goats and sheep Flashcards

1
Q

CAE/MAEDI- VISNA

A

caprine arthritis/encepahlitis
OIE

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2
Q

aetiology of CAE/Maedi

A

, enveloped, single strand RNA, lentivirus from retroviridae fam (small rum lentiviruses)
CAEV
MVV

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3
Q

CAE MOT

A
  • MOT: infected colostrum/milk (pooled colostrum) direct contact, contaminated fomites/needles, experimental = in utero, sexual, during birth
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4
Q

CAE HS

A
  • HS: dairy goats, rare in meat/fibre breeds. Prevalence increase w age. Infected young
    • sero + for life. Seroprevalence = >65% in high income economies
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5
Q

pathogenesis CAE

A
  • unclear
  • infected macrophages absorbed through GI mucosa  spread through body  periodic virus multiplication + macrophage maturation  lymphoproliferative lesions (synovial membrane, choroid plexus, lungs, udder)  humoral and cell immune response but it’s not protective
  • persistence due to CAEV sequestered as provirus in host cells
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6
Q

signs CAE

A

arthritis - swelling of joints, lameness, joint deformities, reduced ROM, pain

enchepalitis - ataxia, weakness, head tilt, tremor/involvuntary movements

mastics - hard swollen udder, reduced milk, lumpy udder

pneumonia - respiratory signs - difficulty breathing, nasal discharge, coughing (respiratory signs are less common)

general signs of infection - weight loss, reduced growth rate, poor coat conditions

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7
Q

diagnosis of CAE/MVV

A
  • presumptive = signs + history
  • VI or PCR. AGID more specific but less sensitive than ELISA + = infection but doesn’t mean signs are caused by CAEV kids at birth get antibodies 4-10w after infection
  • Colostral antibodies can last up to 90d
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8
Q

differentials CAE/MVV

A
  • Mycoplasma/traumatic arthritis, spine abscesses, trauma, listeriosis, Polioencephalomalacia, rabies, caseous lymphadenitis if pulmonary form
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9
Q

treatment CAE/MVV

A
  • No treatment, no vaccine, foot trimming, NSAIDs
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10
Q

MVV

A
  • Maedi visna = Icelandic for laboured breathing + wasting (paralysing meningoencephalitis)
  • Ovine progressive pneumonia (OPP)
  • CAE + MV = small ruminant lentiviruses (SRLVs)
  • 5 genotypes : A-E
    o A (1-13): classical MVV strains. Some infect both sheep and goats
    o B: classical CAEV strains
    o C: both goat and sheep
    o D & E: goat strains
    o Possible recombination between SRLV = new vairnats
  • AB = widespread
  • CDE = specific
    o Genotypes C (Norway), D (Spain and Switzerland) and E (Italy) appear to be limited to small geographic areas in Europe
  • Texel + Leicester most likely to become ill
  • Maedi = most common form, adult sheep. Wasting + progressive dysnpnea, no fever, depress or bronchial exudate. Eventually fatal (anorexia/2nd bact pneumonia)
  • Visna = hindlimb weakness, head tilt, ataxia. Lasts 1y
  • MVV can sometimes cause arthritis
  • PM = enlarged, firm lungs that don’t collapse. Mottled emphysematous with grey/brown consolation
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11
Q

ORF

A

contagious ecthyma

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12
Q

ORF

A
  • Highly contagious, zoonotic, viral pustular dermatitis
  • Usually resolves spontaneously and the mortality rate is generally low
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13
Q

aetiology of ORF

A
  • Parapoxvirus, Family Poxviridae
  • Highly resistant to drying – survives on dry crusts for 12y + wool + hides for 1m after lesions have healed
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14
Q

SOI ORF

A

sick and carrier animals

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15
Q

POE ORF

A

cuts + abrasion of skin

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16
Q

MOT ORF

A

direct contact and fomites

17
Q

HS ORF

A

Sheep and goats (goats more severe), young artificially reared lambs, older lambs autumn on pasture + winter in feedlots. Ungulates (alpaca, reindeer, elk, chamois, humans, rare in dogs + cats)

18
Q

GD ORF

19
Q

pathogenesis ORF

A
  • Papules  vesicle  pustule  encrusts
  • coalesce of multiple discreet lesions  formation of large scabs
  • proliferation of dermal tissue  verrucous mass underneath
  • humans = lesions on hands + face, PPE, mistaken for anthrax
20
Q

signs ORF

A
  • Incubation: 2 to 3 days
  • Hyperaemia + pustules on mucocutaneous junction of lips  extends to mucosa of buccal cavity
  • Pustules  crusts  verrucose mass (2nd bact)
  • Lambs  dams  lesions on udder
  • Lesions on feet + dermatophilus congolensis  strawberry foot rot (lameness)
  • Anorexia, not gaining weight, abandon kid. Uncomplicated resolve in 1-2m
21
Q

diagnosis ORF

A
  • Lesions characteristic, PCR, electron microscopy of scab
22
Q

differentials ORF

A
  • Ulcerative dermatitis (usually older), FMD, bluetongue, staph folliculitis
23
Q

treatment ORF

A
  • supportive care: Tube feeding +Antibiotics as needed for secondary infections
24
Q

control ORF

A

o quarantine new animals, clean + disinfect. Difficult to remove once in herd
o live vaccine for where infections have occurred in past – isolate until vaccine scabs have gone. Not in pregnancy.
o Immunity 18m after natural infection – highly resistant

25
Q

CATS ORF

A
  • Lesions of feet, face of back. Cauliflower like/proliferative ulcerative. Spontaneous healing or euthanasia
26
Q

Dogs ORF

A
  • Circular areas of acute, moist dermatitis with ulcers + scabs around head. Outcome not described
27
Q

caseous lymphadenitis

A
  • chronic infectious disease of sheep and goats
  • manifesting as abscesses of peripheral/internal LN + organs
28
Q

aetiology of caseous lymphadentiis

A
  • Corynebacterium pseudotuberculosis, gram +, non-motile, non-sporulating, non-capsulated
  • 2 biotypes on ability to reduce nitrate-ovis = nitrate neg, equi = nitrate +
  • Exotoxin phospholipase D + virulence factor mucolic acids provides protection
  • Survives in soil 8m, bedding for 2m
29
Q

SOI caseous lymphadenitis

A
  • SOI: sick animals with or without visible clinical symptoms (pus from lesions)
30
Q

POE caseous lymphadenitis

A
  • POE: ski/MM – shedding, castration, tail docking
31
Q

MOT CL

A
  • MOT: direct contact or contaminated environment
32
Q

HS CL

A
  • HS: sheep + goats, prevalence increase w age (shearing) all breeds – merino increase – thinner skin, neck wrinkles
33
Q

pathogenesis CL

A
  • Entry via skin/MM  exotoxin increase vascular permeability  dissemination to LN
  • Survives + replicates in macrophages (helped by mucolic acids)  rupture + bacteria are released
  • Replication, attraction + death of inflam cells  abscesses (onion ring formation)
    o onion ring – concentric bands due to repeated stages of necrosis and capsule formation (green which is debris from cell and bacteria, large amount of eosinophils which is why it’s a little green)
34
Q

signs CL

A
  • incubation 1-3m
  • external form= abscesses on peripheral LN  swollen, firm, fibrous capsule hairless  open draining abscess  purulent w no odour  heal w scarring. Recurrence common
  • internal form = chronic weight loss, thin ewe syndrome. Often lung abscesses so cough, fever, purulent nasal discharge, tachypnoea
35
Q

diagnosis CL

A
  • external abscesses= highly suggestive
  • definitive = culture of pus from intact abscess
  • synergistic haemolysine inhibition test to detect antibodies to exotin – shows exposure not cause
36
Q

differential CL

A
  • morel’s disease = staph aureus subsp anaerobicus
  • t. pyogenes, p. multocida, actinobacillosis, TB, lymphosarcoma, other causes of chronic weight loss
37
Q

treatment CL

A

not curable’ – surgical drainage, atb – difficult to penetrate abscesses, cull

38
Q

control CL

A
  • Cull, strict biosecurity, prevent skin injuries, clean equipment, vaccine
39
Q

public health CL

A
  • Zoonotic potential
  • Rarely long + recurrent lymphadenitis through cuts (farmers + shearers). Ingestion of unpasteurised milk from affected animals