Systemic and local interferon-gamma production following Mycobacterium ulcerans infection.

Buruli ulcer disease (BUD) is an emerging predominantly tropical disease caused by Mycobacterium ulcerans. The initial pre-ulcerative skin lesion often breaks down into an ulcer with undermined edges. Healing is common but may require considerable time, and scarring often results in functional limitations.

A stepwise approach to the laboratory diagnosis of Buruli ulcer disease.

Objective: In view of technical and financial limitations in areas of endemicity, the current practice and recommendations for the laboratory diagnosis of Buruli ulcer disease (BUD) may have to be reconsidered. We reviewed diagnostic results in order to explore options for a modified, more practicable, cost-effective and timely approach to the laboratory diagnosis of BUD.

Methods: Diagnostic specimens from 161 clinically diagnosed BUD patients from four different treatment centres in Ghana were subjected to laboratory analysis.

Cytokine mRNA expression in Mycobacterium ulcerans-infected human skin and correlation with local inflammatory response.

Cytokine mRNA expression in biopsies of Mycobacterium ulcerans-infected human tissue was investigated using real-time PCR, and the findings were correlated with the clinical stages of disease and histopathologies. A broad range of cytokine mRNAs were detected in 16 early nodules and 28 late-stage ulcers, including those for the Th1 cytokines tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) and the Th2 cytokine interleukin 10 (IL-10). IFN-gamma was strongly expressed in both nodules and ulcers, suggesting that a Th1 response begins early in the disease.

Cytokine response to antigen stimulation of whole blood from patients with Mycobacterium ulcerans disease compared to that from patients with tuberculosis.

Mycobacterium ulcerans disease (Buruli ulcer) is a skin-ulcerating infection common in some parts of the tropics. We have investigated cytokine secretion after stimulation of whole blood from Buruli ulcer (BU) patients in a region of endemicity in Ghana with M. ulcerans sonicate or culture filtrate antigens to investigate the development of the response over time and its specificity by comparison with the response to Mycobacterium tuberculosis sonicate in human immunodeficiency virus-negative tuberculosis patients.

Susceptibility to Buruli ulcer is associated with the SLC11A1 (NRAMP1) D543N polymorphism.

Similar to other mycobacterial diseases, susceptibility to Buruli ulcer (Mycobacterium ulcerans infection) may be determined by host genetic factors. We investigated the role of SLC11A1 (NRAMP1) in Buruli ulcer because of its associations with both tuberculosis and leprosy. We enrolled 182 Buruli ulcer patients (102 with positive laboratory confirmation) and 191 healthy neighbourhood-matched controls in Ghana, and studied three polymorphisms in the SLC11A1 gene: 3' UTR TGTG ins/del, D543N G/A, and INT4 G/C.

Sensitivity of PCR targeting the IS2404 insertion sequence of Mycobacterium ulcerans in an Assay using punch biopsy specimens for diagnosis of Buruli ulcer.

Punch biopsy specimens from Mycobacterium ulcerans disease lesions were used to compare the sensitivities and specificities of direct smear, culture, PCR, and histopathology in making a diagnosis of M. ulcerans disease in a field setting. PCR for the insertion element IS2404 was modified to include uracil-N-glycosylase and deoxyuridine triphosphate instead of deoxythymidine triphosphate to reduce the risk of cross contamination.

Efficacy of the combination rifampin-streptomycin in preventing growth of Mycobacterium ulcerans in early lesions of Buruli ulcer in humans.

Mycobacterium ulcerans disease is common in some humid tropical areas, particularly in parts of West Africa, and current management is by surgical excision of skin lesions ranging from early nodules to extensive ulcers (Buruli ulcer). Antibiotic therapy would be more accessible to patients in areas of Buruli ulcer endemicity. We report a study of the efficacy of antibiotics in converting early lesions (nodules and plaques) from culture positive to culture negative.

Risk factors for Buruli ulcer disease (Mycobacterium ulcerans Infection): results from a case-control study in Ghana.

Background: Morbidity due to Buruli ulcer disease (BUD), a cutaneous infection caused by Mycobacterium ulcerans, has been increasingly recognized in rural West Africa. The source and mode of transmission remain unknown.

Methods: To identify BUD risk factors, we conducted a case-control study in 3 BUD-endemic districts in Ghana.

Reliability and validity of the Buruli ulcer functional limitation score questionnaire.

The reliability and validity of the earlier developed Buruli ulcer functional limitation score (BUFLS) questionnaire was assessed. Of 638 former Buruli ulcer patients (of 678 individuals examined), sufficient items on daily activities (>or= 13 of the 19) were applicable to calculate a score. To determine the validity, the functional limitation scores of the 638 individuals were compared with the global impression of the limitations, range of motion (ROM), and the social impact (change of occupation or education) of Buruli ulcer.

Distribution of Buruli ulcer lesions over body surface area in a large case series in Ghana: uncovering clues for mode of transmission.

We studied hospital records of 750 consecutive Buruli ulcer patients in a highly endemic area in Amansie West, Ghana. Although more Buruli ulcer lesions were found on the right side of the body, comparison of lesions on arms and legs showed a bilaterally symmetrical distribution. Upper and lower extremities were affected equally by Buruli ulcers, if correction was made for differences in body surface area.

Buruli ulcer and schistosomiasis: no association found.

Helminth infections elicit an immune response potentially enhancing susceptibility to mycobacterial diseases. Schistosomiasis and infection with Mycobacterium ulcerans show a remarkable similarity in epidemiologic characteristics in Ghana. In 2000, a case-control study was conducted in three districts in Ghana endemic for M.

An outreach education and treatment project in Ghana for the early stage of Mycobacterium ulcerans disease.

Mycobacterium ulcerans disease starts as a painless, subcutaneous nodule, excision of which prevents the development of large Buruli ulcers. An outreach programme was set up in Ghana to promote nodule recognition and excision. The programme was cost-effective and shifted the pattern of disease presentation.

Histopathologic features of Mycobacterium ulcerans infection.

Because of the emergence of Buruli ulcer disease, the World Health Organization launched a Global Buruli Ulcer Initiative in 1998. This indolent skin infection is caused by Mycobacterium ulcerans. During a study of risk factors for the disease in Ghana, adequate excisional skin-biopsy specimens were obtained from 124 clinically suspicious lesions.

Phenolic glycolipid-1 (PGL-1) in Buruli ulcer lesions. First demonstration by immuno-histochemistry.

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.

Malignant melanoma of the buttock presenting as a Buruli ulcer.

We report an unusual case of malignant melanoma clinically diagnosed as Buruli ulcer, that arose in a 13-year-old boy and presented as an ulcerated, fungating 2 cm mass on the right buttock. The tumor showed the histology and immunohistology of a malignant melanoma. We present this interesting case of malignant melanoma of soft tissue, arising in an unusual location of the body.

Socioeconomic implications of Buruli ulcer in Ghana: a three-year review.

This study examines some of the socioeconomic cost of treating 102 cases of Buruli ulcer between 1994 and 1996 at the St. Martin's Catholic Hospital in Agroyesum in the Amansie West district of the Ashanti region of Ghana. Seventy percent of the cases were children (up to 15 years of age).