M. tuberculosis genotypic diversity and drug susceptibility pattern in HIV- infected and non-HIV-infected patients in northern Tanzania
1 Department of Internal Medicine, Endoscopy Unit and Department of Medical Microbiology, Kilimanjaro Christian Medical Centre, Tumaini University, P.O Box 3010, Moshi, Tanzania
2 Microbiology Laboratory Twente, Enschede, The Netherlands
3 Department of Internal Medicine, Division General Internal Medicine, University Nijmegen Medical Centre St-Radboud, PO Box 9101 (484), 6500 HB Nijmegen, The Netherlands
4 Medical Microbiology and Infection Control, Gelre Hospitals, Apeldoorn, The Netherlands
5 Department of Pulmonary Diseases and University Lung Centre Dekkerswald, University Nijmegen Medical Centre St-Radboud, PO Box 9101 (484), 6500 HB Nijmegen, The Netherlands
6 National Institute of Public Health and the Environment (RIVM), Bilthoven, The Netherlands
7 Institut Pasteur de Guadeloupe, Guadeloupe
8 Present address: Unité de Génétique Mycobactérienne, Institut Pasteur, Paris, France
BMC Microbiology 2007, 7:51 doi:10.1186/1471-2180-7-51Published: 31 May 2007
Tuberculosis (TB) is a major health problem and HIV is the major cause of the increase in TB. Sub-Saharan Africa is endemic for both TB and HIV infection. Determination of the prevalence of M. tuberculosis strains and their drug susceptibility is important for TB control.
TB positive culture, BAL fluid or sputum samples from 130 patients were collected and genotyped. The spoligotypes were correlated with anti-tuberculous drug susceptibility in HIV-infected and non-HIV patients from Tanzania.
One-third of patients were TB/HIV co-infected. Forty-seven spoligotypes were identified.
Fourteen isolates (10.8%) had new and unique spoligotypes while 116 isolates (89.2%) belonged to 33 known spoligotypes. The major spoligotypes contained nine clusters: CAS1-Kili 30.0%, LAM11- ZWE 14.6%, ND 9.2%, EAI 6.2%, Beijing 5.4%, T-undefined 4.6%, CAS1-Delhi 3.8%, T1 3.8% and LAM9 3.8%. Twelve (10.8%) of the 111 phenotypically tested strains were resistant to anti-TB drugs. Eight (7.2%) were monoresistant strains: 7 to isoniazid (INH) and one to streptomycin. Four strains (3.5%) were resistant to multiple drugs: one (0.9%) was resistant to INH and streptomycin and the other three (2.7%) were MDR strains: one was resistant to INH, rifampicin and ethambutol and two were resistant to all four anti-TB drugs. Mutation in the katG gene codon 315 and the rpoB hotspot region showed a low and high sensitivity, respectively, as predictor of phenotypic drug resistance.
CAS1-Kili and LAM11-ZWE were the most common families. Strains of the Beijing family and CAS1-Kili were not or least often associated with resistance, respectively. HIV status was not associated with spoligotypes, resistance or previous TB treatment.