Recently, Buruli ulcer is emerging from the West and Central African countries. The disease come up with necrotizing and immno-suppressive type ulcer in the skin, subcutaneous tissue and bone, infected by Mycobacterium ulcerans, and shows indolent chronic course as mycobacterial infection, like tuberculosis and Hansen's disease. After the transmission to human, the lesion is usually single and begin as firm, painless, subcutaneous nodule and on any area of human body skin, though most frequently on lower limbs. In countries of West Africa, it is suspected that the disease should be spreading most widely in Ghana. During April and June 1999, Ghana Health Service pick up the new patients by nation-wide examination. The author visited Ghana twice at March and September 1999 and made on-the-spot inspections not only at a community and Ga district Health Service Center in Accra region but also at St.Martin's hospital in Agroyesum, Amanse west district, Ashanti region. At the time, the author did see the present state of Buruli ulcer, i.e. health and medical enlightenment. This report, includes the results due to undergoing nation-wide examination on Buruli ulcer at 2 District in Ghana (List 1 and 2), the present states of the patients and the enlightenment provided by the staffs of Ga district Health Service Center (Photografs 1 ?? 14). Staffs working for WHO and Ghana Health Service are tackling to Buruli ulcer problems, but conditions of the patiens are very hard because these patients must live in tropical wetlands, poor health, poor medical and poor economic conditions.
Cell surface expression and release of the tumor necrosis factor receptor (TNFR type I) was analyzed after stimulation of peripheral blood mononuclear cells (PBMC) with Mycobacterium leprae (M. leprae) or lipopolysaccharide (LPS). A transient spontaneous expression of TNFR type I on the surface of PBMC was observed. Two hr after activation with LPS, a significant reduction of TNFR type I expression was detected: Release of TNFR type I by M. leprae or LPS-stimulated PBMC was evaluated with an enzyme-linked immunoabsorbent assay. This release occurred relatively later (20 to 40 hr) than the secretion of TNF alpha which reached high levels between 8 to 20 hr after activation. Thalidomide, a potent drug for the treatment of erythema nodosum leprosum episodes by inhibiting TNF alpha production, had no influence on the TNFR type I expression. Similar results were obtained with pentoxifylline. It is concluded that the release of TNFR type I by M. leprae or LPS-stimulated PBMC may counteract the pro-inflammatory activities of TNF alpha, by reducing the systemic toxicity of this cytokine in leprosy.