e-journal
Detection of mutations associated with resistance to rifampicin and isoniazid in Mycobacterium tuberculosis by polymerase chain reaction-ligase detection reaction
Mycobacterium tuberculosis (MTB) infection remains a serious infectious disease worldwide, causing 8.8 million new infections and 1.45 million deaths in 2010. The emergence of drug-resistant strains of MTB poses a significant threat to the control of the disease globally. Multidrugresistant MTB (MDR-TB), defined as being resistant to at least rifampicin (RMP) and isoniazid (INH), and extensively drug-resistant TB (XDR-TB), defined as being additionally resistant to any fluoroquinolone and one injectable secondline drug, are associated with higher treatment failure rates. China is the second largest nation in terms of the number of
the MTB infection, and 9.3% of the cases are MDR-TB. MDR-TB arises from spontaneous chromosomal mutations
at low frequency, but clinical MDR-TB largely occurs as a result of man-made selection during disease treatment of these genetic alterations through erratic drug supply, suboptimal physician prescription, and poor patient adherence. S315T/M mutation in katG and mutations in the promoter region of inhA operon are the main mechanisms of INH resistance. Mutations at positions 516, 526, and 531 in rpoB are the most frequent mutations in RMP-resistantMTB strains. Since the transmission of the selected MDR-TB strains
causes a large number of MDR-TB cases, the need for rapid, reliable, and cost-effective drug susceptibility testing (DST) is urgent.
Tidak ada salinan data
Tidak tersedia versi lain