Group A streptococcus and its antibiotic resistance

Abstract

Acute pharyngo-tonsillitis caused by beta-haemolytic group A Streptococcus is a common disease in childhood. Epithelial cells are the initial sites of the host invasion by group A Streptococcus. Although group A Streptococcus has been considered an extracellular pathogen, recent studies have demonstrated that strains of this bacterium can internalize into epithelial cells both in vitro and in vivo. As adherence to and internalization into host cells significantly contributes to the pathogenesis of group A Streptococcus infections, internalization of group A Streptococcus by human epithelial cells has been extensively studied during the past decade. Multiple mechanisms are involved in this process. Most strains of Streptococcus pyogenes express the fibronectin-binding proteins F1 and F2, which promote bacterial adherence to and entry into human cells. Strains containing the gene for the protein Fl have been proved to be responsible for the failure of antibiotic treatment to eradicate Streptococcus pyogenes. Thus, in a significant number of cases, streptococcal internalization might contribute to eradication failure and persistent throat carriage. Since treatment failure, asymptomatic group A Streptococcus carriers and recurrent group A Streptococcus infections represent the main group A Streptococcus reservoir, from which the bacteria are spread in the general population, the choice of antibiotic is crucial. Beta-lactams select a large number of F1-positive organisms: therefore, macrolides, and, possibly, last generation molecules, are the best and first choice for antibiotic treatment against group A Streptococcus.