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Systemic Pathology II > CNS, Pt. 3 > Flashcards

CNS, Pt. 3 Flashcards

1
Q

What is the most common cause of equine encephalomyelitis? What does it cause?

A

Eastern, Western, and Venezuelan encephalomyelitis viruses in the Togaviridae family spread through mosquitoes

polioencephalomyelitis with prominent lesions in the brainstem

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2
Q

What is the most common histological presentation of equine viral encephalitis?

A

gliosis and perivascular cuffing rich in neutrophils (usually viruses are lymphocytes and plasma cells) caused by advances necrosis

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3
Q

Other than equine encephalitis viruses, what are 2 other important causes of viral-induced inflammatory disease in horses? What is the characteristic lesion?

A
  1. equine herpesvirus 1 - myeloencephalitis (lesion more significant in spinal cord)
  2. West Nile virus - encephalitis (zoonotic)

vasculitis leading to thrombosis and infarction

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4
Q

What are 3 common clinical signs of equine herpesvirus myeloencephalitis?

A
  1. ataxia
  2. paresis
  3. posterior and bladder paralysis - urinary incontinence
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5
Q

What is a common viral cause of encephalitis in cows? What 2 syndromes are most common?

A

bovine herpesvirus —> 5-18 months

  1. bovine necrotizing meningoencephalitis = BHV-5
  2. bovine meningoencephalomyelitis = BHV-1 (infectious bovine rhinotracheitis)
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6
Q

What is the most common cause of encephalitis in dogs? What age is most susceptible?

A

canine herpesvirus 1 —> neonates, resistance after 3 weeks old

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7
Q

How does rabies reach the brain? Where does it most commonly affect the brain in carnivores? How is it diagnosed?

A

replicates at the site of bite from an infected animal and undergoes retrograde transport to the brain, then the salivary glands

limbic system - hippocampus

FAT of the entire brain

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8
Q

Rabies, steer:

A

VERY SUBTLE - minimal inflammation with ONE perivascular cuff

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9
Q

How are neurons affected by rabies infection? What was the past way of diagnosis? Why is this no longer used for definitive diagnosis?

A

normal morphology, with accumulations of eosinophilic intracytoplasmic Negri bodies

Negri body formation - 15-30% of rabies cases lack Negri bodies —> FAT and IHC

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10
Q

What are Negri bodies?

A

eosinophilic, amorphous matrix rich in rabies proteins formed in neuron cytoplasm

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11
Q

What Paramyxovirus commonly affects dogs and ferrets? How does disease progress?

A

canine distemper virus (CDV)

  • primary viremia
  • secondary viremia with systemic epithelial colonization and viral shedding (dogs with proper humoral and cellular immunity may recover)
  • severe disease where CDV spreads hematogenously to the brain and choroid plexus and infects astrocytes and microglia
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12
Q

What is thought to cause CNS histological changes with canine distemper virus infection?

A

white matter vacuolization (intramyelinic edema) results from direct effect of the virus on oligodendrocytes, astrocytes, and glial cells

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13
Q

What does canine distemper virus target? What does this commonly cause?

A

epithelium of multiple body systems

mucosuppurative exudate from the nose and eye, with conjunctivitis

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14
Q

What are 2 common secondary effects of canine distemper virus infection?

A
  1. enamel hypoplasia - targets enamoblasts causing a brownish discoloration at the root
  2. footpad keratosis - marked thickening
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15
Q

Canine distemper virus, dog cerebellum:

A

demyelination - spongiform change

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16
Q

Canine distemper virus, dog:

A
  • astrocytes with inclusion bodies
  • perivascular cuffing
  • vacuolization of white matter (oligodendrocytes)
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17
Q

Canine distemper virus, intranuclear inclusions:

A
  • inclusions in astrocytes in the cerebellar white matter
  • vacuolization
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18
Q

What coronavirus commonly affects cats with the involvement of multiple organs including the CNS?What does it cause? What are the 2 forms?

A

feline infectious peritonitis virus —> pyogranulomatous inflammation that leads to vasculitis, vascular necrosis, and infarction

  1. EFFUSIVE: serositis, fluid accumulation in abdomen, pyogranulomatous inflammation
  2. NON-EFFUSIVE: leptomeningitis, chorioependymitis, focal encephalomyelitis, and ophtalmitis
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19
Q

FIP, dry form:

A
  • pyogranulomatous meningoencephalitis
  • meninges are invaded by macrophages and scattered neutrophils
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20
Q

FIP, cat:

A
  • frozen specimen
  • aquired hydrocephalus: cellular debris clog lateral ventricles
  • ventricular asymmetry
  • dull edges caused by chorioependymitis
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21
Q

What viral infection has significant CNS implications in goats? What does this cause? How is it spread?

A

caprine arthritis encephalitis virus - Lentivirus

  • arthritis, bursitis, pneumonitis, and mastitis in older goats
  • neurological disease is young kids 2-4 months

colostrum, milk, direct contact with infected dams

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22
Q

What CNS lesions are associated with CAE syndrome?

A

demyelinating encephalomyelitis in the caudal brainstem and spinal cord

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23
Q

What viral infection has significant CNS implications in sheep? What else does it cause?

A

Visna-Maedi virus - Lentivirus

ovine progressive penumonia —> lymphoid interstitial pneumonia

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24
Q

What etiology is suspected with CAE syndrome and Visna?

A

immune-mediated

25
Q

What protozoal disease commonly affects the CNS of horses? How does disease progress? What are the characteristic neurologic deficits?

A

Equine Protozoal Myeloencephalitis (EPM) caused by Sarcocystis neurona and Sarcocystis falcatula (opossums!)

sudden or gradual onset of pelvic limb paresis and ataxia

multifocal, asymmetric neurologic deficits

26
Q

How do horses and opossums factor into the life cycle of Sarcocystis?

A

HORSES = dead-end aberrant hosts that develop equine protozoal myeloencephalitis (EPM) when they ingest feed contaminated with opossum feces containing sporocysts or dead birds (IH)

OPOSSUMS = definitive host that houses the sexual stages of the protozoan in their GIT

27
Q

Where does Sarcocystis multiply in equine hosts? What must this disease be differentiated from? What is the gross lesion like?

A

CNS (not muscle)

wobblers and herpesvirus myeloencephalitis, which will usually have symmetric or only mildly asymmetric neurologic deficits

multifocal discoloration in the white and gray matter of the spinal cord —> hemorrhage and necrosis

28
Q

EPM, horse:

A

multifocal hemorrhage and malacia in the spinal cord

29
Q

EPM, inflammatory changes:

A
  • spinal cord and brainstem
  • perivascular cuffing
  • gliosis
  • vacuolization
  • axonal degeneration = empty spaces
  • foci of necrosis (necrotic myeloencephalitis)
30
Q

EPM, horse:

A
  • S. neurona
  • focus of gliosis
  • intralesional protozoa
31
Q

EPM, brainstem:

A
  • S. neurona bradyzoite rosettes
  • difficult to find, PCR and presence of asymmetric lesions are best diagnosis
32
Q

What are the 2 most common causes of verminous encephalomyelitis in horses?

A
  1. Halicephalobus gingivalis - environmental nematode enters through skin lesions
  2. Strongylus vulgaris - thrombosis of cranial mesenteric artery

aberrant larvae migration to CNS

33
Q

Cerebrospinal nematodiasis, horse:

A

aberrant migration of Strongylus vulgaris larvae

    • perivascular cuffing
34
Q

What is the most common cause of non-suppurative meningoencephalitis in cats?

A

Toxoplasma gondii

  • cysts containing bradyzoites
  • no prominent inflammatory response
35
Q

What causes transmissible spongiform encephalopathies? What diseases does this cause in humans?

A

transformation of host prion protein (PrP) into an abnormal isoform (PrPSc), which renders it resistant to protease degradation and allows for acumulation within neurons causing progressive and fatal neurological disease

  • Creutzfeldt-Jakob Disease, Familial Fatal Insomnia, Kuru, Gertsmann-Straussler-Scheinker Disease
36
Q

What are the transmissible spongiform encephalopathies in animals? What are outbreaks associated with? What is its incubation period like?

A
  • Scrapie (OSE) in sheep
  • feline, mink, and bovine spongiform encephalopathy
  • Chronic Wasting Disease (CWD) in deer, elk, and moose

feeding TSE positive meat and brains from infected animals

LONG - 2-8 years

37
Q

What are the most common clinical signs of bovine spongiform encephalopathy?

A
  • aggression
  • incoordination
  • abnormal posture
  • hypermetria
  • progressive weakness
  • decreased milk production
  • emaciation
38
Q

Where are lesions associated with bovine spongiform encephalopathy commonly found?

A

obex - dorsal brainstem where the 4th ventricle enters into the central canal and spinal canal

  • neuronal vacuolization
  • relatively no inflammation
39
Q

Where have BSE agents (prion isoforms) been identified? What organ is considered a specific risk material?

A
  • neural tissue: brain, spinal cord, nerves, ganglia, eyes, peripheral nerves
  • lymphoid tissue: tonsils, bone marrow, GALT

small intestine

40
Q

What is the most common clincial sign of Scrapie? What are some other signs?

A

self-inflicted damage to fleece caused by intense pruritis

  • ataxia, gait abnormalities
  • weight loss
  • behavioral changes
  • scratching and rubbing against fixed objects
41
Q

How does chronic wasting disease present? What human implications are associated?

A

deer/elk that are emaciated, in poor body condition, have gait abnormalities, and lose fear of humans (common in Western Canada - Saskatchewan, Alberta)

consumption of meat is unsafe and can spread disease

42
Q

What 2 rickettsial disease commonly affect the CNS?

A
  1. Rocky Mountain Spotted Fever (RMSF) - Rickettsia rickettsi causes vasculitis. meningitis, and meningoencephalitis
  2. canine ehrlichiosis - Ehrlichia canis causes suppurative meningitis/meningoencephalitis
43
Q

What is the characteristic CNS lesion in Cryptococcus neoformans infection?

A

immunosuppression of the host allows for the extension of the fungi from the nasal cavity and sinus to the brain, where it forma a mucopolysaccharide capsule of yeasts —> viscous mucoid exudate

(cryptococcal meningo-encephalitis)

44
Q

Cryptococcus neoformans, brain, cat:

A

translucent mucoid cavitations

45
Q

Cryptococcosis, cat:

A

mucoid cavitations

46
Q

How does cryptococcus neformans look on histology? What stain is used for diagnosis?

A

yeast surrounded by mucopolysaccharide capsule, non-suppurative inflammation, minimal inflammation

Mucicarmin stains the capsule red, indicating cavitated lesions
(Giemsa can also stain)

47
Q

What primary and secondary neoplasms are commonly seen in the brain?

A

PRIMARY - meningiomas, astrocytomas, oligodendrogliomas, choroid plexus papillomas, ependymomas, medulloblastomas, neuroblastomas

SECONDARY (metastatic) - hemangiosarcomas, mammary adenosarcomas, pulmonary carcinomas, lymphosarcomas, melanomas

48
Q

How do meningiomas present grossly?

A

BENIGN - proliferative, surface lesion that is well-demarcated and grows by expansion, compressing the parenchyma

49
Q

Meningioma, cat:

A

BENIGN, but dangerous —> compresses other structures in the brain —> brainstem compression can lead to cardiorespiratory disruption

50
Q

Malignant meningioma, cat:

A

arose from the surface and infiltrated surrounding parenchyma

51
Q

Malignant meningioma, dog:

A

proliferative lesion destroying the nasal cavity, invading from the cribriform plate

52
Q

Choroid plexus papilloma, dog:

A
  • well-circumscribed, proliferative, expanding
  • granular, dark lesion arising from the choroid plexus of the lateral ventricle
53
Q

Astrocytoma, dog:

A
  • swelling, asymmetry
  • arises from gray matter parenchyma
  • intraventricular hemorrhage with marked dilatation
54
Q

Glioblastoma, 18 m/o Boston Terrier:

A
  • young = more likely to be a primary tumor
  • asymmetry, swelling
55
Q

Where are medulloblastomas more likely to be found? What signs does this cause? What cells do they arise from?

A

cerebellum

unilateral central nervous signs

primitive neurons

56
Q

CNS metastatic mammary carcinoma, dog:

A
57
Q

CNS metastatic hemangiosarcoma, dog:

A

multifocal, cavitating, hemorrhagic lesions

58
Q

CNS metastatic hemagiosarcoma, cat:

A

Systemic Pathology II (24 decks)

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