title: M. tuberculosis genotypic diversity and drug susceptibility pattern in HIV-infected and non-HIV-infected patients in northern Tanzania.
abstract: BACKGROUND
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Internal Medicine, Endoscopy Unit, Kilimanjaro Christian Medical Centre, Tumaini University, Moshi, Tanzania. gkibiki@gmail.com <gkibiki@gmail.com>
authors.forename: Gibson S
authors.initials: GS
authors.lastname: Kibiki
authors.forename: Bert
authors.initials: B
authors.lastname: Mulder
authors.forename: Wil M V
authors.initials: WM
authors.lastname: Dolmans
authors.forename: Jessica L
authors.initials: JL
authors.lastname: de Beer
authors.forename: Martin
authors.initials: M
authors.lastname: Boeree
authors.forename: Noel
authors.initials: N
authors.lastname: Sam
authors.forename: Dick
authors.initials: D
authors.lastname: van Soolingen
authors.forename: Christophe
authors.initials: C
authors.lastname: Sola
authors.forename: Adri G M
authors.initials: AG
authors.lastname: van der Zanden
mesh_terms: D000328:Adult; D000995:Antitubercular Agents / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000235:genetics; D015373:Bacterial Typing Techniques; D001992:Bronchoalveolar Lavage Fluid / Q000382:microbiology; D002374:Catalase / Q000235:genetics; D016000:Cluster Analysis; D004269:DNA, Bacterial / Q000235:genetics; D012321:DNA-Directed RNA Polymerases / Q000235:genetics; D024881:Drug Resistance, Bacterial; D024901:Drug Resistance, Multiple, Bacterial; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000150:complications*; D006801:Humans; D008297:Male; D008826:Microbial Sensitivity Tests; D009154:Mutation; D009169:Mycobacterium tuberculosis / Q000145:classification / Q000187:drug effects* / Q000235:genetics* / Q000302:isolation & purification; D016133:Polymerase Chain Reaction / Q000379:methods; D013183:Sputum / Q000382:microbiology; D013636:Tanzania; D014376:Tuberculosis / Q000150:complications / Q000453:epidemiology / Q000382:microbiology*
chemical_list: D000995:Antitubercular Agents; D001426:Bacterial Proteins; D004269:DNA, Bacterial; D002374:Catalase; C480353:katG protein, Mycobacterium tuberculosis; D012321:DNA-Directed RNA Polymerases; C105078:RNA polymerase beta subunit