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Zuku Top 20s > Ruminant Top 15 Small Ruminant Diseases - Part 3 > Flashcards

Ruminant Top 15 Small Ruminant Diseases - Part 3 Flashcards

1
Q

T/F: cases of polioencephalomalacia in small ruminants usually occurs sporadically or in outbreaks

A

true

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2
Q

what is the classic case presentation of acute polioencephalomalacia?

A

cortical blindness - normal PLR & absent menace

followed by recumbency, tonic-clonic seizures, & coma

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3
Q

what is the classic case presentation of sub-acute polioencephalomalacia?

A

anorexia, facial twitching, elevated head, stands apart from the group, cortical blindness, dorsomedial strabismus, ataxia, head pressing, opisthotonus, bruxism, & rarely progresses to recumbency & seizures

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4
Q

what are the 2 main etiologies of polioencephalomalacia in small ruminants?

A
  1. abnormal thiamine status (thiamine normally made by rumen microbes)
  2. high dietary sulfur intake (or water deprivation, sodium toxicosis, or lead poisoning)
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5
Q

what is the etiology of altered thiamine causing polioencephalomalacia?

A

any alteration in ruminal microbial activity can lead to decreased thiamine production/thiamine destruction

or some plants contain thiaminase (bracken fern)

thiamine deficiency leads to decreased energy availability to the brain/impaired glucose metabolism

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6
Q

what are some examples of high sulfur causing polioencephalomalacia?

A

high molasses-urea diet, corn or sugar cane by products, high sulfur in water, certain plants (alfalfa, canada thistle, kockia, & lambsquarter)

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7
Q

how is polioencephalomalacia diagnosed in small ruminants?

A

measure thiamine, calculate total sulfur intake on a dry matter basis

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8
Q

what is seen on necropsy of an animal with polioencephalomalacia?

A

laminar cerebrocortical necrosis & auto-fluorescent lesions

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9
Q

T/F: regardless of cause, treatment for polioencephalomalacia is the same

A

true

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10
Q

how is polioencephalomalacia treated?

A

thiamine - 1st dose slowly IV then IM for 3-5 days with improvement seen within 24 hours (may not have a complete recovery if advanced state)

+/- dexamethasone to decrease cerebral edema

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11
Q

how is polioencephalomalacia prevented?

A

thiamine supplementation

calculate total sulfur in diet/water & make sure it’s not too high

provide sufficient roughage during outbreaks to maintain happy rumen microbes/prevent ruminal acidosis

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12
Q

what is the pathophysiology of polioencephalomalacia?

A

abnormal cerebral energy metabolism leads to increased intracellular sodium/water leading to cerebral edema which causes cerebral necrosis

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13
Q

polioencephalomalacia affects what animals? what animals are more commonly affected?

A

worldwide in sheep, goats, cattle, deer, & camelids

more common in younger animals on high grain diets

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14
Q

what is another name for border disease?

A

hairy shaker lambs

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15
Q

what is the classic case presentation of border disease in dams?

A

increased number of barren dams & abortion of mummified or macerated fetuses

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16
Q

what is the classic case presentation of lambs with border disease?

A

lambs more often than kids!!

hairy, low birth weight lambs with dark pigmented wool, +/- shortened bones, decreased crown rump length, decreased tibial/radial length, decreased longitudinal axis of the cranium

+/- muscle tremors of the trunk & pelvic limbs that is worse when walking/running

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17
Q

what is the prognosis of border disease in lambs?

A

poor survival rate

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18
Q

what is the etiology of border disease?

A

7 known genotypes of a certain pestivirus (flaviviridae) related to classical swine fever & BVDV

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19
Q

how is border disease in lambs diagnosed?

A

testing must be done BEFORE colostral intake as maternal antibodies can impact test results - take blood from affected lambs & do virus isolation, PCR, fluorescent antibodies, & IHC

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20
Q

how is border disease diagnosed at necropsy?

A

histopathology of CNS lesions are pathognomonic

myelin deficiency, increased interfasicular glial cells with intracellular accumulation of myelin-like lipid droplets - using viral immunocytochemical staining

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21
Q

how is border disease treated?

A

it’s not - they die

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22
Q

how is border disease prevented/controlled?

A

bulk tank milk test for antibodies, serology of dams with affected lambs, mix lambs recovered from infection with breeding stock before breeding season to enhance natural immunity

DO NOT BREED recovered lambs - no effective vaccine

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23
Q

what is the distribution of border disease?

24
Q

how are lambs infected with border disease? what is the problem with lambs that survive border disease?

A

fetus is infected early in pregnancy leads to abortion or widespread distribution in fetal tissues

they are persistently viremic, so virus is present in excretions & secretions including semen

25
is the BVDV vaccine effective for preventing border disease?
NOPE
26
what breeds are predisposed to scrapie?
black faced breeds
27
what is the classic case presentation of scrapie?
progressive weight loss with good appetite, pruritus, progressive ataxia (bunny hopping in pelvic limbs, then high stepping gait in thoracic limbs), fine head tremors especially in the ears, vacant/fixed stare
28
what is the cutaneous sensitivity seen in small ruminants with scrapie?
if you scratch their back, sheep will throw their head back & lick the air or compulsively nibble lower limbs
29
what is the etiology of scrapie?
transmissible spongiform encephalopathy caused by an abnormal prion protein related to BSE & CWD
30
how is scrapie diagnosed?
3rd eyelid or rectal mucosal biopsy for IHC - rectal biopsy is easier/more sensitive necropsy - brain IHC
31
what is the USDA/APHIS scrapie slaughter surveillance program?
brain/lymphoid tissue of black faced sheep & those with clinical signs of scrapie at slaughter are tested by IHC so positives can be traced back to the herd so the herd can be quarantined & test
32
what is the US mandatory scrapie eradication program?
individual & premises identification required for all breeding sheep leaving their premises
33
how does scrapie cause neuro signs?
the abnormal prion is deposited as an amyloid plaque in lymphoreticular & nervous tissue leading to neuro signs
34
how is scrapie transmitted? how long is the incubation period?
transmitted during lambing (NOT IN UTERO) 2-5 year incubation period
35
does scrapie affect humans?
NO
36
where is scrapie found in the world?
everywhere but australia & new zealand
37
T/F: scrapie is rare but possible in goats
true
38
what is the classic case presentation of blue tongue?
cyanotic tongue, fever, serous/mucopurulent nasal discharge, edema of lips/nose/face/submandibular area, reluctance to eat
39
what congenital defects are seen with blue tongue virus?
infection of pregnant dams produces fetuses with hydrancephaly or porencephaly causing ataxic/blind lambs
40
what signs of blue tongue are seen in fine-wool/mutton breeds of sheep?
listlessness, reluctance to move, worse in young lambs (30% mortality), congestion of mouth/nose/nasal cavities/conjunctiva/coronary bands, lameness, depression, & dermatitis with abnormal wool growth
41
what is the etiology of blue tongue?
24 serotypes of the blue tongue virus - genus orbivirus in family reoviridae
42
what are the classic necropsy findings from an animal with bluetongue?
petechia, ecchymoses, or hemorrhages in walls of pulmonary artery & focal necrosis of the papillary muscle of the left ventricle
43
how is blue tongue virus diagnosed?
virus isolation from the blood of febrile animals, PCR to ID specific isolate, & serology (competitive ELISA or AGID)
44
how is blue tongue prevented?
vaccinate in endemic regions - no cross protection between serotypes in non-endemic regions - use serotype-specific inactivated vaccines during outbreaks & use insecticides to control vectors (culicoides spp)
45
how is blue tongue treated?
supportive care - encourage eating, NSAIDS, & deep bedding
46
how does blue tongue virus cause pathology?
virus causes vascular endothelial damage - causing changes to vascular permeability, subsequent intravascular coagulation, leading to edema, congestion, hemorrhage, inflammation, & necrosis
47
T/F: blue tongue also affects wild ruminants
true
48
what are other names for hypomagnesemic tetany?
grass staggers or grass tetany
49
what is the classic case presentation of grass staggers?
lactating ewes that are grazing normally & suddenly throw their heads up, bellowing, galloping in a blind frenzy, falling, & severe paddling/convulsions with repeated episodes & death
50
what are clinical signs seen in less severe cases of grass stagger?
stiffness, hypersensitivity to touch/sound, & frequent urination
51
how is grass staggers diagnosed?
positive response to treatment hypomagnesemia & hypocalcemia (> 0.5 & > 8) post mortem Mg concentrations less than 1.8mg/dl in the vitreous humor
52
how is grass staggers treated?
magnesium & calcium given slowly IV, minimize stimulation as too much can trigger fatal convulsions, follow up with SQ/oral magnesium
53
how is grass staggers prevented?
daily oral magnesium oxide during risk period
54
low magnesium levels in the CSF leads to what?
hyperexcitability, muscle spasms, convulsions, respiratory distress, collapse, & death
55
what are some risk factors for grass staggers?
lactating animals on lush green pastures - lush green gas is low in magnesium & can lead to metabolic alkalosis which causes decreased ionized calcium & magnesium
56
T/F: clinical signs of grass staggers are rare until there is a concurrent hypocalcemia
true

Zuku Top 20s (21 decks)

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