Multidrug resistance in Mycobacterium tuberculosis

被引:22
作者
Heym, B
Cole, ST
机构
[1] INST PASTEUR, UNITE GENET MOL BACTERIENNE, F-75724 PARIS 15, FRANCE
[2] HOP AMBROISE PARE, F-92104 BOULOGNE, FRANCE
关键词
tuberculosis; short course chemotherapy; isoniazid; rifampicin; pyrazinamide; streptomycin; ethambutol; fluoroquinolones;
D O I
10.1016/S0924-8579(96)00356-1
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
All but one of the four major mechanisms of resistance to antimicrobial agents-inactivation of the drug, altered cell wall permeability or drug efflux, drug titration due to target overproduction, and alteration of the target by mutation-appear to be employed by Mycobacterium tuberculosis in its resistance to components of short course chemotherapy regimens. To date no enzymes capable of inactivating any of the frontline drugs have been found. The most common resistance mechanism is alteration of the target leading to inadequate drug binding, or drug activation: as a result of mutations in chromosomal genes. This occurs in the case of the specific antituberculous drugs isoniazid, pyrazinamide and ethionamide as well as in resistance to the broad-spectrum antibiotics, rifampicin, streptomycin and the fluoroquinolones. Overproduction of the drug target also appears to lead to resistance to isoniazid and ethionamide whereas changes in permeability, or the activation of antibiotic-efflux systems, may contribute to the low-level resistance of the tubercle bacillus to streptomycin and fluoroquinolones. (C) 1997 Elsevier Science B.V.
引用
收藏
页码:61 / 70
页数:10
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