PubMed · 15786884
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Renée Ridzon. 2005. Optimal latent TB control methods.. https://pubmed.ncbi.nlm.nih.gov/15786884/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
We report a rare case of infective granulomatous prostatitis caused by Mycobacterium tuberculosis that may be mistaken for prostatic carcinoma, both on clinical examination and transrectal sonography (TRUS). A large hypoechoic mass was detected in the prostate of a 46-year-old man during TRUS and histopathologic examination after TRUS-guided biopsies reported the diagnosis of tuberculous prostatitis. We herein describe the clinical and TRUS findings of this case.
We evaluated the French Azay-Mycobacteria network for surveillance of Mycobacterium tuberculosis drug resistance by matching data with those collected through the mandatory notification (MNTB). Sensitivity of Azay was 96% by capture-recapture analysis. Cases reported to MNTB were more often smear-positive than non-reported cases. Concordance of data collected for common cases was excellent for a majority of variables (k > 0.79), excepted for tuberculosis site (k = 0.52). These results suggest a good quality of the network.
We developed a DNA sequencing-based method to detect mutations in the genome of drug-resistant Mycobacterium tuberculosis. Drug resistance in M. tuberculosis is caused by mutations in restricted regions of the genome. Eight genome regions associated with drug resistance, including rpoB for rifampin (RIF), katG and the mabA (fabG1)-inhA promoter for isoniazid (INH), embB for ethambutol (EMB), pncA for pyrazinamide (PZA), rpsL and rrs for streptomycin (STR), and gyrA for levofloxacin, were amplified simultaneously by PCR, and the DNA sequences were determined. It took 6.5 h to complete all procedures. Among the 138 clinical isolates tested, 55 were resistant to at least one drug. Thirty-four of 38 INH-resistant isolates (89.5%), 28 of 28 RIF-resistant isolates (100%), 15 of 18 EMB-resistant isolates (83.3%), 18 of 30 STR-resistant isolates (60%), and 17 of 17 PZA-resistant isolates (100%) had mutations related to specific drug resistance. Eighteen of these mutations had not been reported previously. These novel mutations include one in rpoB, eight in katG, one in the mabA-inhA regulatory region, two in embB, five in pncA, and one in rrs. Escherichia coli isolates expressing individually five of the eight katG mutations showed loss of catalase and INH oxidation activities, and isolates carrying any of the five pncA mutations showed no pyrazinamidase activity, indicating that these mutations are associated with INH and PZA resistance, respectively. Our sequencing-based method was also useful for testing sputa from tuberculosis patients and for screening of mutations in Mycobacterium bovis. In conclusion, our new method is useful for rapid detection of multiple-drug-resistant M. tuberculosis and for identifying novel mutations in drug-resistant M. tuberculosis.