Small Ruminant Periparturient Diseases Flashcards

1
Q

what are the 3 most common periparturient diseases in small ruminants?

A
  1. pregnancy toxemia
  2. hypocalcemia
  3. hypomagnesemia
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2
Q

what causes peripaturient metabolic diseases in small ruminants?

A

failure to meet nutritional requirements during late pregnancy and/or early lactation

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3
Q

what causes pregnancy toxemia in small ruminants?

A

abnormal metabolism of carbs and fats in last trimester
(rapid fetal growth, increased metabolic demand and competition with fetus for glucose, stress, decreased rumen capacity, genetics)

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4
Q

Name the following TYPE of pregnancy toxemia:

results from a decline in plane of nutrition during late pregnancy or management changes that create a brief period of fasting

A

primary pregnancy toxemia

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5
Q

Name the following TYPE of pregnancy toxemia:

excessively thin ewes resulting from mismanagement or unavailable feed resources following periods of drought, heavy snow, or flooding.

A

starvation pregnancy toxemia

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6
Q

Name the following TYPE of pregnancy toxemia:

sporadic and results from concurrent disease in the affected female

A

secondary pregnancy toxemia

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7
Q

Name the following TYPE of pregnancy toxemia:

results from overconditioning during early pregnancy, sometimes followed by late gestational decline in nutrition. Excess abdominal fat also contributes to reduced rumen capacity.

A

fat ewe/doe pregnancy toxemia

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8
Q

Name a few causes of SECONDARY pregnancy toxemia.

A

this pregnancy toxemia type will result from conditions that cause DECREASED FEED INTAKE and INCREASED ENERGY NEEDS

  • acidosis
  • thin/malnourished animals
  • water deprivation
  • infectious pododermatitis
  • vaginal prolapse
  • poor dentition
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9
Q

what are clinical signs associated with pregnancy toxemia in small ruminants?

A
  • Early: anorexia, depression
  • Advanced: recumbent, listlessness, neuro signs (head pressing, muscle tremors, blindness, star-gazing, ataxia), tachypnea, dyspnea, chewing/teeth grinding, excessive salivation and licking.
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10
Q

How can we diagnose pregnancy toxemia in SR?

A
  • Hx, Sg, and clin signs
  • ketonuria
  • ketonemia ( 1.4-2.4 = suggestive, but >2.4 is diagnostic)
  • elevated liver enzymes and hypocholesterolemia

in advanced stages: hyperglycemia, hypokalemia, hypocalcemia, azotemia, and hypoproteinemia (all d/t fetal death, anorexia, renal and hepatic failure)

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11
Q

how would you treat a mild case of ketosis in a SR?

A

Oral propylene glycol or glycerol

alternatives: Ca-proprionate, Na-proprionate, liquid molasses, Na-lactate, ammonium lactate; but these are not metabolized as quickly and can disrupt NF of the rumen.

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12
Q

How do you treat acidosis, dehydration, and anorexia in cases of ketosis in SR?

A
  • oral dextrose and calf electrolyte solutions
  • appetite stimulant: vit B complex, calcium borogluconate, or oral calcium gel
  • offer high energy feed and limit roughage intake.
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13
Q

How would you treat a mod-to-severe case of ketosis in SR?

A
  • oral/IV fluids + IV dextrose (can do boluses, but its best to hospitalize and do CRI)
  • insulin (will facilitate tissue glucose uptake and inhibit fatty acid mobilization, but requires hospitalization for serial BG monitoring)
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14
Q

what supportive care treatments are utilized for preg toxemia/ketosis in SR?

A
  1. anti-inflammatories (flunixin)
  2. PPN/TTN
  3. Transfauntation
  4. Antioxidants (vit C or BOSE)
  5. Thiamine
  6. Deworming (not with levamisole or albendazole)
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15
Q

what gestational ages would it be SAFE to induce parturition in a SR with pregnancy toxemia?

A

ewe – d140
doe – d143

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16
Q

Parurition induction in SR with pregnancy toxemia may be necessary in order to save the dam. What drugs are used to do this?

A

prostaglandins (dinoprost or lutalyse)
steroids (dexamethasone)

note that emergency c-section or euthanasia may be warrented.

17
Q

how do you prevent pregnancy toxemia from occuring in SR?

A
  • check ketones in last month of pregnancy to ID at-risk females
  • group preg animals by BCS or preg stage for proper nutritional management (top-dress with high-energy supplementary feed, high qual hay and concentrates, proprionic salts)
18
Q

when does hypocalcemia most commonly occur in SR?

A

shortly BEFORE or AFTER parturition

greatest Ca demand in non-dairy animals is 3-4 weeks BEFORE parturition.

19
Q

what are clinical signs associated with hypocalcemia in SR?

A
  • isolate from herd/flock
  • Early on: stiff gait, tremors, hyperesthetic, ataxia
  • Later on: hyposensitive, weak, recumbent, depleted muscle contractions (constipation, bloat, absence of PLR, increased HR and RR, coma)
20
Q

What is involved in the treatment of uncomplicated cases of hypocalcemia in SR?

A
  • IV calcium gluconate (heated to 35-40C before admin and admin slowly while monitoring HR)
  • follow up with SQ or oral Ca gluconate

response will be immediate.

21
Q

What is involved in the treatment of complicated cases of hypocalcemia in SR?

A

Avoid IV administration of Ca solutions in animals with concurrent pregnancy toxemia because this is fatal in animals with impaired liver function.

22
Q

How can you prevent hypocalcemia from occuring in SR?

A
  • pay attention to Ca content of feed
  • avoid unnecessary stressors
  • avoid oxalates in feed because they precipitate formation of non-absorbent compounds with Ca
  • inorganic Ca is more digestible than Ca in feedstuffs.
  • herd/flock management
23
Q

Hypomagnesemia is primarily an issue in SR that graze …

A
  • lush, rapidly growing pastures
  • lush cereal grains (wheat and rye) in early lactation or late gestation
24
Q

What are the main risk factors associated with hypomagensemia in SR?

A
  1. increase K (alfalfa hay / haylage)
  2. reduced Na content + increased milk yield
    reduced Mg absorption from GI tract
25
Q

what is the etiology of hypomagnesemia in SR?

A
  1. stress –> increases FFAs in blood and decreases Mg
  2. poor qual grass hay (low Mg)
  3. poor dentition
26
Q

what are the clinical signs of hypomagnesemia and when does it most commonly occur in SR?

A

most commonly occurs 2-4 weeks post partum

causes: excitability, paddling, convulsions, clonic-tonic muscle spasms, and increased RR, as well as possible sudden death.

27
Q

How do we diagnose hypomagnesemia in SR?

A
  1. Sg, Hx, and response to tx
  2. serum Mg levels (<1.0 mg is diagnostic)
28
Q

how do we treat hypomagenesemia in SR?

A

Immediately:
1. IV 4-5% Magnesium Chloride +
2. 20-25% CMPK

recovery occurs quickly, but relapse may occur, so do additional tx SQ/oral 12-24 hr later.

if this is an outbreak situation, then give magnesium oxide PO to ALL animals (healthy and sick)

29
Q

how do you prevent hypomagnesemia from occuring in SR?

A

appropriate mineral supplementation
balanced fertilizers.