Evolution and Characterization of Penicillin-Resistant Streptococcus pneumoniae in Canadian Hospitals 2007-2010

Abstract

Streptococcus pneumoniae continues to cause considerable morbidity and mortality as a respiratory tract pathogen. Evolution and adaptation of S. pneumoniae occurs in response to antimicrobial use as well as vaccination of children and adults. The evolution of penicillin-resistant and multi-drug resistant (MDR) S. pneumoniae is of considerable concern to scientists and clinicians. In this study, penicillin-resistant isolates of S. pneumoniae were collected from the CANWARD national surveillance study over the years of 2007-2010 inclusive, and were studied to understand their demographic characterization, antimicrobial resistance patterns, serotype distribution, genetic and phenotypic relatedness, and virulence factors. This study determined penicillin-resistant S. pneumoniae from Canadian hospitals to be genetically related and frequently possess a MDR phenotype. These highly pathogenic pneumococci originated from all over Canada, and were isolated from patients from a wide age range in a variety of hospital settings. The emerging serotype 19A represented the most important source of penicillin and MDR strains. Clusters of penicillin-resistant S. pneumoniae isolates were genetically related to each other and to internationally recognized clones, including Taiwan19F-14, Spain9V-3, Spain23F-1, and England14-9. The pilus-encoding genetic islet virulence factors, PI-1 and PI-2 were associated with serotypes 19A, 19F, 9V, 14, and 35B, with PI-2 associated only with 19A and 19F isolates. In conclusion, penicillin-resistant S. pneumoniae accounted for 3.4% of all S. pneumoniae from Canadian hospitals between 2007-2010 and were isolated from patients of a wide age range, from all hospital ward types and all regions across Canada. These virulent S. pneumoniae were represented predominantly by the emerging serotype 19A, commonly exhibited a MDR phenotype, were genetically related and frequently possessed the virulence factors, P1 and P2.