Johne's Disease Flashcards

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1
Q

Johnes first described when? found in NA when?

A

Described 1895
First found in North America in 1908

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2
Q

nature of Johnes disease and species affected? causative agent?

A

Paratuberculosis or Johne‘s Disease (JD) is a chronic bacterial enteric disease of ruminants
Causative Agent: Mycobacterium avium subspecies paratuberculosis (MAP)

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3
Q

geographic spread and prevalence of Johne’s in Ontario

A

Worldwide (Ontario: ~30% of dairy herds, 3-5% within-herd test- positive prevalence)

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4
Q

Johne’s bacterial strains? how well do they survive in environment? what is the organism susceptible to? what about pasteurization?

A
  • Mycobacterium paratuberculosis
  • 3 distinct groups of strains
  • Persist in pasture (without replication) for prolong period (≈ year)
  • Organism is susceptible to: sunlight, drying, high pH, soil calcium content, and contact with urine and feces
  • Can survive pasteurization (i.e. 63°C x 30 minutes)
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5
Q

Johne’s pathogenesis

A
  • Ingestion > organism localizes in: small intestine mucosa, associated lymph nodes, tonsils and supra-pharyngeal lymph nodes
  • Replication in small and large intestine
  • Three possible group of animals:
    > Infected resistant - Develop resistance, control infection, do not shed
    > Intermediate - Partly control the infection, shed the organism
    > Clinical - Organism persist in the intestine and these animals develop clinical disease
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6
Q

what species are affected by Johne’s? what ages? incubation?

A
  • Affects: cattle, sheep, goats, llamas
  • Prenatal infections occur
    > Up to 40% of fetuses from cows with clinical paratuberculosis
    > 18% of asymptomatic but “heavy shedding” cows
    > Rarely from “light shedders”
  • Infection more common after birth
  • Long incubation period
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7
Q

what age group is most susceptible to Johne’s? how does the disease usually present and progress? at what age are clinical signs generally seen, if at all?

A
  • Calves have highest susceptibility
  • Infection progresses very slowly
  • Most MAP infected cows are subclinical
  • Clinical signs usually seen around 3-6 yrs of age
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8
Q

apparent prevalence of Johne’s and individual and herd level in canada

A

individual level ~1%
herd level ~5%

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9
Q

how often is MAP found in the environment?

A
  • ~15% of chute systems down to ~4% of calving pens. Overall present in about ~10% of environmental samples
  • also can be found in worms, ~22% of drone fly larvae, ~2% of other flies…
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10
Q

Johne’s transmission

A
  • Subclinically infected cows can shed MAP in manure, colostrum and milk
  • Transmission: fecal-oral & vertical transmission
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11
Q

risk factors for Johne’s

A
  • Herd size
  • Annual birth rate
  • Annual herd replacement rate
  • Number of infected cows at time zero
  • Number of replacements purchased each year —
  • Risk of purchasing an infected heifer
  • Number of infected cow-calf contacts per year
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12
Q
  • Stages of the Johne’ s disease
A
  • Silent infection (Stage 1)
  • Subclinical (Stage 2)
  • Clinical (Stage 3)
  • Advanced clinical disease (Stage 4)
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13
Q

nature of Johne’s silent infection (stage 1) - what age group and signs, shedding, tests,etc.?

A
  • Animals less than 2 years of age
  • No clinical signs, or changes on body weight or body condition
  • May be shedding the organism
  • Clinico-pathologic tests do not detect infection
  • Fecal or tissue culture may detect the organism
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14
Q

nature of Johne’s silent infection (stage 2) - what age group and signs, shedding, tests,etc.?

A
  • Carrier adult animals
  • No clinical signs but would be affected by other abnormalities such as mastitis or infertility
  • Most of these animals are negative in fecal culture (only 15-25% would culture +)
  • Also, negative to most serological tests
  • Would move to stage 3 if not culled
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15
Q

nature of Johne’s clinical disease (stage 3) - what age group and signs, shedding, tests,etc.?

A
  • “Tip of the iceberg”of the number of affected animals in a herd
  • Clinical signs usually appear after 2 years of age, normally between 2-6 years of age
  • Cases appear sporadically
  • Gradual loss of body weight/normal appetite * Diarrhea
  • Decreased milk production
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16
Q

nature of Johne’s advanced clinical disease (stage 4) - what age signs?

A
  • Emaciation
  • Submandibular edema (bottle jaw)
  • Fluid diarrhea: water hose or pipe stream
  • End result: dehydration, emaciation, weakness…
17
Q

Johne’s Ddx

A
  • Salmonellosis
  • Coccidiosis
  • Gastrointestinal parasitism
  • Secondary copper deficiency
  • Others:
    — Malnutrition, chronic reticuloperitonitis, hepatic abscess, pyelonephritis, lymphosarcoma, amyloidosis.
18
Q

John’es clinical pathology, 4 categories

A
  • Clinical disease + shedding the organism
  • Subclinical infection +shedding the organism
  • Infected - neither ill or shedding (detectable by culture)
  • Uninfected cattle
19
Q

Johne’s macroscopic PM lesions

A
  • Lesions are localized to alimentary tract and
    associated lymph nodes
  • Small intestine, cecum and first part of colon
  • Thick and corrugated mucosa (3-4 times) (not always)
  • Prominent serosal lymphatics
  • Arteriosclerosis
20
Q

Johne’s microscopic PM lesions

A
  • Within lamina propria and
    submucosa
    > Epithelioid macrophages
    > Multinucleated giant cells
  • Granulomatous lymphangitis
21
Q

Diagnosis of Johne’s, gold standard

A
  • Necropsy: Gold Standard
  • Gross Pathology, histology, culture/PCR
  • Se: 100% Sp: 100%
22
Q

Johne’s diagnosis options for live animal

A

Direct Tests for MAP
* Culture or PCR on feces, milk, tissue
> Se: ~ 60%, Sp: <100%
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Indirect tests using immune response
* Serum or milk ELISA tests
* Se: ~ 30%, Sp: 99%
* >85% in animal with clinical disease
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Fecal Culture:
* Se: < 50%, Sp: <100%
Fecal PCR:
* Se: ~ 30 %, Sp: ~99%
Serum and Milk ELISA: —
* Se: ~ 30 %; Sp: 99%

23
Q

overall characteristics of Johne’s live animal diagnostic tests, and consequence

A
  • Tests have low Sensitivity for detection of infection of individual animals (dependent on infection status)
  • Many cows go/shed undetected&raquo_space; pure Test-and-Cull programs do not work
24
Q

Milk ELISA for Johne’s - who should we not forget to test? how do we interpret results?

A
  • Don‘t forget to test 1st lactation cows (1/3 of herd)
  • The higher the titre (optical density)
    > The less likely are cows to change their test result
    > The more likely the cows are shedding MAP
  • Cows are more likely to test positive early in lactation
  • If test-positive despite good milk production, likely a true positive cow
25
Q

Johne’s treatment

A
  • No antimicrobial are approved for M. paratuberculosis
    <><>
  • Streptomycin
    ○ 50mg/kg. Onlyt ransient improvement of clinical signs
  • Isoniazid
    ○ 20mg/kg. Failed to cure clinical signs
  • Clofazimine
    ○ 600mg daily for 10 months. Clinical improvement
26
Q

Johnes Disease Control Programs

A
  1. Test-and-Cull Programs
  2. Vaccination (no licensed vaccine in Canada, do not prevent infection)
  3. Risk Assessment (RA) - based JD Control Program
27
Q

what are risk assessment-based programs for Johne’s prevention?

A
  • Prevention and Control through management practices (MP)
  • Aim: Breaking the infectious cycle from cow to calf
  • Risk Assessment (RA) based JD control programs are used in
    e.g. Australia, Denmark, USA,
  • Canada
28
Q

Top 10 reccomendation for Johne’s transmission prevention

A
  1. Remove newborn calves quickly from maternity pen
  2. Separate newborn calves from cows (create
    minipen)
  3. Feed low-risk colostrum to calves
  4. Feed more colostrum to calves
  5. Feed low-risk milk to calves
  6. Do not feed non-saleable milk to calves
  7. Do not walk through calf pens with cow manure on
    boots
  8. Wash pails/bottles for calves daily
  9. Identify test-positive cows & their offspring
  10. Do not calve JD clinical/test-positive cows in same area as test-negative cows
29
Q

Johne’s zoonotic potential? implications?

A
  • MAP DNA has been detected with variable frequency (46%-100%) in blood and biopsies of Crohn’s disease patients
  • MAP is detected less often in patients with ulcerative colitis

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  • M. paratuberculosis has been isolated from humans with Crohn’s disease
  • But acid-fast microscopy and IHC had not been able to show the organism within disease intestinal tissue
  • No evidence indicating that the incidence of Crohn’s disease is associated with
    exposure to the organism (i.e. farmers, animal care workers)

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  • Meta-analyses have demonstrated that the association of MAP with Crohn’s disease in humans is specific and cannot be denied, although a causal role has not yet been demonstrated. Furthermore, transmission from cattle to humans has never been proven.