Neuro 4 (midterm material including Kahoot)

Question 1

name a small ruminant lentivirus that causes hygromas in goats

Answer 1

caprine arthritis encephalitis virus, CAEV

Question 2

name a small ruminant lentivirus that causes hygromas in sheep

Answer 2

Made Visna virus, MV

Question 3

what is effect of small ruminant lentiviruses on CNS? on joints?

Answer 3

CNS: nonsuppurative leukoencephalomyelitis; joints: arthritis, forms hygromas (flattened cystic subcutaneous division over anterior carpus with inspissated fibrin)

Question 4

you see a hygroma in a joint of a small ruminant. important differentials would be

Answer 4

lentiviruses caprine arthritis encephalitis virus (CAEV), Maedi visna virus (MV) OR brucellosis

Question 5

how does CAEV present in young goats <4 months

Answer 5

neurological disease [+/- pneumonia]

Question 6

how are small ruminant lentiviruses transmitted?

Answer 6

colostrum and milk [and to lesser extent respiratory droplets]

Question 7

how do small ruminant lentiviruses they get into the CNS, and what part of the CNS are they targeting?

Answer 7

infect monocytes/macrophages, so get into CNS by leukocyte trafficking. they target white matter

Question 8

what is one of the most neurotropic viruses globally that can infect any mammal (although uncommon in small rodents and lagomorphs)

Answer 8

rabies

Question 9

describe pathogenesis of rabies

Answer 9

bite or scratch by rabid animal –> local replication in muscle or peripheral nerve –> bind acetylcholine receptors and neuromuscular junction –> fast anterograde transport to CNS –> anterograde axonal transport to salivary gland

Question 10

3 phases of rabies clinical signs are

Answer 10

prodromal, excitatory, paralytic

Question 11

if excitatory clinical signs of rabies predominate, what type of rabies is this

Answer 11

furious form

Question 12

if paralytic clinical signs of rabies predominate, what type of rabies is this

Answer 12

dumb form

Question 13

true or false: rabies histological findings are extensive, AND include characteristic Negri bodies

Answer 13

false: findings can be minimal! Negri bodies part is correct.

Question 14

which prion disease is known to transmit to humans

Answer 14

BSE, bovine spongiform encelopathy

Question 15

what is a prion? include what a normal and abnormal form would be

Answer 15

abnormally folded proteins which are infectious and lack DNA/genome. normal version of protein known as PrPc is found in most living things and abnormal form is PrPsc and is highly resistant to things that would normally degrade DNA and protein

Question 16

prions accumulate as plaques and fibrils causing _____

Answer 16

neurodegenerative disease

Question 17

is PrPsc easily transmitted between species

Answer 17

no, species barrier [because PrPsc is slightly different between species]

Question 18

prion diseases are also known as

Answer 18

transmissible spongiform encelopathies

Question 19

what are 2 ways of acquiring PrPsc in prion diseases? include any subtypes for these 2 ways?

Answer 19

acquired: can be horizontal transmission [through saliva, blood, urine, eg. CWD], ingestion [eg. BSE], or ingestion and possible vertical transmission [eg. scrapie]. or can be spontaneous mutation of a normal protein in the individual.

Question 20

clinical signs, including timing of these signs, of prion diseases in general

Answer 20

variable but PROGRESSIVE clinical signs, can take YEARS to accumulate enough protein to accumulate signs, and eventually FATAL. there is NO immune response [body doesn’t recognize protein as foreign].

Question 21

key histologic findings of prion diseases? why can it be hard to distinguish prion diseases from autolysis?

Answer 21

no inflammation, cytoplasmic vacuolation of neurone and neutrophil [also astrocyte hypertrophy and hyperplasia; targeted location in the brain varies between different TSEs]. vacuolation in brains also occurs in autolysis, but usually not in neurons

Question 22

where should you look for prion diseases in the CNS

Answer 22

obey

Question 23

what prion disease is increasing in prevalence in Alberta? it was found in Calgary in summer 2020 :(

Answer 23

CWD chronic wasting disease

Question 24

the full name for polio is _____. is this the same as human polio?

Answer 24

polioencephalomalacia. no.

Question 25

what 4 things cause polioencephalomalacia? what would be most common in a feedlot?

Answer 25

thiamine (vitamin B1) deficiency is the most common in feedlot. also sulfur toxicity, lead toxicity, salt toxicity/water deprivation

Question 26

where is thiamine produced in adult ruminants? what might disrupt adult ruminants’ production of thiamine?

Answer 26

bacteria in the rumen. grain overload and luminal acidosis disrupting rumen flora and therefore impact thiamine production

Question 27

describe gross changes and a key histological change seen with polioencephalomalacia in herbivores

Answer 27

bilaterally symmetric yellow discolouration of deep gray matter of cerebral cortex. once that discoloration is seen, autofluorescence occurs. histological important finding is laminar cortical necrosis

Question 28

are the gross and histological lesions of polioencephalomalacia the same in herbivores and carnivores?

Answer 28

no

Question 29

describe gross changes seen with polioencephalomalacia in carnivores

Answer 29

bilaterally symmetrical lesions target periventricular matter of brainstem, especially the caudal colliculi

Question 30

is lead toxicity reportable

Answer 30

yes

Question 31

it is hard to distinguish between different causes of polio postmortem. what postmortem test could you do? if you have other living affected animals, what clinical test could you do?

Answer 31

postmortem = salt testing for brain and liver. clinical = response to thiamine supplementation (to rule out thiamine deficiency)

Question 32

how does salt toxicity polio, ie. water deprivation polio, occur in pigs? give 2 ways please and thank you

Answer 32

direct = over-consumption of salt. indirect = water deprivation and then sudden unlimited access to water (eg. if water source freezes in winter).

Question 33

salt toxicity polioencephalomalacia affects which species? which is it most common in

Answer 33

any species, but most common in pigs and poultry

Question 34

what histological finding is seen in salt toxicity in pigs

Answer 34

distinct eosinophilic infiltrate [in meninges and perivascular spaces]

Question 35

a pathogenesis of salt toxicity/water deprivation polioencephalomalacia in pigs, after a period of water deprivation organic osmolytes are formed in the brain to help compensate for high levels of salt in the blood. once given access to water, pigs pigs will consume a lot of water. what then happens to the brain

Answer 35

water moves rapidly into brain causing edema

Question 36

true or false: neurologic disease due to small ruminant lentiviruses is most common in goat kids

Answer 36

false

Question 37

the infectious agent of prion diseases is what: bacteria, amino acid, virus, or protein

Answer 37

protein

Question 38

what disease causes brain autofluorescence

Answer 38

polioencephalomalacia

Question 39

what white blood cell is observed in pigs with salt toxicity which makes them unique

Answer 39

eosinophils

Question 40

true or false: after horizontal transmission, clinical signs of prion diseases develop rapidly

Answer 40

false, develop progressively and can take years