Adult Sheep and Goat Disease Flashcards
a single or small number of ewe(s) present(s) with chronic weight loss. this is a very nonspecific sign… what are a few differentials related to management factors, medical problems, and infectious diseases?
management: inadequate quantity or poor quality diet, inadequate feeder space, poor housing
medical: tooth or oral lesions, lameness (foot rot), parasites eg. Haemonchus
infectious: CLA, OPP, CAE, paratuberculosis
what are the 2 clinical presentations of caseous lymphadenitis? how to confirm this disease?
external vs internal abscesses (internal more common)
culture abscesses (individual) or synergistic hemolysin inhibition test (herd level)
how is caseous lymphadenitis transmitted?
skin and resp route
how is caseous lymphadenitis treated
AMD usually don’t work
external abscess: CULL, or for valuable animals surgically remove, can also try isolation and lancing of abscesses (iodine and chlorhex)
internal abscess: CULL
how is caseous lymphadenitis controlled
purchase from CLA free flock
provide own shearing equipment and dinsinfect
isolation prior to rupture of abscesses
shear affected last, younger animals first
test and cull
vaccinate entire flock if can’t be controlled: Case-Bac, caseous DT Colorado serum cpy
what are the 4 forms of the small ruminant lentiviruses, SRLV (OPP / CAE)? who does each affect?
- chronic pneumonia - sheep
- encephalitic form - lambs and kids <6 mo
the above are grouped as Maedi Visna. - arthritic form - goats, rare in sheep
- hard udder - sheep and goats
how are CAE / OPP transmitted? what kind of virus?
Lentivirus (SRLV)
vertical transmission from colostrum (hardest to control) and milk
horizontal through respiratory (hardest to control), venereal, and lochia
a recently purchased sheep >3 years old with pneumonia gets AMD, seems to improve, then comes back with severe dyspnea, increasing frequency of resp signs, and weight loss. the lungs appear overinflated upon necropsy. what is this a typical presentation of?
Maedi Visna / ovine progressive pleuropneumonia, OPP (a SRLV)
this disease affects mostly goats, sometimes sheep, 1-6 years old. joints are enlarged, most often the carpal joints, and animals can be on knees. weight loss. joint tap reveals 90% monocytes and lymphocytes. what is likely disease?
caprine arthritis and encephalitis - arthritis form
Ddx could be septic arthritis, but we would see degenerate neutrophils on joint tap.
this disease affects sheep and goats 1-6 months old. ataxia rear > forelimbs, paresis, and rarely blindness, head tilt, head tremors.
encephalitis form of SRLV (CAE / OPP)
this disease affects sheep and goats. lymphocytic filtration of mammary tissue causing mastitis “hard udder”
SRLV (CAE / OPP) hard udder form
how are SRLV (OPP / CAE) tested?
PCR, ELISA on serum, culture
how are SRLV (OPP / CAE) treated?
no treatment
how are SRLV (OPP / CAE) controlled?
highly infected: remove newborns, heat treated colostrum or even use cow colostrum, pasteurized milk, serologic surveillance
moderately infected: separate and remove, then milk serological. negatives first, mate sero- to sero- , select for resistant breed
this disease is transmitted through FECAL-ORAL route as well as MILK/COLOSTRUM. bacteria can survive 9 months in manure. disease interferes with nutrient absorption and causes granulomatous inflammation of intestine (see SI images, bottom has this disease)
Johne’s disease or paratuberculosis caused by Mycobacterium avium paratuberculosis
how is paratuberculosis / Johne’s disease diagnosed
PCR on FECES most commonly done
culture of limited benefit (takes too long)
AGID, ELISA detects on 60% of clinically affected animals
how to control paratuberculosis / Johne’s disease
identify and cull
dispose manure
vaccines are not available in Canada
how does contagious ecthyma / sore mouth / off present
young / naivee adults with crusty lesions at mucocutaenous junctions (nose, lips, udder). not distinguishable from other vesicular diseases (FMD, vesicular stomatitis)
how is contagious ecthyma treated
nutritional/fluid support, do not remove crust, course of disease is 1 month
ZOONOTIC! careful
how is contagious ecthyma prevented
maintain virus free herd, closely examine new additions
no vaccine in Canada
describe rumen acidosis pathophysiology
- fermentable substrates release VFAs
- when there is sudden change in ration, interruption after a sale, or an excessive amount of rapidly digestible carbs ingested, there is a large amount of VFA released
- pH drops and Strep. bovis proliferates, produce DL lactic acid
- causes further drop in pH, and Lactobacilli proliferate and make more lactic acid
- lactic acidosis, shock, colic, diarrhea, dehydration can occur
how is rumen acidosis diagnosed
sudden C/S and rapid evolution:
rapid death
severe dehydration
prerenal azotemia
metabolic acidosis with increased plasma lactate
how is rumen acidosis treated
fluids: for CV shock, dehydration, prerenal azotemia
add 5% bicarb or in mild cases MgSO4 to fluids for metabolic acidosis
NSAIDs, AMD (procaine penicillin?), thiamine
grass hay, water until rumen function restored
transfaunation
how is rumen acidosis prevented
slow introduction of concentrate over 2-3 weeks
if high grain ration, use a rumen buffer - sodium bicarb or Mg oxide
