Group A Streptococcus (GAS)

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Streptococcus pyogenes, also known as Group A streptococcus (GAS), is a β-hemolytic, Gram-positive bacterium that most commonly causes respiratory disease, including pharyngitis or tonsillitis, as well as skin infections such as impetigo and cellulitis. The organism is transmitted via respiratory droplets or by contact with fomites, and commonly infects young children. In addition to the common clinical presentations associated with S. pyogenes, some individuals develop the postinfectious sequelae of rheumatic fever and glomerulonephritis. Due to the severity of these medical consequences, prophylactic antibiotic use is often recommended for any patients with otherwise mild S. pyogenes infections (21).
In addition to its traditional clinical manifestations, GAS can also cause serious invasive disease such as necrotizing fasciitis, colloquially known as the flesh-eating disease. First broadly reported during the Civil War, when it was known as gangrene, necrotizing fasciitis occurs when an individual’s subcutaneous fat and superficial fascia become rapidly necrotic. Though incidence data is limited, one study estimated that, worldwide, there are approximately 660,000 cases of invasive GAS disease per year, with 97% of those cases occurring in low-income populations (4). Many microorganisms other than GAS have been linked with necrotizing fasciitis, including Staphyloccocus aureus, Escherichica coli, and Klebsiella pneumoniae, and the disease is often caused by a polymicrobial infection. However, the most well known causative agent in necrotizing fasciitis cases is usually Group A streptococci (6). Although risk factors for necrotizing fasciitis include diabetes, old age, and immunosuppression, nearly half of all infections occur i...

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...ly 24 hours postinfection, during the late exponential and early stationary phases, SpeB is dramatically upregulated as tissue invasion occurs and the bacteria disseminate (13). It is speculated that this upregulation occurs so that SpeB can cleave the GAS adhesive molecules and allow the bacteria to spread throughout the tissue during invasive infections (20). Following the dissemination of GAS in this stage, SpeB expression is once again downregulated as the bacterium invades the bloodstream. GAS selects for mutations in the CovRS regulatory system, which result in reduced expression of SpeB and a simultaneous enhancement of the production of another virulence factor, Sda1. Sda1 helps avoid host neutrophil extracellular traps, allowing the bacterium to survive in the bloodstream and produce the bacteremia and sepsis characteristic of invasive GAS infections (26).

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