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Cigarette smoking is a well-recognized risk factor for development of severe, invasive pneumococcal disease. However, little is known about the direct effects of exposure to cigarette smoke on the virulence mechanisms of the pathogen, particularly in respect of resistance to macrolide antibiotics, which are widely used in the treatment of pneumococcal infection. This study aimed to investigate the effects of exposure to cigarette smoke condensate (CSC, 80 and 160 mg/L) and clarithromycin (2 and 8 mg/L), alone and in combination  in vitro , on expression of the  erm (B) and  mef (A) macrolide resistance genes of strains 2507 and 521 (both serotype 23F), respectively, of the pneumococcus.    METHODS  Following exposure to CSC or clarithromycin, individually and in combination,  erm (B) and  mef (A) gene expression were measured by sequential extraction of RNA, conversion to and amplification of cDNA, and detection by qRT-PCR.    RESULTS  As expected, exposure of both test strains of the pneumococcus to clarithromycin resulted in substantial upregulation of both macrolide resistance genes, which was significantly (p<0.001) augmented by prior exposure to CSC in the case of  erm (B), but not  mef (A). Somewhat unexpectedly, exposure of strain 2507 to CSC (160 mg/L) alone (in the absence of clarithromycin) also resulted in significant (p<0.05) expression of the  erm (B) gene.    CONCLUSION  Although the possible clinical significance remains to be established, these findings suggest that smoking may impede the efficacy of macrolide-based antimicrobial therapy by accelerating the onset and magnitude of  erm (B)-mediated resistance, representing a novel pro-infective mechanism of smoking.

Cigarette smoke exposure induces expression of the pneumococcal <i>erm</i>(B) macrolide resistance gene