L5 Molecular Epidemiology of Penicillin- (PEN), Clarithromycin- (CLR), Ciprofloxacin- (CIP), Tetracycline- (TET) and Trimethoprim/Sulfamethoxazole-Resistant (SXT-R) Streptococcus pneumoniae (SPN) in Canada 
K.A. Nichol*, D.J. Hoban, G.G. Zhanel, Health Sciences Centre and University of Manitoba, Winnipeg, MB.

Background: The increasing incidence of antibiotic-resistant SPN worldwide has emphasized the need for epidemiological surveillance of this important pathogen.  Genetic lineages that have achieved unusually wide geographic spread across both national and international borders have been identified.  The purpose of this study was to examine the molecular epidemiology of PEN-R, CLR-R, CIP-R, TET-R and/or SXT-R SPN from across Canada.

Methods: 813 resistant isolates of SPN were selected from among 8957 clinical isolates collected between 1997 and 2003 as part of an ongoing national respiratory organism surveillance study.  Susceptibilities to PEN, CLR, CIP, TET and SXT were determined by broth microdilution as specified by the NCCLS (2003).  The genetic relatedness between isolates was evaluated by PFGE of SmaI digests.  Serotyping was performed by the Quellung reaction.

Results: Of the 813 SPN isolates, 455 were PEN-R (MIC ³ 2 mg/ml), 419 were CLR-R (MIC ³ 1 mg/ml), 135 were CIP-R (MIC ³ 4 mg/ml), 133 were TET-R (MIC ³ 8 mg/ml) and 416 were SXT-R (MIC ³ 4 mg/ml).  Dendrogram analysis revealed 3-4 major PFGE types (21-119 isolates each) among the SXT- and PEN-R isolates.  Predominant serotypes included 9V, 14, 19F and 23F.  8 epidemiologic clusters (³ 80% genetic relatedness), including 4 PEN-R clusters related to known international clones, were identified among the CLR-R isolates.  Associations between TET or CIP resistance and PFGE type were not observed.

Conclusions: The close genetic relatedness among SXT- and PEN-R isolates demonstrates the important contribution of clonal spread to the overall increase of PEN-R and SXT-R SPN in Canada.  Increases in macrolide resistance appear to involve both the dissemination of resistant clones and de novo acquisition of CLR resistance determinants.  The emergence of TET- and CIP-R SPN in Canada is currently not attributable to clonal dissemination.