Pathology
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 deformity.
Th1-mediated immune responses are protective against M. ulcerans infection, whereas Th2-mediated responses are not.
Read more about this topic: Buruli Ulcer
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