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Moving Exam 3 > La Ortho - MS Disease Sheep/goats > Flashcards

La Ortho - MS Disease Sheep/goats Flashcards

1
Q

Foot disorders & problems

A

Environment, nutritional, management, genetic factors
Hooves grow rapidly
Wet, muddy conditions = Increased predisposition
BIOSECURITY - disease walks on all 4 legs

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2
Q

Contributing factors to foot health

A

Foot trimming - every 2-3 months (depends on terrain)
Nutrition
Genetics !!! Poor conformation

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3
Q

Pathogenesis of foot abscess

A

Moisture
Softening hoof keratin or interdigital skin
Invasion of Actinomyces
Foot abscess

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4
Q

Pathogenesis of foot scald

A

Moisture trauma
Softening of keratin or interdigital skin
Invasion of fusobacterium necrophorum
Invasion of D. Nudosus w aprB2
Foot scald / benign foot rot

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5
Q

Characterization of foot scald

A
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6
Q

Contagious foot rot

A

Interdigital necrobacillosis - not interdigital

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7
Q

Epidemiology of contagious foot rot

A
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8
Q

Pathogenesis of foot rot

A
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9
Q

Where is lesion found in foot rot

A
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10
Q

Bacteria that causes foot problems

A
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11
Q

Treatment /prevention for foot diseases

A

Can treat equally due to anaerobic bacteria
Treat with systemically antibiotics
Foot baths
Hoof trimming
Segregation
Improve environmental conditions

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12
Q

Prevention for contagious foot rot

A

Feet trimmed
Moving to dry area /improve moisture
Vaccination (shorten course of disease)
Culling (genetic, chronic carrier animal)
Avoid contaminated facilities
Grime new additions/quarantine for 30 days

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13
Q

Contagious (virulent) foot rot eradication

A

Endemic in herds - nearly impossible
Trim soak vaccine
Trim soak vaccine antibiotics
Segregated affected
Cull

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14
Q

Foot bathes /topicals

A

10-15% Zinc sulfate
5-10% copper sulfate
5% for Aline
Not super common in smaller flocks/farms

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15
Q

Foot abscess

A

Bacteria enter into hoof via puncture injury or WLD
Can occur above the hoof then migrate into hoof = severe lameness
Treat by opening/removal

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16
Q

Which type of foot bath is preferred for foot rot

A

Zinc sulfate !!!
Copper can be ingested = copper toxicity
Formalin = helps harden hoof, temperature sensitive

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17
Q

CAE

A

Caprine arthritis encephalitis
Retrovirus - integrated into host genome
Chronic multi systemic disease
Seroprevalence 38-81%
Small ruminants lentivirus

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18
Q

CAE epidemiology

A

Transmission thru infected macrophages in fluids
Verticals - colostrum or milk
Horizontal - physical contact, milking equipment, semen, surgical equipment

19
Q

infection of CAE

A

Infects monocytes & macrophages, induces a persistent lifelong infection
Not all infected animals develop disease

20
Q

CAE clinical syndromes

A
  1. Arthritis (most common)
    25% of seropositive animals
    >6 months of age
  2. Leukoencephalomyelitis in kids
  3. Mastitis, interstitial pneumonia
  4. Old goat encephalitis
21
Q

Diagnosing CAE

A

Serologic testing
- Elisa - more sensitive than AGID, great specificity (100%, 99.6%)
- AGID - fair sensitive, good specificity (85-90%, 100%)
- biosecurity panel (CAE, CL, Johne’s, Q fever)

22
Q

What is the best prevention if you have a seropositive doe (CAE) that you don’t want to cull?

A

Don’t use her colostrum = how the disease spreads

23
Q

Prevention of CAE

A

Feed CAE free milk/colostrum
Separated infected
Milk non infected first
Use seronegative bucks
Disinfect equipment between animals
Cull positive animals

24
Q

Septic arthritis prevalence

A

Bacterial infection of joints

25
Q

Age of infected animals and origin of infects for SA

A

Young animals
Carpus, hip, fetlock
Environmental, gi tract, resp tract, transdermal
Lesions can occur without being systemically sick

26
Q

Pathogenesis of SA

A

Septicemia
Hematogenous seeding of joints
Synovitis
Joint pain, heat, swelling, synovial effusion
Damage to articular cartilage +subchondral bone
Chronic changes - thickening of synovial tissue/fibrosis of jC
Degenerative joint disease

27
Q

Why are young animals effected?

A

Failure of passive transport
Or secondary diseases

28
Q

Clinical signs for SA

A

Lameness - very lame NWB
Warm swelling near effected area
Possibly febrile & anorexia
Signs of septicemia - Fever, lethargy, hypovulemic, red eyes,

29
Q

Joints common for SA

A

Carpus, tarsus, stifle most common

30
Q

Diagnosing SA

A

Radiographs (can take a few weeks to see periarticular changes)
Ultrasound
Joint tap of synovial fluid - consistency & color
Pleocytosis & neutrophilia

31
Q

Treatment/prevention of SA

A

Antibiotics systemically or intra articularly
Lavage joint
Arthotomy
Regional limb perfusion
Adequate colostrum intake

32
Q

Mycoplasma poly arthritis : goats

A

Same as respiratory agent
Mycoplasma mycoides subspecies capri (most common)
M. Capricolum, M. Agalactaie, M. Putrefaciens
Typically infected by colostrum & milk

33
Q

Clin pres Mycoplasma poly arthritis : goats

A

3-8 weeks in kids (highly fatal)
High fever, lameness
Painful joints
Meningitis, conjunctivitis, pneumonia
Mastitis (adults)

34
Q

Treatment & prevention of mycoplasma polyarthisis : goat

A

Florfenicol, tylosin
Pasteurize milk/colostrum /feed kids
Culture doe’s & bulk tank

35
Q

Chlamydial polyarthritis : sheep

A

Chlamydophila pecorum
1-8 month lambs, feedlot (high morbidity)
High fever, lameness, enlarged joints, conjunctivitis

36
Q

Treatment for chlamydial polyarthisis

A

Florfenicol, tetracycline

37
Q

White muscle disease

A

Deficiency in selemium or vitamin e
- skeletal form
- cardiac form

38
Q

Cardiac form of WMD

A

Labored breathing, tachypnea, tachycardia, nasal discharge, heart murmur

39
Q

Skeletal form of WMD

A

Stiff gait, trembling when standing, recumbent, weakness and unable to nurse

40
Q

Common age demographic for WMD

A

Young, rapidly growing animals

41
Q

Diagnosing WMD or NMD

A

CK and AST levels elevated
Whole blood levels of Se and plasma levels of Vit E
Necropsy ( whitish streaks in muscle fibers)

42
Q

Treating WMD

A

Vit E and Se injections
Vit E not super bioavailability as injectable

43
Q

Prevention of WMD

A

Mineral salts
VIT E and Se injections shortly after birth

Moving Exam 3 (34 decks)

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