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The Role of Bacteriophage in Group A Streptococcal Pathogenesis, Page 1 of 2
< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555815851/9781555814694_Chap05-1.gif /docserver/preview/fulltext/10.1128/9781555815851/9781555814694_Chap05-2.gifAbstract:
Group A streptococci (e.g., Streptococcus 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 streptococcus 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.