Neuro 4 Flashcards
What are the two big small ruminant Lentiviruses that we need to know?
Caprine arthritis encephalitis virus (CAEV)
Maedni Visna (MV)
who does caprine arthritis encephalitis virus affect?
goats
who does Maedni visna virus affect? what is the other name for the disease?
Sheep
ovine progressive pleuropneumonia
What are the 4 body systems that small ruminant lentiviruses target?
CNS, lung, joints, mammary gland
what do small ruminant Lentiviruses do to the CNS?
nonsuppurative leukoencephalomyelitis
Lentiviruses form _____ in joints.
Hygromas
what are two ddx’s for a hygroma?
Brucella, Lentivirus
true or false: Lentivirus infection is a lifelong virus
true
what is this?
hygroma
Small ruminant lentiviruses:
1) how are they transmitted?
2) infect what cell type
3) what is the important signalment for CAEV that we need to know?
4) what type of tissue does it impact in CNS?
1) colostrum/milk > resp droplets
2) monocytes/macrophages
3) goat kids <4mo old –> neuro disease ± pneumonia
4) white matter (demyelinating disease)
who is affected by rabies?
all mammals!
what is the pathogenesis of rabies?
1) bitten/scratched by rabid animal
2) local replication in muscle or peripheral nerve
3) binds acetylcholine receptors at neuromuscular junction
4) fast retrograde axonal transport to CNS
5) antergrade axonal transport to salivary gland
what re the 3 phases of rabies? what are the two forms and what do they mean?
phases: prodromal, excitatory, paralytic
forms:
- furious form –> excitatory predominates
- dumb form –> paralytic predominates
what are the important gross and histo findings of rabies?
gross: none
histo: Negri bodies, can be minimal!
Prion diseases are also known as ______.
Transmissible Spongiform Encephalopathies (TSE)
what causes prion disease?
prions (infectious proteins)
abnormal folding, don’t have DNA/genome
1) The normal version of prion proteins, ____, is coded from a highly conserved gene and is found ______.
2) the abnormal version, _____, is _____ resistant to things that would normally degrade DNA and protein.
1) PrPc, in most living things
2) PrPSc, highly
Prions cause _______ disease.
neurodegenerative
PrPSc has a species barrier. what does that mean?
PrPSc is slightly different in each species and doesn’t easily transmit between different species
what are the two ways of acquiring PrPSc?
Acquired and spontaneous mutation
what are the 3 acquired prion diseases that we need to know and how are they transmitted?
chronic wasting disease (CWD) - horizontal transmission (saliva, blood, urine, etc)
bovine spongiform encephalopathy (BSE) - ingestion
Scrapie - ingestion and possible vertical transmission
Prion diseases:
1) it can take ____ for enough atypical protein to accumulate to cause clinical disease.
2) is there an immune response to prion diseases? why/why not/
3) eventually ____, C/S variable but ____
1) years
2) no. body doesn’t recognize protein as foreign
3) fatal, progressive
what are the gross and histo findings of prion diseaseS?
gross: none
histo: no inflammation, vacuolation of neutrons and neuropil
What are the 4 causes of polioencephalomalacia?
- thiamine deficiency (Vit B1)
- sulfur toxicity
- lead toxicity
- salt toxicity/water deprivation
in adult ruminants, thiamine is produced by _____ in _____.
bacteria, rumen
what is the important way that thiamine deficiency happens in ruminants?
disruption of rumen flora production of thiamine (ruminant acidosis, grain overload, for ex)
true or false: for polioencephalomalacia, the gross + histo lesions are the same for carnivores and herbivores.
false. they are different!
what are the gross lesions of polioencephalomalacia in herbivores?
targets deep gray matter of the cerebral cortex
bilaterally symmetric
yellow discolouration (can be autofluorescence)
what most likely caused this lesion? ruminant brain
polioencephalomalacia