Ruminant Top 15 Small Ruminant Diseases - Part 2

Question 1

what is the classic case of CAE in an adult small ruminant?

Answer 1

progressive polysynovitis/arthritis - swollen joints (especially the carpus), lameness, weight loss, poor hair coat, indurative mastitis (hard udder), agalactia, & dyspnea due to interstitial pneumonia

Question 2

what is the classic case presentation of CAE in a 2-4 month old kid?

Answer 2

encephalomyelitis - weakness, ataxia, placing deficits in pelvic limbs, hypertonia, hyperreflexia, & may progress to para or tetraparesis or paralysis

Question 3

what is the etiology of CAE?

Answer 3

enveloped single stranded RNA lentivirus similar to ovine progressive pneumonia/maedi visna - family retroviridae

Question 4

what testing is used for herd control programs of CAE?

Answer 4

serology - agar gel immunodiffusion (AGID) more specific - ELISA is more sensitive

Question 5

how is a definitive diagnosis of CAE made?

Answer 5

biopsy or necropsy shows characteristic lymphoproliferative mononuclear cell infiltration

virus isolation or pcr

Question 6

what is the prevalence of CAE in dairy goats?

Answer 6

wide spread, 65% prevalence in US herd with only 20% of infected goats ever showing clinical signs

Question 7

how is CAE prevented?

Answer 7

isolate kids at birth & feed heat treated colostrum, pasteurized milk

serology of herd biannually - separate seropositive & seronegative animals & eventually cull seropositive animals

Question 8

when are most goats infected by CAE?

Answer 8

infected when young through colostrum or milk - clinical signs develop much later

horizontal transmission within the herd is possible

Question 9

what is the classic case presentation of pregnancy toxemia in small ruminants?

Answer 9

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

Question 10

what lab abnormalities are seen on a small ruminant diagnosed with pregnancy toxemia?

Answer 10

ketosis (increased serum beta-hydroxybutyric acid) & increased urine ketones), hypoglycemia, hypocalcemia, increased non-esterified fatty acids

Question 11

what is seen on necropsy of a small ruminant that died from pregnancy toxemia?

Answer 11

hepatic lipidosis, adrenal enlargement - increased BHB in aqueous humor or CSF

Question 12

what is the treatment for mild cases of pregnancy toxemia in small ruminants?

Answer 12

enteral/oral therapy - propylene glycol, +/- calcium, potassium, & inducing parturition with steroids

Question 13

what is the treatment for severe cases of pregnancy toxemia in small ruminants?

Answer 13

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

Question 14

how can feeding management be improved for preventing pregnancy toxemia in small ruminants?

Answer 14

provide adequate space, sort animals by BCS, ration formulation, & forage analysis

Question 15

how is pregnancy toxemia prevented?

Answer 15

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

Question 16

how is herd screening used to prevent pregnancy toxemia in small ruminants?

Answer 16

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)

Question 17

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?

Answer 17

ionophores - monensin

don’t give to goats

Question 18

why does pregnancy toxemia develop in small ruminants?

Answer 18

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

Question 19

what is the prognosis for pregnancy toxemia in small ruminants?

Answer 19

good if ambulatory with mild clinical signs

guarded to poor if recumbent or comatose

Question 20

what is the classic case presentation of a small ruminant with a partial urethral obstruction due to urolithiasis?

Answer 20

dribbling urine, hematuria/stranguria, & mineral crystals on hair around urethral orifice

Question 21

what is the classic case presentation of a small ruminant with a complete urethral obstruction due to urolithiasis?

Answer 21

tenesmus, tail swishing, colic, weight shifting, bloat, rectal prolapse, inappetence, depression

Question 22

what is the classic case presentation of a small ruminant with a urethral/bladder rupture due to urolithiasis?

Answer 22

abdominal swelling, preputial swelling, necrosis of the ventral abdomen skin with pseudourethral development

Question 23

how is a ruptured bladder in a small ruminant diagnosed?

Answer 23

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

Question 24

what uroliths can be diagnosed off of radiographs in small ruminants? which ones are not?

Answer 24

radiopaque - calcium carbonate & calcium oxalate calculi

radiolucent - struvite

Question 25

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?

Answer 25

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

Question 26

what surgery can be done for a blocked small ruminant due to urolithiasis? what is a common long term complication?

Answer 26

perineal urethrostomy done to bypass urolith strictures!!!

Question 27

what treatment is done for a small ruminant with a ruptured urethra/bladder due to urolithiasis?

Answer 27

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

Question 28

why are uroliths more of a problem in male small ruminants?

Answer 28

they have a long urethra with a sigmoid flexure - more places to get blocked

Question 29

what diets predispose small ruminants to developing urolithiasis?

Answer 29

high grain diets with a 1:1 calcium:phosphorus ratio or diets high in magnesium

Question 30

where do small ruminants often get blocked due to urolithiasis?

Answer 30

most often at sigmoid flexure & urethral process

Question 31

what is the most common type or urolith to cause issues in small ruminants?

Answer 31

urethroliths

Question 32

what diet predisposes small ruminants to develop struvite crystals/uroliths?

Answer 32

magnesium-ammonium-phosphate stones - due to lots of grain with low calcium:phosphorus ratio

Question 33

what diet predisposes small ruminants to develop silica crystals/uroliths?

Answer 33

associated with grazing on silica-rich soil

Question 34

what diet predisposes small ruminants to develop calcium crystals/uroliths?

Answer 34

due to high calcium diets

Question 35

T/F: urolith type in small ruminants is based on diets

Answer 35

true

Question 36

what is the classic presentation of acute copper toxicity in sheep?

Answer 36

gi pain, diarrhea, anorexia, dehydration, & shock

Question 37

which is more common - acute or chronic presentations of copper toxicity in sheep? why?

Answer 37

chronic is more common - no signs until they have an ACUTE hemolytic crisis

Question 38

what is the classic case presentation of chronic copper toxicity in sheep?

Answer 38

depression, lethargy, weakness, recumbency, rumen stasis, anorexia, thirst, dyspnea, pale mucus membranes, hemoglobinuria, jaundice, photosensitization, & if the animal survives, renal failure

Question 39

what is seen at necropsy in a sheep that died from acute copper toxicity?

Answer 39

blue-green ingesta, gun metal colored kidneys, & enlarged spleen

Question 40

what is seen at necropsy in a sheep that died from chronic copper toxicity?

Answer 40

increased blood & liver copper concentrations & need to measure molybdenum levels

Question 41

T/F: treatment for copper toxicity is rarely successful & carries a poor prognosis

Answer 41

true

Question 42

what is the acute treatment used for copper toxicity in sheep?

Answer 42

gi sedative & shock treatment, penicillamine to enhance copper excretion, & vitamin c as an antioxidant for erythrocyte damage

Question 43

what are some preventative medications used for copper toxicity in sheep?

Answer 43

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

Question 44

T/F: copper toxicity is a world wide problem & sheep are uniquely sensitive

Answer 44

true

Question 45

T/F: sheep will have increase liver enzymes for weeks before an acute crisis from copper toxicity occurs

Answer 45

true

Question 46

what are the factors that affect copper metabolism in sheep?

Answer 46

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

Question 47

what are some examples of stress that may incite a copper toxicity crisis in sheep?

Answer 47

transportation, handling, pregnancy, lactation, deteriorating plane of nutrition, weather conditions, & strenuous exercise

Question 48

what is the pathophysiology of copper toxicity in sheep?

Answer 48

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

Question 49

what breeds most commonly are affected by polled intersex syndrome?

Answer 49

western european breeds - toggenburg, saanen, & alpine

Question 50

what is the classic case presentation of polled intersex syndrome?

Answer 50

usually male phenotype, female genotype with testes/ovotestes & dysfunctional penis (rare is a female phenotype with enlarged clitoris & hypospadias)

Question 51

why should you never breed polled homozygous male goats?

Answer 51

they have increased fertility because of segmental epididymal aplasia

Question 52

how is polled intersex syndrome diagnosed? how is it treated?

Answer 52

thorough physical exam CULL THEM DO NOT BREED

Question 53

T/F: polledness is an autosomal dominant trait in male & females while intersexism is a recessive trait only seen in polled females

Answer 53

true

Question 54

how are intersex goats characterized?

Answer 54

homozygous for polled trait genetically female with male traits (developed testes) most are NOT true hermaphrodites (true testes & ovarian structure)

Question 55

T/F: polled intersex syndrome is very rare in cattle & sheep

Answer 55

true

Question 56

what causes freemartinism in goats?

Answer 56

occurs in 20% of opposite sex sheep twins - arteriovenous anastomoses between their placentas leads to masculinization of the female twin

Question 57

what animals are most affected by pizzle rot?

Answer 57

male small ruminants - especially castrated males

Question 58

what is the classic case presentation of a mild pizzle rot? what about a severe case?

Answer 58

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

Question 59

what are some other names for pizzle rot?

Answer 59

enzootic posthitis/vulvitis, enzootic balanoposthitis

Question 60

how do females present with pizzle rot?

Answer 60

swelling, redness of vulva/clitoris & scabs & ulcers of vulva/vestibule, & caudal vagina with yellow exudate

Question 61

what is the etiology of pizzle rot in small ruminants?

Answer 61

corynebacterium renale - gram negative diphtheroid bacterium that hydrolyzes urea

Question 62

how is pizzle rot diagnosed?

Answer 62

clinical signs & culture

Question 63

how is pizzle rot treated in small ruminants?

Answer 63

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)

Question 64

what is the pathophysiology of pizzle rot?

Answer 64

high protein diet that leads to increased urea in urine causing increased ammonia produced by c. renale which causes penile/urethral irritation

Question 65

what are predisposing factors for pizzle rot?

Answer 65

dirt caked in hair around prepuce preputial hairs too short or long - alters urine flow away from urethral orifice

Question 66

T/F: there is seasonal incidence associated with high protein feed intake & pizzle rot

Answer 66

true