Molecular mechanisms of macrolide resistant invasive Streptococcus pneumoniae isolates from Alaska, 1986 to 2010.

Rudolph K, Bulkow L, Bruce M, Zulz T, Reasonover A, Harker-Jones M, Hurlburt D, Hennessy T.

Source

Arctic Investigations Program, Centers for Disease Control and Prevention, 4055 Tudor Centre Drive, Anchorage, Alaska 99508, USA.

Abstract

Rapid emergence of antibiotic resistant pneumococcal strains has reduced treatment options. The aim of this study was to determine antimicrobial susceptibilities, serotype distributions and molecular resistance mechanisms among macrolide resistant invasive pneumococcal isolates in Alaska from 1986-2010. We identified cases of invasive pneumococcal disease in Alaska from 1986-2010 through statewide population-based laboratory surveillance. All invasive pneumococcal isolates submitted to the Arctic Investigations Program laboratory were confirmed by standard microbiological methods and serotyped by slide agglutination and the Quellung reaction. Minimal inhibitory concentrations were determined by the broth microdilution method and macrolide resistant genotypes determined by multiplex PCR. Among 2923 invasive pneumococcal isolates recovered from 1986-2010, 270 (9.2%) were non-susceptible to erythromycin; 177 (66%) erythromycin non-susceptible isolates demonstrated co-resistance to penicillin and 167 (62%) were multidrug resistant. The most frequent serotypes among the macrolide-resistant isolates were 6B (23.3%), 14 (20.7%), 19A (16.7%), 9V (8.9%), 19F (6.3%), 6A (5.6%) and 23F (4.8%). Mef and ermB genes were detected in 207 (77%) and 32 (12%) of isolates, respectively. Nineteen (7%) of the erythromycin non-susceptible isolates contained both mef and ermB genotypes; 15 were serotype 19A. There was significant year-to-year variation in the proportion of isolates that were non-susceptible to erythromycin (p< 0.001).Macrolide resistance among pneumococcal isolates from Alaska is predominantly mediated by mef genes and this has not changed significantly over time. However, there was a statistically significant increase in the proportion of isolates that possess both ermB and mef, primarily due to serotype 19A isolates.