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Emergence of a Bacterial Clone with Enhanced Virulence by Acquisition of a Phage Encoding a Secreted Phospholipase A2

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Specialty Science
Date 2006 Oct 18
PMID 17043230
Citations 32
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Abstract

The molecular basis of pathogen clone emergence is relatively poorly understood. Acquisition of a bacteriophage encoding a previously unknown secreted phospholipase A(2) (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 DeltaslaA 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.

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References
1.
Shelburne 3rd S, Granville C, Tokuyama M, Sitkiewicz I, Patel P, Musser J . Growth characteristics of and virulence factor production by group A Streptococcus during cultivation in human saliva. Infect Immun. 2005; 73(8):4723-31. PMC: 1201272. DOI: 10.1128/IAI.73.8.4723-4731.2005. View

2.
Davies H, McGeer A, Schwartz B, Green K, Cann D, Simor A . Invasive group A streptococcal infections in Ontario, Canada. Ontario Group A Streptococcal Study Group. N Engl J Med. 1996; 335(8):547-54. DOI: 10.1056/NEJM199608223350803. View

3.
Sumby P, Porcella S, Madrigal A, Barbian K, Virtaneva K, Ricklefs S . Evolutionary origin and emergence of a highly successful clone of serotype M1 group a Streptococcus involved multiple horizontal gene transfer events. J Infect Dis. 2005; 192(5):771-82. DOI: 10.1086/432514. View

4.
Bricker A, Cywes C, Ashbaugh C, Wessels M . NAD+-glycohydrolase acts as an intracellular toxin to enhance the extracellular survival of group A streptococci. Mol Microbiol. 2002; 44(1):257-69. DOI: 10.1046/j.1365-2958.2002.02876.x. View

5.
Lukomski S, Sreevatsan S, AMBERG C, Reichardt W, Woischnik M, Podbielski A . Inactivation of Streptococcus pyogenes extracellular cysteine protease significantly decreases mouse lethality of serotype M3 and M49 strains. J Clin Invest. 1997; 99(11):2574-80. PMC: 508102. DOI: 10.1172/JCI119445. View