Veterinary Parasitology 100 Quiz

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#1. Which of the following is considered the pathognomonic gross pathological lesion of chronic hepatic fasciolosis in cattle, characterized by calcification and thickening of the bile duct walls?💡 Click for ExplanationIn chronic cases of Fasciola hepatica/gigantica in cattle, the constant irritation by the flukes leads to severe thickening and fibrosis of the bile ducts, followed by calcium deposition. This makes the bile ducts prominent, hard, and white, resembling the stems of clay pipes, a condition classically known as ‘pipe stem liver’ or ‘piped stem liver’.

Morocco leather liver

Pipe stem liver

Nutmeg liver

Milky white spotted liver

#2. Acute fasciolosis in sheep and goats is primarily caused by which of the following processes?💡 Click for ExplanationAcute fasciolosis is essentially a traumatic hepatitis occurring 6 to 8 weeks post-infection, caused by the burrowing and migration of a large number of immature flukes through the liver parenchyma. This causes extensive tissue destruction, rupture of the liver capsule, severe parenchymal hemorrhages, and often sudden death.

Severe calcification of the major bile ducts and gallbladder

The mechanical damage and hemorrhages caused by the simultaneous migration of large numbers of immature flukes through the liver parenchyma

Extensive egg deposition in the portal vein leading to portal hypertension

Severe enteritis due to immature flukes plucking the intestinal mucosa

#3. In veterinary medicine, what is the estimated volume of host blood ingested daily by a single adult Fasciola fluke within the bile ducts?💡 Click for ExplanationStudies on the pathophysiology of fasciolosis demonstrate that adult liver flukes are active hematophages inside the bile ducts. A single adult fluke (Fasciola spp.) sucks blood from the host’s biliary capillaries at an average rate of approximately 0.2 ml per day, contributing significantly to the development of microcytic hypochromic anemia.

0.05 ml

0.2 ml

0.8 ml

1.5 ml

#4. During urine analysis of an animal suffering from clinical fasciolosis, which of the following biochemical profiles is expected?💡 Click for ExplanationIn clinical fasciolosis, bile ducts are occluded by adult flukes, causing obstructive jaundice. This prevents bilirubin from entering the intestine, meaning no urobilinogen is formed (urobilinogen test is negative). However, conjugated bilirubin regurgitates into the blood and is excreted in the urine, making the test for bile pigment positive.

Bile pigment test is positive, and urobilinogen test is negative

Bile pigment test is negative, and urobilinogen test is positive

Both bile pigment and urobilinogen tests are highly positive

Both bile pigment and urobilinogen tests are completely negative

#5. Which of the following anthelmintics is highly specific and uniquely effective against very young, immature Fasciola flukes (1 to 6 weeks old) in ruminants?💡 Click for ExplanationDiamphenitide (administered @ 100 mg/kg b.wt. orally) is a highly unique fasciolicide because it possesses exceptional efficacy against very young immature flukes (from 1 to 6 weeks of age) migrating through the liver parenchyma, whereas most other standard drugs like oxyclozanide or carbon tetrachloride are only effective against mature flukes.

Carbon tetrachloride

Rafoxanide

Oxyclozanide

Diamphenitide

#6. Which fluke has a life cycle involving two intermediate hosts—a terrestrial snail as the first and the brown ant (Formica fusca) as the second—and is transmitted when the final host ingests ants containing metacercariae?💡 Click for ExplanationDicrocoelium dendriticum (the lancet fluke) has a unique land-based life cycle. The first intermediate host is a land snail, which voids cercariae in ‘slime balls’. These are eaten by the second intermediate host, the ant Formica fusca, where they develop into metacercariae (some migrate to the subesophageal ganglion, altering the ant’s behavior to stay on grass tips). The host is infected by ingesting these ants.

Fasciola gigantica

Dicrocoelium dendriticum

Schistosoma nasale

Gigantocotyle explanatum

#7. In ruminant amphistomiasis, where are the mature and immature stages of the flukes respectively located within the host?💡 Click for ExplanationThe adult amphistomes (stomach flukes) reside in the rumen and reticulum where they attach to the mucosa and are considered relatively non-pathogenic. However, the immature flukes migrate and reside in the duodenum and small intestine, where they cause severe mechanical damage, enteritis, and clinical disease.

Mature flukes in the liver; immature flukes in the bile ducts

Mature flukes in the abomasum; immature flukes in the small intestine

Mature flukes in the rumen and reticulum; immature flukes in the duodenum and small intestine

Mature flukes in the portal veins; immature flukes in the nasal cavity

#8. What is the primary pathogenic mechanism responsible for the high morbidity and mortality (up to 40-60%) seen in acute immature amphistomiasis in young ruminants?💡 Click for ExplanationThe immature amphistomes in the duodenum attach to the mucosal lining using their powerful posterior suckers, drawing and plucking plugs of the mucosa. This leads to extensive necrosis, mucosal sloughing, severe hemorrhagic enteritis, profuse foul-smelling diarrhea, hypoproteinemia (leakage of plasma proteins), severe dehydration, shock, and death.

Severe calcification of the ruminal wall leading to indigestion

Immature flukes attaching to the duodenal mucosa and plucking mucosal plugs, causing severe hemorrhagic enteritis and protein loss

Complete blockage of the bile duct leading to liver failure

Migration of the young flukes into the cerebral capillaries causing encephalitis

#9. Which of the following drugs is highly effective and widely considered the drug of choice for the treatment of clinical immature amphistomiasis in cattle and sheep?💡 Click for ExplanationNiclosamide (administered @ 90-100 mg/kg b.wt. orally after overnight fasting) is highly effective and considered the premier drug of choice against the highly pathogenic immature amphistomes present in the small intestine, whereas drugs like carbon tetrachloride are mostly limited to mature rumen flukes.

Niclosamide

Carbon tetrachloride

Levamisole

Piperazine

#10. What is the specific etiological agent of nasal schistosomiasis (nasal granuloma or snoring disease) in cattle, and where does it localize?💡 Click for ExplanationNasal schistosomiasis (snoring disease) is caused by the blood fluke Schistosoma nasale (previously Schistosoma nasalis). The adult male and female worms live in copula within the nasal veins of the nasal cavity of cattle, buffaloes, and occasionally sheep and goats.

Schistosoma spindale in the mesenteric veins

Schistosoma bovis in the portal veins

Schistosoma nasale in the nasal veins of the nasal cavity

Schistosoma indicum in the pelvic veins

#11. In puppies, what is the most common and clinically significant mode of transmission for Toxocara canis that leads to heavy infection at birth?💡 Click for ExplanationThe most important transmission routes for Toxocara canis in young puppies are prenatal (transplacental) migration of third-stage larvae from the pregnant bitch to the fetal lungs, and transcolostral/transmammary transmission where larvae are shed in the colostrum/milk for up to 3 to 4 weeks postpartum.

Ingestion of sporulated eggs from the soil

Ingestion of paratenic hosts like earthworms

Prenatal/transplacental transmission of migrating larvae from the dam, as well as transcolostral/transmammary transmission

Percutaneous penetration of the skin by infective L3 larvae

#12. Somatic larval migration of Toxocara canis in adult dogs and bitches is characterized by which of the following features?💡 Click for ExplanationIn dogs older than 5 weeks, and especially in adult dogs, larvae of T. canis fail to complete the tracheal migration pathway. Instead, they enter the systemic circulation and undergo somatic migration, distributing into various organs (liver, muscles, brain) where they remain dormant as hypobiotic larvae until reactivated during pregnancy.

Larvae continuously migrate through the trachea and are coughed up and swallowed to mature in the gut

Larvae fail to undergo tracheal migration; instead, they migrate into somatic tissues (liver, heart, kidneys, muscles) and remain dormant as dormant third-stage larvae

Larvae migrate directly to the esophagus and form fibrous nodules

Larvae undergo sexual reproduction in the liver parenchyma

#13. A necropsy of a growing pig reveals multiple fibrotic, milky-white focal lesions on the liver capsular surface, commonly described as ‘milky white spots’. This lesion is pathognomonic for the migration of which parasite?💡 Click for ExplanationThe ‘milky white spotted liver’ is a classic pathognomonic lesion in swine caused by the migration of Ascaris suum larvae. As the larvae migrate from the portal vein through the hepatic parenchyma, they cause focal tissue damage and necrosis. This resolves as chronic granulomatous inflammation and focal fibrosis, appearing as white spots.

Stephanurus dentatus

Trichinella spiralis

Ascaris suum

Metastrongylus apri

#14. During the lung migration phase of Ascaris suum in young pigs, what is the characteristic clinical syndrome produced?💡 Click for ExplanationThe migration of large numbers of Ascaris suum larvae through the pulmonary capillaries into the alveoli causes severe tissue damage, alveolar hemorrhages, and interstitial pneumonia. This results in a clinical respiratory syndrome in piglets known as ‘thumps’, characterized by rapid, shallow, spasmodic breathing and double expiratory efforts.

Louder, deep snoring sounds

'Thumps' - characterized by severe dyspnea with rapid, spasmodic raising and falling of the rib cage

Chronic dry coughing only during the night

Bilateral purulent ocular discharge

#15. Severe adult Ascaris suum infection in pigs can sometimes lead to which of the following post-mortem or clinical findings, apart from intestinal blockage?💡 Click for ExplanationAdult Ascaris suum worms are notorious for wandering from their normal habitat in the small intestine. They frequently enter the duodenum and crawl up the common bile duct, causing complete mechanical blockage. This leads to biliary stasis, liver damage, and the development of severe obstructive jaundice.

Hypertrophic pulmonary osteoarthropathy of the long bones

Migration of adult worms into the bile ducts, causing biliary stasis and obstructive jaundice

Thickening of the abomasal wall giving a Morocco leather appearance

Development of coenurus cysts in the brain

#16. Which of the following hookworm species is the primary cause of severe ancylostomosis in dogs, possessing three pairs of sharp ventral teeth in its well-developed buccal capsule?💡 Click for ExplanationAncylostoma caninum is the highly pathogenic hookworm of dogs. It is characterized morphologically by a large, wide-open buccal capsule containing three pairs of sharp ventral teeth that it uses to bite and attach to the small intestinal mucosa to suck blood.

Ancylostoma braziliense

Ancylostoma tubaeforme

Ancylostoma caninum

Uncinaria stenocephala

#17. What is the primary physiological mechanism by which Ancylostoma caninum causes severe, life-threatening anemia in young puppies?💡 Click for ExplanationAncylostoma caninum is a highly destructive blood-sucker, with each adult worm capable of ingesting up to 0.8 ml of blood per day. The worms constantly change attachment sites and secrete a powerful anticoagulant that prevents clotting, leading to persistent hemorrhaging from the vacated bites, culminating in severe anemia and hypoproteinemia.

By destroying the erythropoietin-producing cells in the kidneys

By actively sucking blood (up to 0.8 ml per worm daily) and producing an anticoagulant that leads to continuous hemorrhage from attachment sites

By suppressing the bone marrow directly via toxic excretions

By causing intravascular hemolysis through autoimmune antibody production

#18. What is the etiological agent of canine spirocercosis, and what is its characteristic physical appearance in fresh specimens?💡 Click for ExplanationSpirocerca lupi (the esophageal worm of dogs) is a highly distinctive nematode. In fresh necropsy specimens, the worms are bright red or pinkish in color, and their body is typically coiled in a spiral or circular shape.

Dirofilaria immitis, which is long, white, and hair-like

Spirocerca lupi, which is bright red or pinkish in color and spirally coiled

Toxocara canis, which is large, white, and translucent

Ancylostoma caninum, which is small and gray-colored with a hooked anterior end

#19. Which of the following outlines the complex larval migration pathway of Spirocerca lupi within the canine host?💡 Click for ExplanationSpirocerca lupi has a unique migration. The infective L3 larvae are released in the stomach, penetrate the gastric mucosa, and migrate within the walls of the gastric and gastro-epiploic arteries to the coeliac artery, and then to the aorta. After developing in the aortic wall, they migrate across the connective tissue space (tunneling) to the adjacent esophageal wall.

Ingested larvae penetrate the stomach wall → coeliac artery → aorta → tunnel to the esophageal wall

Ingested larvae penetrate the intestinal mucosa → portal vein → liver → lungs → trachea → reswallowed to esophagus

Ingested larvae penetrate the skin → cutaneous veins → vena cava → right heart → lungs

Ingested larvae remain in the stomach mucosa and develop locally without migrating

#20. Which of the following neoplastic conditions is classically associated as a direct sequela of chronic Spirocerca lupi infection in dogs?💡 Click for ExplanationSpirocerca lupi is one of the few helminths proven to be oncogenic. The persistent irritation and chronic granulomatous inflammation induced by the adult worms in the esophageal wall can trigger a neoplastic transformation of the local connective tissue, leading to the development of highly malignant esophageal fibrosarcomas or osteosarcomas.

Hepatic cholangiocarcinoma

Esophageal fibrosarcoma or osteosarcoma

Pulmonary adenocarcinomatosis

Gastric adenocarcinoma

#21. In dogs, Spirocerca lupi infection often leads to hypertrophic osteopathy (also known as hypertrophic pulmonary osteoarthropathy or Marie’s disease). What is the main clinical manifestation of this condition?💡 Click for ExplanationHypertrophic osteopathy (HPOA) is a common paraneoplastic or neurogenic sequela of S. lupi. It is characterized by progressive, bilateral, non-edematous periosteal thickening and new bone formation along the diaphyses of the long bones of the limbs, causing swelling, pain, and lameness.

Severe osteoporosis of the skull bones

Extensive periosteal new bone formation and thickening of the long bones of the limbs

Complete ankylosis of the cervical vertebrae

Severe atrophy and necrosis of the skeletal muscles

#22. In canine heartworm disease, a hyperacute, life-threatening clinical syndrome known as ‘Caval Syndrome’ (or vena cava syndrome) develops under which of the following circumstances?💡 Click for ExplanationCaval Syndrome is a critical, acute phase of heartworm disease. It occurs when a large burden of adult worms moves from the pulmonary arteries into the right atrium and vena cava. This obstructs blood flow, causes severe tricuspid valve insufficiency, massive mechanical destruction of RBCs (hemoglobinuria), acute icterus, hepatic/renal failure, and rapid cardiovascular collapse.

When larvae migrate into the cerebral ventricles, causing sudden coma

When a massive volume of adult worms backs up and obstructs the posterior vena cava and right atrium, leading to acute tricuspid regurgitation, intravascular hemolysis, and hepatic/renal failure

When a single worm ruptures inside the aorta, causing anaphylactic shock

When microfilariae clog the glomerular capillaries, causing acute renal shut-down

#23. Which of the following lungworms is the primary etiological agent of verminous bronchitis (‘husk’ or ‘hoose’) in young calves, causing consolidations and emphysema?💡 Click for ExplanationDictyocaulus viviparus is the highly pathogenic lungworm of cattle and buffaloes. It infects the trachea, bronchi, and bronchioles, causing verminous bronchitis, atelectasis, emphysema, and a characteristic spasmodic coughing syndrome known as ‘husk’ or ‘hoose’.

Dictyocaulus filaria

Dictyocaulus viviparus

Metastrongylus apri

Protostrongylus rufescens

#24. In bovine parasitic gastroenteritis (PGE), chronic infection with Ostertagia ostertagi produces a highly characteristic gross abomasal mucosal lesion described as:💡 Click for ExplanationThe larval stages of Ostertagia ostertagi invade and develop within the gastric glands of the abomasum. This causes severe proliferation and hyperplasia of the surrounding mucosal epithelial cells, resulting in the formation of thousands of small, circular nodules (2-3 mm) with a central opening. Collectively, this gives the abomasal mucosa a classic ‘Morocco leather’ or ‘cobblestone’ appearance.

White 'milky spot' granulomas

Punched-out 'button-like' necrotic ulcers

'Morocco leather' or 'cobblestone' appearance due to numerous hyperplastic mucosal nodules

Thin, branching 'pipe stem' tracts

#25. Which of the following gastrointestinal nematodes is classically known as the ‘barber’s pole worm’ or ‘wire worm’ of ruminants, residing in the abomasum and causing severe anemia?💡 Click for ExplanationHaemonchus contortus is known as the ‘barber’s pole worm’ because the white, ovaries-filled uterus wraps spirally around the blood-filled intestine in the female worm, resembling a barber’s pole. It lives in the abomasum of sheep, goats, and cattle, sucking blood.

Trichostrongylus axei

Ostertagia ostertagi

Haemonchus contortus

Oesophagostomum columbianum

#26. Which of the following represents the largest tapeworm of ruminants (sheep, goats, cattle) caused by ingestion of Oribatid mites containing cysticercoids?💡 Click for ExplanationMoniezia expansa (in sheep) and Moniezia benedini (primarily in cattle) are large, broad cestodes that can measure up to 600 cm (6 meters) in length. Ruminants get infected by ingesting the intermediate host—free-living Oribatid mites on pasture—which harbor the infective cysticercoid stage.

Taenia hydatigena

Moniezia expansa

Stilesia globipunctata

Thysanosoma actinioides

#27. What is the etiological agent of the common double-pored dog tapeworm, and which vectors serve as the intermediate hosts in its life cycle?💡 Click for ExplanationDipylidium caninum is the double-pored tapeworm of dogs and cats. Its life cycle requires an arthropod intermediate host, primarily the dog and cat fleas (Ctenocephalides canis and C. felis) or the biting louse (Trichodectes canis). Pups get infected by swallowing these insects during grooming.

Taenia ovis; intermediate host is sheep

Dipylidium caninum; intermediate hosts are fleas (Ctenocephalides spp.) and the dog louse (Trichodectes canis)

Echinococcus granulosus; intermediate host is wild rodents

Diphyllobothrium lotum; intermediate hosts are copepods and fish

#28. The clinical condition known as ‘Gid’, ‘staggers’, or ‘turnsugar’ in sheep is caused by the space-occupying fluid-filled larval cyst of which canine tapeworm in the brain?💡 Click for ExplanationGid (or staggers) is caused by Coenurus cerebralis, the larval stage of the canine tapeworm Taenia multiceps. When sheep ingest T. multiceps eggs, the oncospheres migrate to the central nervous system (brain and spinal cord) and develop into large, fluid-filled coenurus cysts. These exert severe pressure on the brain parenchyma, destroying tissue and causing characteristic circling, head tilting, staggering, and blindness.

Cysticercus tenuicollis (larva of Taenia hydatigena)

Coenurus cerebralis (larva of Taenia multiceps)

Hydatid cyst (larva of Echinococcus granulosus)

Cysticercus ovis (larva of Taenia ovis)

#29. Which of the following defines the morphology and developmental characteristics of the larval stage of the tiny canine tapeworm, Echinococcus granulosus, in its intermediate hosts?💡 Click for ExplanationThe larval stage of Echinococcus granulosus is the hydatid cyst. It is a highly complex, slow-growing structure with a thick outer cuticular layer and an inner germinal layer. This germinal layer buds off brood capsules, each containing numerous infective scolices (hydatid sand), suspended in hydatid fluid.

Coenurus cyst, which is a large cyst with a single invaginated scolex

Hydatid cyst, which is a slow-growing, fluid-filled cyst containing an inner germinal layer that buds off 'brood capsules' containing multiple infective scolices

Cysticercus cellulosus, which is a small vesicle with a single head

Plerocercoid, which is a solid, worm-like larval form

#30. Which tiny poultry tapeworm (measuring less than 4 mm in length) is highly pathogenic to young chickens, utilizing land slugs as intermediate hosts, and causes severe hemorrhagic enteritis?💡 Click for ExplanationDavainea proglottina is a minute but highly pathogenic tapeworm of poultry. It lives deep within the duodenal mucosa, utilizing slugs as intermediate hosts. Its active movements and attachment cause severe necrosis and hemorrhagic enteritis, leading to high mortality.

Amoebotaenia cuneata

Choanotaenia infundibulum

Davainea proglottina

Raillietina echinobothrida

#31. Apart from blood loss and disease transmission, certain female hard ticks can induce a severe neurological condition in livestock and dogs known as ‘Tick Paralysis’. What is the primary cause of this condition?💡 Click for ExplanationTick paralysis is a non-infectious, toxic, progressive neurological disease. It is caused by a neurotoxin secreted in the saliva of certain engorging female ticks (like Dermacentor or Rhipicephalus species) during a blood meal. The toxin inhibits acetylcholine release at neuromuscular junctions, leading to a classic flaccid, ascending motor paralysis that starts in the hindlimbs and progresses cranially.

Blockage of the spinal cord capillaries by migrating larval ticks

Injection of a salivary neurotoxin produced in the tick's ovaries during engorgement, which blocks acetylcholine release at the neuromuscular junction, causing ascending motor paralysis

Severe calcium and magnesium depletion in the host's blood

Autoimmune destruction of the host's myelin sheath

#32. Which tick-borne metabolic/systemic disturbance, classically transmitted by Hyalomma truncatum, is characterized by profuse, generalized moist eczema, shedding of fleece, and high mortality in calves?💡 Click for ExplanationSweating sickness is a highly acute, tick-produced disease of cattle, sheep, and pigs, particularly calves. It is caused by a epitheliotropic toxin injected by the tick Hyalomma truncatum. Clinical signs are characterized by high fever, hyperemia of visible mucous membranes, hyperesthesia, and a profuse, moist, generalized eczema with a sweetish, sickly odor, leading to skin necrosis and fleece/hair loss.

Sweating sickness

Red water fever

Tick pyemia

Gid

#33. In veterinary entomology, how are sucking lice (such as Haematopinus and Linognathus) primarily differentiated from chewing/biting lice (such as Damalinia and Bovicola)?💡 Click for ExplanationThis morphological distinction is highly important. Sucking lice (Anoplura) feed on the host’s blood and lymph, possessing a pointed head narrower than the thorax. Chewing/biting lice (Mallophaga) have a broad, rounded head wider than the thorax and feed on skin scales, scabs, and hair, causing intense pruritus but not anemia.

Sucking lice are only found on dogs, while biting lice are found on ruminants

Sucking lice have a narrow head that is narrower than the thorax and possess piercing-sucking mouthparts to feed on blood/lymph, whereas chewing lice have a broad head (wider than the thorax) and feed on epidermal debris

Sucking lice are microscopic mites, while biting lice are macroscopic flies

Sucking lice undergo indirect life cycles involving snails, while biting lice have direct cycles

#34. Which of the following mange mites is a burrowing mite that excavates deep tunnels within the stratum corneum of the epidermis, and is characterized morphologically by having short legs with long, unsegmented pedicels?💡 Click for ExplanationSarcoptes scabiei is the classic burrowing mange mite. The fertilized female uses its sharp mouthparts to burrow into the epidermis, feeding on tissue fluids and laying eggs in tunnels. Morphologically, Sarcoptes has short legs, and its anterior two pairs of legs in females (all legs in males) terminate in pretarsi with long, unsegmented pedicels.

Psoroptes ovis

Sarcoptes scabiei

Demodex canis

Chorioptes bovis

#35. Which non-burrowing mange mite is highly contagious and responsible for the highly destructive disease ‘Sheep Scab’, and is morphologically characterized by long legs with three-segmented pedicels?💡 Click for ExplanationPsoroptes ovis is the cause of ‘Sheep Scab’, a highly severe, contagious disease. The mites are non-burrowing and feed superficially on the skin, causing severe exudative dermatitis, crusting, intense pruritus, and loss of wool. Morphologically, Psoroptes has long, prominent legs, and its pretarsi possess long, three-segmented pedicels.

Sarcoptes scabiei

Psoroptes ovis

Chorioptes bovis

Otodectes cynotis

#36. Which of the following mange mites has a unique elongated, cigar-like or alligator-like appearance and resides within the hair follicles and sebaceous glands of domestic animals?💡 Click for ExplanationDemodex species (such as Demodex canis) are highly unique follicular mites. Morphologically, they are small (0.2-0.3 mm), elongated, cigar-shaped mites with short, stubby legs on the anterior part of the body, adapted for living inside hair follicles and sebaceous glands.

Notoedres cati

Demodex canis

Otodectes cynotis

Cnemidocoptes mutans

#37. A cat presents with intense head shaking, ear scratching, and a diagnostic bilateral accumulation of copious, dark brown-to-black crumbly ear wax (‘coffee-ground’ discharge) within the external auditory canals. What is the etiological agent?💡 Click for ExplanationOtodectes cynotis is the ear mite of dogs and cats. It infests the external ear canal, feeding on tissue fluids and inducing a hypersensitivity reaction characterized by intense pruritus and the production of a copious, dark, crumbly ceruminous discharge resembling coffee grounds.

Notoedres cati

Otodectes cynotis

Sarcoptes scabiei

Demodex cati

#38. The highly destructive condition known as ‘obligatory cutaneous myiasis’ in domestic animals in Asia, Africa, and the Middle East is primarily caused by the larvae of which blowfly species?💡 Click for ExplanationChrysomya bezziana (the Old World screw-worm fly) is an obligatory parasite of warm-blooded animals in Africa and Asia. The adult female flies lay eggs strictly on fresh, living wounds. The hatched larvae (maggots) burrow deep into the living tissue, causing massive liquefaction necrosis and cavernous lesions.

Lucilia cuprina

Chrysomya bezziana

Cochliomyia hominivorax

Musca domestica

#39. During the clinical examination of a deep, necrotic wound on a calf, which of the following larval characteristics would confirm a Chrysomya bezziana infestation?💡 Click for ExplanationChrysomya bezziana (screw-worm) larvae have a classic wood-screw appearance. Mature third-instar larvae are 1-2 cm long, pinkish, with rows of dark spines on the anterior of each segment. A key diagnostic feature is the presence of two dark, heavily-pigmented main tracheal trunks running forward from the posterior spiracles along the dorsal surface.

Tiny, transparent, round larvae with no visible spines

Mature pinkish larvae (1-2 cm long), pointed anteriorly and blunt posteriorly, with prominent bands of dark fine spines on each segment and two dark parallel tracheal trunks visible posteriorly

Flattened, oval larvae with lateral leaf-like projections

Highly coiled, bright red worm-like larvae

#40. In sheep-rearing countries, which of the following environmental and management factors is a major predisposing trigger for ‘blowfly strike’ (cutaneous myiasis caused by Lucilia cuprina)?💡 Click for ExplanationCutaneous myiasis (blowfly strike) is highly attracted to moist, decomposing wool. Conditions like ‘fleece rot’ (bacterial dermatitis during prolonged rains) or wool heavily soiled with feces and urine provide an ideal, moist, alkaline medium that releases specific volatile odors, highly attractive to gravid Lucilia cuprina blowflies.

Housing sheep in dry, concrete-floored pens in winter

'Fleece rot' and urine/feces-soiling of the breech wool during wet summer months, which releases alkaline-decomposing odors that attract gravid flies

Feeding diets containing high levels of calcium

Regular shearing of wool before the onset of rains

#41. Tropical Bovine Theileriosis (Bovine Tropical Theileriosis) in the Indian subcontinent is primarily caused by which protozoan pathogen, and what is its principal tick vector?💡 Click for ExplanationTropical Bovine Theileriosis is caused by the intracellular apicomplexan protozoan Theileria annulata. In India and surrounding regions, the principal vector responsible for transmitting this pathogen is the multi-host hard tick Hyalomma anatolicum (previously Hyalomma anatolicum anatolicum).

Theileria parva; vector Rhipicephalus appendiculatus

Theileria annulata; vector Hyalomma anatolicum

Theileria mutans; vector Boophilus microplus

Babesia bigemina; vector Rhipicephalus microplus

#42. During the diagnostic evaluation of a cow suspected of having acute Theileria annulata infection, the detection of ‘Koch’s Blue Bodies’ (macroschizonts or microschizonts) is considered diagnostic. In which cells are they located?💡 Click for ExplanationKoch’s Blue Bodies represent the intra-lymphocytic schizont stage of Theileria. Sporozoites injected by the tick vector invade host lymphocytes and monocytes, developing into multinucleated schizonts (Koch’s blue bodies). These are detected in aspiration smears of superficial lymph nodes (like the prescapular lymph node) and are diagnostic.

Inside mature erythrocytes (RBCs)

In the cytoplasm of host lymphocytes and monocytes/macrophages in lymph node or spleen biopsy smears

Inside the cytoplasm of neutrophilic granulocytes

Free-floating in the blood plasma

#43. What is the primary pathological mechanism responsible for the severe, progressive anemia observed in cattle suffering from Tropical Bovine Theileriosis?💡 Click for ExplanationThe anemia in bovine theileriosis is primarily autoimmune-mediated. The intra-erythrocytic piroplasms modify the RBC surface antigens. The host’s immune system recognizes these altered RBCs as foreign, producing autoantibodies that bind to them. This antigen-antibody complex is then recognized and phagocytized by splenic and hepatic macrophages, leading to massive extravascular hemolysis.

Direct mechanical lysis of RBCs by rapidly multiplying merozoites

Autoimmune-mediated erythrophagocytosis, where the surface antigen of host RBCs is modified by the parasite and recognized as foreign by host macrophages

Severe iron-deficiency anemia due to dietary block

Complete hypoplasia of the bone marrow due to leukopenia

#44. A classical, pathognomonic necropsy finding in the gastrointestinal tract of a crossbred cow that died of acute Tropical Bovine Theileriosis is the presence of:💡 Click for ExplanationAt necropsy, bovine theileriosis is characterized by petechiae and ecchymoses across serosal surfaces. A highly classic, diagnostic gross lesion is the presence of multiple, sharply circumscribed, punched-out, ‘button-like’ necrotic ulcers (which may bleed or show mucosal sloughing) in the mucosa of the abomasum and occasionally small intestine.

Thick, corrugated mucosal folds in the colon resembling a washboard

Punched-out, button-like necrotic ulcers in the abomasal mucosa

Extensive calcification and pipe-stem lesions of the rumen

Cauliflower-like granulomatous lesions lining the esophagus

#45. Which of the following represents the highly specific, gold-standard therapeutic agent used for the treatment of Tropical Bovine Theileriosis in cattle?💡 Click for ExplanationBuparvaquone (available commercially as Butalex @ 50 mg/ml) is a highly specific, second-generation hydroxynaphthoquinone with exceptional efficacy against both the schizont and piroplasm stages of Theileria. It is administered @ 2.5 mg/kg b.wt. i/m (deep i/m, usually in the neck muscles). A single dose is curative, though severe cases may require a second dose after 48-72 hours.

Diminazene aceturate (Berenil) @ 3.5 mg/kg i/m

Buparvaquone (Butalex) administered @ 2.5 mg/kg body weight intramuscularly

Piperazine citrate @ 100 mg/kg orally

Thiacetarsamide sodium @ 1.0 mg/lb i/v

#46. How are the bovine hemoprotozoan parasites Babesia bigemina and Babesia bovis differentiated microscopically on a Giemsa-stained thin blood smear?💡 Click for ExplanationThis morphological distinction is highly diagnostic. Babesia bigemina is a ‘large Babesia’ (pear-shaped, 4-5 µm, longer than RBC radius), typically found as pairs joined at a sharp acute angle within the erythrocyte. Babesia bovis is a ‘small Babesia’ (1.5-2.0 µm, shorter than RBC radius), often paired at a wide obtuse angle.

B. bigemina is small and round, while B. bovis is large and flagellated

B. bigemina is a large Babesia (longer than the radius of RBC) typically occurring as pairs joined at an acute angle, whereas B. bovis is a small Babesia (shorter than RBC radius) typically paired at an obtuse angle

B. bigemina is found only inside neutrophils, while B. bovis is in lymphocytes

B. bigemina forms rosette-like schizonts, while B. bovis is extra-erythrocytic

#47. The transmission of Babesia bigemina by its vector, the one-host tick Rhipicephalus (Boophilus) microplus, involves which of the following biological pathways?💡 Click for ExplanationBecause Rhipicephalus microplus is a one-host tick (completing its entire larval, nymphal, and adult life on a single host), it cannot transmit Babesia transstadially to another animal. Therefore, Babesia must undergo transovarian transmission—migrating to the tick’s ovaries and infecting the eggs—so that the next generation of tick larvae (seeded onto pastures) can transmit the protozoa when they feed.

Only mechanical transmission via biting stable flies

Transstadial (stage-to-stage) and transovarian transmission, where the parasite infects the tick ovary and is passed to the next generation of tick larvae

Development of metacercariae on water plants ingested by the tick

Sexual reproduction within the host's lymphatic ducts

#48. A dairy cow presents with a sudden onset of extremely high fever (106°F), severe pale-to-icteric mucous membranes, rapid heart rate, and the passage of distinct dark coffee-colored (or red-colored) urine. What is the most likely diagnosis?💡 Click for ExplanationThese are the classic, cardinal clinical signs of bovine babesiosis (tick fever or red water fever). The rapid multiplication of Babesia piroplasms inside erythrocytes causes extensive intravascular hemolysis. The released hemoglobin exceeds the blood haptoglobin-binding capacity, leading to severe hemoglobinuria (giving urine a dark-red or coffee color), accompanied by severe icterus and high fever.

Rumen acidosis

Bovine Tropical Theileriosis

Bovine Babesiosis (Red water fever)

Chronic immature amphistomiasis

#49. What is the etiological agent of the extracellular protozoan disease ‘Surra’ in animals, and how is it primarily transmitted?💡 Click for ExplanationSurra is caused by Trypanosoma evansi, a monomorphic, extra-erythrocytic flagellate protozoan. Unlike African trypanosomes, T. evansi has lost its ability to develop biologically in tsetse flies; instead, it is transmitted mechanically by the biting mouthparts of hematophagous flies, principally horseflies (Tabanus) and stable flies (Stomoxys).

Trypanosoma equiperdum; transmitted via coitus

Trypanosoma evansi; transmitted mechanically by the biting stable flies (Tabanus and Stomoxys)

Trypanosoma cruzi; transmitted by kissing bugs

Leishmania donovani; transmitted by sandflies

#50. Which of the following Eimeria species causes highly fatal ‘Cecal Coccidiosis’ in young poultry, and what is its pathognomonic gross lesion seen at necropsy?💡 Click for ExplanationEimeria tenella is the etiological agent of cecal coccidiosis in chickens, which is highly fatal. At necropsy, the ceca are markedly distended, turgid, and dark-red, filled completely with frank clotted blood and yellowish, cheesy caseous debris resulting from the complete destruction of the cecal mucosa.

Eimeria acervulina; ladder-like white transverse bands in the duodenum

Eimeria necatrix; 'salt and pepper' white and red spots on the mid-small intestine

Eimeria tenella; severely distended ceca filled with clotted blood, fluid, and yellowish cheesy/caseous necrotic material

Eimeria maxima; severe thickening of the middle jejunum with pink mucoid exudate

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