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Small ruminants > Thin sheep and goats > Flashcards

Thin sheep and goats Flashcards

1
Q

When is it a flock problem (BCS)

A

If more than 5% have BCS<2.0 or the range of BCS is wide

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2
Q

Dental conditions causing weight loss in sheep and goats

A

Premature loss of incisor teeth
Broken teeth
Excessively worm teeth
Caries and periodontitis of molar teeth
Dietary/secondary hyperparathyroidism
Dentigenous cysts
Congenital malformations

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3
Q

Chronic diseases causing weight loss

A

Johnes disease
MV/CAE
CLA
OPA
TB
Scrapie
Chronic pneumonia, pleural abscess, hepatic abscess, chronic focal peritonitis, endocarditis
Parasites
Ruminal impaction, abomasal emptying syndrome
Tumours
Lameness

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4
Q

Pleural abscesses

A

Variable in size and position
Capsule of varying thickness
Inspissated pus more echo dense
Gas bubbles (if present) are very hyperechoic
Prognosis: small abscesses treated successfully with prolonged course of procaine penicillin

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5
Q

Fibrinous pleurisy

A

Fibrin tags visible attached to both the parietal and visceral pleura
Hypoechoic exudate between pleural surfaces
Areas of organising fibrin with fluid pockets have a ‘spider’s web’ appearance
Prognosis: guarded, some cases have recovered after prolonged antibiotic therapy

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6
Q

Premature loss of incisor teeth (broken mouth, periodontal disease)

A

Gingivitis that progresses to periodontitis
Bacterial infection (Fusobacterium, Bacteroides)
Destruction of periodontal ligament supporting the tooth
No routine treatment

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7
Q

Broken teeth

A

Lambs fed root crops first winter, especially if frosted

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8
Q

Excessively worn teeth

A

Sandy pastures

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9
Q

Caries and periodontitis of molar teeth

A

Tooth loss, abscessation, commonly a cause of individual weight loss in older ewes
Often show cud staining of the chin, or cheek packing as well as weight loss
Cull affected animals

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10
Q

Dietary/secondary hyperparathyroidism

A

Reported in dairy goats fed excessive levels of grain
Often show bent limbs, the ‘rachitic rosary’ on the ribs and swollen mandible

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11
Q

Dentigerous cysts

A

Solitary, unilateral, mandibular incisors adult sheep
Contain milky or caseous material

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12
Q

Congenital malformations of teeth

A

Result in malocclusions

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13
Q

Aetiology of Johne’s disease

A

Mycobacterium avium paratuberculosis
Bacteria ingested and enters M cells in Peyer’s patches
Macrophages produce granulomatous inflammation
Latent period
Progresses to diffuse, severe granulomatous enteritis
Paucibacillary form - mainly Th1 response
Multibacillary form - mainly Th2 response

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14
Q

Clinical signs of Johne’s

A

Adults, usually >3yrs
Progressive weight loss and increasing lethargy
Decreased production
Diarrhoea is not usually a feature
Anaemia and hypoproteinaemia

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15
Q

PM findings of Johne’s

A

Thickened ileum, may be yellow, enlarged, mesenteric LNs, gelatinous atrophy of fat, effusions in body cavities
May see caseation/calcification

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16
Q

Diagnosis of Johne’s disease

A

Serology - highest sensitivity, best for screening flocks
Faecal culture, direct faecal smear (MZN) or PCR
PM ileocaecal/mesenteric LN enlarged and oedematous

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17
Q

Treatment of Johne’s

A

None

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18
Q

Control of Johne’s

A

Very difficult to eradicate
- Snatch births
- Vaccination
- Do not pool colostrum
- Cull suspect cases and do not retain their last 2 offspring in the flock/herd
- Lamb/kid younger animals separately and keep replacements only from those animals
- Regular cleaning and disinfection of kidding accomodation

19
Q

Aetiology of Maedi-visna (sheep)

A

Maedi is pulmonary form - chronic progressive pneumonia
Visna is chronic meningo-encephalitic form - progressive paralysis resulting in death
MV is a non-oncogenic lentivirus in the retrovirus group
RNA viruses
Do not target T cells
Cross transmission between sheep and goats is possible
Slowly developing disease

20
Q

Pathogenesis of MV

A

Close contact via respiratory route, via colostrum/milk
May die of secondary pasteurellosis

21
Q

Clinical signs of MV

A

Usually older animals
Weight loss and exercise intolerance
Dyspnoea
Coughing and nasal discharge may occur
Arthritis occurs rarely

22
Q

Diagnosis of MV

A

Serology - ELISA
PM: lungs increased weight, non-compliant

23
Q

Control of MV

A

Eradication: if high prevalence depop-repop, if not test and cull, snatch lambing etc.
Control: Slaughter affected animals, do not breed from affected ewes, keep a young flock, source from accredited free flocks, test on arrival

24
Q

Aetiology of CAE

A

Lentivirus closely related to MV but different tropism

25
Q

Clinical signs of CAE

A

Many goats are symptomless carriers
- Affects synovial membranes - arthritis
- Hard udder or chronic progressive pneumonia
- Encephalitis
- Progressive weight loss

26
Q

Diagnosis of CAE

A

Serology
CSF or synovial fluid analysis
PM: unilateral brownish areas of malacia in spinal cord, perivascular mononuclear cell infiltration and demyelination of white matter

27
Q

Treatment of CAE

A

NSAIDs may be used to relieve pain from arthritis
Cull affected animals

28
Q

Aetiology of Caseous Lymphadenitis (CLA)

A

Corynebacterium pseudotuberculosis
Enters through skin wounds or oral/nasal cavity
Lesions in LNs

29
Q

Pathogenesis of CLA

A

Local infection then spread to regional lymph nodes
Localises and forms ‘onion ring’ abscess - primarily neutrophils
Can disseminate to other LNs or the lungs
Spread due to animals with lung lesions, coughing up aerosols of bacteria

30
Q

Clinical signs of CLA

A

Causes chronic weight loss, possibly with coughing if lungs involved
Commonly seen in rams, maybe due to fighting

31
Q

Diagnosis of CLA

A

Culture from samples taken from LNs
Serology - ELISA

32
Q

Treatment of CLA

A

None
Ripe abscesses may be lanced and flushed with iodine or chlorhexidine

33
Q

Control of CLA

A

Eradication: test and cull
Control in flock: Shear young to old, check flock LNs, isolate and cull affected, avoid dipping if present, reduce period of time crowded after shearing, etc.
Prevention of entry: source from free flock, test pre-sale, test after purchase
Low risk of zoonosis

34
Q

Aetiology of OPA/SPA/Jaagsiekte

A

Oncogenic retrovirus
Oncogenic transformation of type II pneumocytes
Development of adenocarcinoma

35
Q

Transmission of OPA

A

Respiratory route
In late stage milk and colostrum
Infects WBCs and travels in blood stream

36
Q

Clinical signs of OPA

A

Caused by loss of effective lung tissue and accumulation of lung secretions
Weight loss
Breathlessness
Lagging when driven
Soft, wet cough
Clear nasal discharge

37
Q

Diagnosis of OPA

A

Auscultation: increased, wet lung noise, increased resp rate and effort
US scan: consolidated lung in CrVe regions has hepatoid appearance
Wheelbarrow test: pick up hindlegs and lung surfactant comes out of nose. Low sensitivity, euthanase immediately if positive
PM: solid lung tumours, usually CrVe distribution, grey-purple appearance

38
Q

Treatment of OPA

A

None, cull

39
Q

Control of OPA

A

Eradication: snatch and rear separately
Control: Cull thin sheep, scan all adults, do not house/trough feed/water troughs
Prevent introduction

40
Q

Aetiology of tuberculosis

A

Very rare in sheep
More common in goats
Spillover hosts

41
Q

Clinical signs of tuberculosis

A

Weight loss
May have extensive lesions and remain in good BC
Chronic pneumonia with a moist productive cough

42
Q

Diagnosis of tuberculosis

A

Notifiable
PM: granulomatous lesions of lungs and thoracic LNs
Intradermal tuberculin tests

43
Q

Control of TB

A

Whole herd SICCT if detected, repeat every 60 days until 2 clear
Limit goat contact with cattle and badgers
Zoonotic risk

44
Q

Aetiology of liver fluke

A

Fasciola hepatica
Lifecycle requires mud snail Galba truncatula
Migrate through liver parenchyma, causing haemorrhage and inflammation to the bile ducts
Can have black disease due to the activation of Clostridium novyi spores in the damaged liver parenchyma

Small ruminants (14 decks)

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