000151297 001__ 151297
000151297 005__ 20181203021959.0
000151297 022__ $$a0924-8579
000151297 02470 $$2PMID$$a18611785
000151297 0247_ $$2doi$$a10.1016/S0924-8579(96)00356-1
000151297 037__ $$aARTICLE
000151297 245__ $$aMultidrug resistance in Mycobacterium tuberculosis
000151297 269__ $$a1997
000151297 260__ $$c1997
000151297 336__ $$aJournal Articles
000151297 520__ $$aAll but one of the four major mechanisms of resistance to antimicrobial agents-inactivation of the drug, altered cell wall permeability or drug efflux, drug titration due to target overproduction, and alteration of the target by mutation-appear to be employed by Mycobacterium tuberculosis in its resistance to components of short course chemotherapy regimens. To date no enzymes capable of inactivating any of the frontline drugs have been found. The most common resistance mechanism is alteration of the target leading to inadequate drug binding, or drug activation, as a result of mutations in chromosomal genes. This occurs in the case of the specific antituberculous drugs isoniazid, pyrazinamide and ethionamide as well as in resistance to the broad-spectrum antibiotics, rifampicin, streptomycin and the fluoroquinolones. Overproduction of the drug target also appears to lead to resistance to isoniazid and ethionamide whereas changes in permeability, or the activation of antibiotic-efflux systems, may contribute to the low-level resistance of the tubercle bacillus to streptomycin and fluoroquinolones.
000151297 700__ $$aHeym, B
000151297 700__ $$g177247$$aCole, S T$$0243892
000151297 773__ $$j8$$tInternational journal of antimicrobial agents$$k1$$q61-70
000151297 909C0 $$xU11742$$0252302$$pUPCOL
000151297 909CO $$pSV$$particle$$ooai:infoscience.tind.io:151297
000151297 937__ $$aEPFL-ARTICLE-151297
000151297 973__ $$rREVIEWED$$sPUBLISHED$$aOTHER
000151297 980__ $$aARTICLE