Recovery of susceptibility to penicillin G in clinical isolates of Streptococcus pneumoniae despite increased accumulation of pbp gene alterations

Abstract

Two hundred consecutive clinical isolates of Streptococcus pneumoniae isolated in 2005 and 2006 were analysed for susceptibility to various antimicrobials, pbp gene alterations and macrolide resistance gene expression (2007 analysis) and the results were compared with previous data (2003 analysis). The average minimum inhibitory concentration (MIC) of penicillin G in isolates with 1a m /2x m /2b m decreased from 1.135 ± 0.503 mg/L in the 2003 analysis to 0.872 ± 0.540 mg/L in the 2007 analysis ( P = 0.0046). The prevalence of isolates with 1a m /2x m /2b m increased from 30.5% to 32.3%, but the difference was not statistically significant ( P = 0.6979). The prevalence of isolates with a clarithromycin MIC ≥ 1.0 mg/L increased from 65.9% to 80.0% ( P = 0.0005). Isolates expressing ermB increased from 46.6% to 62.6% ( P = 0.0004). We conclude that the decrease in penicillin resistance of S. pneumoniae does not correlate with a decrease in pbp mutations; on the contrary, the prevalence of isolates with pbp mutations increased. A decrease in penicillin resistance in S. pneumoniae with pbp mutations appears to explain the present results regarding the recovery of penicillin susceptibility. Our results suggest that the spread of mutated pbp genes among S. pneumoniae itself is not responsible for acquisition of the penicillin-resistant phenotype. Use of β-lactams, especially oral cephalosporins, appears to be responsible for the acquisition of penicillin resistance.