Serologic response to culture filtrate antigens of Mycobacterium ulcerans during Buruli ulcer disease.
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Buruli ulcer (BU) is an emerging necrotic skin disease caused by Mycobacterium ulcerans. To assess the potential for a serodiagnostic test, we measured the humoral immune response of BU patients to M. ulcerans antigens and compared this response with delayed-type hypersensitivity responses to both Burulin and PPD. The delayed-type hypersensitivity response generally supported the diagnosis of BU, with overall reactivity to Burulin in 28 (71.8%) of 39 patients tested, compared with 3 (14%) of 21 healthy controls. However, this positive skin test response was observed primarily in patients with healed or active disease, and rarely in patients with early disease (p=0.009). When tested for a serologic response to M. ulcerans culture filtrate, 43 (70.5%) of 61 BU patients had antibodies to these antigens, compared with 10 (37.0%) of 27 controls and 4 (30. 8%) of 13 tuberculosis patients. There was no correlation between disease stage and the onset of this serum antibody response. Our findings suggest that serologic testing may be useful in the diagnosis and surveillance of BU. (+info)
Pulmonary mycobacteriosis caused by rifampicin-resistant Mycobacterium szulgai.
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We describe a rare case of pulmonary mycobacteriosis infected with rifampicin (RFP)-resistant Mycobacterium szulgai that was successfully eradicated with clarithromycin (CAM) treatment. An 80-year-old man was admitted to our hospital with a 4-week history of high fever, productive cough and malaise. Chest roentgenogram showed an infiltrative shadow in the left lower lung field. Isolated bacteria from sputum were acid-fast bacilli and identified as M. szulgai by the DNA-DNA hybridization method. Drug susceptibility tests showed resistance to RFP (MIC>100 microg/ml). Combined treatment with ethionamide, streptomycin and isoniazid based on the results of drug susceptibility tests resulted in clinical and radiologic improvement within two years. Additional treatment with CAM for another year resulted in complete eradication of the mycobacterium. (+info)
Disseminated Mycobacterium terrae infection in a patient with advanced human immunodeficiency virus disease.
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Mycobacterium terrae has been rarely implicated in human disease and never in patients infected with human immunodeficiency virus (HIV). We describe an HIV-infected patient with disseminated infection by M. terrae with pulmonary and cutaneous clinical manifestations. M. terrae was isolated from both sputum and urine, and identified by both conventional tests and high-performance liquid chromatography. Clinical and microbiological characteristics of this case are compared with those reported in the literature. (+info)
Granuloma-specific expression of Mycobacterium virulence proteins from the glycine-rich PE-PGRS family.
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Pathogenic mycobacteria, including the agent of tuberculosis, Mycobacterium tuberculosis, must replicate in macrophages for long-term persistence within their niche during chronic infection: organized collections of macrophages and lymphocytes called granulomas. We identified several genes preferentially expressed when Mycobacterium marinum, the cause of fish and amphibian tuberculosis, resides in host granulomas and/or macrophages. Two were homologs of M. tuberculosis PE/PE-PGRS genes, a family encoding numerous repetitive glycine-rich proteins of unknown function. Mutation of two PE-PGRS genes produced M. marinum strains incapable of replication in macrophages and with decreased persistence in granulomas. Our results establish a direct role in virulence for some PE-PGRS proteins. (+info)
High intracellular level of guanosine tetraphosphate in Mycobacterium smegmatis changes the morphology of the bacterium.
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Almost one-third of the world population today harbors the tubercle bacillus asymptomatically. It is postulated that the morphology and staining pattern of the long-term persistors are different from those of actively growing culture. Interestingly, it has been found that the morphology and staining pattern of the starved in vitro population of mycobacteria is similar to the persistors obtained from the lung lesions. In order to delineate the biochemical characteristics of starved mycobacteria, Mycobacteria smegmatis was grown in 0.2% glucose as a sole carbon source along with an enriched culture in 2% glucose. Accumulation of the stringent factor guanosine tetraphosphate (ppGpp) with a concomitant change in morphology was observed for M. smegmatis under carbon-deprived conditions. In addition, M. smegmatis assumed a coccoid morphology when ppGpp was ectopically produced by overexpressing Escherichia coli relA, even in an enriched medium. The Mycobacterium tuberculosis relA and spoT homologue, when induced in M. smegmatis, also resulted in the overproduction of ppGpp with a change in the bacterium's growth characteristics. (+info)
Mycobacterium kansasii infections in patients with cancer.
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Mycobacterium kansasii was isolated from 25 patients with cancer who were cared for at the University of Texas M. D. Anderson Cancer Center (Houston) from January 1987 through December 1996. Two patients (8%) had disseminated disease, and 23 (92%) had pleuropulmonary isolates only. Signs and symptoms of mycobacterial infection at the time of diagnosis were often minimal or absent despite substantial radiographically evident involvement. The infections responded well to rifampin-based antimycobacterial regimens. M. kansasii is an infrequent but serious cause of pulmonary and, occasionally, disseminated disease in patients with cancer. (+info)
We report four cases of pulmonary mycobacterial disease (three due to Mycobacterium malmoense and one to Myco- bacterium avium intracellulare) complicated by the development of chronic necrotising pulmonary aspergillosis. Difficulties with treatment and the potential benefits of steroids are discussed. (+info)
Identification of Mycobacterium ulcerans in the environment from regions in Southeast Australia in which it is endemic with sequence capture-PCR.
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We recently described the use of PCR to identify the environmental source of Mycobacterium ulcerans during an outbreak of ulcerative disease that occurred in a localized region of southeast Australia. The PCR used was based on amplification of the M. ulcerans-specific insertion sequence, IS2404. In this study we developed a new test that is a substantial improvement over the original PCR method in terms of sensitivity, reliability, and ease of use. In the new method magnetic bead sequence capture-PCR is used to detect two M. ulcerans sequences (IS2404 and IS2606) and total mycobacterial 16S ribosomal DNA. We used sequence capture-PCR to test water and plant material collected over a 12-month period during 1998 and 1999 from sites near the centers of two distinct foci of M. ulcerans infections. A golf course irrigation system in one area and a small shallow lake in another area repeatedly were PCR positive for M. ulcerans. Nearby sites and sites unrelated to the endemic areas were negative. Based on the PCR data, a most-probable-number method was used to estimate the concentration of M. ulcerans cells in positive samples from both regions. This procedure resulted in average concentrations of 0.5 cell per 100 ml of water and 40 cells per 100 g of detritus. Loss of the PCR signal coincided with a decrease in ulcerative disease in each area. These results provide further evidence that M. ulcerans may be transmitted from a point environmental source and demonstrate the utility of magnetic bead sequence capture-PCR for identification of nonculturable microbial pathogens in the environment. (+info)