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ZUKU NAVLE PREP > Ruminant Top 15 Small Ruminant Diseases - Part 2 > Flashcards

Ruminant Top 15 Small Ruminant Diseases - Part 2 Flashcards

1
Q

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

A

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

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2
Q

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

A

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

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3
Q

what is the etiology of CAE?

A

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

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4
Q

what testing is used for herd control programs of CAE?

A

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

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5
Q

how is a definitive diagnosis of CAE made?

A

biopsy or necropsy shows characteristic lymphoproliferative mononuclear cell infiltration

virus isolation or pcr

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6
Q

what is the prevalence of CAE in dairy goats?

A

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

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7
Q

how is CAE prevented?

A

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

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

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8
Q

when are most goats infected by CAE?

A

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

horizontal transmission within the herd is possible

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9
Q

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

A

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

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10
Q

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

A

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

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11
Q

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

A

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

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12
Q

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

A

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

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13
Q

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

A

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

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14
Q

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

A

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

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15
Q

how is pregnancy toxemia prevented?

A

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

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16
Q

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

A

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)

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17
Q

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?

A

ionophores - monensin

don’t give to goats

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18
Q

why does pregnancy toxemia develop in small ruminants?

A

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

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19
Q

what is the prognosis for pregnancy toxemia in small ruminants?

A

good if ambulatory with mild clinical signs

guarded to poor if recumbent or comatose

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20
Q

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

A

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

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21
Q

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

A

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

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22
Q

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

A

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

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23
Q

how is a ruptured bladder in a small ruminant diagnosed?

A

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

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24
Q

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

A

radiopaque - calcium carbonate & calcium oxalate calculi

radiolucent - struvite

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25
Q

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?

A

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

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26
Q

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

A

perineal urethrostomy done to bypass urolith

strictures!!!

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27
Q

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

A

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

28
Q

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

A

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

29
Q

what diets predispose small ruminants to developing urolithiasis?

A

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

30
Q

where do small ruminants often get blocked due to urolithiasis?

A

most often at sigmoid flexure & urethral process

31
Q

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

A

urethroliths

32
Q

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

A

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

33
Q

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

A

associated with grazing on silica-rich soil

34
Q

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

A

due to high calcium diets

35
Q

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

A

true

36
Q

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

A

gi pain, diarrhea, anorexia, dehydration, & shock

37
Q

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

A

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

38
Q

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

A

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

39
Q

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

A

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

40
Q

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

A

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

41
Q

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

A

true

42
Q

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

A

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

43
Q

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

A

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

44
Q

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

A

true

45
Q

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

A

true

46
Q

what are the factors that affect copper metabolism in sheep?

A

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

47
Q

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

A

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

48
Q

what is the pathophysiology of copper toxicity in sheep?

A

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

49
Q

what breeds most commonly are affected by polled intersex syndrome?

A

western european breeds - toggenburg, saanen, & alpine

50
Q

what is the classic case presentation of polled intersex syndrome?

A

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

51
Q

why should you never breed polled homozygous male goats?

A

they have increased fertility because of segmental epididymal aplasia

52
Q

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

A

thorough physical exam

CULL THEM DO NOT BREED

53
Q

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

A

true

54
Q

how are intersex goats characterized?

A

homozygous for polled trait

genetically female with male traits (developed testes)

most are NOT true hermaphrodites (true testes & ovarian structure)

55
Q

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

A

true

56
Q

what causes freemartinism in goats?

A

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

57
Q

what animals are most affected by pizzle rot?

A

male small ruminants - especially castrated males

58
Q

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

A

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

59
Q

what are some other names for pizzle rot?

A

enzootic posthitis/vulvitis, enzootic balanoposthitis

60
Q

how do females present with pizzle rot?

A

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

61
Q

what is the etiology of pizzle rot in small ruminants?

A

corynebacterium renale - gram negative diphtheroid bacterium that hydrolyzes urea

62
Q

how is pizzle rot diagnosed?

A

clinical signs & culture

63
Q

how is pizzle rot treated in small ruminants?

A

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)

64
Q

what is the pathophysiology of pizzle rot?

A

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

65
Q

what are predisposing factors for pizzle rot?

A

dirt caked in hair around prepuce

preputial hairs too short or long - alters urine flow away from urethral orifice

66
Q

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

A

true

67
Q
A

ZUKU NAVLE PREP (178 decks)

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