Targeting Antibiotic Resistance Mechanisms in Mycobacterium tuberculosis

Recharging the Old Magic Bullets

Liem Nguyen

Disclosures

Expert Rev Anti Infect Ther. 2012;10(9):963-965. 

In This Article

Introduction

Tuberculosis (TB) is an ancient disease. This 'White Plague' came and went throughout the history of mankind as unavoidable visits from Death until the recent era of antibiotics, starting some 80 years ago. The discovery of these 'magic bullets' brought a sudden great victory to our battle against the TB etiological agent, Mycobacterium tuberculosis.[1] Thanks to these powerful chemicals, TB has become a curable disease. Although it remains one of the most difficult infections to treat, the current Direct Observed Treatment Short regimen, which usually takes 6–9 months of continuous chemotherapy, is quite effective in treatment of drug-susceptible TB. The arising problem now lies in the emergence and wide spread of drug-resistant forms of the disease. Mutations in drug target genes have contributed to the evolution of M. tuberculosis strains that are resistant to the handful of currently available first- and second-line TB antibiotics.[2,3] Repeated misuse of these few drugs has led to the sequential accumulation of the mutations that result in the emergence of strains simultaneously resistant to multiple existing TB drugs. These multidrug resistant, extensively drug-resistant, and most recently totally drug-resistant M. tuberculosis strains pose a serious threat to public health if alternative therapeutic options do not quickly become available.[4,5] It's clear now that the current 'magic bullets' are losing their magic power. What are we going to do to contain these multidrug resistant, extensively drug-resistant and totally drug-resistant M. tuberculosis strains?

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