Johne's Disease Flashcards
Causative agent of Johne’s
Mycobacterium avium subspecies paratuberculosis
Route of transmission of Johne’s
Faecal-oral transmission
Infection acquired at young age via ingestion of faeces/milk from infected animals
In utero transmission has been reported but importance as a means of spread is unclear
When do cattle typically present with Johne’s?
2+ years old
Some infected animals are sub clinical carriers so do not show signs but shed the mycobacteria intermittently.
Clinical signs of Johne’s in cattle
Diarrhoea, initially intermittent but then persistent and profuse
Progressive weight loss without loss of appetite
Post-mortem findings of cattle with Johne’s
Mucosa of terminal small intestine and large intestine usually thickened and folded in transverse corrugations
Enlarged and oedematous mesenteric and ileocaecal lymph nodes
Clinical signs of Johne’s in sheep, goats and deer
Sheep and goats: diarrhoea is less marked than in cattle and may be absent
Deer: rapid weight loss, sudden onset of diarrhoea, death in 2-3 weeks or extreme emaciation developing over months without evidence of diarrhoea
Postmortem findings of deer, sheep and goats with Johne’s disease
In sheep, thickening of mucosa may be less marked than in cattle, but necrosis and caseation may be present in regional lymph nodes
Lesions in deer are similar to those in sheep
How should milk be treated to prevent transmission of Johne’s?
Should be pasteurised
Describe the pathogenesis of Johne’s disease?
Bacterium = intracellular pathogen. Organisms cross the epithelial layer thorough the M cell route and interfere with the phagosome-lysosome fusion hence they survive.
Cell-mediated reactions are mainly responsible for enteric lesions.
As the disease progresses, granulomatous reaction develops I.e. accumulation of lymphocytes and macrophages in the lamina propria and submucosa.
The resulting enteropathy leads to loss of plasma proteins and malabsorption of nutrients and water.
What is another name for Johne’s?
Paratuberculosis
Terminal ileum of a cow with Johne’s. What are the circled structures?
Granulomatous inflammation
Granulomatous formation in Johne’s is an example of what type of hypersensitivity?
Type IV
What is the difference between Type I, II and III and then Type IV hypersensitivity?
Type I, II and III = antibody-mediated
Type IV = cell mediated
How do you test for Johne’s?
Blood test for antibody to the MAP bacteria
Faecal test to identify the shedding/presence of MAP bacteria
How does TB testing impact on Johne’s detection?
TB testing can result in a cross-reaction with antibodies to Johne’s
Therefore, either sample for Johne’s before TB testing, of 3 months after last TB test
Why might a PCR of faeces from an infected animal return a negative result?
MAP bacteria may be intermittently shed, thus producing a false negative result for an animal that is infected with Johne’s
Why might a blood test for antibodies produce a negative result for an infected cow?
Antibody response is variable and may be absent in the later stages of infection when the immune system becomes overwhelmed
Is it a risk to spread slurry from a Johne’s positive farm onto silage fields?
Technically there is an increased risk, but if carried out properly, the ensuring process effectively kills MAP bacteria
Can MAP survive on pasture and if so for how long?
Yes it can - sometimes for several years in cool damp climates and certain soil conditions
What should you do if you have identified a Johne’s positive cow in the herd?
Ideally cull ASAP
Remove calf immediately after birth and pasteurise milk/feed it milk from a Johne’s-negative dam
Which staining methods do you use to differentiate Mycobatceria from other bacteria?
Ziehl-Nielsen staining method (=a type of acid fast staining)
Describe the M cell route of antigen sampling from the gut?
M cells overlying Peyer’s patches take up particulate antigens and deliver them to the subepithelial dendritic cells
