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Archives de pédiatrie
Volume 21, n° S2
pages 54-61 (novembre 2014)
Doi : 10.1016/S0929-693X(14)72261-4
Facteurs de pathogénicité de Streptococcus pyogenes
Streptococcus pyogenes pathogenic factors
 

Ph. Bidet 1, 2, , S. Bonacorsi 1, 2
1 Université Paris-Diderot, PRES Sorbonne-Paris-Cité, 46, rue Henri-Huchard, 75018 Paris, France 
2 Service de microbiologie, hôpital Robert-Debré (AP-HP), 48, boulevard Sérurier, 75019 Paris, France 

*Auteur correspondant.
Résumé

Le pouvoir pathogène du streptocoque ß-hémolytique du groupe A (SGA) est particulièrement vaste, allant des infections bénignes, comme l’angine ou l’impétigo, à des pathologies post-streptococciques potentiellement invalidantes, et jusqu’aux infections invasives sévères, comme la fasciite nécrosante ou le redoutable syndrome de choc toxique streptococcique. Cette variété d’expressions cliniques, souvent radicalement différentes chez des individus infectés par une même souche, résulte d’une interaction complexe entre les facteurs de pathogénicité de la bactérie, le mode d’infestation et le système immunitaire de l’hôte. Les progrès en génomique comparative ont permis de mieux comprendre comment, au terme de cette confrontation, le SGA s’adapte à la pression du système immunitaire, soit de manière pacifique, en diminuant l’expression de certains facteurs de pathogénicité pour aboutir à un portage asymptomatique, ou au contraire en les surexprimant de manière démesurée, avec pour conséquence les formes les plus sévères d’infection invasives.

The full text of this article is available in PDF format.
Summary

The pathogenicity of ß-hemolytic group A streptococcus (GAS) is particularly diverse, ranging from mild infections, such as pharyngitis or impetigo, to potentially debilitating poststreptococcal diseases, and up to severe invasive infections such as necrotizing fasciitis or the dreaded streptococcal toxic shock syndrome. This variety of clinical expressions, often radically different in individuals infected with the same strain, results from a complex interaction between the bacterial virulence factors, the mode of infection and the immune system of the host. Advances in comparative genomics have led to a better understanding of how, following this confrontation, GAS adapts to the immune system's pressure, either peacefully by reducing the expression of certain virulence factors to achieve an asymptomatic carriage, or on the contrary, by overexpressing them disproportionately, resulting in the most severe forms of invasive infection.

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