[Study on the molecular mechanism of multi-drug resistance in clinical isolates of Mycobacterium tuberculosis]

Zhonghua Jie He He Hu Xi Za Zhi. 1997 Dec;20(6):332-5.
[Article in Chinese]

Abstract

Objective: To study the molecular mechanism of multi-drug resistance in M. Tuberculosis, and to develop a new method for detecting genes related with multi-drug resistance.

Method: The ropB, rpsL, katG genes and inhA regulatory sequence in clinical isolates of M. tuberculosis were analyzed with PCR and PCR-SSCP techniques.

Result: The sensitivity of amplifing the drug-resistant genes with PCR was 1-10 pg DNA. Of the 20 multiple resistant strains with reduced sensitivity to streptomycin, rifampin and isoniazid, 90% showed mutations in more than two genetic markers associated with resistance to each of these three drugs, 10% revealed only mutations in rpoB gene.

Conclusion: Multi-drug resistance in M. tuberculosis could be caused by an accumulation of mutations in chromosomal genes encoding drug targets or an alteration at a single multiple resistance locus. PCR and PCR-SSCP techniques might become simple, rapid and reliable diagnostic tests for multi-drug resistance.

Publication types

  • English Abstract

MeSH terms

  • Antitubercular Agents / pharmacology
  • Drug Resistance, Microbial / genetics*
  • Drug Resistance, Multiple / genetics*
  • Genes, Bacterial*
  • Humans
  • Isoniazid / pharmacology
  • Mutation
  • Mycobacterium tuberculosis / drug effects
  • Mycobacterium tuberculosis / genetics*
  • Polymerase Chain Reaction
  • Polymorphism, Single-Stranded Conformational
  • Rifampin / pharmacology
  • Streptomycin / pharmacology
  • Tuberculosis, Multidrug-Resistant / microbiology*

Substances

  • Antitubercular Agents
  • Isoniazid
  • Rifampin
  • Streptomycin