goats and sheep

Question 1

CAE/MAEDI- VISNA

Answer 1

caprine arthritis/encepahlitis
OIE

Question 2

aetiology of CAE/Maedi

Answer 2

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

Question 3

CAE MOT

Answer 3

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

Question 4

CAE HS

Answer 4

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

Question 5

pathogenesis CAE

Answer 5

• 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

Question 6

signs CAE

Answer 6

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

Question 7

diagnosis of CAE/MVV

Answer 7

• 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

Question 8

differentials CAE/MVV

Answer 8

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

Question 9

treatment CAE/MVV

Answer 9

• No treatment, no vaccine, foot trimming, NSAIDs

Question 10

MVV

Answer 10

• 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

Question 11

ORF

Answer 11

contagious ecthyma

Question 12

ORF

Answer 12

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

Question 13

aetiology of ORF

Answer 13

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

Question 14

SOI ORF

Answer 14

sick and carrier animals

Question 15

POE ORF

Answer 15

cuts + abrasion of skin

Question 16

MOT ORF

Answer 16

direct contact and fomites

Question 17

HS ORF

Answer 17

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)

Question 18

GD ORF

Answer 18

worldwide

Question 19

pathogenesis ORF

Answer 19

• 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

Question 20

signs ORF

Answer 20

• 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

Question 21

diagnosis ORF

Answer 21

• Lesions characteristic, PCR, electron microscopy of scab

Question 22

differentials ORF

Answer 22

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

Question 23

treatment ORF

Answer 23

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

Question 24

control ORF

Answer 24

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

Question 25

CATS ORF

Answer 25

- Lesions of feet, face of back. Cauliflower like/proliferative ulcerative. Spontaneous healing or euthanasia

Question 26

Dogs ORF

Answer 26

- Circular areas of acute, moist dermatitis with ulcers + scabs around head. Outcome not described

Question 27

caseous lymphadenitis

Answer 27

- chronic infectious disease of sheep and goats - manifesting as abscesses of peripheral/internal LN + organs

Question 28

aetiology of caseous lymphadentiis

Answer 28

- 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

Question 29

SOI caseous lymphadenitis

Answer 29

- SOI: sick animals with or without visible clinical symptoms (pus from lesions)

Question 30

POE caseous lymphadenitis

Answer 30

- POE: ski/MM – shedding, castration, tail docking

Question 31

MOT CL

Answer 31

- MOT: direct contact or contaminated environment

Question 32

HS CL

Answer 32

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

Question 33

pathogenesis CL

Answer 33

- 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)

Question 34

signs CL

Answer 34

- 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

Question 35

diagnosis CL

Answer 35

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

Question 36

differential CL

Answer 36

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

Question 37

treatment CL

Answer 37

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

Question 38

control CL

Answer 38

- Cull, strict biosecurity, prevent skin injuries, clean equipment, vaccine

Question 39

public health CL

Answer 39

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