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FAMS > Small Ruminant Lameness > Flashcards

Small Ruminant Lameness Flashcards

1
Q

What is infectious foot rot in small ruminants?

A

Severe contagious disease that causes significant economic loss

70-80% all herd lameness

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2
Q

What is the infectious agent of foot rot in small ruminants?

A

Dichelobacter nodosus

Fusobacterium necrophorum plays a role

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3
Q

What conditions are perfect for footrot?

A

Warm, wet, overstocked, poor generics, poor trimming schedule

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4
Q

Where do animals get footrot from?

A

Soil and carriers

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5
Q

What are clinical signs of footrot?

A

Benign - foot scald, just D. nodosus, interdigital lesion, horn underun

Virulent - with F. necrophorum, severely lame, underrun hard horn, horn separates, exudate smelly

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6
Q

How do you prevent footrot?

A

proper trimming, proper Quarantine new animals, foot baths

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7
Q

How do you treat footrot?

A

Topicals: Powder tetracycline, zinc sulfate, foot bath with zinc
Injectables: Oxytetracyiline, nuflor, zactran

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8
Q

How fast should you ideally treat foot rot?

A

3 days

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9
Q

How long should you quarantine new animals?

A

30-60 days

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10
Q

What does CAE stand for?

A

Caprine arthritis and enecphalitis

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11
Q

What kind of virus is CAE and who does it commonly effect?

A

Retrovirus/Lentivirus
Goat
38-81% prevenance

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12
Q

How is CAE transmitted?

A

Fluids with infected macrophages
-Colostrum
-Milkers
-Venereal
Uninfected convert

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13
Q

Where does CAE localize?

A

Macrophages of synovium, lung, CNS, and mammary gland
Lymphocytes in joints, mammary gland, lung, brain

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14
Q

What are the 4 clinical syndromes of CAE?

A

Arthritis, Leukoencephomyelitis, Mastitis and Interstitial Pneumonia

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15
Q

Who and where does the arthritis version of CAE effect?

A

> 6 month old goats
Carpal joints, hock, stifle, hip, atlantooccipital
Swelling wax and wanes

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16
Q

Who and how does the neurlogic version of CAE work?

A

1-5 months
Demyelinating leukoencephalomyelitis
Choppy gait, unilateral or bilateral paresis and ataxia

17
Q

How do you get rid of CAE in your herd?

A

Test and cull (positive antibody = infection)
Manage colostrum - separate kid and dam, heat or pasteruize colostrum
Test every 6 months

18
Q

How do you diagnose CAE?

A

Clinical signs
Postmortem: nonsuppurative, demyelinating encephalomyelitis and lymphocytic infiltration of any target tissue

19
Q

What is OPP? What is its name in other countries?

A

Ovine Progressive Pneumonia

Maedi-visna

20
Q

What are the common presentations of OPP?

A

Pneumonia and mastitis (hard bag), arthritis and encephalitis possible

21
Q

Who does it normally effect and when?

A

Older sheep
Long incubation
0.5-49% prevalence

22
Q

What is the pathophysiology of the virus?

A

Stimulate reticular cells and lymphocytes to proliferat causing thickening of intra-alveolar septa and produced adenomatosis of alveolar lining

23
Q

What is the layman’s term for nutritional muscular dystrophy?

A

White muscle disease

24
Q

What is white muscle disease?

A

Deficiency of selenium or vitamine E

Effect skeletal and cardiac muscle in young rapidly growing animals

Ill thrift and repro losses

25
Q

Where is white muscle prevalent?

A

All over us bc Se deficient (check hay)

26
Q

What causes WMD?

A

Poor se in nutrition
-Poor hay
<0.1PPM

27
Q

What is the pathophysiology of WMD?

A

Selenium and VE are antioxidants, when diets defiecnet there is oxidative damage that leads to mucse degeneration

Scary when effect diaphragm and cardia

28
Q

Who is commonly effected by WMD?

A

Young animals 2-4 months of age

29
Q

What are clinical signs of WMD?

A

Cardiac: recumbency, resp distress, death

Respiratory: tachypnea, frothy nasal dischatge, pulmonary edema

Skeletal muscle: stiff gait, tremble while stand, hunched, weak and unable to nurse

30
Q

How do you diagnose SE WMD?

A

Clinical signs, whole blood or tissue at necropsy
-Pale streaks - bilateral

31
Q

How do you treat WMD?

A

Inject VE/Selenium (not too much or toxicosis)
-Give dam mineral mix 30 days before lambing

FAMS (41 decks)

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