Pathogenesis of group A streptococcal infections

Authors
Citation
Mw. Cunningham, Pathogenesis of group A streptococcal infections, CLIN MICROB, 13(3), 2000, pp. 470
Citations number
564
Language
INGLESE
art.tipo
Review
Categorie Soggetti
Microbiology
Journal title
CLINICAL MICROBIOLOGY REVIEWS
ISSN journal
0893-8512 → ACNP
Volume
13
Issue
3
Year of publication
2000
Database
ISI
SICI code
0893-8512(200007)13:3<470:POGASI>2.0.ZU;2-3
Abstract
Group A streptococci are model extracellular gram-positive pathogens respon sible for pharyngitis, impetigo, rheumatic fever, and acute glomerulonephri tis. A resurgence of invasive streptococcal diseases and rheumatic fever ha s appeared in outbreaks over the past 10 years, with a predominant M1 serot ype as well as others identified with the outbreaks. emm (M protein) gene s equencing has changed serotyping, and new virulence genes and new virulence regulatory networks have been defined. The emm gene superfamily has expand ed to include antiphagocytic molecules and immunoglobulin-binding proteins with common structural features. At least nine superantigens have been char acterized, all of which may contribute to toxic streptococcal syndrome. An emerging theme is the dichotomy between skin and throat strains in their ep idemiology and genetic makeup. Eleven adhesins have been reported, and surf ace plasmin-binding proteins have been defined. The strong resistance of th e group A streptococcus to phagocytosis is related to factor H and fibrinog en binding by M protein and to disarming complement component C5a by the C5 a peptidase. Molecular mimicry appears to play a role in autoimmune mechani sms involved in rheumatic fever, while nephritis strain-associated proteins may lead to immune-mediated acute glomerulonephritis. Vaccine strategies h ave focused on recombinant M protein and C5a peptidase vaccines, and mucosa l vaccine delivery systems are under investigation.