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Chapter 5 : The Role of Bacteriophage in Group A Streptococcal Pathogenesis

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The Role of Bacteriophage in Group A Streptococcal Pathogenesis, Page 1 of 2

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Abstract:

Group A streptococci (e.g., pyogenes) are strictly human pathogens that are responsible for a number of suppurative infections, including scarlet fever, toxic shock syndrome, necrotizing fasciitis, impetigo, erysipelas, cellulitis, and pharyngitis. Early progress on group A streptococcal phage research was slow, partly due to poor plaque formation as a result of the streptococci’s fastidious growth requirements. Some of the first papers began to appear in the 1950s, with the introduction of a dialysate medium which helped to overcome this obstacle. But even then, studies on group A streptococcal phage were not extensive over the ensuing decades. Although it was well known that group A streptococci have an elaborate bacteriophage system, suggesting that phage may play an important role in the disease potential of these bacteria, it was not until 2001, when the first complete genome sequence of an M1 strain (SF370) was reported by Ferretti and coworkers that the true impact phage has on streptococcal pathogenicity was realized. To determine the nature of the events necessary for phage induction in the presence of pharyngeal cells, the necessity of contact between streptococci and pharyngeal cells can be ruled out since phage and Spd-1 could be induced when the pharyngeal cells were covered with a membrane before the addition of the streptococci. The frequency of lysogeny increases with the amount of free prophage mixed with recipient bacteria.

Citation: Fischetti V. 2007. The Role of Bacteriophage in Group A Streptococcal Pathogenesis, p 69-74. In Brogden K, Minion F, Cornick N, Stanton T, Zhang Q, Nolan L, Wannemuehler M (ed), Virulence Mechanisms of Bacterial Pathogens, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815851.ch5

Key Concept Ranking

Toxic Shock Syndrome
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Sodium Dodecyl Sulfate
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Streptococcus pyogenes
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FIGURE 1

Hypothetical model based on present data describing the in vivo induction of prophage and the infection of local sensitive streptococci. The pharyngeal mucosas in up to 30% of the population could be colonized with group A streptococci ( ). A lysogenized streptococcus ( ) could enter the oral cavity through exposure to contaminated saliva or another source and settle down on the pharyngeal mucosal surface ( ). It would come in contact with SPIF (boxes) produced by the pharyngeal cells, resulting in the induction of the lysogen and the production of progeny phage ( ). Upon lysis, progeny phage and other bacterial contents would be released onto the mucosal surface, including phage-encoded proteins such as toxin, DNase (SpeC and Spd-1), and hypothetical proteins ( ). The released Spd-1 would digest the viscous DNA of the lysing bacteria for better phage dissemination. The released proteins may enhance the infection process, allowing the incoming streptococcus to become better established in the human host ( ). Phage, released in the process, may encounter colonizing streptococci ( ), creating a new lysogen ( ), and resulting in a new strain of streptococcus, in some rare cases, a more virulent disease strain.

Citation: Fischetti V. 2007. The Role of Bacteriophage in Group A Streptococcal Pathogenesis, p 69-74. In Brogden K, Minion F, Cornick N, Stanton T, Zhang Q, Nolan L, Wannemuehler M (ed), Virulence Mechanisms of Bacterial Pathogens, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815851.ch5
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References

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