Objectives: In humans, enterococci are among the most important opportunistic pathogens. This study aims to compare invasive isolates obtained from blood cultures of patients with sepsis and endocarditis with colonizing isolates obtained from healthy donors’ stool samples. Methods: A case-by-case assessment was conducted on invasive infection cases to determine whether enterococci were involved in their pathogenesis. They were tested for the presence of virulence factor genes, β-hemolysis on agars supplemented with human and sheep blood, and biofilm forming capacity. Results: Three species of enterococci were identified among invasive isolates: Enterococcus faecalis, Enterococcus faecium, and Enterococcus durans. All endocarditis isolates were biofilm producers. Genes esp, gelE, asa1, ace, hyl, cylB, and cylA were present in 7 (41.2%), 11 (64.7%), 11 (64.7%), 13 (76.5%), 0, 3 (17.6%), and 1 (5.9%) invasive isolate, but none of them could be linked to a particular infection (sepsis or endocarditis). Colonizing isolates proved to have had more virulence factor genes, but the differences were not statistically significant. Members of that group produced a greater amount of biofilm when the ace gene was absent (p = 0.047). The production of β-hemolysis by noninvasive strains was detected more frequently when agar was supplemented with human blood (p = 0.021). In general, the presence of either cyl gene on that specific agar was in direct connection with the production of β-hemolysis: cylA (p = 0.047) or cylB (p = 0.020). Conclusion: We have been unable to establish any correlation between invasive isolates and any virulence gene carriage and biofilm formation. β-hemolysis was produced significantly more often by colonizing strains when agar had been supplemented with human blood.
CITATION STYLE
Jovanović, M., Velebit, B., Tošić, T., Maki, G., Pavić, S., Jovanović, S., … Zervos, M. J. (2023). Comparative study of virulence factor genes, β-hemolysis and biofilm production in invasive and colonizing enterococci. European Journal of Inflammation, 21. https://doi.org/10.1177/1721727X231156333
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