Small Ruminant Lameness Flashcards

(31 cards)

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
Where is white muscle prevalent?
All over us bc Se deficient (check hay)
26
What causes WMD?
Poor se in nutrition -Poor hay <0.1PPM
27
What is the pathophysiology of WMD?
Selenium and VE are antioxidants, when diets defiecnet there is oxidative damage that leads to mucse degeneration Scary when effect diaphragm and cardia
28
Who is commonly effected by WMD?
Young animals 2-4 months of age
29
What are clinical signs of WMD?
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
How do you diagnose SE WMD?
Clinical signs, whole blood or tissue at necropsy -Pale streaks - bilateral
31
How do you treat WMD?
Inject VE/Selenium (not too much or toxicosis) -Give dam mineral mix 30 days before lambing