Adult Sheep & Goats (marin's FCs) Flashcards

1
Q

you are presented with a thin sheep, “thin ewe syndrome”, what are your differentials

A

poor diet: not enough, bad quality, not enough feeder space
teeth problems, lameness, parasites

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2
Q

caseous lymphadenitis is caused by ______ and what are the 2 forms?

A

corynebacterium pseudotuberculosis

external and internal abscesses (the ones with internal abscesses lose weight)

transmitted via skin/contact with infected animals

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3
Q

this goat is losing weight. differentials? how will you confirm?

A

caseous lymphadenitis, could also be abscesses of other causes or a cysts, possibly wasting diseases like parasites

culture the abscess (individual test) or synergistic hemolysin inhibition test (herd level test)

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4
Q

how do you treat caseous lymphadenitis?

A

antibiotics dont work!!

if they have external abscesses, cull them, or isolate and lance the abscesses, surgery removal only for valuable animals

if they have internal: cull them

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5
Q

a new sheep farmer is concerned about the risk of caseous lymphadenitis. what recommendations do you have for him to control the disease?

A

purpose CLA free flocks, disinfect shearing equipment, isolate affected animals before rupturing them, shear any affected animals last

can do a SHI Test and ELISA (test and cull)

there is a vaccine, but only use it if it can’t be controlled in the flock; it doesn’t eliminate disease, it will just reduce the number of animals with abscesses

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6
Q

what are the 4 clinical forms of ovine progressive pneumonia (OPP) & Caprine arthritis and encephalitis (CAE)?

A

chronic pneumonia (sheep)
encephalitic form (lambs and kids)
arthritis form (goats)
hard udder (both sheep and goats)

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7
Q

how are OPP and CAE transmitted? what kind of virus is it?

A

lentivirus transmitted via colostrum and milk, respiratory is also possible

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8
Q

a 5 yo ewe that recently lambed a few days ago presents with severe dyspnea and has lost weight. She is in very rough shape and you decide to cull her. On necropsy, her lungs do not deflate as they should. What is this disease most likely and what would you expect to see on histo?

A

OPP

alveoli are filled with cellular infiltrates, mostly macrophages and lymphocytes

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9
Q

a 4 yo goat presents with swollen carpal joints and the goat is “on its knees” as per the producer. The goat also seems to have lost some weight. What would you expect to see on a joint tap based on your top dx?

A

CAE

monocytes and lymphocytes in the joint most likely

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10
Q

a 4 month old sheep presents with ataxia mainly in the hind end, and there seems to be some paresis as well. dx?

A

OPP/CAE

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11
Q

“hard udder” is caused by…

A

OPP/CAE

lymphocytic infiltration causes the udder to become “hard”

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12
Q

a farmer has a few sheep suspected to have OPP/CAE. what diagnostic and treatment options are there? How can this farmer prevent any more cases of this disease?

A

testing: PCR, ELISA on serum, culture

no treatment

prevention: remove any infected newborns from their mothers, heat treat colostrum, pasturize milk fed to babies, serologic surveillance

other options for more moderately infected flocks: milk negative first and positive last, mate neg with neg to breed it out, select for resistant breeds

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13
Q

true or false: most SR with johne’s will have diarrhea

A

false, only 20% do

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14
Q

you are presented with a very thin adult goat with chronic weight loss, but the producer says the goat is eating very well still. The goat does not have diarrhea and is UTD on parasite prevention. most likely diagnosis?

A

johne’s/paratuberculosios

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15
Q

how is johne’s transmitted?

A

milk/colostrum
feco-oral

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16
Q

a producer has many suspected cases of johne’s in his herd and wants to test them for it. what options are there?

A

ELISA
PCR

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17
Q

a young goat presents with these oral lesions. based on your top differential, what other location would you expect to see lesions besides the oral cavity?

A

contagious ecthyma/orf

the udder and possibly the nose

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18
Q

orf doesn’t really have a “treatment” and the disease usually goes away in a month, but can still cause some weight loss. What is one other reason you do NOT want it in your herd, and how can you prevent this disease?

A

it is zoonotic!!!!

prevention: maintain a virus free herd, closely examine new additions to the herd

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19
Q

briefly explain the pathogenesis of rumen acidosis

A

lots of fermentable feed creates lots of VFAs, which leads to a drop in pH, which changes the microbe population in the rumen, S. bovis proliferates and produces a lot of lactic acid causing the pH to drop more, which allows lactobacilli to proliferate, producing more lactic acid, resulting in a self feeding cycle

20
Q

clinical signs of rumen acidosis include

A

shock, colic, diarrhea, dehydration, lactic acidosis, rapid death, pre-renal azotemia, metabolic acidosis

21
Q

a herd of 3 yo ewes present for diarrhea, colic, and severe dehydration. The producer says they are new to farming and just barely got his sheep a few days ago. He is very worried about his sheep. You find out that the producer gave the sheep their concentrate just last night, and when you asked how much, the producer said he let them “eat as much as they wanted”. Based on your top dx, what treatment is best for the ewe?

A

rumen acidosis
fluids with 5% bicarbonate to correct acidosis, consider NSAIDs, antibiotics, thiamine (risk for PEM;bacteria eat up all the thiamine), only feed the ewe grass hay and water until she’s better. could consider rumen juice transplant too

22
Q

how will you instruct the new producer to prevent rumen acidosis in the future?

A

slow introduction of concentrate, or if the sheep are on a high grain ration, add in a rumen buffer like sodium bicarb of magnesium oxide to help neutralize the acidity

23
Q

listeriosis causes

A

multifocal encephalitis, septicemia, abortion

24
Q

a herd of sheep presents for head tilt, depression, and a recent increase in the number of abortions. some of the ewes have also been found dead on pasture. It has been an exceptionally wet season this year. these sheep are being fed a mix of grass hay and silage. based on your top dx, what treatment is best?

A

listeriosis (L monocytogenes)

procaine penicillin or oxytet, fluid support

25
Q

sheep/goats infected with listeriosis shed it via

A

feces, MILK, tears, and uterine fluid

26
Q

tetanus in sheep is often associated with

A

castration and tail docking

sometimes shearing, umbilical infection, post partum metritis

mostly unvaccinated animals

27
Q

in order to prevent tetanus in sheep/goats, you should vaccinate who and when?

A

ewes pre lambing (so its in colostrum)
AND vaccinate lambs

28
Q

what is scrapie? why does it happen?

A

transmissible spongiform encephalopathies similar to BSE and CWD

it is an infectious prion that accumulates in neurons

29
Q

scrapie is transmitted vis

A

ingestion of placenta and amniotic fluid
feces and milk
urine

30
Q

clinical signs of scrapie include

A

rubbing of flanks against objects, loss of wool, bruxism and/or lip licking, nibbling of feet, trembling, ataxia, weakness, excitable, over reactive to stimuli, dropping ears, aggression, weight loss, death

31
Q

what is the scratch test for scrapie?

A

scratch their back and they go nuts=scrapie

32
Q

for genotyping scrapie, the codons of interest are

A

171, 154, and 136

33
Q

for codon 171, if arginine (R)= _____ and if glutamine (Q)=_______

for codon 136, if alanine (A)=______ and if valine (V)=______

so therefore, an AARR genotype means ___ and a VVQQ genotype means___

A

resistance, susceptible

resistance, suscpetible

R and A are resistant

Q and V are susceptible

not susceptible at all
very susceptible

34
Q

what is atypical scrapie?

A

usually only 1 case in a herd

ataxia, weight loss, weird behavior

no lesions in the obex on pathology/histo

35
Q

foot rot is a painful contagious disease of the feet and can cause severe lameness, causing weight loss. How is this disease best treated?

A

examine feet of all animals carefully!
for severely affected animals=cull

for the exposed group: trim feet, foot bath, clean ground housing

for the lame group: extensive feet trimming, antibiotic LA, footbath for 1hr, clean pasture

36
Q

how is footrot prevented?

A

avoid introduction of disease! quarantine animals for 30 days, regular foot trimmings, foot baths with zinc/sulfur

vaccines DO NOT work for foot rot

37
Q

who is more susceptible to copper toxicity

A

sheep (young lambs moreso than adults)

38
Q

what are some potential sources of copper in regards to copper toxicity?

A

swine, equine, or cattle feed
trace mineral supplements
foot baths with copper sulfate
fertilized pasture with chicken or pig manure

39
Q

what are the 3 scenarios for copper toxicity?

A

acute poisoning: high amount of copper suddenly
primary chronic: accumulation over time in the liver and then sudden release (MOST COMMON)
secondary chronic: plants promote accumulation of copper or hepatotoxic plants

40
Q

pathogenesis of copper toxicity?

A

copper builds up in the liver, suddenly copper is released into blood, causes hemolysis=anemia, hemoglobinuria/emia, and hemoglobinuric nephrosis

41
Q

clinical signs of copper toxicity?

A

acute: salivation, abdominal pain, diarrhea
chronic: pale, icterus, weakness, anorexia, trambling

42
Q

the “gun metal kidney” is pathogneumiiicncbefiuefubfbfkc for

A

copper toxicity

43
Q

can copper toxicity be treated?

A

not really

can try ammonium tetrathiomolybdate to lower copper stores

supportive therapy like fluids to help kidneys

44
Q

urolithiasis in SR is commonly caused by _______. What are some risk factors?

A

calcium salts and phosphatic complexes

risk factors: high concentrate low roughage feed, feedlot or show rams, limited water, early castration (makes urethra smaller)

45
Q

you are called out to a sheep feedlot where one of the breeding rams is “colicky”. When you get there you see he is struggling to urinate, he is teeth grinding, and you see a little drop of blood coming out as he strains to pee. Based on the top dx, what will you recommend to this producer for this ram and for future rams?

A

urolithiasis

to fully diagnose: sedate, exteriorize the penis, ultrasound to check for ruptured bladder, rectal palp/pulsations (idk what this means)

treatment: urethral process removal, catheter + retrograde flushing, perineal urethrostomy (salvage procedure), cyctotomy and flushing, etc.

prevention: more water access, balance Ca:P ratio, add ammonium chloride to the diet to decrease urine pH