Abstract
We believe Helen Cox and colleagues’ proposal to restrict moxifl oxacin use to multidrug-resistant tuberculosis is based on fl awed logic. In a clinical trial of the present fi rst-line regimen for drug-susceptible tuberculosis, cure rates were greater than 95% and no new regimen is likely to improve on this rate. However, reducing treatment duration with moxifl oxacincontaining regimens would lead to a decreased risk of default and consequent drug resistance. Moxifl oxacin-containing regimens render sputum cultures sterile more rapidly than standard therapy, and so reduce onward transmission. A resultant decline in incident cases has been estimated by modelling studies. Cox and colleagues suggest that reserving moxifl oxacin for use in drugresistant tuberculosis will decrease future drug resistance. Restriction might be feasible in government programmes but is unrealistic in private practice, which is a common setting for tuberculosis treatment in countries with a high tuberculosis burden, including India. Furthermore, that all drugs in this class can be restricted is unlikely because of their widespread use and low cost. Those drugs with poorer anti-tuberculosis activity are more likely to select for resistance—for example, exposure to subinhibitory ciprofl oxacin concentrations increased mycobacterial mutation rates by up to 200 times compared with the rates without the antibiotic. Cross-resistance among fl uoroquinolones is common. Therefore, restriction of one drug in the class would not achieve a useful result. Cox and colleagues note that treatment-shortening trials are underway, and we advocate that patients with uncomplicated susceptible disease should not be treated with moxifl oxacin until results of these trials are known. In cases of drug resistance or poor tolerance, fl uoroquinolones should be used only in settings where susceptibility results are available to prevent the risk of increasing resistance.
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