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PathogenesisThe incubation period of BU varies from approximately 2 weeks to 3 years, with an average of 2 to 3 months. Following inoculation into the skin, M. ulcerans proliferates and elaborates a toxin that causes necrosis of the dermis, panniculus, and fascia. Undefined host factors and variations in the etiologic agent may play a role in determining the type of pathologic changes. In localized disease, necrosis in the deepest layers of the skin forms a nodule that eventually erodes through the skin surface, leaving a well-demarcated ulcer with a necrotic slough in the base and widely undermined edges. Some infections spread rapidly along the fascia-subcutaneous tissue plane and bypass the localized nodular ulcerative stage. This disseminated form results in edematous plaques that, if untreated, lead to ragged ulcers. The etiologic agent may spread, presumably by lymphatic and hematogenous pathways, to distant foci, usually skin and bone. Severe osteomyelitis is well-known. If invaded by M. ulcerans, regional lymph nodes become necrotic. Inflammatory cells are scarce in active lesions, probably from the combined tissue necrosis and the immunosuppressive activity of the M. ulcerans toxin. Lesions tend to heal after months or years by a cell-mediated granulomatous response and ultimate scarring. Early organization in healing lesions is characterized by loosely arranged lymphocytes, epithelioid and giant cells with scarce or absent acid-fast bacilli (AFB). Well-organized delayed-type hypersensitivity granulomas and scarring are characteristic of late organization in healing lesions. While HIV infection may not predispose to BU, it can make the disease more aggressive.Based on clinicopathologic studies of more than 4,000 patients with BU accessioned at the AFIP, a schema (left) of active M. ulcerans disease was developed. |
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