Thin sheep and goats Flashcards
When is it a flock problem (BCS)
If more than 5% have BCS<2.0 or the range of BCS is wide
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
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
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
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
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
Broken teeth
Lambs fed root crops first winter, especially if frosted
Excessively worn teeth
Sandy pastures
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
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
Dentigerous cysts
Solitary, unilateral, mandibular incisors adult sheep
Contain milky or caseous material
Congenital malformations of teeth
Result in malocclusions
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
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
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
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
Treatment of Johne’s
None
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
