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What is a significant clinical sign of lead toxicosis in cattle?
Which of the following is a source of lead toxicosis in birds?
What are the gross lesions typically associated with salt toxicity in pigs?
Which systemic feature is least affected by lead toxicosis in animals?
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Which statement accurately describes Clostridium botulinum?
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Which type of botulinum is most prevalent in the mid-Atlantic states to Kentucky for horses?
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What is the primary clinical outcome of botulism in horses?
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Which age group of pigs is primarily affected by edema disease caused by E. coli?
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What is a characteristic gross lesion observed in the brain due to edema disease?
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What type of toxin is associated with Centaurea spp. and its effects in animals?
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What is the primary cause of Feline Ischemic Encephalopathy?
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Which age group of cattle is most commonly affected by Vitamin B1 deficiency?
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What is a common clinical sign of sodium chloride toxicity?
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Which lesion is primarily associated with Polioencephalomalacia due to Vitamin B1 deficiency?
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In which species are thiaminase-containing plants particularly problematic for causing thiamine deficiency?
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What type of necrosis is primarily noted in Vitamin B1 deficiency in ruminants?
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What histopathological changes are commonly seen in Feline Ischemic Encephalopathy?
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What dietary factor mainly contributes to Vitamin B1 deficiency in young ruminants?
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Which of the following clinical signs is NOT typically associated with Thiamine deficiency in carnivores?
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What is a potential consequence of rapid rehydration following sodium chloride toxicity?
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What is a characteristic of Hansen Type I Intervertebral Disc Disease?
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Which breed is most commonly associated with Hansen Type I Intervertebral Disc Disease?
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What age group is most commonly affected by meningiomas in dogs?
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What is a common microscopic feature of meningiomas?
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In which part of the body do hemangiosarcomas primarily form?
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What is the primary cause of glaucoma related to aqueous humor?
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What is the typical age range for cats affected by meningiomas?
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Which type of canine breed is more likely to suffer from Hansen Type II Intervertebral Disc Disease?
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What is a common clinical consequence of increased intraocular pressure due to glaucoma?
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What are the characteristics of the lesions associated with meningiomas in dogs?
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What is the primary pathological change observed in Nigropallidal encephalomalacia?
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Which clinical sign is most commonly associated with Nigropallidal encephalomalacia in horses?
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What type of lesions do cholesteatomas typically form in horses?
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In lysosomal storage diseases, what is the primary consequence of the inability to degrade substrates?
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Which breed is commonly associated with Globoid Cell Leukodystrophy due to its autosomal recessive inheritance?
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What is the consequence of deficient galactosylceramidase activity in Globoid Cell Leukodystrophy?
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Which characteristic change is seen histologically in lysosomal storage diseases?
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What does hypomyelinogenesis refer to?
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What structural change is associated with cholesteatomas in horses?
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Which condition is specifically linked with the development of space-occupying lesions due to cholesterol deposits in the brain?
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What common zoonotic condition is associated with the reduction in myelin formation during fetal development?
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Which of the following histopathological findings indicates Globoid Cell Leukodystrophy?
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Which statement about lysosomal storage diseases is incorrect?
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Study Notes
Feline Ischemic Encephalopathy
- Caused by the aberrant migration of Cuterebra fly larvae into the nasal cavity and brain.
- Larvae can migrate and cause parasitic infarcts, primarily affecting the middle cerebral artery.
- Affecting any age, characterized by unilateral, white, and gray matter necrosis and hemorrhages in the CNS or leptomeninges.
- Histological findings include vasculitis, thrombosis, ischemia, infarction, cerebral cortical atrophy, and destruction of brain architecture.
- Clinical signs: depression, mild ataxia, seizures, behavioral changes, and blindness, typically seen during summer months.
Vitamin B1 (Thiamine) Deficiency
- Results in polioencephalomalacia (PEM), characterized by necrosis and softening of the brain.
- Primarily affects cattle and sheep more than goats.
- Three main causes: decreased ruminal thiamine, inactive thiamine analogues, and overgrowth of thiaminase-producing microbes.
- Cattle are susceptible due to high-carbohydrate diets and low roughage intake, leading to ruminal acidosis and microflora changes.
- Young ruminants are more susceptible to thiamine deficiency as their rumen is not fully populated with the necessary microbes.
- Thiaminase-containing plants like Bracken Fern can lead to thiamine deficiency.
- Salt, lead, and sulfur toxicosis can also contribute by cleaving thiamine.
- Histological findings include laminar cortical necrosis, edema, and astrocytic swelling.
- Neuronal necrosis with a preference for the cortex is prominent.
- Gross lesions are limited to the cerebral cortex, often exhibiting swelling and brain displacement.
- Autofluorescence under UV light reveals a bilaterally symmetrical laminar pattern, indicating areas of gray matter necrosis.
- Clinical signs: depression, stupor, ataxia, head pressing, cortical blindness, opisthotonos, convulsions, recumbency, paddling, and death.
- In carnivores, an absolute dietary requirement for thiamine exists.
- Diets containing thiaminase or inadequate thiamine supplementation can lead to deficiency.
- Gross and histological lesions include bilateral focal necrosis in the thalamus, midbrain, or colliculi, accompanied by neuronal vacuolation, degeneration, necrosis, hemorrhage, astrogliosis, and gitter cells.
- Clinical signs: vomiting, wide-based stance, ataxia, spastic paresis, circling, seizures, recumbency, opisthotonos, coma, and death.
Sodium Chloride Toxicity – Salt Toxicosis
- Affects primarily pigs and poultry, sometimes ruminants.
- Overconsumption of sodium chloride coupled with limited drinking water leads to severe dehydration.
- Salt toxicity results in hyperosmolarity and hypernatremia due to excessive sodium intake or dehydration.
- When rehydrated with water, a rapid shift in sodium levels from hypernatremia to hyponatremia occurs.
- Brain swelling results due to water entering the brain to offset the osmotic stress.
- Histological findings include cerebrocortical laminar neuronal necrosis similar to PEM.
- In pigs, perivascular eosinophils with laminar cortical necrosis are indicative of salt toxicity.
- Gross lesions: cerebral and leptomeningeal congestion and edema.
- Clinical signs: inappetence, dehydration, head pressing, incoordination, blindness, circling, paddling, convulsions, and sometimes sudden death.
Lead Toxicosis
- Affects cattle and other species, with sources including car batteries, lead paint, and fishing sinkers.
- Can be peracute, acute, subacute, or chronic.
- Affects CNS, PNS, liver, kidneys, GI tract, bone marrow, blood vessels, reproductive system, and endocrine system.
- Gross lesions may include battery pieces or paint flakes in the rumen, resembling PEM.
- CNS lesions are typically absent, requiring differentiation from other causes of PEM.
- In dogs, lesions resemble those in cattle, but with more vascular damage.
- Clinical signs in cattle: depression, diarrhea, teeth grinding (bruxism), circling, head pressing, incoordination, and blindness.
- Clinical signs in small animals (dogs): ataxia, tremors, clonic-tonic seizures, blindness, and deafness.
- In horses, cranial neuropathy can lead to laryngeal and facial paralysis.
Microbial Toxins – Botulism (CNS & PNS)
- Caused by Clostridium botulinum, a gram-positive anaerobic bacterium.
- Spores are found in soil and germinate in necrotic tissue.
- Neurotoxin of C. botulinum type A, B, or C is prevalent in North America.
- Affects horses in various forms: contaminated forage (adult horses) and toxicoinfectious botulism (foals).
- Pathogenesis involves toxin production, binding to receptors at myoneural junctions, inhibiting acetylcholine release, and causing flaccid paralysis.
- Death typically occurs due to paralysis of the diaphragm.
- No microscopic or gross lesions are typically observed.
- Horses exhibit progressive paralysis of muscles, including limbs, pharynx, eyelids, tongue, and tail.
Microbial Toxins – Edema Disease (Enterotoxemic Colibacillosis)
- Caused by strains of E. coli producing a Shiga-like toxin.
- Affects rapidly growing, healthy feeder pigs on high-energy rations.
- Lesions involve angiopathy, leading to leaky vessels, edema, and hypoxic-ischemic injury.
- Gross lesions include facial edema, gastric submucosal edema, colonic mesentery edema, lung congestion, thoracic effusion, pericardial sac effusion, and spongiosis of CNS parenchyma.
- Characteristic brain lesions include bilaterally symmetrical foci of necrosis in the caudal medulla.
- Inflammation is not a primary process, but endothelial cells become swollen.
- Clinical signs: initial ataxia, followed by lateral recumbency, paddling limbs, coma, and death within 24 hours.
- Surviving pigs often develop CNS lesions.
Plant Toxins – Centaurea spp. Poisoning
- Yellow Star Thistle and Russian Knapweed cause nigropallial encephalomalacia.
- Histological findings: necrosis and loss of neurons, necrotic axons, glia, and blood vessels.
- Gross lesions: bilateral or unilateral sharply demarcated foci of yellow discoloration and malacia in the globus pallidus (pallidal) and substantia nigra (nigro).
- Clinical signs: lip/tongue paralysis, reduced jaw tone, persistent chewing, difficulty with prehension of feed and water.
- Death can occur due to emaciation and starvation.
Cholesteatomas (Cholesterol Granulomas)
- Form in the choroid plexuses of lateral ventricles in horses.
- Age-related and often incidental, but can occlude CSF flow, leading to acquired hydrocephalus.
- Gross lesions: tan to yellow-brown, firm masses with a smooth surface, often containing mineral deposits.
- Result from edema and minor hemorrhages within the choroid plexuses, leading to cholesterol deposits.
- Elicit a foreign body granuloma.
- Can be confused with choroid plexus tumors.
Lysosomal Storage Diseases (LSDs)
- Result from the accumulation of undigested substrates in lysosomes due to enzyme deficiencies.
- Can affect neurons or myelinating cells, leading to substrate release into adjacent tissue and macrophage phagocytosis.
- Causes include reduced enzyme synthesis, synthesis of inactive proteins, enzyme misdirection, lack of enzyme activator, lack of substrate activator protein, and lack of transport protein.
- Cell swelling and cytoplasmic vacuolation are general characteristics.
- Many lipids and glycolipids are unique to the nervous system, making neural cells susceptible to substrate accumulation.
- Gangliosidoses are inherited autosomal recessive disorders.
- Age of onset varies between different LSDs and enzymes.
- Histological findings: neurons with foamy, finely vacuolated, or granular cytoplasm.
- Gross lesions vary among LSDs, with brain atrophy occurring in globoid cell leukodystrophy and ceroid-lipofuscinosis.
LSD: Globoid Cell Leukodystrophy
- Principal lesion: primary demyelination of oligodendrocytes (CNS) and Schwann cells (PNS).
- Autosomal recessive inheritance, affecting Cairn Terriers, West Highland Terriers, Beagles, Mini Poodles, Bassets, Pomeranians, Blueticks, and cats.
- Primarily affects animals under one year old.
- Sequence of events: normal myelination followed by disruption due to deficient galactosylceramidase activity, leading to psychosine accumulation and primary demyelination.
- Recruitment of phagocytes leads to globoid cell formation by macrophages phagocytosing myelin byproducts.
- Histological findings: loss of myelin, globoid cells containing galactocerebroside, and PAS-positive staining.
- Gross lesions: discoloration of white matter, particularly in cerebral hemispheres and spinal cord.
- Clinical signs: ataxia, limb weakness, paralysis, muscular atrophy, and blindness.
- Affecting peripheral nerves, lesions include primary demyelination and axonal degeneration.
- Diagnosis is through biopsy of peripheral nerves.
- Microscopic findings show significant loss of myelin and abundant globoid cells.
- Gross lesions are not evident.
Hypomyelinogenesis (Hypomyelination)
- Underdevelopment of myelin.
- Classical swine fever (hog cholera), a pestivirus, can cause hypomyelinogenesis in fetuses.
- Other lesions include cerebellar hypoplasia and microencephaly.
- Border disease virus (in lambs and goats), also a pestivirus, can cause hypomyelinogenesis, primarily affecting the white matter of the cerebrum and cerebellum.
- Gross lesions make it difficult to differentiate between white and gray matter.
- PNS is unaffected.
- Other lesions in lambs: early inflammation, porencephaly-hydranencephaly, cerebellar hypoplasia, microencephaly, and smaller spinal cord diameter.
Intervertebral Disc Disease (IVDD)
- Disc herniations occur dorsally in dogs, resulting in diverse neurological signs.
- Hansen Type I: affects chondrodystrophic breeds like Dachshunds and Pekingese.
- Characterized by acute, progressive disc degeneration, often triggered by trauma.
- Genetic chondroid metaplastic change of the nucleus pulposus, starting around 6 months of age.
- Loss of elasticity in the nucleus pulposus compresses blood vessels and the spinal cord segment, causing ischemia, neuronal endotoxicity, and necrosis.
- Stress on the annulus fibrosus can lead to severe spinal cord damage.
- Multiple discs can be affected.
- Hansen Type II: progressive and degenerative, occurring in non-chondrodystrophic breeds like German Shepherd Dogs, Labrador Retrievers, Dobermans, and obese dogs.
- Slower degeneration leads to gradual loss of elasticity, placing mechanical stress on the annulus fibrosus, resulting in protrusion and compression of the spinal canal.
- Less painful than Type I.
- Occurs in older dogs, typically 8-10 years old.
Meningiomas
- The most common CNS neoplasm in dogs and cats, rare in horses and ruminants.
- In dogs, they occur between 7-14 years old, while in cats, they are more common in animals over 10 years old.
- Locations: brain, spinal cord, retrobulbar (optic nerve sheath) in dogs, 3rd ventricle, cerebral hemispheres, along the cerebri, cerebellum, tentorium, and base of the brain in cats.
- Can compress or invade surrounding CNS parenchyma.
- Gross lesions: solitary, well-defined, spherical, lobulated, firm, encapsulated, gray-white masses, often with areas of hemorrhage and necrosis in dogs.
- In cats, multiple lesions (mm to 2 cm in diameter) can be incidental findings.
- Microscopic subtypes include transitional, meningothelial, psammomatous, fibrous, atypical, malignant.
- Most meningiomas typically contain features of meningothelial or transitional types, with psammoma bodies being a common characteristic.
Hemangiosarcoma
- Often metastases from other organs like the right auricle or spleen.
- More prevalent in dogs compared to other species.
- Lesions: solitary, expansile, red to dark red-black masses within the cerebral cortex.
- Differential diagnosis: primary or metastatic melanoma.
Ophthalmic System
- Aqueous humor is formed by the ciliary epithelium and circulates through the posterior chamber, anterior chamber, and exits through the iridocorneal angle.
- Drainage occurs through the scleral venous plexus.
- Glaucoma, an enlargement of the globe, is linked to many diseases.
- Increased intraocular pressure due to decreased drainage of aqueous humor damages the optic nerve and retina, leading to blindness.
- Glaucoma is a painful condition.
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Description
Explore the intricate details of Feline Ischemic Encephalopathy caused by aberrant migration of Cuterebra fly larvae, leading to significant neurological deficits. Additionally, delve into Vitamin B1 deficiency and its impact on cattle and sheep, characterized by polioencephalomalacia. This quiz covers clinical signs, causes, and histological findings of both conditions.
