Services on Demand
Journal
Article
Indicators
Cited by SciELO
Related links
Similars in SciELO
uBio
Share
Acta bioquímica clínica latinoamericana
Print version ISSN 0325-2957On-line version ISSN 1851-6114
Abstract
BERARDINELLI, Elena María and LOPARDO, Horacio Ángel. Estreptococos del grupo Streptococcus anginosus Parte II. Patogenia y sensibilidad a los antibióticos. Acta bioquím. clín. latinoam. [online]. 2021, vol.55, n.1, pp.61-77. ISSN 0325-2957.
This second part of the review about Streptococcus anginosus group streptococci (SAG) describes their virulence factors and their antimicrobial susceptibility. SAG are common colonizers of the oropharyngeal, intestinal, and genitourinary mucosa, but are increasingly recognized as human pathogens. Among their virulence factors, enzymes such as hyaluronidase, chondroitin sulfatase and nucleases (DNases and RNases) have been described. Superantigenic exoenzymes homologous to those of Streptococcus pyogenes have also been detected in some strains. The role of hemolysins (cytolysins) is notable, and specifically that of intermedilysin in Streptococcus intermedius, one of the three species of the group. SAG present low percentages of non-sensitivity to beta-lactams (penicillin: 0–15%, cefotaxime: 0 - 3% and carbapenems: 0-3%) with very few exceptions and very few resistant isolates. Instead, they are naturally resistant to metronidazole and nitrofurans. High percentages of resistance to macrolides, clindamycin and tetracycline have been reported (in some cases up to more than 50%). Fluoroquinolone resistance is variable, but it is very low for levofloxacin. SAG are generally susceptible to vancomycin and/or teicoplanin with minimal inhibitory concentrations (MICs)≤1 μg/mL, although the isolation of a few isolates with decreased sensitivity to vancomycin, one of them carrying the vanG gene, is notable. Resistance to other antibiotics was observed only sporadically.
Keywords : Streptococcus anginosus; Streptococcus intermedius; Streptococcus constellatus; Streptococcus milleri; Pathogenesis; Antimicrobial resistance.