During the 1990s, multidrug-resistant tuberculosis (MDR-TB), resistant to at least isoniazid and rifampin, emerged as a great threat to global tuberculosis (TB) control [1]. For most MDR-TB patients, the World Health Organization (WHO) recommends a treatment regimen including second-line anti-TB drugs [2]. One of the most effective second-line drugs is fluoroquinolone [3]. During the treatment, MDR-TB may develop resistance to fluoroquinolone, or even become extensively drug-resistant (XDR-TB), which is resistant to both fluoroquinolone and at least one of three injectable second-line drugs [4]. The main genetic mechanism of fluoroquinolone resistance lies in the mutations in the quinolone-resistance-determining region of gyrA and gyrB [5].
from # All Medicine by Alexandros G. Sfakianakis via alkiviadis.1961 on Inoreader http://ift.tt/2B9oUIr
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