Abstract
Background: Staphylococcus epidermidis is the predominating etiology of neonatal septicemia in industrilized countries, but specific virulence factors associated with S. epidermidis are incompletely described. The aim of the present study was to investigate possible virulence factors representing different pathogenetic steps in neonatal blood isolates of S. epidermidis: a) Up-regulation of inflammatory activity in endothelial cells b) the ability to express bacterial surface proteins and biofilm of importance for bacterial colonization and c) antibiotical resistance.
Methods: All blood isolates of S. epidermidis collected at the neonatal intensive care unit, Örebro University Hospital, Sweden 1990 – 97 were classified as representing sepsis (n=12) or contaminants (n=38) and compared according to endothelial activation and to the prevalence of genes encoding for biofilm-production (ica ABD), fibrinogen-binding protein (fbe) and meticillin resistance (mecA). Endothelial cells were prepared from umbilical veins (HUVEC) and challenged by the different bacterial strains. The endothelial release of Intracellular Adhesion Molecule 1 (ICAM-1), endothelial selectin (E-selectin), vascular cell adhesion molecule 1 (VCAM-1) and interleukin-8 (IL-8) was investigated by an ELISA-assay. Endothelial cell death was determined by light microcopy. The genes of ica ABD, fbe and mecA were detected by PCR and biofilm-production was investigated by trypan-blue-staining.
Results: The sepsis-strains of S. epidermidis induced a significantly higher endothelial release of ICAM-1 (p=0.021, Mann-Whitney-U), E-selectin (p=0.002) and IL-8 (p=0.010) compared to the contaminants. The sepsis-strains also turned out to be more cytotoxic to HUVEC; Nine out of twelve sepsis strains induced > 50% cytotoxicity to HUVEC compared to 15/38 contaminant strains (p=0.047, Fischer's exact test). The prevalence of the icaoperon, biofilm-production, fbe- or mecA-genes did not discriminate between sepsis- and contaminants strains. None of the investigated bacterial strains induced endothelial release of VCAM-1.
Conclusion: Sepsis strains of S. epidermidis induced a higher endothelial release compared to contaminants of inflammatory mediators involved in the recruitment of cirkulating neutrophils. This might reflect important steps in the pathogenesis of neonatal S. epidermidis sepsis. In neonatal infections biofilm-producing properties of S. epidermidis might be less important.
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Bjorkqvist, M., Soderquist, B. & Schollin, J. 32 Virulence Factors in Neonatal Blood Isolates of Staphylococcus Epidermidis. Pediatr Res 56, 469 (2004). https://doi.org/10.1203/00006450-200409000-00055
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DOI: https://doi.org/10.1203/00006450-200409000-00055
