BACKGROUND: As the immunocompromised population has increased in recent years, the number of cutaneous nontuberculous mycobacterial (NTM) infections has also risen. However, since this affliction has no pathognomonic clinical or histological features, the diagnosis and treatment of cutaneous NTM infections are often delayed. OBJECTIVE: The aim of this study was to investigate the microbiological, clinical, and histological findings of cutaneous NTM infections. METHODS: We reviewed medical records and histologic slides of 10 patients diagnosed with cutaneous NTM infections confirmed by culture or polymerase chain reaction. RESULTS: All patients except one were immunocompetent, and 5 of 10 patients had preceding factors including trauma, liposuction, and intralesional triamcinolone injection. Microbiologically, of the 10 infections, 5 were caused by Mycobacterium marinum, 3 by Mycobacterium fortuitum, and 1 each by Mycobacterium chelonae and Mycobacterium ulcerans, respectively. Of the 5 patients with M. marinum, 2 had a fish-related job and 1 reared fish at a home aquarium. The most common clinical presentation was erythematous nodules (7/10). Histologically, irregular acanthosis (4/10), mixed cell infiltrate of lymphocytes, histiocytes, neutrophils (9/10), suppurative granuloma (7/10), microcysts lined by neutrophils (5/10), fibrosis (4/10), and panniculitis (7/10) were identified. CONCLUSION: We found microcysts lined by neutrophils in 50% of the samples and considered this finding to be a diagnostic marker of NTM infection. These clinicopathologic features will assist clinicians in diagnosing NTM infection more rapidly and accurately.
Diagnosis ; Fibrosis ; Granuloma ; Histiocytes ; Humans ; Lipectomy ; Lymphocytes ; Medical Records ; Mycobacterium chelonae ; Mycobacterium fortuitum ; Mycobacterium marinum ; Mycobacterium ulcerans ; Neutrophils ; Nontuberculous Mycobacteria ; Panniculitis ; Polymerase Chain Reaction ; Triamcinolone

Mycolactone is a recently reported lipid toxin of Mycobacterium ulcerans that causes Buruli ulcer, a severe human skin disease. However, the mechanism of cell death by mycolactone is still unclear. In this paper, we demonstrate that mycolactone induces apoptosis in Hep 3B hepatocellular carcinoma (HCC) cells. Morphological and biochemical evidences of apoptosis, such as membrane blebbing, cell shrinkage, increase of TUNEL-positive cells and a sub-G 1 cell population, were observed. To explain the mechanism of mycolactone-induced apoptosis, we examined the expression of Bcl-2 family genes. The mRNA expression of anti-apoptotic BclXL gene was decreased after 8 hours, while that of Mcl-l, another anti-apoptotic gene, was slowly decreased with an initial increase at second hour after treatment. Bcl-2 gene expression was extremely low both in the presence and absence of mycolactone. The expression of other Bcl-2 family genes, such as Bclw, Bad, Bak, and Bax, was not affected. By Western blotting analysis, Mcl-1 expression (not BclXL) was down-regulated. Our results suggest that the down-regulation of Mcl-1 protein expression is involved in the apoptosis of Hep 3B cells by mycolactone.
Apoptosis ; Blister ; Blotting, Western ; Buruli Ulcer ; Carcinoma, Hepatocellular* ; Cell Death ; Down-Regulation ; Genes, bcl-2 ; Humans ; Membranes ; Mycobacterium ulcerans ; RNA, Messenger ; Skin Diseases

Adult ; Aged ; Aged, 80 and over ; Buruli Ulcer ; pathology ; surgery ; DNA, Bacterial ; analysis ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Mycobacterium ulcerans ; genetics ; isolation & purification ; Tuberculosis, Cutaneous ; pathology