ABSTRACT
Buruli ulcer, caused by Mycobacterium ulcerans, is emerging as the third most common mycobacterial disease after leprosy and tuberculosis in some tropical regions. Although a toxin of the polyketide family is central to the pathogenesis of the disease, there are still several parameters that need clarification. Among them and of crucial interest are the curative drug treatment and the test for early detection of the disease. In this study, we used mouse monoclonal antibodies, raised against synthetic sugars of the terminal trisaccharide of M. leprae PGL-1, to detect the immunoreactivity of this antigen in tissue infected with M. ulcerans. Thirty specimens of skin tissue from Buruli ulcer patients (3 plaques, 10 nodules, 1 ulcerated nodule, 7 deep ulcer beds and 9 ulcers in healing) were obtained from Ghana. Eighty-three percent of the submitted cases were compatible with the lesions of Buruli ulcer. AFB were positive in 33% of plaques, 40% of nodules, 44% of actives ulcers and 22% of the ulcer in healing stage. Immunohistochemically, phenolic glycolipid-1 (PGL-1) was detected in all AFB-positive cases. This observation implies that Mycobacterium ulcerans may express an M. leprae PGL-1-like substance and should tentatively emulate research to further characterize such a substance. The search for an early diagnostic tool for the Buruli disease may benefit from such investigations.
Subject(s)
Glycolipids/isolation & purification , Mycobacterium Infections, Nontuberculous/metabolism , Mycobacterium ulcerans , Antibodies, Monoclonal , Antigens, Bacterial/metabolism , Ghana , Glycolipids/metabolism , Humans , ImmunohistochemistryABSTRACT
"AFIP classification" by light microscopy was of help to analyze the skin lesions of Buruli ulcer, in which the histopathology were classified into 6 stages i.e. active, healing, active but healing, consistent with active and chronic stages. In this paper, skin lesions biopsied from 41 cases of Buruli ulcer were observed by light microscopy. Those were sent from Benin in west Africa at 1997, and under the control of Armed Forces Institute of Pathology(AFIP) in Washington DC, USA. Each age, sex, biopsy lesions and histopathological stage and corresponding characteristic histopathological findings of 41 cases except that of chronic stage were analyzed and herewith reported by this paper.
Subject(s)
Mycobacterium Infections/pathology , Skin Diseases, Bacterial/pathology , Skin Ulcer/pathology , Adolescent , Adult , Age Factors , Aged , Benin/epidemiology , Child , Child, Preschool , Female , Humans , Infant , Male , Middle Aged , Mycobacterium Infections/classification , Mycobacterium Infections/microbiology , Mycobacterium ulcerans/isolation & purification , Skin/microbiology , Skin/pathology , Skin Diseases, Bacterial/classification , Skin Diseases, Bacterial/microbiology , Skin Ulcer/classification , Skin Ulcer/microbiologyABSTRACT
Buruli ulcer, caused by Mycobacterium ulcerans, is emerging as the third most common mycobacterial disease after leprosy and tuberculosis in some tropical regions. Although a toxin of the polyketide family is central to the pathogenesis of the disease, there are still several parameters that need clarification. Among them and of crucial interest are the curative drug treatment and the test for early detection of the disease. In this study, we used mouse monoclonal antibodies, raised against synthetic sugars of the terminal trisaccharide of M. leprae PGL-1, to detect the immunoreactivity of this antigen in tissue infected with M. ulcerans. Thirty specimens of skin tissue from Buruli ulcer patients (3 plaques, 10 nodules, 1 ulcerated nodule, 7 deep ulcer beds and 9 ulcers in healing) were obtained from Ghana. Eighty-three percent of the submitted cases were compatible with the lesions of Buruli ulcer. AFB were positive in 33% of plaques, 40% of nodules, 44% of actives ulcers and 22% of the ulcer in healing stage. Immunohistochemically, phenolic glycolipid-1 (PGL-1) was detected in all AFB-positive cases. This observation implies that Mycobacterium ulcerans may express an M. leprae PGL-1-like substance and should tentatively emulate research to further characterize such a substance. The search for an early diagnostic tool for the Buruli disease may benefit from such investigations.
