Fluoroquinolones for treatment of community-acquired pneumonia and tuberculosis: putting the risk of resistance into perspective.

Community-acquired pneumonia (CAP) is a common and important disease that occurs in all age groups worldwide. Strep-tococcus pneumoniae is the most common cause of CAP and is the pathogen associated with the greatest morbidity and mortality [1]. High-level penicillin-resistant and drug-resistant S. pneumoniae infections are now a global problem; thus, the number of therapeutic options for the empirical treatment of CAP is limited. The fluoroquinolones for treatment of respiratory diseases, including gatifloxacin, moxifloxacin, and levofloxacin, have an excellent spectrum, providing coverage for the most important respiratory pathogens, including drug-resistant S. pneumoniae and atypical pathogens. The rate of fluo-roquinolone-resistant pneumococcus infection is !3% in most countries [2–4]. As a result, the fluoroquinolones for treatment of respiratory diseases have been recommended and are increasingly being used as preferred or alternative therapy for the treatment of CAP [1, 5]. Given that an estimated one-third of the world's population is infected with My-cobacterium tuberculosis and ∼1.6 million deaths worldwide in 2006 were attributable to tuberculosis (TB), TB remains a major public health concern. Fluoroquin-olones have excellent in vitro activity against M. tuberculosis. They are one of the most important drug classes for the treatment of multidrug-resistant TB and of patients who experience severe adverse effects of first-line anti-TB therapy [6, 7]. Furthermore, fluoroquinolone-containing regimens are likely to be proved to be effective for shortening the treatment duration for drug-susceptible disease [6]. Depending on the prevalence of TB in a specific region, a percentage of patients with CAP who are empirically treated with a fluoroquinolone will actually have pulmonary TB with or without infection due to a copathogen. In a study of CAP in adult patients in Asian countries, Song et al. [8] found that the etiology was M. tuberculosis in 3.3% of cases. There's the rub. Monotherapy with a fluoroquinolone may temporarily improve the patient's symptoms and, therefore, delay diagnosis [9– 12] and/or may select for fluoroquino-lone-resistant M. tuberculosis strains. In this issue of Clinical Infectious Diseases, Long et al. [13] put the threat of the emergence of fluoroquinolone resistance into perspective. With access to 2 large provincial TB registries with linkages to corresponding prescription drug plans, the authors found that, although outpatient fluoroquinolone use (ostensibly for CAP) was not uncommon among patients with pulmonary TB, fluoroquinolone-resistant M. tuberculosis was identified infrequently; only 3 of 74 patients who had been treated with a fluoroquinolone prior to the diagnosis of pulmonary TB were infected with …