Emergence of a bacterial clone with enhanced virulence by acquisition of a phage encoding a secreted phospholipase A2

Izabela Sitkiewicz, Michal J. Nagiec, Paul Sumby, Stephanie D. Butler, Colette Cywes-Bentley, James M. Musser

Research output: Contribution to journalArticle

65 Scopus citations

Abstract

The molecular basis of pathogen clone emergence is relatively poorly understood. Acquisition of a bacteriophage encoding a previously unknown secreted phospholipase A2 (designated SlaA) has been implicated in the rapid emergence in the mid-1980s of a new hypervirulent clone of serotype M3 group A Streptococcus. Although several lines of circumstantial evidence suggest that SlaA is a virulence factor, this issue has not been addressed experimentally. We found that an isogenic ΔslaA mutant strain was significantly impaired in ability to adhere to and kill human epithelial cells compared with the wild-type parental strain. The mutant strain was less virulent for mice than the wild-type strain, and immunization with purified SlaA significantly protected mice from invasive disease. Importantly, the mutant strain was significantly attenuated for colonization in a monkey model of pharyngitis. We conclude that transductional acquisition of the ability of a GAS strain to produce SlaA enhanced the spread and virulence of the serotype M3 precursor strain. Hence, these studies identified a crucial molecular event underlying the evolution, rapid emergence, and widespread dissemination of unusually severe human infections caused by a distinct bacterial clone.

Original languageEnglish (US)
Pages (from-to)16009-16014
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume103
Issue number43
DOIs
StatePublished - Oct 24 2006

Keywords

  • Bacteria
  • Group A Streptococcus
  • Streptococcus pyogenes

ASJC Scopus subject areas

  • Genetics
  • General

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