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ZUKU NAVLE PREP > 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?

A

worldwide

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
Q

is the BVDV vaccine effective for preventing border disease?

A

NOPE

26
Q

what breeds are predisposed to scrapie?

A

black faced breeds

27
Q

what is the classic case presentation of scrapie?

A

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
Q

what is the cutaneous sensitivity seen in small ruminants with scrapie?

A

if you scratch their back, sheep will throw their head back & lick the air or compulsively nibble lower limbs

29
Q

what is the etiology of scrapie?

A

transmissible spongiform encephalopathy caused by an abnormal prion protein related to BSE & CWD

30
Q

how is scrapie diagnosed?

A

3rd eyelid or rectal mucosal biopsy for IHC - rectal biopsy is easier/more sensitive

necropsy - brain IHC

31
Q

what is the USDA/APHIS scrapie slaughter surveillance program?

A

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
Q

what is the US mandatory scrapie eradication program?

A

individual & premises identification required for all breeding sheep leaving their premises

33
Q

how does scrapie cause neuro signs?

A

the abnormal prion is deposited as an amyloid plaque in lymphoreticular & nervous tissue leading to neuro signs

34
Q

how is scrapie transmitted? how long is the incubation period?

A

transmitted during lambing (NOT IN UTERO)

2-5 year incubation period

35
Q

does scrapie affect humans?

A

NO

36
Q

where is scrapie found in the world?

A

everywhere but australia & new zealand

37
Q

T/F: scrapie is rare but possible in goats

A

true

38
Q

what is the classic case presentation of blue tongue?

A

cyanotic tongue, fever, serous/mucopurulent nasal discharge, edema of lips/nose/face/submandibular area, reluctance to eat

39
Q

what congenital defects are seen with blue tongue virus?

A

infection of pregnant dams produces fetuses with hydrancephaly or porencephaly causing ataxic/blind lambs

40
Q

what signs of blue tongue are seen in fine-wool/mutton breeds of sheep?

A

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
Q

what is the etiology of blue tongue?

A

24 serotypes of the blue tongue virus - genus orbivirus in family reoviridae

42
Q

what are the classic necropsy findings from an animal with bluetongue?

A

petechia, ecchymoses, or hemorrhages in walls of pulmonary artery & focal necrosis of the papillary muscle of the left ventricle

43
Q

how is blue tongue virus diagnosed?

A

virus isolation from the blood of febrile animals, PCR to ID specific isolate, & serology (competitive ELISA or AGID)

44
Q

how is blue tongue prevented?

A

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
Q

how is blue tongue treated?

A

supportive care - encourage eating, NSAIDS, & deep bedding

46
Q

how does blue tongue virus cause pathology?

A

virus causes vascular endothelial damage - causing changes to vascular permeability, subsequent intravascular coagulation, leading to edema, congestion, hemorrhage, inflammation, & necrosis

47
Q

T/F: blue tongue also affects wild ruminants

A

true

48
Q

what are other names for hypomagnesemic tetany?

A

grass staggers or grass tetany

49
Q

what is the classic case presentation of grass staggers?

A

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
Q

what are clinical signs seen in less severe cases of grass stagger?

A

stiffness, hypersensitivity to touch/sound, & frequent urination

51
Q

how is grass staggers diagnosed?

A

positive response to treatment

hypomagnesemia & hypocalcemia (> 0.5 & > 8)

post mortem Mg concentrations less than 1.8mg/dl in the vitreous humor

52
Q

how is grass staggers treated?

A

magnesium & calcium given slowly IV, minimize stimulation as too much can trigger fatal convulsions, follow up with SQ/oral magnesium

53
Q

how is grass staggers prevented?

A

daily oral magnesium oxide during risk period

54
Q

low magnesium levels in the CSF leads to what?

A

hyperexcitability, muscle spasms, convulsions, respiratory distress, collapse, & death

55
Q

what are some risk factors for grass staggers?

A

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
Q

T/F: clinical signs of grass staggers are rare until there is a concurrent hypocalcemia

A

true

ZUKU NAVLE PREP (178 decks)

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