllobothrium latum
3 Nematodes-General characteristics
4 Strongylus-Chabertia
5 Oesophagostomum-Syngamus
6 Hookworms-Ancylostoma (missing)
7 Haemonchus
8 Teladorsagia
9 Ostertagia
10 Trichostrongylus
11 Cooperia-Nematodirus
12 Dictyocaulus
13 Spirocerca lupi-Gnathostoma
14 Habronema-Draschia-Thelazia
15 Toxocara-VLM (missing)
16 Ascaris-Parascaris
17 Dirofilaria
18 Heterakis, Ascaridia and Anisakis (missing)
19 Pinworms
20 Trichuris
21 Capillaria_Trichinella
22 Dioctophyma
23 Dracunculus medinensis
24 Integerated Parasite Management

Teachers:
Prof.Imran Rasheed Prof.Oneeb Prof.Haroon Akbar

Credits:
M Saad (2019-DVM-86) Haroon Qaiser Ch (2020-DVM-113)
Rana Ehtisham (2020-DVM-109) Gulam Gaus (2020-DVM-063)

Special thanks to Fazal Elahi (2020-DVM-032), Shah Jahan (2020-DVM-102) and Fath-e-din Hameed
(2020-DVM-091)

Edited and complied by M Ibraheem Saeed

If there are some mistakes in these notes or some changes are required or for any query REACH ME AT
+92321-4725769 or 2019-dvm-102@uvas.edu.pk
 Raillietina tetragona, Davainea proglottina
Parasitic class: Cestode
Family: Davaineidae
Raillietena is the commonest cestode of poultry and and 2nd one is daivenia.

Raillietena tetragina Davainea Proglattina

Predilection site site posterior half of small intestine duodenum
 Metacestode is cysticercoid
 Same final Host (Gallinaceous birds)
 Both cestodes are very important for poultry especially for
Similarities
gallinaceous birds which include pigeon turkey, guinea fowls. Hicken
etc.
 Both are non-zoonotic and have worldwide prevalence.
 Davaniea are small and raillietena are large in size.
 Different I.Hs
 I.H of Davainea are gastropods and mollusks which include snail and
Dissimilarities
sluvge. These are gastropods molluscs. Both have predilection site of
small intestine.
 I.H of Raillietena is ants.

Breaking in the case study:

1st case reported from Nigeria which has Ailletena, Echinobothria and Choanotenia infundibulum.

What happen to chicken in case study?

Chicken died due to these cestodes. Death is uncommon with cestode infestation and causes weakness,
debilitation.

How can you measure debilitation in chicken?

 In background poultry, weakness in chicken can be measured by muscle on the kneel bone
(chest bone). This is a parameter; More mass on kneel bone, more is the chicken healthy.
 FCR practical with commercial chicken poultry farms.

Spirometra mansni & Diphyllobothrium latum

Order Pseudophyllidea: Similar to cyclophillidea
Distinct features:
1. Scolex has no suckers and instead has two longitudinal grooves or bothria, which becomes
flattened to forms organs of attachment.
2. Eggs shells are thick, brown and operculate, and the coracidium. Which emerges after hatching,
is an oncosphere with an embryophore which is ciliated for mobility in water.
Pseudophillidean life cycle uses two intermediate hosts. The coracidium must first be ingested by a
crustacean in whose body cavity a larval pro-cercoid develops. Subsequently, if a crustacean is eaten by
a freshwater fish, the procercoid is liberated, and in muscles of new host develops into a second larval
stage, a plerocercoid, which possesses the characteristic scolex; it is only this stage which is infective to
the final host.

Bothria (from Greek bothrion = small pit, diminutive of bothros = pit/trench) are elongate dorsal or ventral
longitudinal grooves on scolex of cestoda. They have week muscle but are capable of some sucking action.

Genus Species Final host Intermediate host Metacestode Predilection site

Man,dog, 1st: Copepods Abdominal
Diphyllobothrium latum nd
pig, cat 2 : Fish cavity, muscles
Dogs, cats,
wild
1st: Copepods Plerocercoid Muscles,
carnivores, nd
Spirometra mansoni 2 : Amphibians, subcutaneous
&
Reptiles, birds tissues
occasionally
man
The genus diphyllobothrium is an important cestode of human and fish eating mammals. They are long
tapeworms with unarmed scolex, with two muscular bothria.

Spirometra mansoni
Spirometra are tapeworms of dogs, cats and wild carnivores and an occasional human zoonosis
(sparganosis).
Plerocercoid: is called as spargana, are white, ribbon like crinckled and can measure 300-400 mm.

Geographical distribution: South America and Asia

Pathogenesis & pathology: The tapeworms usually causes little effect in the intestine of dogs and cats.

Clinical signs: Usually asymptomatic in animals

Diphyllobothrium latum
Common name
Predilection site
Class
Family
Final hosts
Intermediate host
Geographical distribution
Pathogenesis & clinical signs
Broad tapeworm
small intestine
Cestode
Diphyllobothriidae
Man, fish eating mammals, such as dog, cat, pig, and polar bear
(1) copepods (2) fresh water fish (pike, trout, perch)
Parts of Scandinavia, Russia, Japan, North America
In man, infection is usually asymptomatic but there can be fatigue

Life Cycle:
Eggs are continuously discharged from the genital pore of attached gravid segment of strobila and pass
to exterior in the feces. They resemble F.heptica eggs being yellow and operculate. The eggs must
develop in a water and within a few weeks each hatches to liberate motile ciliated coracidium, which if
ingested by a copepod, develops into in to the first parasitic larval stage, a procercoid. When the copepods
ingested by a fresh water fish, the procercoid migrates to the muscles or viscera to form the second larval
stage, the plerocercoid; this solid larval metacestode is about 5 mm long and possesses the characteristic
scolex. The life cycle is completed when the infected fish is eaten raw, or insufficiently cooked by the final
host. Development to patency is rapid, occurring within four weeks of ingestion of plerocercoid. However,
if the infected fish is eaten by a larger fish, the plerocercoid has ability to establish itself in new host.
 Nematodes-General characteristics

A worm of the large phylum Nematoda, such as a roundworm or threadworm

The phylum Nemathelminthes has six classes but only one of these, the Nematoda.
Most nematodes have a cylindrical form, tapering at either end, and the body is covered by a colorless,
somewhat translucent, layer: the cuticle.

Divided into bursate and non-bursate groups.

 LIFE CYCLE
 In the Nematoda, the sexes are separate.
 The males are generally smaller than the females.
 During development, a nematode moults at intervals, shedding its cuticle.
 In the complete life cycle there are four moults.
 L1, L2, L3, L4 and finally L5, which is the immature adult.
 They could have direct life cycle or an indirect life cycle. Can have intermediate host and cannot
have one.
 In the common form of direct life cycle, the free-living larvae undergo two moults after
hatching.
 Infection is by ingestion of the free L3.
 Infection sometimes being by larval penetration of the skin or by ingestion of the egg containing
a larva.

 In indirect life cycles, the first two moults usually take place in an intermediate host
 Infection of the final host is either by ingestion of the intermediate host or by inoculation of the
L3

Strongylus-Chabertia
Superfamily strogyloidea
With the exception of three genera, syngamus, mammomonogamus & cyathostoma which are parasitic
in trachea and major bronchi and stephanurus found in peri-renal area all other important parasites of
veterinary importance of this this superfamily are found in the intestine and can be conveniently divided
into two groups, the strongyles and hook worms.

Strongylus vulgaris
Common name large strongyles
Predilection site large intestine
Parasite class nematode
Family strogylidea
Host Horse, donkey
 Lesions due to migrating larvae are most common in the cranial
mesenteric artery and its main branches, and consist of thrombus
Pathology
formation provoked by larvae damage to the endothelium together with
marked inflammation and thickening of arterial wall.
Anemia, poor condition and performance, varying degree of colic
Clinical signs temporary lameness, intestinal stasis, sometime intestinal rupture and
death
Colic due to verminous arteritis may be associated with a palpable, painful
Diagnosis
enlargement at root of mesentery

Life cycle
 The adult parasite live in cecum
 The free living state is as described for S.edentatus.
 Following ingestion L3 penetrates the intestinal mucosa and moult to L4 in the submucosa 7 days
later.
 These then enter small arteries and migrate on the endothelium to their predilection site in the
cranial mesenteric artery and its branches.
 After a period of development of several month the larvae moult to L5 and return to intestinal
wall via the arterial lumina.
 Nodules are formed around the larvae mainly in the wall of cecum and colon when due to their
size, they can travel no further within the arteries and subsequent rupture of these nodules
releases the young adult parasite into lumen of intestine. Prepatent period is 6-7 months

Chabertia ovina
Common name large mouthed bowel worm
Predilection site large intestine
Superfamily strongyloidea
Host Sheep, goat, occasionally deer, cattle and other ruminants
Pathology There are potential hemorrhages in the mucosa of the colon due to
immature, and immature and adult worms are found in the gut lumen.
The major pathogenic effect is caused by L5 stage larvae and by mature
adults, there are local hemorrhages and loss of proteins through mucosal
damages, burden of 300 worms is considered pathogenic.
Clinical signs Moderate infections are asymptomatic. In severe infections there is diarrhea
with blood and mucous in which worms may be found. Sheep becomes
anemic and suffer weight loss.
Diagnosis Fecal egg count is very low, but in diarrheic phase worms are expelled and
easily recognized.
Treatment Anthelmintic therapy with broad spectrum anthelmintics (benzimidazole,
levamisole, avermectins)

Life cycle
The life cycle is direct. Eggs are passed in the feces and hatch on the ground releasing the first stage
larvae, which, moults to second stage and then to infective third stage. The host is infected by ingestion
of larvae with herbage. In the parasitic phase L3 enters mucosa of small intestine and occasionally that
of cecum and colon; and after a week they moult the L4 emerge on to mucosal surface and migrate to
congregate in the cecum where development to L5 is completed about 25 days after ingestion. The
young adult then travel to colon. There is no migration stage in the body. The prepatent period is 6-7
weeks.

Oesophagostomum-Syngamus
 Oesophagostmum radiatum in large ruminants
 Oesophagostmum bifurcum (zoonotic) in monkeys and man

Oesophagostmum radiatum

Common name Nodular worms

Parasite class nematode
Superfamily strongyloidea
Predilection site large intestine
Host Cattle and buffalo
Geographical distribution worldwide
Clinical signs In acute infection there is anemia edema and diarrhea.
The presence of P-shaped nodules in the intestinal wall on postmortem
is indication of nodular worm infection.
Diagnosis:
In the chronic disease eggs are present and L3 can be identified
following fecal culture.
Anthelmintic therapy with broad spectrum anthelmintic (
Treatment
benzimidazoles , levamisole and ivermectins )is highly effective.
Life cycle:
 The preparasitic phase is typically strongyloid and infection is by ingestion of L3 which enter the
mucosa in any part of small or large intestine forming nodules in which the moult to L4 takes
place.
 These L4 then emerges on the mucosal surface migrate to the colon and develop to the adult
stage.
 On reinfection larvae may arrested as L4 in nodules up to 1 year.
 The prepatent period is about 40 days.

Syngamus trachea >>> birds

Syngamus laryngeus (zoonotic) >>> man, cattle, goat, sheep, deer

Worms are typical joined male and female giving Y shaped, male and female are join together and gives
Y shaped appearance.
Syngamus trachea
Synonym syngamus parvis, syngamus gracilis
Common name Gapeworm
Parasite class Nematode
Super family Strongyloidea
Predilection site Trachea or lungs
Hosts Chicken, Turkey, Game birds, pigeon and various wild birds
 Pneumonia during the prepatent period may cause the signs of dyspnea, and
depression , whereas presence of adult and excess mucous in the trachea leads
to signs of the respiratory distress, asphyxia or suffocation with the bird gasping
for the air, often there is always great deal of head shaking and coughing as it
Clinical Signs
tries to rid itself of the obstruction. The clinical picture of gapes may thus range
from gasping, dyspnea and death to, in less severely affected animals weakness,
anemia and emaciation.
This based on clinical signs and the finding of eggs in the feces. Disease is best
Diagnosis confirmed by postmortem examination of selected cases when reddish worms
will be found attached the tracheal mucosa.
 In feed modern benzimidazoles are effective administered over period
Treatment of several days.
 Nitroxynil and levamisole are also efficacious when given in water.
Life Cycle:
 Unlike other strogyloids the L3 develops within the egg. Infection may occur by one of three ways,
firstly by ingestion of L3 in the egg, secondly by ingestion of the hatched L3, or thirdly by ingestion
of transport or paratenic host containing the L3.
 The most common paratenic host is the common earthworm, but a variety of other invertebrates
including slugs, snails, beetles, and some flies may act as transport host.
 After penetrating the intestine of final host the L3 travel via the liver to the lungs.
 The two parasitic moults takes place in the lungs. Copulation occurs around day 7 in the trachea
or bronchi after which the female grows rapidly.
 The prepatent period is 16-20 days. Longevity is around 9 months.

Control:
 Young birds should not be reared with adults, especially turkeys, and to prevent infection
becoming established runs or yards must be kept dry and contact with wild birds prevented.
 Avoid the continuous rearing birds on same ground. Drug prophylaxis may be practiced over the
period when outbreaks are normally expected. It is not usually feasible to eliminate paratenic
hosts.

HAEMONCHUS
It is the very important disease of livestock camels and large ruminants.
 Buccal cavity small
 Direct lifecycle
 L3 is the infective stage, usually non migratory
SUPER FAMILY: Tricostrongalidae (The trichostrongyloids are small, often hair-like, worms in the bursate
group, which, with the exception of the lungworm Dictyocaulus, parasitise the alimentary tract of animals and
birds. Structurally they have few cuticular appendages and the buccal capsule is vestigial.)
PARASITE CLASS: Nematode. Bursate nematodes (those having bursa)
Haemonchus Placie - nematode of large ruminants
Haemonchus Contortus - parasite of small ruminants
SYNONYM: Haemonchus placei
COMMON NAME: Barber's pole worm
(Both have common name of barbers pole worm morphologically similar to the barbers pole (in which
blood filled intestines have wrapping signs white ovaries) that gives indication of barbers pole.)
PRE DILECTION SITE: Abomasum.
They are blood suckers small thread like worms reddish appearance because of blood tekkens.
IMPORTANCE:
Their importance is that they are cause of mortalities especially in small ruminants. cause disease
Haemonchusis.
It is the number one cause of anaemia in small roomants thats why death occurs if you give repeatedly
enthlmantic these ones are more likely to develop drug resistance.
How will you evaluate that there is drug resistance?
Resistance develops due to change of drug treatment molecule mutation. it is also for survival and lethal
DIAGNOSIS:
 Fecal Egg Count
 Reduction Test.
Polymorphism Y shape of single in population. So if change of one nucleotide, change of AA ( AA are
present on by nucleotide) if one nucleotide change in mRNA change in A from hydrophobic to
hydrophyllic protein will occur and changes dimensionally, there are depths and prominent areas that
organised drug accounts if control change drug change its target and resistance is developed.

Teladorsagia Cicumcincta
Common Name: Brown stomach worm
Superfamily: Trichostronyloidea
Morphological Characteristics:
 Adults are slender
 Reddish brown worms with short buccal cavity
 Smaller than 1cm
 Difficult to visible with naked eye
Predilection site: Abomasum
Morocco Leather appearance: It is observed in abomasum (tan color) in this disease
Four parts of compound stomach
 Rumen, Reticulum, Omasum, Abomasum
 Rumen is largest
 Abomasum have acidic pH rest 3 have basic pH

Biology
 Three living stages in environment L1, L2, L3
 L3 is Infective stage. Ingested during grazing.
 Moult into L4 (may be dormant for many months)
 L5 is pathogenic stage which transforms into adult and pass egg in feaces.

Differentiate between susceptible and resistant parasite: If the difference between post treatment and
pretreatment efficiency is greater than 97% then it is susceptible, if less than 97% it is resistant. But also
it depends on alpha value (error) 99% confidence 1% alpha value.
 Ostertagia
 Ostertagia ostertagi
 Synonym: ostertagia lyrata, Skrjabinagia lyrata
 Common name: brown stomach worm
 Predilection site: Abomasum
 Parasite class: Nematode
 Superfamily: strongyloidea
 Host: Cattle, deer, and occasionally goats
 Geographical distribution: worldwide (especially important in temperate climates and in
subtropical regions with winter rainfall)
Life cycle
The life cycle is direct. Eggs are passed in feces and under optimal condition develop within fecal part to
infective third stage within 2 weeks. When moist conditions prevail, L3 migrate from feces to herbage.
After ingestion of the L3 larval stage, the L3 exsheath in the rumen and further development takes place
in the lumen of abomasal gland. The two parasitic moults occur before the L5 stage emerges from the
gland around 18 days after infection to become sexually mature on the mucosal surface. The entire
parasitic life cycle usually takes 3 weeks, but under certain circumstances the ingested L3 become
arrested in development at early fourth stage EL4 for period of upto 6 month also called as hypobiosis.

Diagnosis
 The clinical signs of in appetence, weight loss and diarrhea
 The season, for example type-I occurs in from July to September while type-II from March to
May.
 The grazing history; in type-I the calves have usually been set stocked in one area for several
months, while in type-II history often tells that calves have been grazed on a field from spring to
mid-summer and moved and brought back to original field in autumn.
 Fecal egg count; in Type-I there are usually 1000 eggs per gram while in type-II count is highly
variable.
Treatment
 Modern benzimidazoles , the pro benzimidazoles ( febantel , netobimine and thiophanate ) ,
levamisoles, or avermectins at standard dosages.

Trichostrongylus
Synonym: Trichostrongylus extenuates
Common name: stomach hairworm
Class: Nematode
Superfamily: trichostrongylidea
Host: cattle, sheep, goat, deer, horse, donkey, pig, occasionally man
Life cycle:
 Life cycle is direct and pre-parasitic phase is typically trichostrongylidoies.
 Pre-patent period in sheep is 3 weeks
 
L3 is infected stage
Geographical distribution: world wide
Pathogenesis:
 the extent of lesion in abomasum or stomach is dependent on the size of the worm population.
 Lesions may be present in pyloric and fundic region
 These lesions are about 1-2 cm in diameter have been termed plaques or ringworm lesions
 In heavy infection shallow ulcers may be seen
 These changes induced in gastric mucosa are similar to those of ostertagia with an increase pH
and increase in permeability of mucosa
Clinical signs:
 In heavy infection rapid weight loss and diarrhea, dehydration.
 In low level of infection in appetence and poor growth rates
 Sometimes accompanied by soft feces
Diagnosis:
Based on clinical signs, seasonal occurrence of disease and if possible lesions at postmortem
Fecal egg count is useful aid
Fecal culture
At necropsy T.axei is easily identified from washing and digest of abomasum or stomach
Control: If parasite of sheep and cattle are different then this work – rotational grazing
Trichostrongyloides eggs are similar to strongyloide egg
Confirmation is obtained only by pcr
Morocco leather appearance in ostertagia
Plaqus ring worm lesion in trichostrongylus

1 Cooperia curticei
2 Cooperia onchophora
3 Cooperia punctate
4 Cooperia pectinata
Cooperia
Trichostrongyloidea Sheep, Goat, Deer
Trichostrongyloidea Cattle, Sheep, Goat, Deer
Trichostrongyloidea Cattle, Deer
Trichostrongyloidea Cattle, Deer

Cooperia
Parasite Cooperia onchophora Cooperia punctate Cooperia surnabada
pectinata
Common name Cattle bankrupt worm
Predilection
Small intestine
site
Hosts Cattle, Sheep, Goat, Deer Cattle, Deer Cattle, Deer Cattle, Sheep, Camel
Geographical Parts of Europe, north
Worldwide
distribution America and Australia
Loss of appetite poor Loss of appetite
weight gain intermittent Poor weight gain Similar to
Clinical signs
diarrhea in heavy Diarrhea C.punctata
infection Submandibular edema

Generally considerd as
mild pathogenin calves,
associated with in
appetence and poor
Pathogenesis
weight gain, partial
immunity develops after
8-12 month of exposure
of infective larvae.
Eggs of cooperia spp. are
all very similar in
Diagnosis morphology, fecal culture
helps to identify infective
larvae.
Treatment Same as ostertagia
Control Same as ostertagia
Penetrates the
epithelial surface of
small intestine and
cause disruption
similar to intestinal Similar to
trichostrongylid C.punctata
species, leading to
villous atrophy
reducing area for
absorption
Fecal Culture

Life Cycle C. onchophora

This is direct and typical of superfamily trichstrogyloidea. Ingested L3 ex-sheath, migrate into intestinal
crypts for two moults and then the adults develop on the surface of the intestinal mucosa. The prepatent
period is around 3 weeks. The bionomic requirements of free living stages are similar to those of
ostertagia.

Life cycle of C.Punctata

Similar to C.onchophora but the adults remains closely associated with mucosa and surface epithelium.
Prepatent period is around 2-3 weeks. Bionomic requirements are same as for Haemonchus.

Life cycle of C.pectinata

Same as for C.punctata

Life cycle of C.surnabada

Similar to C.punctata and C.pectinata. The bionomic requirements are of free living stages concur with
those for Haemonchus.

Nematodirus
Parasite Nematodirus helvetianus Nematodirus battus
Common name Thread necked worm Thread necked worm
Class Nematode Nematode
Superfamily Trichstrongylidea Trichstrongylidea
Predilection site Small intestine Small intestine
Cattle, occasionally sheep, goat and other
Hosts Sheep, goat & occasionally cattle (calves)
ruminants
Pathogenesis Ingestion of large number of L3 causes
This parasite has been incriminated in
disruption in intestinal mucosa,
outbreaks of bovine parasitic gastroenteritis
particularly in ileum, there is
 but experimental attempts to produce
disease have been unsuccessful.
Low to moderate infection may produce no
Clinical signs clinical signs but severe infection diarrhea
occurs in young animals.
Diagnosis Fecal examination , large colorless eggs
Treatment Avermectin ,benzimidazole
development of L4 & L5 coinciding with
damage to villi and erosion of mucosa
leading to villus atrophy. The ability to
exchange fluid is greatly disturbed
leading to diarrhea.
In severe infection, yellow green
diarrhea, animal becomes thirsty
Because clinical signs appear during
prepatent period, fecal egg counts are of
little value in early diagnosis which is best
made on grazing history. If possible a
postmortem examination. Nematodirosis
must be differentiated from coccidiosis
Avermectin benzimidazole

Life cycle of N.helvetianus

The preparasitic phase is almost unique in the trichostrongyloids in that the development to L3 takes place
within the egg shell. N.helvetianus does not have the same critical hatching requirements as N.battus and
so the larvae often appears on the pasture within 2-3 weeks of the eggs being excreted in feces. More
than one annual generation is possible. The parasitic phase within host is similar to that of N.battus. The
prepatent period is about 3 weeks.

Dictyocaulus (Dictyocaulosis)
Parasite Dictyocaulus viviparus
Common name Bovine Lung worm, verminous pneumonia
Superfamily Trichostrongyloidea
Predilection site
Bronchi, Trachea
Host Cattle, Buffalo, Deer, Camel
Importance Worldwide, 3 imp. Species (D.viviparus, D.filaria, D.arnfieldi)
Phases Pathogenesis is divided into 3 phases
(1) Pre-patent phase: around days 8-25. (Disease caused by L5 larvae).
(2) Patent phase: around days 26-60. (Disease caused by adult worm)
(3) Post-patent phase: around days 61-90. (L1 larvae which hatch in trachea)
Role of Fungus This fungus, Pilobolus, is commonly found growing on the surface of bovine fecal
in epidemiology pats about 1 week after deposition. The larvae of D. viviparus migrate in large
numbers up the stalks of the fungi on to, and even inside, the sporangium or seed
capsule. When the sporangium is discharged it is projected a distance of up to 3 m
in still air to land on the surrounding herbage.
Signs/Symptoms Coughing, Cracking sound in lungs
Treatment Ivermectin or benzimidazoles

Biology:
The female worms are ovo-viviparous, producing eggs containing fully developed larvae, which hatch
almost immediately. The L1, migrate up the trachea, are swallowed and pass out in the feces. The larvae
are unique in that they are present in fresh feces, are characteristically sluggish, and their intestinal cells
are filled with dark brown food granules. In consequence the preparasitic stages do not require to feed.
Under optimal conditions the L3 stage is reached within 5 days, but usually takes longer in the field. The
L3 leave the fecal pat to reach the herbage either by their own motility or through the agency of the
ubiquitous fungus, Pilobolus. After ingestion, the L3 penetrate the intestinal mucosa and pass to the
mesenteric lymph nodes where they moult. The L4 then travel via the lymph and blood to the lungs, and
break out of the capillaries into the alveoli about 1 week after infection. The final moult occurs in the
bronchioles a few days later and the young adults then move up the bronchi and mature. The prepatent

period is around 3-4 weeks.

Spirocera lopi
 Non Bursate Nematodes of spiral shape
 With indirect life cycle
Predilection site: Aorta, Oesophagus, Stomach
Parasitic class: Nematodes
Super family: Spiruriodae
Final Host: Dog but occasionally Cat
Intermediate Host: Dung Beatles
Paratenic Host: Rodents and Birds
Life Cycle:
 Eggs are passed through faces or vomit.
 Eggs have larva L1. Egg DO NOT hatch in ENVIRONMENT.
 Eggs are eaten up by Intermediate host which is DUNG BEATLES.
 There they develop into L3.
 They can be eaten up by some other animal called as Paratenic host.
 That paratenic host is eaten up by our Final Host.
 L3 hence is the infective stage.
  L3 enters in stomach mucosa from there they enter aorta and can cause perforation thus called
aneurism.
 From there they move to the oesophagus and shed eggs in the lumen which come out of faces
or they vomit them out.

Pathology:
 Carcoma of Oesophagus
 Blockage of oesophagus
 Formation of fibrotic nodules in the inner wall of aorta which will cause Rupture

Treatment: Difficult to treat.

Gnathostoma spinigerum
Zoonotic, Coiled nematodes
Neurognathostomiasis in a young child

Predilection site: Stomach

Final Host: Cat, Dog, Man
Intermediate Host: Host 1- Crustacians
Host 2-Mammals , birds, reptiles

Life Cycle:
 Unembryonated Egg are released in feces.
 Hatch In the ENVIRONMENT
  L1 enter into 1st Host Crustaceans
 L2 enter into 2nd Host
 Develops into L3.
 L3 is the infective stage.
 Enten up by Final Host.
 Resides in its Stomach Nodules
 Release eggs in the Lumen of stomach

Pathology:
Nodule formation in Stomach
Gastric Perforation

Habronema-Draschia-Thelazia
Draschia megastoma
Synonyms Habronema megastoma
Predilection site Stomach
Superfamily Spiruroidea
The presence of adult worms in the stomach causes very little clinical
disturbance. Cutaneous habronematidosis presents as intense itching of
Clinical signs
the affected skin. Non-healing granulomatous lesions, raised above the
surface of the skin may be a feature.
Usually only low numbers of eggs or larvae are present in the feces. Eggs
may be demonstrated in gastric lavage taken via a stomach tube.
Diagnosis
Sometimes larvae can be identified in the small granulomatous skin
lesions.
Disease Cutaneous habronemiasis also called “Summer sores”
Final hosts Horse and other equines
Intermediate hosts Dipteran flies of the genera Musca, Stomoxys and Haematobia (Lyperosia)
Treatment Broad spectrum anthelmintics

Life cycle:
Eggs or L₁ are passed in the faeces and the L₁ are ingested by the larval stages of various muscid flies that
are often present in faeces. Development to L3 occurs synchronously with the development to maturity
 of the fly intermediate host. When the fly feeds around the mouth, lips and nostrils of the horse, the
larvae pass from its mouthparts on to the skin and are swallowed. Alternatively, infected flies may be
swallowed whole in feed and drinking water. Development to adult takes place in the stomach where
the larvae burrow into the glandular area of the mucosa and induce the formation of nodules. The
worms develop to mature adults within the nodules in about 8 weeks. When Draschia larvae are
deposited on a skin wound or around the eyes they can invade the tissues; they do not complete their
development but may cause granulomatous skin lesions.

Habronema microstoma
Synonym Habronema majus
Predilection site Stomach
Superfamily Spiruroidea
These are usually absent in gastric habronematidosis. Lesions of cutaneous
habronematidosis are most common in areas of the body liable to injury and
occur during the fly season in warm humid countries, although it also occurs in
temperate regions. During the early stages, there is intense itching of the
infected wound or abrasion, which may cause further self-inflicted damage.
Subsequently a reddish brown, non-healing cauliflower-like granuloma
Clinical signs
develops that protrudes above the level of the surrounding skin. These lesions
are known as 'summer sores' in acute cases. Later the lesion may become more
chronic, fibrous and inactive, but will not heal until the advent of cooler
weather when fly activity ceases. Invasion of the eye produces a persistent
conjunctivitis with nodular ulcers. Sometimes larvae invade the skin of the
prepuce and glans penis of stallions.
This is based on the finding of non-healing, reddish cutaneous granulomas. The
larvae, recognized by spiny knobs on their tails, may be found in material from
Diagnosis
these lesions. Gastric infection is not easily diagnosed since Habronema eggs
and larvae are not readily demonstrable in the feces by routine techniques.
Final hosts, Intermediate hosts, Life cycle, Treatment are same as that of Draschia megastoma

Thelazia lacrymalis Thelazia callipaeda

Eye worm
Common name Equine eye worm
(PARASITES OF THE NERVOUS SYSTEM)
Predilection site Eye, conjunctival sac and lachrymal duct Eye, conjunctival sac and lachrymal duct
Superfamily Spiruroidea
Final hosts Horse and other equids Dog, cat, occasionally sheep and deer
Muscid flies, particularly Musca, Fannia
Intermediate hosts Muscid flies, particularly Fannia spp
and Morellia
The worms are viviparous. The L1, passed The worms are viviparous. The L, passed by
by the female worm into the lachrymal the female worm into the lachrymal
secretion is ingested by the fly secretion is ingested by the fly
Life cycle intermediate host as it feeds. intermediate host as it feeds. Development
Development from L1, to L3 occurs in the from L, to L3 occurs in the ovarian fol licles
ovarian follicles of the fly in 15-30 days of the fly during the summer months. L3
during the summer months. L3 migrate to migrate to the mouthparts of the fly and
 the mouthparts of the fly and are are transferred to the final host when the
transferred to the final host when the fly fly feeds.
feeds. Development in the eye takes
place without further migration and the
prepatent period is between about 3-6
weeks.
Heavy infestations can cause
lachrymation, conjunctivitis and
photophobia. Flies are usually clustered
Clinical signs around the eye because of the excessive Conjunctivitis, excessive lachrymation
secretion. In severe cases the eyes may
be swollen, with keratitis, corneal
ulceration with a purulent exudate.
This is based on observation of the parasites in the conjunctival sac. Examination of the
Diagnosis
lachrymal secretion may reveal first-stage larvae.
Ivermectin at 0.2 mg/ kg has been reported
Treatment Fenbendazole
to be effective.

Ascaris
More than 1 billion children in developing countries affected
Effects of ascaris in Children: Malnutrition, Weakness, loss of memory, loss of cognition
Biology:

Constipation vs Obstipation:
Constipation is a condition in which animal passes feces less often or in smaller amounts than normal.
Obstipation occurs when severe constipation makes defecation impossible or nearly impossible. It is an
emergency.

Points of awareness in case study: Community based awareness about complications, damages of
disease and how it spreads

SDG
This is particularly important in the context of achieving the ambitious target of the sustain able
development goal (SDG) 3.3 which seeks to eradicate neglected tropical diseases by 2030.

Parascaris equorum
Basically, it is disease of foals (young horses) because of eating soil.
It is important in pedigree (thorough bred) horses.
Predilection site: small intestine
Signs: thriftiness, anxiety, stress

Why foal died even after giving treatment of colic in case study?
Because of chronic colic, surgeon advised to do laparotomy (costly), owner denied because of high cost.

Older horses are more likely to develop pulmonary and hepatic signs rather than gastrointestinal tract
signs, why?
Because of immunity development, larva stages are in Liver and Lungs and less adult worms in intestine

What is reason not to develop parascariasis in foals under one month of age?
Because there is no trans mammary transmission

What is the reason to develop parascariasis in foals after 4 months till 12 months of age?
 Infection in 1st month
 Incubation period 3 months
 So, 4 months at least for disease to develop.

Dirofliariasis
Causative agent: Dirofilaria immitus (Not common in Pak)

→A dog was presented with history of soft, dry cough and exercise intolerance

 Shortness of breath
 Weakness
 Loss of stamina

Prognosis: Might be Respiratory system affected.

Diagnosis: By wet smear (take one drop of blood and cover with cover slip then examine under
microscope)

Heart worms (Dirofilaria immitus) lives in heart chambers + Pulmonary artery / vein
Size: Couple of centimeters. Transmission: By Mosquito

Host: Cat, Dog, Human(Zoonotic) Affected parts: Lungs, Liver, Kidney

It can affect lungs badly by microfilariae

Treatment: First paralyze worms then do surgery to remove adults and use ivermectin for microfilariae
Melarsomine (1st shot ----wait for 30 days---two shots on 31st day)

Life Cycle
During a blood meal, an infected mosquito introduces third-stage filarial larvae of Dirofilaria
immitis into the skin of the definitive host

. In the definitive host, the L3 larvae undergo two more molts into L4 and adults. Adults reside in
pulmonary arteries, and are occasionally found in the right ventricle of the heart .Adults can live for 5
– 10 years. In the heart, the female worms are capable of producing microfilariae over their lifespan. The
microfilariae are found in peripheral blood . A mosquito ingests the microfilariae during a blood meal
. After ingestion, the microfilariae migrate from the mosquito’s midgut through the hemocoel to the
Malpighian tubules in the abdomen . There the microfilariae develop into first-stage larvae and
subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the
mosquito’s proboscis and can infect another definitive host when it takes a blood meal . In
humans , D. immitis larvae tend to follow the same migratory pathway as in the canine host, ending
up in the lungs, where they often lodge in small-caliber vessels, causing infarcts and typical “coin
lesions” visible on radiographs.
 PINWORM INFECTION
Super family: Oxyuroidea
Genus:
 Oxyuris
 Probstmayria
 Skrjabinema
 Paraspidodera
 Enterobius
 Aspicularis
 Passalurus
 Syphacia
Known as pinworm bcz of pointed tail (which cause irritation, pleuritis, pinning effects around anal
areas) of female parasite
 They have a double bulb esophagus and a direct life cycle.
 The genera of veterinary interest are Oxyuris and Probstmayria, both parasitic in the horse
 Skrjabinema-parasite of ruminants.
 Paraspidodera-guinea pigs
 Subulura (Subuluroidea)-parasites of poultry.
 Enterobius-common human pinworm.
(different parasite in casse of each specie)
OXYURIS EQUII SKRJABINEMA OVIS
COMMON NAME Equine pinworm, Rat tail Pinworms
PREDILECTION SITE Ceacum, Colon, Rectum Ceacum, colon
HOST Horse, Donkey Sheep, goat
GEOGRAPHICAL
Worldwide Worldwide
DISTRIBUTION
PREPATENT PERIOD 05 months 25 days

LIFE CYCLE
 The life cycle is direct.
  The adult worms are found in the lumen of the caecum and large Colon
 After fertilisation the gravid female migrates to the anus, extrudes her anterior end and lays her
eggs
 Unembryonated eggs passes out in feces in clumps (up to 50 000 eggs per female), seen grossly
as yellowish white gelatinous streaks on the perineal skin or perianal region.
 Development is rapid, and within 45 days the egg contains the infective L3,
 Eggs are rubbed off and contaminate the environment.
 Infection is by ingestion of embryonated eggs on fodder, grass, bedding etc.
 The larvae are released in the small intestine, move into the large intestine and migrate into the
mucosal crypts of the caecum and colon where development to L4 takes place within 10 days.
 The L4 then emerge and feed on the mucosa before maturing to adult stages that inhabit the
lumen and feed on intestinal contents.
 L4 is pathogenic
 Eggs congaining L3 doesnt hatch in environment
Biology in man is same as in equine
SIGNS & SYMPTOMS:
 Signs of anal pleuritis
 Tail rubbing
 Greyish yellow eggs
 Female worm (long tail) in feces
 Rat tail like appearance
 Sloughing of hair around anas
 Animal rubs with wall which leads to sloughing of hair around that area
 Eggs are streaky laid in clumps which causes irritation
 Irritation is caused by eggs which leads to pleuritis
SIZE:
 Male-1-2cm
 Female-10-12cm(bcz of its long hair size is long)rat tail might be due to rhisy
DIAGNOSIS:
 Fecal examination if positive maybe due to eggs stick to stool during defecation
 Sellotape test is used for diagnosis -stick tape on anal area and observed in microscopy
IMPORTANCE:
 It causes restlessness in animals and humans
 We can’t get Maximum work from animals
SWEET ITCH:
 Loss of hair on neck due to bite of some flies (black flies cause irritation and cause hair loss on
neck)
 When during grooming they may transfer their eggs on neck
 It may happen during cause of oxyuriasis
 When the eggs are passed from anal region to neck during grooming it resembles sweet itch
TREATMENT:
Effective anthelmintics include ivermectin,moxidectin, the benzimidazoles (fenbendazole, oxfendazole,
oxibendazole) and pyrantel.
Moxydectin - reported to use against this drug
 Why didn’t this work?
 Resistance
 Drug absorbed in small intestine while parasite is in large intestine

Trichuris vulpis
(Common in Pak)
Superfamily→ Trichuridae
Common name→ Canine Whipworms (because of long tail like whip)

Host → Dog, fox, cat

Predilection site: Large intestine Infective Stage: L1
Eggs: Lemon shaped / barrel (drum) shaped
Zoonosis: Only 1 specie is zoonotic (Capillaria aerophila ) that’s why differential diagnosis is important

Q:What does the following sentence convey the meaning stated in the case study "canine whipworm
is a ubiquitous parasite infesting all categories of dogs with high prevalence all over the World"?
Ubiquitous means universal
All categories → stray dogs. kennelled dogs (kept in cages)

Life Cycle
The unembryonated eggs are passed with the stool 1. In the soil, the eggs develop into a 2-cell stage 2:
an advanced cleavage stage 3: and then they embryonate 4; eggs become infective in 15 to 30 days.
After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release
larvae 5: that mature and establish themselves as adults in the colon 6: The adult worms (approximately
4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with
the anterior portions threaded into the mucosa. The life span of the adults is about 1 year.
What is Moulting? shedding of cuticle …. further development to other stage is called moulting/
Sign/Symptoms: watery diarrhea, dysentery, inflammation of large intestine
Remarkable features: mixed of 3 species infection in dog
Diagnosis: by fecal sample (eggs lemon shape … egg has rings + plugs)
Copromicroscopic: fecal examination through microscope
Morphometric analysis: Use of micrometer in microscope

Trichuris Capillaria
On basis of Symmetry Symmetrical No Symmetry
Rings in Plug 3 Rings No Ring
Length (72-94 micro meter) Length (60-65 micro meter)
Micrometry
Width (31-42 micro meter) Width (25-40 micro meter)

Capillaria – Trichinella
Capillaria hepatica
Biology:
Capillaria hepatica has a direct life cycle, with no intermediate host. It can develop with only one
definitive host, but likely requires two hosts to complete the life cycle.
The eggs trapped in the parenchyma cannot be passed in the feces of the host, and remain in the liver
until the animal dies, or more likely, is eaten by a predator or scavenger. Eggs ingested by scavengers
are unembryonated (not infectious) and are passed in through the digestive tract into and out in feces,
providing an efficient mechanism to release eggs into the environment; this is ecologically the most
likely primary route of transmission. Eggs embryonate in the environment, where they require air and
damp soil to become infective. Under natural conditions, embryonation is slow and may take between 6
weeks and 5 months. The cycle continues when embryonated eggs are eaten by a suitable mammalian
host. Infective eggs hatch in the intestine, releasing first stage larvae. The larvae penetrate the intestinal
wall and migrate via the portal vein to the liver parenchyma within 3-4 days. Larvae take about 3-4
weeks to mature into adults and mate. Humans are usually infected after ingesting embryonated eggs in
fecally-contaminated food, water, or oil

Cannibalism: eating another member of same specie

Zoonotic: yes (Man-→dead end host) Predilection site Liver - Small intestine

Host → Rodents, squirrels, Mustelide occasionally dog, Cat, man

Question: Can Man be infected by eating of liver of horse infected with Capillaria hepatica?
No, for infection embryonated eggs are required (happen in environment)

Importance: zoonotic, worldwide

Can we diagnose capillariasis through fecal examination?

through fecal sample → No, because for infective animal there are no eggs in feces

How can diagnosis of Capillariasis caused by Capillaria hepatica be done?

Elisa(serology), necropsy of live , liver function test
Can capillariasis be spread by eating of carcass/ cannabolism? Yes

Would a patient have the infection who is shedding the eggs?

No, egg are ingested un embryonated And same pass in feces

What is the breaking in the given case? First infection in horse in Japan

Trichinella spiralis
Common name Muscle worm
Predilection site Small intestine, Muscle
Host Pig , rat, man, and most mammals
Zoonosis Food borne
Why Trichinella spiralis is called Muscle Because larva is in striated Muscles
worm?
What are Trichinae? (singular: Trichina) L1 Larva
Infective Stage L1
Muscle cells that welcome L1 larvae and feed it with
Nurse cells
independent blood circulation.
No intermediate or final host though life Cycle is indirect
Exceptional in Life Cycle  No free living Stage
 No stage in environment
Diagnosis Serological test

Biology
. After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the
small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2
mm. The life span in the small bowel is about four weeks. After 1 week, the females release
larvae that migrate to striated
muscles where they encyst .
Diagnosis is usually made based
on clinical symptoms, and is
confirmed by serology or
identification of encysted or non-
encysted larvae in biopsy or
autopsy specimens
 DIOCTOPHYMA
 Very large worms
 Life cycle indirect
 infection by L3 in aquatic annelids
DIOCTOPHYMA RENALE
SYNONYM Dictophyme renale, Eustrongylus gigas
COMMON NAME Giant kidney worm
PREDILECTION SITE Kidney parenchyma, abdominal cavity
SUPERFAMILY Dioctophymatoidea
Aquatic oligochaetes (annelids), e.g.
INTERMEDIATE HOSTS
Lumbriculus variegatus
Dog, fox, mink, ferret, otter, pine marten, polecat, mink; sporadically
FINAL HOSTS
reported in the cat, pig, horse, cattle and man.
Temperate and subarctic Areas, Its main endemic area is the northern part
GEOGRAPHICAL DISTRIBUTION
of North America, chiefly Canada.
CONTROL: Elimination of raw fish from the diet.
 Dioctophyma (red scourge) infection in man: this has been mainly
recorded in N. America, but other cases have occurred throughout
the world.
 Annelid intermediate hosts in the drinking water are infective and
NOTE:
uncooked frogs and fish act as paratenic hosts.
 The adult worms are found in a thick-walled cyst in the kidney
(usually the right) and may cause loin pain and haematuria.

LIFE CYCLE
 The worms are oviparous.
 The eggs, in the single-
cell stage, are passed in
the urine in clumps or
chains, and are
ingested by the annelid
intermediate
 The development
phase in the annelid is
about 2—4 months.
 The final host is
infected by swallowing
the annelid with the
drinking water, or by
the ingestion of a
paratenic.
 host, such as a frog or
fish, which has itself eaten the
  infected annelid.
 In the final host, the infective larvae
 penetrate the intestinal wall, enter the peritoneal cavity
 and eventually penetrate the kidney.

The prepatent period is about 6 months but has been observed to be as long as 2 years.

DRANCULULUS MEDINENSIS
 Largest tissue parasite affecting human (600-800mm approx 1 meter)
 Prevalent all over the world
 is caused by the nematode (roundworm)
 Neglected tropical disease
 New emerging with old history
 It is snake like

DISEASE NAME: Dracunculiasis PREDILECTION SITE: subcut tissue, connective tissue

INTERMEDIATE HOST: crustacean (fish are paratenic host

FINAL HOST: man, dog

COMMON NAME: Guinea worm disease (guinea is name of country in Africa from where the parasite
maybe discovered)

IMPORTANCE:
 zoonotic
 Water borne zoonosis
 Food borne

SIGN AND SYMPTOMS:

 Cause of weakness
 lethargy
 dizziness
 vomiting
 Diarrhea
 skin rashes(urticaria)

BIOLOGY:
 There are no eggs
 Parasite is larveparous
 Female lay eggs directly on water
 Female is long it searches skin near foot where it penetrates and comes out creating irritation
and burning sensation due to which infected person puts foot in water so female lays L1 larvae
directly in water
 L1 larvae is ingested by crustaceans (IM host)
  Where further molting to L2 To L3 Larvae occurs
 Crustacean harbor L3 larvae
 Fish ingest crustacean and is paratenic host
 Man is infected by ingesting crustacean or under cooked fish or contaminated water
 When a person drinks contaminated water from ponds or shallow open wells, the cyclops is
dissolved by the gastric acid of the stomach and the larvae are released and migrate through the
intestinal wall
 L3 larvae from stomach moves to Connective tissue or subcut tissue
 After 100 days, the male and female meet and mate. The male becomes encapsulated and dies
in the tissues while the female moves down the muscle planes. After about one year of the
infection, the female worm emerges, usually from the feet, releasing thousands of larvae and
thus repeating the life cycle
 After male dies it takes 1 year for female to reach foot

DIFFERENTIAL DIAGNOSIS: tuberculosis

We cannot say this parasite CLM (cutaneous larval migrants)
In the last there is ulcer formation

RISK FACTOR:
 Contaminated water
  Undercooked(man) fish, uncooked(dog)

TREATMENT:
 Ivermectin/Albendazole/Surgical operation

DIAGNOSIS:
 Serology at initial stage
 Water contaminated test

CONTROL: Filter water or sterilized water

Integrated Helminth Management

Helminths: Challenges
1. Loss of productivity caused by the slow killers
Weakness, loss of fertility, Culling of animal
2. Sewage water for drinking
Contaminated water mixed with drinking water
3. Stagnant water
4. Rice cultivation Versus snail population
5. Lack of availability of vaccines
6. Parasite Zoonoses
7. Mixed Farming system
In small level farming
8. Free access of stray and farm dogs
Do spaying
9. Rodents as reservoir hosts
10. No availability of confirmatory Diagnostic tools in developing countries
11. Irrational use of anthelmintics
12. Drug resistance
13. Interaction with Wild-animals

Following is the vision of helminth control in farmed ruminants by 2030, bringing to bear progress in:
1. Diagnostic tools,
2. Innovative control approaches based on vaccines and selective breeding,
3. Anthelmintics, by sustainable use of existing products and potentially new compounds,
4. Rational integration of future control practices.

Three main principles of action which can be exploited to disrupt the parasite’s life cycle
1. To reduce the contact between the host and the parasite’s infective
stage
2. To stimulate the host response,
3. To eliminate the worms in the host.

Strategies to Control parasites

1. Pasture Rotation/rotational grazing
2. Knowing the Pasture Contamination –A Vicious Cycle
3. Multi-Specie Grazing
4. Zero- Grazing
Not using pasture will increase cost and no fresh environment available

5. Alternate Forages
Sorghum
Pasture with Tannin

6. Biological Control (use of organisms to control helminths)

A. Duddingtonia flagrans
B. Dung beetles
C. Plough Earthworms
7. Nutritional Management
 Balance diet
 Protein supplementation
 High fat diet during pregnancy
 Nutrition supplementation
8. Housing Management
V/S
9. Rationale use of anthelmintic
A. Anti-parasitic drugs are still
important
B. Avoid Drug resistance (Screen
animals for the resistance having less
than FECRT 95%)
 C. Avoid injudicious use of anthelmintics as it is being used irrationally 4 times per year in our
local settings.
D. Treat those which need treatment
10. Refugia: Refugia-based strategies are intended to help slow the development of anthelmintic
resistance by leaving a population unexposed to a treatment.

11. Use of full dose of Anti-parasitic drugs/don’t use under dose

12. Use of Alternative dewormers
A. Charcoal.
B. Garlic
C. Pumpkin seeds.
D. 1%solution of Copper Sulphate.
E. Wild Ginger.
(https://eap.mcgill.ca/agrobio/ab370-04e.htm)
13. Genetic Selection
Breeding
-Raise or introduce a more resistant breed.
-Raise crossbred animals for breed selection
Selection
-Cull animals that require frequent deworming and/or have consistently high or higher fecal egg counts.
-Select animals with lower fecal egg counts and lower FAMACHA© Scores and productivity.
14. Use of Vaccines
Types of vaccines against helminths
A. Live-attenuated
B. Soluble secretory or excretory products.
C. Somatic antigens (antigen bound to surface of parasite).
D. Hidden antigens (antigens that are not exposed to immune system).
E. Recombinant vaccines (rec-protein, rec-DNA, vectored vaccines)
List of commercial vaccines
A. HuskVac
Vaccine against Dictyocaulus viviparus infection in cattle. The vaccine, which contains live,
irradiation-attenuated L3 larvae, was developed in England and was originally marketed as Dictol.
This was the first commercial vaccine designed for use against any parasitic disease.
B. BarberVaX
Against Haemonchus contortus:
  Vaccination of lambs and kids against the intestinal aminopeptidase called H11.
 These interfere with worm digestion and reduce both parasite numbers and fertility.
C. Cysvax
Against Taenia spp:
 Recombinant vaccine
 This vaccine contains a cloned oncosphere antigen (To45W for T. ovis and TSOL18 for T.
solium).
 Prevents parasite penetration of the intestinal wall.
D. EG95
Against Echinococcus granulosa:
 Single-antigen recombinant vaccines are highly effective against E. granulosus (EG95) in
sheep and cattle.

What are the Hindrances in the development of vaccine against helminthes

Helminth vaccines are not yet widely employed because farmers are reluctant to change established
control procedures.
Other factors:
Complex life cycles of helminthes
Complex antigenic profiles
Immune escape mechanisms
Rapid evolution – genetic diversity
Lack of animal models.

THE END
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