2. STRONGYLOSIS
Definition
• 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
3. • 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
4. 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
5. HOOK WORM INFECTIONS
ANCYLOSTOMIASIS
Synonym: Hook worm disease
Definition
• Ancylostomiasis is seen in all animals except in horses and
are blood suckers causing chronic haemorrhagic anaemia.
Aetiology
• A.caninum and A. braziliense in dog and cat
• Bunostomum phlebotomum – cattle
• B.trigonocephalum – sheep and goat
6. 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
Haemorrhagic enteritis
8. BUNOSTOMIASIS
Synonym : Hook worm disease
Definition
• Hook worm disease of cattle, sheep and pigs caused by
Bunostomum sp. present in the small intestine characterized by
poor growth and blood loss with anaemia and anasarca.
Aetiology
• Bunostomum phlebotomum -Cattle
• Bunostomum trigonocephalum –Sheep
Incidence
• Calves 4-12 months of age are most commonly affected and it is
more in winter months
9. Life cycle
• Life cycle is direct
• The egg hatch and larva is produced.
• The larvae enter through the skin and also through the mouth.
• After skin penetration, enter the blood stream
• Then carried to the heart, lungs, enter the alveoli where the fourth
stage larvae develop
• The larvae moved to the pharynx, are swallowed and reach
intestine
• The larvae then penetrate the intestinal wall and return to its lumen
without further migration
• The prepatent period of B.phlebotomum is about 8 months
10. Pathogenesis
• Hookworms are blood suckers and cause severe anaemia
• More number of worms are present may cause death in young cattle
• Hypoproteinaemic oedema and mild or intermittent diarrhoea
Clinical signs
• Constipation, unthrifty and anaemia
• In severe infestations, pale mucous membrane, anasarca under the jaw and along the belly,
prostration and death in 2 to 3 days in cattle
Gross lesions
• Worms are found in the first few feet of the small intestine
• Deeply blood stained intestinal contents
• In calves, 100 or more worms present in the intestine, suggest a significant level of infestation
• Over 2000 worms, indicates degree of infestation likely to be fatal
Diagnosis
• Demonstration of blunt ends and deeply pigmented embryonic cells of hookworm eggs in the
faeces
11. HAEMONCHOSIS
Definition
• Under the family of Trichostrongyloidea, Haemonchus contortus is the worm seen
in the abomasum of cattle, sheep and goat.
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
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
12. 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.
Diagnosis
• Symptoms
• Demonstration of ova
13. SPIROCERCOSIS
Definition
• 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
Clinical signs
• Oesophagel obstruction may cause persistent vomition
• Sudden death due to rupture of aortic wall
14. 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.
Sprocercosis-Dog- Worm with eggs
15. Diagnosis
• Small gelatin capsule shaped eggs with the
coiled larva inside
• Post mortem demonstration of lesions in the
aorta and oesophagus
16. DIROFILARIASIS
Synonym: Canine filariasis, Heart worm disease
Definition
• 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
Aetiology
• Two species Dirofilarai immitis and D.ripens affect dogs, foxes, cats etc.
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
17. 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
18. Diagnosis
• Demonstration of microfilaria in the
peripheral blood
• ELISA and indirect immunoflouorescent
assays, for adults or microfilarial antigens, are
both sensitive
Dog - Microfilaia in peripheral blood
19. SETARIASIS
Definition
• Filariad worms of the genus Setaria are commonly found in the peritoneal cavity of
most domestic animals
Aetiology
• Setaria digitata a parasite of the peritoneal cavity of cattle causes cerebrospinal
nematodiasis
Pathogenesis
• Usually neither the adults nor the circulating microfilariae cause serious disease
• The parasites are found in the pleural cavity or eye
• It is a parasite of the peritoneal cavity of cattle causes cerebrospinal nematodiasis
when it invades into the central nervous system of other animal species such as
sheep, goat and horses and cause paralysis and blindness
20. Clinical signs
• Incordination, weakness and paralysis
• In sheep and goats this is known as lumbar
paralysis and in horses ‘ kumri’( weakness of
loin). The disease is prevalent in India
• In young horses and mules of one to two years of
age, animals move with difficulty and on motion
sway (wobble) from side to side.
• They may fall frequently and show difficulty in
rising which might be due to trauma of spinal
cord at the cervical region
21. Gross and microscopic Lesions
• Lesions are found in the brain and spinal cord and the severity
depends on the number of parasites present
• Narrow tortuous tracks of haemorrhages and softening may be
found denoting the path taken by the parasite
• Immature worms wander randomly throughout the brain leaving
necrotic paths
• Bilateral symmetrical areas of malacia
• Gitter cells and infiltration of eosinophils and neutrophils surround
the tracts
Diagnosis
• Careful microscopic examination of the central nervous system
tissue and cerebrospinal fluid is necessary to see the larvae
22. COCCIDIOSIS
Definition
• Coccidiosis is an acute or chronic haemorrhagic enteritis affecting cattle,
rabbit and poultry characterized by invasion and destruction of intestinal
epithelium, diarrhoea, dysentry caused by coccidia
Aetiology
• Eimeria zurnii and E.bovis - caecum, colon and ileum of cattle
• E.arloingi –Small intestine of sheep and goat
• E.canis and Isospora bigemina – Small intestine dog and cat
• E.stiedae – Intra hepatic bileduct of rabbit
• E.tenella – caecum of fowl
• E.necatrix – Small intestine of fowl
• Eimeria burneti -Rectal coccidiosis
• E.debleicki and Isospora suis- Small intestine of swine
• E.truncata - Renal tubule of geese
23. Pathogenesis and life cycle
• Oocyst which are the resistant, mature coccidia are voided
in faeces
• Inside oocysts, sporozoites develops which is ingested by a
susceptible animal
• The sporozoites escape out of oocyst and invade the
intestinal epithelium and multiply asexually called
schizogony, forming merozoites
• Later, asexual multiplication stops and merozoites
differentiates into male (microgametocyte) and female
(macrogametocyte).
• The union of these two produces oocyst which ruptures
epithelium and is passed out by the faeces.
Eimeria sp.- Oocyst
24. Clinical signs
• Dysentry with tenesmus leading on to anaemia,
dehydration and emaciation
Lesions
• The harm done to the host by the destruction of epithelial
cells
• The surviving epithelium proliferate and hyperplasia
manifested by enlargement of villi which may show
papillary projections and these cells are full of parasites
• Mucous membrane is thickened, oedematous, denuded
and haemorrhagic
25. In rabbits
• E.stiedae affects intrahepatic biliary epithelium of rabbits
• Cocidiosis of liver or intestine may be observed
• Liver is studded with small to larger nodules which may be
round and grey in colour
• The liver is necrosed with nodules containing large number
of coccidia.
• In the early lesions, there is a destruction of biliary
epithelium but when the course of the disease is longer,
proliferation of the epithelium is the main feature and this
may be thrown into papillary folds resembling
adenomatous hyperplasia
Hepatic coccidiosis- Oocysts and schizonts
were seen
26. In birds
• Mortality may be 90 – 100%
• E. tenella is most pathogenic
Diagnosis
• Dysentry with straining
• Demonstration of oocysts in the faeces and
tissue sections.
27. BABESIOSIS
Synonym : Piroplasmosis, tick fever
Definition
• Babesia occurs in erythrocytes, destroy them
giving rise to fever, anaemia, jaundice and
haemoglobinuria
Aetiology
• Babesia sp.
28. Incidence
• In cattle, severity of infection also depends on the
breed. Bos indicus breeds are relatively resistant
because of their resistance to heavy infestations
with ticks
• The disease may have seasonal incidence if the
tick population varies with climate
Transmission
• Ticks are the intermediate hos
29. Cattle (Bovine piroplasmosis, tick fever, texas
fever or red water)
• It is a an acute or chronic disease of cattle and
buffaloes characterized by fever,
haemoglobinuria caused by B.bigemina, B.
bovis etc.
• B.bigemina is the most common in India and
occurs in the erthrocytes as pear shaped
forms in pairs.
Babesia bigemina-Pear shaped forms in pairs
30. Pathogenesis
• Multiplication is by cell division during which it destroys the
host cells and invade another causing haemoglobinaemia,
haemoglobinuria
• The vector is : Boophilus annulatus
Clinical signs
• The clinical manifestation are variable. The common signs
being fever, anorexia, depression initially and icterus,
haemoglobinuria and ascites later
• Haemolytic anaemia is manifested by thin watery blood
with a fall in haemoglobin, erythrocytes and packed cell
volume
31. Gross lesions
• Emaciated carcass with oedema, haemorrhages in subcutaneous,
subserous and intramuscular regions.
• Spleen and liver are enlarged. Gall bladder distended with dark
green bile
Microscopic lesions
• Haemoglobinuric nephrosis also known as lower nephron
nephrosis, centrilobular and paracentral necrosis of the liver,
oedema, excess fluid in the peritoneal, pericardial and pleural
cavities
• Babesia can be demonstrated in capillaries in the brain
• Equine babesiosis is caused by B.caballi and B. equi of which the
latter is more pathogenic
32. • Canine babesiosis is caused by B.canis and
B.gibsoni
• B.canis is larger and haemoglobinuria is
constant while B.gibsoni is smaller and chronic
form of disease with haemoglobinuria and
jaundice are not seen
B.canis-Larger pear shaped
B.gibsoni-Smaller and ring form
33. Babesiosis in sheep and goats
– B.motasi is longer and virulent
– B. ovis causes a less severe conditon.
• Babesia are easily differentiated from
Plasmodium sp. by the absence of
haemoglobin derived pigment. Babesia
completely catabolize haemoglobin whereas
plasmodium retain the brownish pigment
(Haemozoin)
34. Immune response in Babesia
• The sporozoites attack red blood cells. This invasion involves
activation of the alternate complement pathway. Infected
erythrocytes incorporate babesia antigen into their membranes.
These, in turn induce antibodies which opsonize the red cells and
lead to their removal by the mononuclear phagocyte system. In
addition to the humoral response, infected red blood cells may also
be destroyed by antibody dependent cell mediated cytotoxicity
(ADCC). The babesia antigen-opsonizing antibody complex on the
surface of infected erythrocytes can be recognized by macrophages
and cytotoxic lymphocytes
• Premunition is a form of immunity that is dependent on the
continued presence of parasite in the host. The resistance that is
established after the primary infection has become chronic
35. Diagnosis
• Indentification of babesia in blood smears
• Enzyme immunoassay
• ELISA
• DNA probes are also used to detect specific
parasitaemias at very low levels of infection
36. THEILERIOSIS
Definition
• Theileriosis is an acute disease of cattle characterized by high fever,
swelling of the superficial lymph gland, rough hair coat, salivation,
respiratory distress caused by various species of Theileria
Aetiology
• Theileria parva – causes East coast fever in Africa, not recorded in
India
• T.lawrencei affects cattle and buffaloes and causes Buffalo disease
in Africa
• T.annulata is seen in India
• T.mutans is seen in India without any symptoms
37. Transmission
• It is transmitted through ticks
Pathogenesis
• Theileria may appear as rod shaped, coma shaped or ring shaped
forms.
• Schizogony takes place in lymphocytes and monocytes
• It is transmitted through ticks and on entry into blood of host infect
lymphocytes and monocytes of blood, lymph gland and spleen
where they develop
• The schizonts are called koch’s blue bodies and are pathognomonic
of the disease and may be seen in biopsy material from lymph
gland. Following break up of koch's blue bodies they enter
erythrocytes
38. Gross lesions
• Enlargement of the lymph nodes, white foci of various sizes in renal cortex
and punched out ulcers in the abomasum.
• Pulmonary oedema, emphysema, subcutaneous and intramuscular
oedema and excessive pericardial and pleural fluid, spleen may be
enlarged, enlarged liver
• Meninges may be congested and focal haemorrhages are seen in the brain
• Respiratory distress may follow pulmonary oedema and death may be
result from asphyxia
Microscopic lesions
• Proliferation of lymphatic cells in the lymph nodes, spleen and peyer’s
patches may be observed with the presence of koch's blue bodies
• Effect of anaemia is evident in bone marrow
39. Immune mechanisms
• Animal that survive an infection have a solid immunity
• The parasite can invade both T cells and B cells
• The parasite then triggers certain pathways result in the
production of interleukin 2 and its receptors.
• The schizont stage of Theileria develops within the
lymphocyte, the infected lymphocytes enlarge to form
lymphoblasts and begin to proliferate.
• Since the parasite divides along the host cell, this leads to
very rapid clonal expansion of parasitized cells. In most
cattle, this results in overwhelming infection and death.
• Cytotoxic CD 8+ cells kill infected lymphoblasts.
40. Diagnosis
• Demonstration of the organisms in the
erythrocytes and lymphocytes (Koch's blue
bodies)
• ELISA test is being used increasingly for
seroepidemiological studies
