Buruli ulcer pathophysiology
|
Buruli ulcer Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Buruli ulcer pathophysiology On the Web |
|
American Roentgen Ray Society Images of Buruli ulcer pathophysiology |
|
Risk calculators and risk factors for Buruli ulcer pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Buruli ulcer is an infectious disease caused by the tuberculous agent Mycobacterium ulcerans. The infection causes painless swelling, with lesions developing in the skin later on.
Pathophysiology
Being one of the less known diseases caused by mycobacteria, means of Buruli ulcer infection are not completely clear. However, the mycobacterium has been identified in stagnant or slowly moving water sources in endemic areas and in aquatic insects (Naucoridiae). Transmission to man may be by means of insects or by a contaminated aerosol generated from decaying vegetation in the water source. Infection in Australia has occurred in an alpaca, in koalas, possums and other marsupials.
The disease is primarily an infection of subcutaneous fat, resulting in a focus of necrotic (dead) fat containing myriads of the mycobacteria in characteristic spherules formed within the dead fat cells. Skin ulceration is a secondary event. The mycobacterium produces a toxin, named mycolactone, which causes this fat necrosis and inhibits an immune response. Healing may occur spontaneously but more often the disease is slowly progressive with further ulceration, granulation, scarring, and contractures. Secondary infection may occur with other nodules developing and infection may occur into bone. Although seldom fatal, the disease results in considerable morbidity and hideous deformity.
Th1-mediated immune responses are protective against M. ulcerans infection, whereas Th2-mediated responses are not.