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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
What protozoal disease commonly affects the CNS of horses? How does disease progress? What are the characteristic neurologic deficits?
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
How do horses and opossums factor into the life cycle of Sarcocystis?
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
Where does Sarcocystis multiply in equine hosts? What must this disease be differentiated from? What is the gross lesion like?
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
EPM, horse:
multifocal hemorrhage and malacia in the spinal cord
29
EPM, inflammatory changes:
- spinal cord and brainstem - perivascular cuffing - gliosis - vacuolization - axonal degeneration = empty spaces - foci of necrosis (necrotic myeloencephalitis)
30
EPM, horse:
- S. neurona - focus of gliosis - intralesional protozoa
31
EPM, brainstem:
- S. neurona bradyzoite rosettes - difficult to find, PCR and presence of asymmetric lesions are best diagnosis
32
What are the 2 most common causes of verminous encephalomyelitis in horses?
1. Halicephalobus gingivalis - environmental nematode enters through skin lesions 2. Strongylus vulgaris - thrombosis of cranial mesenteric artery aberrant larvae migration to CNS
33
Cerebrospinal nematodiasis, horse:
aberrant migration of Strongylus vulgaris larvae - + perivascular cuffing
34
What is the most common cause of non-suppurative meningoencephalitis in cats?
Toxoplasma gondii - cysts containing bradyzoites - no prominent inflammatory response
35
What causes transmissible spongiform encephalopathies? What diseases does this cause in humans?
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
What are the transmissible spongiform encephalopathies in animals? What are outbreaks associated with? What is its incubation period like?
- 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
What are the most common clinical signs of bovine spongiform encephalopathy?
- aggression - incoordination - abnormal posture - hypermetria - progressive weakness - decreased milk production - emaciation
38
Where are lesions associated with bovine spongiform encephalopathy commonly found?
obex - dorsal brainstem where the 4th ventricle enters into the central canal and spinal canal - neuronal vacuolization - relatively no inflammation
39
Where have BSE agents (prion isoforms) been identified? What organ is considered a specific risk material?
- neural tissue: brain, spinal cord, nerves, ganglia, eyes, peripheral nerves - lymphoid tissue: tonsils, bone marrow, GALT small intestine
40
What is the most common clincial sign of Scrapie? What are some other signs?
self-inflicted damage to fleece caused by intense pruritis - ataxia, gait abnormalities - weight loss - behavioral changes - scratching and rubbing against fixed objects
41
How does chronic wasting disease present? What human implications are associated?
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
What 2 rickettsial disease commonly affect the CNS?
1. Rocky Mountain Spotted Fever (RMSF) - Rickettsia rickettsi causes vasculitis. meningitis, and meningoencephalitis 2. canine ehrlichiosis - Ehrlichia canis causes suppurative meningitis/meningoencephalitis
43
What is the characteristic CNS lesion in Cryptococcus neoformans infection?
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
Cryptococcus neoformans, brain, cat:
translucent mucoid cavitations
45
Cryptococcosis, cat:
mucoid cavitations
46
How does cryptococcus neformans look on histology? What stain is used for diagnosis?
yeast surrounded by mucopolysaccharide capsule, non-suppurative inflammation, minimal inflammation Mucicarmin stains the capsule red, indicating cavitated lesions (Giemsa can also stain)
47
What primary and secondary neoplasms are commonly seen in the brain?
PRIMARY - meningiomas, astrocytomas, oligodendrogliomas, choroid plexus papillomas, ependymomas, medulloblastomas, neuroblastomas SECONDARY (metastatic) - hemangiosarcomas, mammary adenosarcomas, pulmonary carcinomas, lymphosarcomas, melanomas
48
How do meningiomas present grossly?
BENIGN - proliferative, surface lesion that is well-demarcated and grows by expansion, compressing the parenchyma
49
Meningioma, cat:
BENIGN, but dangerous ---> compresses other structures in the brain ---> brainstem compression can lead to cardiorespiratory disruption
50
Malignant meningioma, cat:
arose from the surface and infiltrated surrounding parenchyma
51
Malignant meningioma, dog:
proliferative lesion destroying the nasal cavity, invading from the cribriform plate
52
Choroid plexus papilloma, dog:
- well-circumscribed, proliferative, expanding - granular, dark lesion arising from the choroid plexus of the lateral ventricle
53
Astrocytoma, dog:
- swelling, asymmetry - arises from gray matter parenchyma - intraventricular hemorrhage with marked dilatation
54
Glioblastoma, 18 m/o Boston Terrier:
- young = more likely to be a primary tumor - asymmetry, swelling
55
Where are medulloblastomas more likely to be found? What signs does this cause? What cells do they arise from?
cerebellum unilateral central nervous signs primitive neurons
56
CNS metastatic mammary carcinoma, dog:
57
CNS metastatic hemangiosarcoma, dog:
multifocal, cavitating, hemorrhagic lesions
58
CNS metastatic hemagiosarcoma, cat:

Systemic Pathology II (24 decks)

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