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Buruli Ulcer

Buruli Ulcer. J.A.G. a.k.a. Mycobacterium ulcerans. Drew Simmelink. Non-ulcerative form. Ulcerative form. So what does it look like?. SEM of M. ulcerans 10D w/o ECM, scale = 5µm. SEM Bacilli isolated w/ immunomagnetic beads, scale = 1µm. 85% progressive disease

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Buruli Ulcer

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  1. Buruli Ulcer J.A.G. a.k.a. Mycobacterium ulcerans Drew Simmelink

  2. Non-ulcerative form

  3. Ulcerative form

  4. So what does it look like? SEM of M. ulcerans 10D w/o ECM, scale = 5µm SEM Bacilli isolated w/ immunomagnetic beads, scale = 1µm • 85% progressive disease • Division time is 3-4 days

  5. BU Prevalence • Occurs with environmental changes such as the development of water storages, sand mining and irrigation.

  6. World Wide = ~7000

  7. Age distribution Why so small? Why more likely with age? Unlike TB or leprosy, the infection is acquired from the environment, not patients IS2404  detection of IS in carnivorous water bugs, as well as mollusks, fish that don’t develop the disease, but some develop natural infections and some are resistant. Clustering!

  8. This is why it’s so small IgG antibody tests in MU/healthy shows common bands of 30, 70-80 kDa. IgM antibody tests in MU/healthy shows bands in only infected patients. (Arrows = common to both IgG and IgM.) So there is some innate immunity to exposure!

  9. What’s the virulence factor? • Mycolactone • Geographical regions  diff. mycolactonesdiff. Presentation/virulence • Major constituent of ECM. • HydrophobicityPassesthrough plasma membrane and interacts with cytosolic target.

  10. Why is it painless? Control (ethanol) mouse footpad. 7D inj. hemorrhage 42D inj.inflammation with damage remaining unchanged

  11. But can the tissue heal? LDH measured w/ Promega assay to determine cytotoxicity. Apoptosis measured w/ ELISA kit. NOPE!

  12. What else is ruined?

  13. What about immediate treatment? • First—A combination of rifampicin and streptomycin for eight weeks. • RIF inhibits DNA-dependent RNA polymerase in prokaryotes by binding its beta-subunit. • SCN binds to the S12 Protein of the 30S subunit of the bacterial ribosome, interfering with the binding of f-met-tRNA to the subunit.

  14. What happens after the drugs? • Surgery mainly to remove necrotic tissue, cover skin defects and correct deformities. • Interventions to minimize or prevent disabilities. • However, even with simple lesions excised early had a recurrence rate of 16% one year after.

  15. So is there a vaccine? • There is a vaccine—the Mycobacterium bovis BCG “BacilleCalmette-Guérin” a.k.a. the TB vaccine (they share same genus). • But this doesn’t inoculate against the ulcer, but rather it helps protect children against M. ulceransosteomyelitis. • Some studies suggest it is effective for only 6 months. Any organizations to help? • The Global Buruli Ulcer Initiative (1998)—40 nongovernmental organizations, research institutions, and foundations. • In 2004, a WHO resolution was passed to increase surveillance and control, local and international cooperation and for intensified research to develop tools to diagnose, treat and prevent the disease. • In reality, not much can be done because of the under-reporting of the disease, insufficient knowledge among health workers and public, people affected live in rural remote areas w/ little access and clinical presentation varies widely and is mistaken for other ulcers.

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