Journal
CURRENT OPINION IN INFECTIOUS DISEASES
Volume 27, Issue 2, Pages 155-164Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QCO.0000000000000047
Keywords
complement; fibrinolysis; Streptococcus dysgalactiae; Streptococcus pyogenes
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Funding
- Leukaemia and Lymphoma Research
- UK NIHR Biomedical Research Centre
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Purpose of reviewIncreasing disease caused by beta-haemolytic streptococci indicates the need for improved understanding of pathogenesis.Recent findingsStreptococcus pyogenes, or group A Streptococcus (GAS), causes significant disease worldwide. The closely related Streptococcus dysgalactiae subspecies equisimilis (SDSE) is increasingly recognized as causing a similar disease spectrum. Whole-genome sequencing applied to the study of outbreaks may reveal factors that contribute to pathogenesis and changes in epidemiology. The role of quorum sensing in biofilm formation, and interspecies communication with other streptococci, is discussed. GAS has evolved multiple mechanisms to evade the humoral arm of innate immunity, including complement, which is well known in protecting the host from bacteria, and the coagulation-fibrinolytic system, which is increasingly recognized as an innate immune effector.SummaryMolecular biology has enhanced our understanding of the intricate balance of host-pathogen interactions that result in clearance or establishment of invasive streptococcal infection. Although the skin and oropharynx remain the usual ecological niche of GAS and SDSE, occasionally the bacteria find themselves within deeper tissues and blood. Recent research has armed us with better knowledge of bacterial adaptations to this alternative environment. However, the challenge is to translate this knowledge into clinical practice, through the development of novel therapeutic options and ultimately a vaccine against GAS.
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