Chronic wasting in sheep and goats Flashcards

1
Q

Presentation of chronic wasting: Individual animal

A
  • Syndrome – many causes of a similar presentation
  • Adults over one year, typically 3 – 5 years
  • Affects single to few animals at a time but
    > Several individuals over time
    > May indicate a higher proportion of flock infected
  • Thinner than cohorts
  • Thinner than expected
    > BCS goals/scoring info available (supplemental)
  • Fail to respond to good nutrition
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2
Q

Presentation of chronic wasting: Group or flock level

A
  • If group is too thin
  • Inadequate nutrition for stage of production
  • Feeding management
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3
Q

Common causes of chronic wasting

A
  • Competition
  • Dental disease
  • Retroviral diseases > Maedi visna (sheep), Caprine arthritis encephalitis (goats)
  • Paratuberculosis (Johne’s disease)
  • Caseous lymphadenitis
  • Enzootic nasal adenocarcinoma
  • GI parasitism (more common in adult goats than sheep)
  • Lameness (will cover in another section)
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4
Q

Competition - ways it arises

A
  • Inadequate feeder space
    > Pregnancy status
    > Ad-lib versus limit fed
  • Mixing (size, age, pregnancy status)
  • Horned versus no horns
  • Species
  • Breed
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5
Q

Dental disease
- presenting complaint
- epidemiology

A
  • “broken mouth”
  • Presenting complaint & history
    > Adult usually 4 years or older
    > Sporadic, low incidence
  • Epidemiology
    > Some farms worse than others
    > Risk factors not well understood
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6
Q

Dental disease - Pathogenesis, clinical presentation

A
  • Normally OK until 7 or 8 years of age
  • Primary gingivitis
  • Tooth loss and abnormal wear
  • Secondary osteomyelitis
    <><><><>
    Clinical Presentation
  • Thin, ≤ BCS 2
  • Appetite but slow eating
  • Decreased cud chewing
  • Swellings on jaw
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7
Q

Dental disease – Clinical exam

A
  • Pull down lower lip
    > Loss of incisors – broken mouth
    > Clinical significance? depends on diet, worse for pasture
    <><>
  • Palpate dental arcade for uneven wear
    <><>
  • Osteomyelitis associated with dental disease
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8
Q

Dental disease – Post mortem findings

A
  • Tooth loss and uneven wear
  • Osteomyelitis
  • Long stems in rumen (poor mastication)
  • Soft tissue infection
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9
Q

Dental disease – Treatment & control

A

Treatment
* Usually none
> Pets: rasp premolars and molars
* Recognize and cull or euthanize depending on fitness for transport
<><>
Control
* Grazing poor quality soil
* Thistles and awns in hay

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10
Q

Maedi Visna - Epidemiology
- geography
- prevalence
- effect on production

A
  • Widespread throughout the world
    > Except Australia and New Zealand
    <><>
  • Canada – high prevalence
  • Within flock seroprevalence
    > 20 to 40% up to 90-100%
    <><>
  • Seroprevalence increases with age
    <><>
    Effect on productivity:
  • Reduced reproductive performance
  • Early culling of adults
  • Reduced lamb growth & survival
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10
Q

Maedi Visna (aka Ovine Progressive Pneumonia)
- what does it mean??
- nature of the pathogen
- presenting complaint and history

A
  • Maedi = dyspnea
  • Visna = neurological disease with wasting (but neorologic signs are rare)
    <><>
  • Small ruminant lentivirus
  • Two groups (one common in sheep, one in goats) but each can infect the other
    <><>
  • Presenting complaint and history:
  • Adult sheep
  • Dyspnea / productive cough
  • Exercise intolerance
  • Hard udders at lambing with insufficient milk
  • Often unrecognized
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11
Q

Maedi Visna
- Pathogenesis
- target tissues

A
  • Chronic active inflammatory process
    > Virus targets macrophages, stimulates lymphocytic proliferation
    <><><>
    Target tissues:
  • Mammary gland
  • Lungs
  • CNS
  • Joints
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12
Q

Maedi Visna - Transmission

A
  • Aerosol – respiratory secretions !!!!!!!!!!
  • Colostrum !!!!
  • Milk !!
  • In utero transmission !!
  • Blood contaminated instruments / needles +/-
  • Semen – white blood cells +/-
    <><><><>
  • Can be infected multiple times!
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13
Q

Maedi Visna – Presentation – Respiratory disease

A
  • Common presentation
  • Afebrile, bright and alert
  • Productive cough
  • Exercise intolerance
  • No response to treatment
  • Progressive & 100% fatal
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14
Q

Maedi Visna – Presentation – Udder

A
  • Lymphocytic mastitis
  • Common presentation
  • “hard bag”
    > Udder uniformly firm to touch
    > Milk normal but decreased
    > Negative CMT
  • Lambs hungry
    > Steal milk or starve
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15
Q

Maedi Visna – Less common presentations

A

Neurological (Visna)
* Hind end ataxia and paresis – paralysis
* Circling, head tilt
* Fine tremor of lips
<><>
Arthritis
* Carpus, stifle, hock
* Uncommon except in some flocks

16
Q

Maedi Visna – Diagnostics

A

Serology – ELISA
> Good sensitivity and specificity
* Seroconversion variable time
> 2 weeks to 6 months
* Offered by the AHL (Guelph)

17
Q

Maedi Visna – PM lesions

A

Postmortem
* Lungs are tanned coloured, highly cellular, firm, heavy
* Worse affected dorsally
* Histopathology reveals lymphoid follicles
* Large, heavy lungs ,imprint of esophagus, thick mucous in trachea

18
Q

Maedi Visna – Treatment and Control

A

Treatment
* None - euthanize
* Necropsy adults with chronic wasting & non-responsive pneumonia
<><><><>
Control
* Serological testing of adult sheep
* Culling to slaughter
* Market this year’s offspring of seropositive ewes
* Test all replacement stock
<><><><>
* Ontario Maedi Visna Flock Status program

19
Q

Caprine Arthritis Encephalitis (CAE)
* Presenting complaint and history
* etiology? pathogens?

A
  • Goats with enlarged joints, lameness – may progress to recumbency
  • Chronic wasting
    <><><><>
    Etiology
  • Caprine arthritis encephalitis virus (CAEV)
  • Genus lentivirus – small ruminant lentivirus (SRLV) * Possible for cross-infection with sheep to occur
20
Q

Caprine Arthritis Encephalitis (CAE)
- common in what animals?
- prevalence
- pathogenesis? similar to?

A
  • Very common in dairy and meat
  • High seroprevalence
  • Similar pathogenesis as for Maedi Visna
21
Q

Caprine Arthritis Encephalitis (CAE)
- transmission?

A
  • Aerosol, saliva & genital secretions (esp. confinement) !!!!!!!!!!!!
  • Colostrum & milk of infected does (1 mL)!!!!
  • Milking equipment (adults)!!
  • In utero transmission (3 to 6%)!!
  • Blood contaminated instruments, needles +/-
22
Q

Caprine Arthritis Encephalitis (CAE)
* Clinical findings

A
  • Arthritis and bursitis
    > Carpus, stifle, scapula, occipital joint
  • Arthritis progresses to contracted tendons secondary to recumbency
  • Udder
    > As for MV
    > Hard at freshening
    > Little milk but normal appearing
    > CMT normal
  • Milk production ~ 10% less than non-infected does
    <><><><><><><>
    (uncommon)
  • Neurological
    > Kids 1 to 5 months
    > Posterior paresis > Uni- or bilateral progresses to tetraparesis
    > Torticollis
  • Progressive Pneumonia
    > Like MV
23
Q

Caprine Arthritis Encephalitis (CAE)
Diagnostics

A
  • Serology
  • Note: seroconversion can be delayed
24
Q

Caprine Arthritis Encephalitis (CAE)
PM findings

A
  • Synovium inflamed, thickened, scarred
  • Eroded cartilage
  • Lung, CNS and udder
    > Similar to MV lesions
    > Lymphoid follicles and scarring
25
Q

Caprine Arthritis Encephalitis (CAE)
* Treatment and control

A

Treatment
* NSAIDS for lameness
* Long term – pet goats?
* Euthanasia
<><>
Control
* Serological testing and removal
* Prevention of vertical transmission
> Snatch at birth and remove
> Heat-treat colostrum & pasteurize milk
> Segregation of youngstock from adults

26
Q

Paratuberculosis (Johne’s Disease)
* Presenting complaint and history
* pathogen, types?

A

Presenting complaint and history
* Annoying level of animals with chronic wasting
* Often not acted upon until 2 year olds affected
* Little diarrhea compared to cattle
<><>
Etiology
* Mycobacterium (avium) paratuberculosis (MAP)
* Can be infected by cattle strain (Type II), or other strains
* Type I – sheep
* Type III – sheep and goats

27
Q

Paratuberculosis (Johne’s Disease)
- who gets it?
- risk factors? spread? transmission?

A
  • Common in dairy sheep and goats
    > Likely also common in meat sheep and goats
  • Spread and risk factors similar to cattle
  • Environmental contamination high risk factor
    > Fecal-oral (manure meal)
    > Milk and colostrum
    > In utero
  • Transmission to adults
    > Less disease but may shed
  • Survival of M. paratuberculosis
    > Months in the environment
28
Q

Paratuberculosis (Johne’s Disease)
- iceberg disease! one clinically infected sheep means…

A
  • More mildly-affected sheep infected & shedding
  • Many more healthy-looking sheep infected & shedding
  • Many, many more healthy-looking sheep infected but not yet shedding
29
Q

Paratuberculosis (Johne’s Disease)
Diagnostics

A
  • Fecal culture – 4 months+
  • Fecal PCR – poor sensitivity (< 50%)
  • Prev. serology – poor sensitivity in pre-clinical
  • ‘Paracheck’ ELISA – better performance (milk/sera)
  • Post mortems – best diagnostics
  • More subtle lesions than cattle, variable (disease type)
  • Thickening of distal ileum, dilated lymphatics (SI), enlarged ileo-caecal and mesenteric lymph nodes
30
Q

Paratuberculosis (Johne’s Disease)
Control

A
  • Reduce risk from environmental contamination
  • Test and remove – only detects a portion of infected
  • Prevention transmission to offspring (similar to CAE)
  • Vaccination of high prevalence flocks / herds
  • Killed Gudair ® (Zoetis) vaccine shown to reduce clinical disease and decreased but not eliminate shedding (not available in Canada)