Ruminant Top 15 Small Ruminant Diseases - Part 2 Flashcards
what is the classic case of CAE in an adult small ruminant?
progressive polysynovitis/arthritis - swollen joints (especially the carpus), lameness, weight loss, poor hair coat, indurative mastitis (hard udder), agalactia, & dyspnea due to interstitial pneumonia
what is the classic case presentation of CAE in a 2-4 month old kid?
encephalomyelitis - weakness, ataxia, placing deficits in pelvic limbs, hypertonia, hyperreflexia, & may progress to para or tetraparesis or paralysis
what is the etiology of CAE?
enveloped single stranded RNA lentivirus similar to ovine progressive pneumonia/maedi visna - family retroviridae
what testing is used for herd control programs of CAE?
serology - agar gel immunodiffusion (AGID) more specific - ELISA is more sensitive
how is a definitive diagnosis of CAE made?
biopsy or necropsy shows characteristic lymphoproliferative mononuclear cell infiltration
virus isolation or pcr
what is the prevalence of CAE in dairy goats?
wide spread, 65% prevalence in US herd with only 20% of infected goats ever showing clinical signs
how is CAE prevented?
isolate kids at birth & feed heat treated colostrum, pasteurized milk
serology of herd biannually - separate seropositive & seronegative animals & eventually cull seropositive animals
when are most goats infected by CAE?
infected when young through colostrum or milk - clinical signs develop much later
horizontal transmission within the herd is possible
what is the classic case presentation of pregnancy toxemia in small ruminants?
late gestation pregnancy (last 1-2 weeks) with an over-conditioned or under-conditioned dam likely with multiple fetuses
partial anorexia/depression, bruxism, aimless pacing, muscle tremors, opisthotonus, blindness, ataxia, recumbency, coma, & death
what lab abnormalities are seen on a small ruminant diagnosed with pregnancy toxemia?
ketosis (increased serum beta-hydroxybutyric acid) & increased urine ketones), hypoglycemia, hypocalcemia, increased non-esterified fatty acids
what is seen on necropsy of a small ruminant that died from pregnancy toxemia?
hepatic lipidosis, adrenal enlargement - increased BHB in aqueous humor or CSF
what is the treatment for mild cases of pregnancy toxemia in small ruminants?
enteral/oral therapy - propylene glycol, +/- calcium, potassium, & inducing parturition with steroids
what is the treatment for severe cases of pregnancy toxemia in small ruminants?
maybe euthanasia
check fetal viability with u/s - if alive & within 3 days of due date, c-section, if dead, induce with steroids
IV therapy - dextrose, insulin, calcium, flunixin, & maybe give oral potassium
how can feeding management be improved for preventing pregnancy toxemia in small ruminants?
provide adequate space, sort animals by BCS, ration formulation, & forage analysis
how is pregnancy toxemia prevented?
assess BCS at breeding & at mid-gestation pregnancy check - take 6 weeks to raise BCS by 1 point, improve feeding management, DO NOT ENTER LAST 6 WEEKS OF PREGNANCY WITH BCS LESS THAN 2.5
how is herd screening used to prevent pregnancy toxemia in small ruminants?
screen 20% of the flock - serum BHB levels should be less than 0.8mmol/L
(0.8-1.6mmol/L is a moderate risk - higher than 1.7mmol/L is a high risk)
what drug may be used to help late gestation ewes to improve feed efficiency to prevent pregnancy toxemia that should not be used in goats?
ionophores - monensin
don’t give to goats
why does pregnancy toxemia develop in small ruminants?
develops when there is inadequate nutrition in late gestation in the face of increased metabolizable energy requirements
mobilized fat stores & increased liver gluconeogenesis passes glucose to the fetus - can overwhelm the liver leading to hepatic lipidosis/ketosis
what is the prognosis for pregnancy toxemia in small ruminants?
good if ambulatory with mild clinical signs
guarded to poor if recumbent or comatose
what is the classic case presentation of a small ruminant with a partial urethral obstruction due to urolithiasis?
dribbling urine, hematuria/stranguria, & mineral crystals on hair around urethral orifice
what is the classic case presentation of a small ruminant with a complete urethral obstruction due to urolithiasis?
tenesmus, tail swishing, colic, weight shifting, bloat, rectal prolapse, inappetence, depression
what is the classic case presentation of a small ruminant with a urethral/bladder rupture due to urolithiasis?
abdominal swelling, preputial swelling, necrosis of the ventral abdomen skin with pseudourethral development
how is a ruptured bladder in a small ruminant diagnosed?
abdominal ballotment of fluid wave, large volume of hypoechoic fluid in the abdomen seen on u/s, creatinine of abdominal fluid is 2x more than that of peripheral blood off of abdominocentesis, & on bloodwork, low sodium/chloride, high phospate, & metabolic alkalosis
what uroliths can be diagnosed off of radiographs in small ruminants? which ones are not?
radiopaque - calcium carbonate & calcium oxalate calculi
radiolucent - struvite
if a small ruminant presents obstructed due to urolithiasis but is not ruptured, what is the preferred treatment? if it is an early/mid/partial obstruction? blocked at urethral process?
tube cystotomy - calculi are expelled spontaneously over time
early/mid/partial - try antispasmodics/tranquilizers to relax sigmoid flexure of penis
blocked at urethral process - amputate
what surgery can be done for a blocked small ruminant due to urolithiasis? what is a common long term complication?
perineal urethrostomy done to bypass urolith
strictures!!!
what treatment is done for a small ruminant with a ruptured urethra/bladder due to urolithiasis?
drain uroperitoneum slowly via teat cannula or trocar, IV normal saline to correct electrolyte abnormalities/dehydration/acid base abnormalities
PU as salvage procedure - cannot repair the bladder, but may repair on its own
usually culled within 3-4 months
why are uroliths more of a problem in male small ruminants?
they have a long urethra with a sigmoid flexure - more places to get blocked
what diets predispose small ruminants to developing urolithiasis?
high grain diets with a 1:1 calcium:phosphorus ratio or diets high in magnesium
where do small ruminants often get blocked due to urolithiasis?
most often at sigmoid flexure & urethral process
what is the most common type or urolith to cause issues in small ruminants?
urethroliths
what diet predisposes small ruminants to develop struvite crystals/uroliths?
magnesium-ammonium-phosphate stones - due to lots of grain with low calcium:phosphorus ratio
what diet predisposes small ruminants to develop silica crystals/uroliths?
associated with grazing on silica-rich soil
what diet predisposes small ruminants to develop calcium crystals/uroliths?
due to high calcium diets
T/F: urolith type in small ruminants is based on diets
true
what is the classic presentation of acute copper toxicity in sheep?
gi pain, diarrhea, anorexia, dehydration, & shock
which is more common - acute or chronic presentations of copper toxicity in sheep? why?
chronic is more common - no signs until they have an ACUTE hemolytic crisis
what is the classic case presentation of chronic copper toxicity in sheep?
depression, lethargy, weakness, recumbency, rumen stasis, anorexia, thirst, dyspnea, pale mucus membranes, hemoglobinuria, jaundice, photosensitization, & if the animal survives, renal failure
what is seen at necropsy in a sheep that died from acute copper toxicity?
blue-green ingesta, gun metal colored kidneys, & enlarged spleen
what is seen at necropsy in a sheep that died from chronic copper toxicity?
increased blood & liver copper concentrations & need to measure molybdenum levels
T/F: treatment for copper toxicity is rarely successful & carries a poor prognosis
true
what is the acute treatment used for copper toxicity in sheep?
gi sedative & shock treatment, penicillamine to enhance copper excretion, & vitamin c as an antioxidant for erythrocyte damage
what are some preventative medications used for copper toxicity in sheep?
ammonium tetrathiomolybdenate - decreases liver copper absorption & increases liver copper excretion (withdrawal period of 10)
molybdenum - top-dress pasture, supplement feed
zinc acetate, sodium thiosulfate - feed supplements that both help to decrease copper absorption
T/F: copper toxicity is a world wide problem & sheep are uniquely sensitive
true
T/F: sheep will have increase liver enzymes for weeks before an acute crisis from copper toxicity occurs
true
what are the factors that affect copper metabolism in sheep?
low molybdenum in diet - leads to excess copper retention
low sulfur, zinc, calcium in diet
subterranean clover - excess copper retention
plants, heliotropium europaeum or senecio, hepatotoxic alkaloids that cause liver disease - release of copper into bloodstream & hemolysis
what are some examples of stress that may incite a copper toxicity crisis in sheep?
transportation, handling, pregnancy, lactation, deteriorating plane of nutrition, weather conditions, & strenuous exercise
what is the pathophysiology of copper toxicity in sheep?
excessive copper ingestion for long periods lead to copper build up in the liver & then stress causes a sudden release leading to an acute hemolytic crisis
what breeds most commonly are affected by polled intersex syndrome?
western european breeds - toggenburg, saanen, & alpine
what is the classic case presentation of polled intersex syndrome?
usually male phenotype, female genotype with testes/ovotestes & dysfunctional penis (rare is a female phenotype with enlarged clitoris & hypospadias)
why should you never breed polled homozygous male goats?
they have increased fertility because of segmental epididymal aplasia
how is polled intersex syndrome diagnosed? how is it treated?
thorough physical exam
CULL THEM DO NOT BREED
T/F: polledness is an autosomal dominant trait in male & females while intersexism is a recessive trait only seen in polled females
true
how are intersex goats characterized?
homozygous for polled trait
genetically female with male traits (developed testes)
most are NOT true hermaphrodites (true testes & ovarian structure)
T/F: polled intersex syndrome is very rare in cattle & sheep
true
what causes freemartinism in goats?
occurs in 20% of opposite sex sheep twins - arteriovenous anastomoses between their placentas leads to masculinization of the female twin
what animals are most affected by pizzle rot?
male small ruminants - especially castrated males
what is the classic case presentation of a mild pizzle rot? what about a severe case?
mild - preputial swelling
severe - preputial swelling plus straining to urinate, scabs/ulcers around preputial orifice, urine accumulation in prepuce, & fatal if urinary blockage due to chronic scarring
what are some other names for pizzle rot?
enzootic posthitis/vulvitis, enzootic balanoposthitis
how do females present with pizzle rot?
swelling, redness of vulva/clitoris & scabs & ulcers of vulva/vestibule, & caudal vagina with yellow exudate
what is the etiology of pizzle rot in small ruminants?
corynebacterium renale - gram negative diphtheroid bacterium that hydrolyzes urea
how is pizzle rot diagnosed?
clinical signs & culture
how is pizzle rot treated in small ruminants?
isolate animal, feed low-protein diet, clean/clip around prepuce, make sure urethra is patent (watch for urination & pass catheter past scarring), & abx (cephalosporin or penicillin)
what is the pathophysiology of pizzle rot?
high protein diet that leads to increased urea in urine causing increased ammonia produced by c. renale which causes penile/urethral irritation
what are predisposing factors for pizzle rot?
dirt caked in hair around prepuce
preputial hairs too short or long - alters urine flow away from urethral orifice
T/F: there is seasonal incidence associated with high protein feed intake & pizzle rot
true
