Johne's Disease Flashcards
Johnes first described when? found in NA when?
Described 1895
First found in North America in 1908
nature of Johnes disease and species affected? causative agent?
Paratuberculosis or Johne‘s Disease (JD) is a chronic bacterial enteric disease of ruminants
Causative Agent: Mycobacterium avium subspecies paratuberculosis (MAP)
geographic spread and prevalence of Johne’s in Ontario
Worldwide (Ontario: ~30% of dairy herds, 3-5% within-herd test- positive prevalence)
Johne’s bacterial strains? how well do they survive in environment? what is the organism susceptible to? what about pasteurization?
- 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)
Johne’s pathogenesis
- 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
what species are affected by Johne’s? what ages? incubation?
- 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
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?
- Calves have highest susceptibility
- Infection progresses very slowly
- Most MAP infected cows are subclinical
- Clinical signs usually seen around 3-6 yrs of age
apparent prevalence of Johne’s and individual and herd level in canada
individual level ~1%
herd level ~5%
how often is MAP found in the environment?
- ~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…
Johne’s transmission
- Subclinically infected cows can shed MAP in manure, colostrum and milk
- Transmission: fecal-oral & vertical transmission
risk factors for Johne’s
- 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
- Stages of the Johne’ s disease
- Silent infection (Stage 1)
- Subclinical (Stage 2)
- Clinical (Stage 3)
- Advanced clinical disease (Stage 4)
nature of Johne’s silent infection (stage 1) - what age group and signs, shedding, tests,etc.?
- 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
nature of Johne’s silent infection (stage 2) - what age group and signs, shedding, tests,etc.?
- 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
nature of Johne’s clinical disease (stage 3) - what age group and signs, shedding, tests,etc.?
- “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
nature of Johne’s advanced clinical disease (stage 4) - what age signs?
- Emaciation
- Submandibular edema (bottle jaw)
- Fluid diarrhea: water hose or pipe stream
- End result: dehydration, emaciation, weakness…
Johne’s Ddx
- Salmonellosis
- Coccidiosis
- Gastrointestinal parasitism
- Secondary copper deficiency
- Others:
Malnutrition, chronic reticuloperitonitis, hepatic abscess, pyelonephritis, lymphosarcoma, amyloidosis.
John’es clinical pathology, 4 categories
- Clinical disease + shedding the organism
- Subclinical infection +shedding the organism
- Infected - neither ill or shedding (detectable by culture)
- Uninfected cattle
Johne’s macroscopic PM lesions
- 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
Johne’s microscopic PM lesions
- Within lamina propria and
submucosa
> Epithelioid macrophages
> Multinucleated giant cells - Granulomatous lymphangitis
Diagnosis of Johne’s, gold standard
- Necropsy: Gold Standard
- Gross Pathology, histology, culture/PCR
- Se: 100% Sp: 100%
Johne’s diagnosis options for live animal
Direct Tests for MAP
* Culture or PCR on feces, milk, tissue
> Se: ~ 60%, Sp: <100%
<><>
Indirect tests using immune response
* Serum or milk ELISA tests
* Se: ~ 30%, Sp: 99%
* >85% in animal with clinical disease
<><>
Fecal Culture:
* Se: < 50%, Sp: <100%
Fecal PCR:
* Se: ~ 30 %, Sp: ~99%
Serum and Milk ELISA:
* Se: ~ 30 %; Sp: 99%
overall characteristics of Johne’s live animal diagnostic tests, and consequence
- Tests have low Sensitivity for detection of infection of individual animals (dependent on infection status)
- Many cows go/shed undetected»_space; pure Test-and-Cull programs do not work
Milk ELISA for Johne’s - who should we not forget to test? how do we interpret results?
- 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
Johne’s treatment
- 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
Johnes Disease Control Programs
- Test-and-Cull Programs
- Vaccination (no licensed vaccine in Canada, do not prevent infection)
- Risk Assessment (RA) - based JD Control Program
what are risk assessment-based programs for Johne’s prevention?
- 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
Top 10 reccomendation for Johne’s transmission prevention
- Remove newborn calves quickly from maternity pen
- Separate newborn calves from cows (create
minipen) - Feed low-risk colostrum to calves
- Feed more colostrum to calves
- Feed low-risk milk to calves
- Do not feed non-saleable milk to calves
- Do not walk through calf pens with cow manure on
boots - Wash pails/bottles for calves daily
- Identify test-positive cows & their offspring
- Do not calve JD clinical/test-positive cows in same area as test-negative cows
Johne’s zoonotic potential? implications?
- 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
<><>
- 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)
<><>
- 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.
