Diseases caused by parasites(Helminths)
1. Fascioliasis
Fascioliasis is a very important disease of cattle and is caused by Fasciola hepatica and
Fasciola gigantica
Fascioloides magna, a large liver fluke occurs in the liver of cattle,sheep, horse,deer and
raely pigs.
Etiology:-Fasciola hepatica and Fasciola gigantic
Host responsibility:-It mostly affect cattle,sheep and goat.
Transmission:-The metacercariae larvae form get entry into host plants or grass blades at
which it is present in encysted form.
After getting entry into body the cyst wall is disolved and young flukes burrow through the
intestinal mucosa and the wall and emerge on the peritoneum.sometimes they reach upto
bile duct and mesentric lymphatic glands.
Pathogenesis:-Infection is by ingestion
It is a hermaphrodite and reproduces by depositing ova in the biliary passages, through
which they reach the intestine and are then passed in the faeces
Intermedaite host: Lymnaea sp.
Following ingestion, infective metacercariae encyst in the duodenum, penetrate wall and
reach peritoneum causes peritonitis and penetrate the liver reach bile duct where they
become mature flukes cause chloangiohepathitis, irritate and obstruct the bile duct and
predispose to bacterial infection.
Fascioloides magna, the infective forms penetrate the intestineal wall, and wander around
in the peritoneal cavity before invading the liver.
Gross lesions:-May be due to the adult fluke in the bile duct(obstructive jaundice) or due to
wandering ones in through parenchyma.
Wandering flukes produces lesions of traumatic nature which appear as haemorrhagic foci
and in the form of tortuous tunnels.
Liver is firmer and harder to the touch and cuts with difficluty.
The bile ducts in advanced cases especially in cattle, are hard and calcified - Pipe stem
appearance or clay pipe liver and when cut, a grating sound is elicited.
In early cases, hepatic cells show degenerative changes and eosinophilic inflammation and
later histiocyte and giant cells invades the necrotic area of coagulative type.
Cyst formation with calcification may also be seen.
Chronic obstruction of biliary passage may result in “clay pipe cirrhosis".
Microscopic lesions:-Cholangiohepatitis, biliary epithelium is stimulted to papillary and
glandular hyperplasia.
The walls of the ducts become infiltrated with eosinophils, lymphocytes, and macrophages
and ultimately become thickened from fibrous proliferation.
Extensie fibrosis and calcification of te bile ducts give rise to the term "pipe stem
liver" /"clay pipe liver"
Small granulomas may form around eggs that become lodged in small bile ducts.
Since clostridium novyi thrives well in the lesions caused by wandering flukes 'black disease'
is usually associated with liver fluke infection in sheep.
Clinical signs:-Acute, subacute and chronic forms. Subacute and acute forms in sheep are
usaually fatal- Damage to liver but death due to haemorrhages and anaemia
Chronic: Anaemia, unthriftiness, submandibular oedema (bottle jaw) and reduced milk
secretion.
Diagnosis:-Identification of characteristic ova in the faeces- oval, pedunculated, golden
brown eggs
Postmortem lesions in the liver.
2.Amphistomiasis
It is also known as stomach fluke disease, the intestinal phase of
amphistomiais is a common parasitic disease of cattle, and to lesser
extent sheep.
It is caused by Paramphistome flukes and characterised by severe
enteritis
Eggs - Big operculated egg with distinct yolk.
Etiology:-Paramphistomum epiclitum
Host responsibility:-usually affects cattle and some extend to sheep.
Transmission:-By ingestion of metacercariae larvae.
Pathogenesis:-Adult flukes are non pathogenic.
Metacercariae swallowed and young flukes reach the intestine, later
migrate to rumen and reticulum via duodenum and abomasum,
before becoming mature in 6 weeks to 4 months
The immature flukes attach to the intestinal mucosa causing irritation
resulting in enteritis.
Gross lesions:-The duodenum and jejunum contain numerous flesh
coloured flukes.
Subcutaneous edema is present together with ascites and
hydropericardium.Fat depots are gelatinous.
The mucosa of duodenum is thickened and show fibro-cattarrhal
inflammation.
Microscopic lesions:-The immature flukes may be seen in the deeper
layers of the mucosa and in the wall of the gut.
Clinical signs:-The clinical condition caused by immature parasite is
known as “immature amphistomiasis” manifested by persistent
foetid diarrhoea, bottle jaw and emaciation.
Diagnosis:-
1.observe the operculated eggs with distinct yolk and germ cells in
the dung.In heavy infection immature amphistomes are also seen in
the faeces.
2.Symptoms of emasication,diarrhoea,and bottle jaw in sheep must
always make one suspect amphistomiasis,especially if mortality is
heavy in flock.
3.Schistosomiasis
Schistosomes are elongated flukes living in the veins of various
animals.These are 1.5-2.0 cm long in length.
Adult female lays egg in the small venules.
S. nasale in the veins of nasal mucosa of cattle and buffalo causes
snoring disease.
S. spindale and S.indicum in mesenteric and portal veins of cattle,
buffalo, sheep and goat
S. incognitum in protal veins of pigs and dogs
S. nairi in elephants
S.japonicum – Hepatocellular carcinoma in human
S.haematobium - Urinary bladder carcinoma in man
The ova excreted through faeces develops into miracidium outside
and enter suitable intermediate host, a snail.
Within the body of snail, it releases numerous cercariae which
emerge into surrounding water.
Upon entering the suitable definitive host through skin they form
metacercariae and reach vein and attain adult form at the site of
predilection.
Route of infection:- The cercariae pierce through the intact skin and
visible mucosa of host. They entre the small cutaneous veins and are
thus swept away by venous circulation. They reach the nasal mucosa
and become mature and lay eggs.
Lesions:-Adult blood flukes in the vein of nasal mucosa causes nasal
granuloma or snoring disease in cattle but no such symptoms are
seen in buffaloes
The adult worms may cause phlebitis and venous thrombosis
They consume erythrocyte causing anaemia and the blood pigments
discharged are engulfed by macrophages ( Bilharzial pigment)
Dead disintegrated worm may set up toxic reaction
Injury caused by ova are more severe
The eggs in the venule adhere to the endothelium, rupture and reach
tissues where they form pseudotubercles. This consists of
schistosome eggs in the centre surrounded by pink stained area is
known as “actinobody”
Cutaneous lesions develop in humans and animals from penetration
of the skin by the cercariae.
Urticaria, itching and the formation of tiny nodules which raises the
epidermis were observed.
Cercariae even have the ability to penetrate the epidermis of hosts in
which complete development of the fluke does not occur
Cercaria dies in the dermis. This is the basis of “cercarial dermatitis”
also known as “swimmer’s itch”, “collector’s itch” and “swamp itch”
It is observed in agricultural workers, swimmers.
Diagnosis:- Examine the nasal discharge for the characterstic
boomrang shaped ova which have a spine at one end.
Nasal washings examined for napolean cap shaped S.nasale eggs.
Histopathological examination of biopsy specimens of rectal mucosa,
liver or other affected organs.
4.Ascariasis(Round worm disease)
Ascarids are extremely common round worms found in the
gastrointestinal tract of birds and mammals and are host specific.
Pathogenesis:There are three type of larvae classification on basis of
penetration ability and pathogenesis:-
The infective larvae are released into the gut following ingestion of
the embryonated eggs by the host.
First type
In some larvae penetrate the intestinal wall pass through the liver,
lung bronchiole, trachea –Swallowed into the alimentary tract where
the adults develops. eg. A.lumbricoides in man and pigs, Parascaris
equorum in horses and Toxocara canis in dogs
Second type
In others larvae migrates not only through the liver and lungs but
also through somatic tissues sometimes causing prenatal infection of
the foetus.e.g. T.canis and Neoascaris vitulorum in cattle
Third type
Larvae penetrates the intestinal wall and without migrating to other
tissues returns back to the lumen of intestine to become adults eg.
Toxascaris leonina and T.cati seen in cats, lion, dogs etc.
Most of the ascarids does not require intermediate host for
development
prepatent period: Interval between the ingestion of infective form
and appearance of eggs in the faeces - Varies for different species of
worms
In poultry – A. galli is seen in the intestine and Heterakis gallinae in
the caeca, of which the former is more pathogenic.
Lesions:-
Adult ascarids feed on to intestinal contents and sometimes moves
into stomach, hepatic or pancreatic duct
If in bile duct, it causes “ jaundice "
Large number of worms may cause obstruction of the intestinal
lumen, intussusception and even rupture
Penetrating worms may cause “peritonitis "
In liver, as the larvae burrow through the parenchyma is destroyed
and the tract formed thus is filled by blood and debris. Neutrophils
and eosinophils crowd around such a track. Healing by sacr tissue
occurs and the foci appear as " milk spots' on the capsular surface. In
heavy infection, the lesions may become confluent and fibrosis may
occur to such a degree as to obliterate the whole lobules.
Adult worms cause inanition and retardation of growth.
The infective larvae due to their migration causes damage in the
various tissues with central caseous necrosis surrounded by
epithelioid cells, eosinophils, lymphocytes and neutrophils.
In the lung of swine, larvae causes haemorrhages, dyspnoea and
cough described as “thumps”
Toxocara larvae migrating in abnormal hosts like man and other
animals is desribed as “visceral larval migrans”
Diagnosis:-
Eggs are thick shelled with unsegmented yolk.
5.Hemonchosis:-
Under the family of Trichostrongyloidea, Haemonchus contortus is
the worm seen in the abomasum of cattle, sheep and goat.
Etiology:-
H.contortus - In cattle,sheep and goats.
H.similar- Cattle
H.longistipes -Sheep and camel
Mecistocirrus digitatus - Cattle,sheep and goats.
Ostertagia ostertagi- cattle,sheep and goat.
Hysostrongylus rubidus - swine( diphtheritic gastritis)
Pathogenesis:-
They have direct life cycle
The ingested larva mature in the abomasum and attach themselves
to the mucosa and sucks blood
By piercing the mucosa for blood they cause lacerations predisposing
to gastritis.
Gross lesions:-
Anaemia is manifested by pale mucous membrane and viscera.
Abomasal mucosa reveals shallow ulcers and haemorrhages
Ascites, hydropericardium and hydrothorax.
Hyperplastic changes in the bone marrow.
Clinical signs:-
Anaemia is the most outstanding symptom and is associated with
oedematous swelling under the jaw and ventral abdomen
Diarrhoea with progressive weakness and emaciation results.
Self cure phenomenon might occur due to the animal developing
immunity.
Diagnosis:-
Symptoms
Demonstration of ova
6.Ancylostomiasis (Hook worm disease)
Ancylostomiasis is seen in all animals except in horses and are blood
suckers causing chronic haemorrhagic anaemia.
Etiology:-
A.caninum and A. braziliense in dog and cat
Bunostomum phlebotomum – cattle
B.trigonocephalum – sheep and goat
Pathogenesis, clinical signs and lesions:-
Infected larva released outside, penetrate the skin causing severe
dermatitis
They may even enter through the skin of aberrant host producing a
specific dermatitis ( creeping eruption)
The skin becomes thickened and scaly - 'Cooly's itch,water itch,
ground itch'
The larva reach lungs through veins and break into the alveoli
causing haemorrhages and secondary bacterial infection may lead on
to pneumonia with fibrosis
Larvae are coughed up, swallowed and reach the small intestine
The adult hook worm have buccal tooth like structures and powerful
oesophagus with which it draws bits of inflammatory mucosa into
their buccal cavity damaging the epithelium and sucks blood.
An anticoagulant secreted causes flow of blood even after the worm
changes position.
Bacteria may also enter through the denuded epithelium.
Each parasite may suck 0. 8 to 1ml of blood in 24 hours and the
erythrocyte count may drop to 25 per cent of normal.
Anaemia is hypochromic, microcytic and hyperplasia of the
haematopoietic region are seen
Diarrhoea with dark tarry coloured faeces
Hyperaemia, emaciation and weakness in chronic cases.
Diagonsis:-
Symptoms of bottle jaw condition.
Demonstration of eggs in faeces.
7.Spirocercosis
The bright red coloured Spirocerca lupi adult worms are found in
nodules in the wall of the oesophagus and aorta of dog, fox, wolf and
cat.
Pathogenesis:-
Embryonated eggs passed in the faeces are ingested by intermediate
host, coprophagus beetles in which the larvae develop.
If the beetle is eaten by a transport host such as frog, snake, lizzard
or birds they remain in them
When the infected beetle or transport host is eaten by the final host,
the larvae penetrate the stomach and through blood reach the wall
of the aorta where they localize in the upper thoracic portion
After a period of development, they move to the adjacent
oesophagus and develop in cystic nodules.
Through a small pore in the nodule, the eggs are released into
oesophagus.
Gross and microscopic lesions:-
Principal lesions are produced by the adult worms localized in the
aorta and oesophagus
Nodules on the aortic wall initiates the formation of aneurysm which
may rupture ending in fatal haemorrhges
The intimal surface of the aorta may be roughened
Nodules on the thoracic portion, oesophagus near the cardiac region
of stomach may contain one or several worms.
A granuloma with central worm surrounded by connective tissue and
infiltration of neutrophils, macrophages, lymphocytes, plasma cells
may be observed.
Eosinophils are usually absent.
Exostoses of thoracic vertebrae may be due to the aberrant location
of the larvae
“Fibrosarcoma" and “osteosarcoma" near the spirocercal lesion is
reported to be their metastasis.
Diagnosis:-
Small gelatin capsule shaped eggs with the coiled larva inside
Post mortem demonstration of lesions in the aorta and oesophagus.
8.Thelaziasis
It is present in the conjuctivital sacs of animals.
Etiology:-
Thelazia rhodesii - cattle,buffalo,sheep and goat
T.lacrymalis - Horses
T.callipadea - Dogs
T.leesi - camel
Oxyspirura mansoni - Fowl
The flies are intermediate host for all except oxyspirura mansoni
(host cockroach) which deposits the larvae in the conjuctivital sac of
animals while feeding around eyes.Usually no harm is done but in
heavy infection conjuctivitis and opthalmia is there.
9.Filiariasis
Synonym: Canine filariasis, Heart worm disease
The heart worm Dirofilaria immitis is an important filarid parasite. It
infects dogs, cats, foxes, wolves and rarely other species such as
horses and human.
Etiology:-
Two species Dirofilarai immitis and D.ripens affect dogs.
Pathogenesis:-
They are slender filariad worms.
After copulation, microfilaria are shed which circulate in blood
They are ingested by mosquitoes when they bite the hosts and
development takes place in their body cavities in about 10 days
The infective larvae migrate to the mouth parts of mosquitoe
When this bites a fresh host the infective larvae enter the subcutis
and muscles where they grow for 3 to 4 months
Later they enter the veins and reach the right ventricle where they
may live for many years.
Gross and microscopic lesions:-
Mild infections causes no great damage
Large numbers of the worms cause obstruction to the flow of blood
and so hypertrophy of right ventricle and chronic venous congestion
of the liver, spleen and lungs.
Ascites may result.
Dead worms form emboli and cause pulmonary infarctions.
Worms in the pulmonary arteries may cause fibrosis of the intima
and hypertrophy of the arteries
Microfilaria circulate in the blood do not cause any disturbances.
If they die, small foci of granulomatous inflammation occurs
Immune complex glomerulonephritris is a complication of
dirofilariasis.
Diagnosis:-
Demonstration of microfilaria in the peripheral blood.
ELISA and indirect immunoflouorescent assays, for adults or
microfilarial antigens, are both sensitive.
10.Strongylosis
The adult worms are found in the caecum and large colon of equines.
The life cycle is direct with involving any intermediate host
The large strongyles includes Strongylus vulgaris, S.edentatus and
S.equinus are blood suckers.
While small strongyles are less injurious but are more in number.
Pathogenesis and lesions:-
S. vulgaris
It is double toothed, seen attached to the caecal mucosa
The developing larva migrate into the arterioles (superior mesenteric
artery and aorta)
Along the tract of movement deposits of thrombus is seen and may
occlude the lumen of artery
Thrombosis and aneurysm of aorta and iliac arteries may cause
weakness of hind limbs and severe abdominal pain.
Verminous enteritis and verminous aneurysm are the most common
lesions encountered
S.equinus
It is triple toothed found in caecum and rarely in the colon of
equines.
The ingested larvae penetrate intestine reach blood stream migrate
through liver, heart, lung coughed up swallowed to reach large
intestine
The larvae burrowing through the wall of caecum and colon forms
nodules (worm nests)
S. edentatus
It is toothless.
Adult worms are seen attched to the mucosa of caecum and colon of
equines
The ingested larvae penetrate the wall of ventral colon and gets
encysted in the abdominal wall for a long time
Later they reach the serosa of small intestine where they produce
subserous small raised nodules consisting of a central caseous
necrotic area surrounded by erythrocytes, leucocytes, macrophages
and oedema. Later, the larva penetrate the wall of intestine and
enter the lumen of large intestine
Diagnosis:-
Examine faeces and identify the eggs
Worm burden may be assessed before treating the animal since light
infections do not harm the animals and every animal harbours a few
parasites
11.Tape worm Infection
Tapeworm disease is caused by cestodes and tapeworm infection
causes more damage only in young animals.
MONIEZIASIS AND TAENIASIS
Etiology
M. expansa – Cattle
M. benedini and M. expansa– Sheep and goat
Dipylidium caninum, Taenia pisiformis, T. hydatigena, Multiceps
multiceps, Diphyllobothrium latum – Dogs
Pathogenesis:-
Tape worms cause damage to the host by
Injury and enteritis – by suckers and hooks.
Absortion of the nutrients in gastrointestinal tract
Obstruction and voluulus
Macrocytic anaemia – by d. latum which absorbs vit b12, folic acid
and iron
Clinical signs:-
Diminished appetite and in dogs due to severe irritation of anus
drags themselves sitting on their buttocks.
Lesions:-
The larval stage or bladder worm of the parasite produces more
damage
Cysticercus cellulosae is the bladder worm of Taenia solium in man
which infects shoulder, neck, diaphragm, tongue, intercostal,
abdominal and cardiac muscle of pigs
The affected meat is called 'measly pork'
Cysticercus bovis is the bladder worm of human adult tape worm – T
saginata found in the muscles, liver, heart etc. of cattle
The affected meat is known as ‘measly beef’.
Coenurus cerebralis is the bladder worm of dog tape worm
M.multiceps found in the central nervous system of sheep causing
'Gid'
Cysticercus ovis is the bladder worm of dog tape worm T.ovis seen in
the muscle of sheep and goat
C.tenuicollis is the bladder worm of T. hydatigena found in the
liver,mesentery and omentum of sheep, goat and pigs
Hydatid cysts is the bladder worm stage of genus Echinococcus found
in the liver,lungs and other important organs and the condition is
called as echinococcosis or hydatid disease
Two species of E.granulosus and E.multilocularis occurs. Dogs and
wild carnivors act as a final host of E.granulosus whose larvae occurs
in sheep and it also infect cattle, horse, pig,monkey, rodents and
human and other species.
Foxes, dogs and cats act as a final host of E.multilocularis whose
larvae occurs in various rodents and human.
Diagnosis:-
Examination of eggs or segments of parasites in the faeces
Hydatid cyst can be identified by histopathological examination,
complement fixation test, delayed hypersensitivity test,
haemagglutination tests and fluorescent antibody test.
