Group A Streptococcus infections in children: from virulence to clinical management

Abstract

A greater understanding of GAS virulence strategies, and their associated clinical manifestations, may be obtained by shifting our research scope toward virulence determinant interactions and cooperation rather than focusing on individual virulence factor or specific strain characterization only.

Group A Streptococcus invasive infection in children: Epidemiologic changes and implications

“…Disease onset and progression can be very rapid, with high fatality rates, especially in young children and elderly, patients with comorbidities (diabetes or cardiovascular disease), immunocompromised, alcohol abuse, intravenous drug users, pregnant women and previous varicella infection [ 1 , 10 ]. Environmental factors such as number of household inhabitants and residential overcrowding have also been associated with iGAS [ 1 ]. Concomitant respiratory viral infection might also play a role on the incidence and severity of iGAS, particularly in children.…”

“…Other virulence factors of GAS include the hyaluronic capsule, streptolysin O, streptolysin S, streptococcal pyrogenic exotoxins A and B, and NAD glycohydrolase NADase. Bacterial exotoxins act as superantingens to trigger polyclonal T-lymphocyte activation by binding to class II major histocompatibility complex molecules, leading to an excessive release of proinflammatory cytokines and subsequent shock [ 1 , 10 ].…”

“…Linezolid and daptomycin are active in vitro , but clinical experience in treating invasive GAS infections is limited [ 10 ]. The addition of and antitoxin antibiotic such as clindamycin or linezolid is recommended, particularly if necrotizing fasciitis, STTS, or clinical signs of toxin production by SGA (rash, gastrointestinal signs, hemodinamic instability) [ 1 ]. The optimal duration of adjunctive clindamycin is uncertain as data are limited, but at least a minimum duration of 3 to 5 days is recommended [ 10 ].…”

Invasive Group A Streptococcal Infections: Benefit of Clindamycin, Intravenous Immunoglobulins and Secondary Prophylaxis

“…Exotoxins that act as superantigens and activate the immune system were associated with several clinical syndrome including STSS (1,5). The M protein promotes GAS infection by various means including the inhibition of phagocytosis (6). GAS also produces enzymes that prevent GAS from being killed like SpeB, a protease degrading host and bacterial components (7), Sda1, a DNAse destroying neutrophils extracellular traps (8), and toxins like Streptolysin O (SLO) cytotoxic for macrophages and neutrophils (6).…”

“…The M protein promotes GAS infection by various means including the inhibition of phagocytosis (6). GAS also produces enzymes that prevent GAS from being killed like SpeB, a protease degrading host and bacterial components (7), Sda1, a DNAse destroying neutrophils extracellular traps (8), and toxins like Streptolysin O (SLO) cytotoxic for macrophages and neutrophils (6). Appropriate diagnostic and rapid treatment based on β-lactam antibiotics and supportive care are the most important factors in reducing mortality (9).…”