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
Age of infected animals and origin of infects for SA
Young animals Carpus, hip, fetlock Environmental, gi tract, resp tract, transdermal Lesions can occur without being systemically sick
26
Pathogenesis of SA
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
Why are young animals effected?
Failure of passive transport Or secondary diseases
28
Clinical signs for SA
Lameness - very lame NWB Warm swelling near effected area Possibly febrile & anorexia Signs of septicemia - Fever, lethargy, hypovulemic, red eyes,
29
Joints common for SA
Carpus, tarsus, stifle most common
30
Diagnosing SA
Radiographs (can take a few weeks to see periarticular changes) Ultrasound Joint tap of synovial fluid - consistency & color Pleocytosis & neutrophilia
31
Treatment/prevention of SA
Antibiotics systemically or intra articularly Lavage joint Arthotomy Regional limb perfusion Adequate colostrum intake
32
Mycoplasma poly arthritis : goats
Same as respiratory agent Mycoplasma mycoides subspecies capri (most common) M. Capricolum, M. Agalactaie, M. Putrefaciens Typically infected by colostrum & milk
33
Clin pres Mycoplasma poly arthritis : goats
3-8 weeks in kids (highly fatal) High fever, lameness Painful joints Meningitis, conjunctivitis, pneumonia Mastitis (adults)
34
Treatment & prevention of mycoplasma polyarthisis : goat
Florfenicol, tylosin Pasteurize milk/colostrum /feed kids Culture doe’s & bulk tank
35
Chlamydial polyarthritis : sheep
Chlamydophila pecorum 1-8 month lambs, feedlot (high morbidity) High fever, lameness, enlarged joints, conjunctivitis
36
Treatment for chlamydial polyarthisis
Florfenicol, tetracycline
37
White muscle disease
Deficiency in selemium or vitamin e - skeletal form - cardiac form
38
Cardiac form of WMD
Labored breathing, tachypnea, tachycardia, nasal discharge, heart murmur
39
Skeletal form of WMD
Stiff gait, trembling when standing, recumbent, weakness and unable to nurse
40
Common age demographic for WMD
Young, rapidly growing animals
41
Diagnosing WMD or NMD
CK and AST levels elevated Whole blood levels of Se and plasma levels of Vit E Necropsy ( whitish streaks in muscle fibers)
42
Treating WMD
Vit E and Se injections Vit E not super bioavailability as injectable
43
Prevention of WMD
Mineral salts VIT E and Se injections shortly after birth