Thin sheep and goats Flashcards by Josie Campbell

When is it a flock problem (BCS)

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

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Dental conditions causing weight loss in sheep and goats

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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Chronic diseases causing weight loss

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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Pleural abscesses

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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Fibrinous pleurisy

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

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

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Broken teeth

Lambs fed root crops first winter, especially if frosted

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Excessively worn teeth

Sandy pastures

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Caries and periodontitis of molar teeth

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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Dietary/secondary hyperparathyroidism

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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Dentigerous cysts

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

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Congenital malformations of teeth

Result in malocclusions

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Aetiology of Johne’s disease

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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Clinical signs of Johne’s

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

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PM findings of Johne’s

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

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Diagnosis of Johne’s disease

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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Treatment of Johne’s

None

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Control of Johne’s

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

Aetiology of Maedi-visna (sheep)

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

Pathogenesis of MV

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

Clinical signs of MV

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

Diagnosis of MV

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

Control of MV

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

Aetiology of CAE

Lentivirus closely related to MV but different tropism

Clinical signs of CAE

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

Diagnosis of CAE

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

Treatment of CAE

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

Aetiology of Caseous Lymphadenitis (CLA)

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

Pathogenesis of CLA

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

Clinical signs of CLA

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

Diagnosis of CLA

Culture from samples taken from LNs Serology - ELISA

Treatment of CLA

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

Control of CLA

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

Aetiology of OPA/SPA/Jaagsiekte

Oncogenic retrovirus Oncogenic transformation of type II pneumocytes Development of adenocarcinoma

Transmission of OPA

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

Clinical signs of OPA

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

Diagnosis of OPA

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

Treatment of OPA

None, cull

Control of OPA

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

Aetiology of tuberculosis

Very rare in sheep More common in goats Spillover hosts

Clinical signs of tuberculosis

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

Diagnosis of tuberculosis

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

Control of TB

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

Aetiology of liver fluke

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