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Production of icaADBC-encoded polysaccharide intercellular adhesin and therapeutic failure in pediatric patients with Staphylococcal device-related infections.

ABSTRACT: BACKGROUND: Biofilm production has been established as a virulence factor which allows Staphylococcus to adhere and persist in medical devices. The objective was to determine whether therapeutic failure in patients infected with Staphylococcus spp. is linked to biofilm production, the presence of the ica operon, and the bacterial insertion sequence element IS256. METHODS: Staphylococcus spp. isolates from patients with device-related infections were collected. Therapeutic failure with proper antimicrobial treatment was registered. Biofilm phenotype was determined by Congo red test agar and Christensen assay. Presence of the ica operon genes A-D and IS256 was detected by PCR. Differences were compared through x2. RESULTS: 100 isolates from staphylococcal infections episodes were included: 40 sepsis/bacteremia, 32 ependymitis, and 28 peritonitis. 73.77% of CoNS and 79.5% of S. aureus isolates harbored the icaD gene, 29% of all isolates IS256-A+ IS256-D genes, icaA and icaB genes were only found in CoNS (27.8% and 21.3% respectively). Therapeutic failure occurred in 95.4.% of patients with a positive IS256-A+ IS256-D S. epidermidis isolate, RR 5.49 (CI 95% 2.24-13.44 p < or = 0.0001), and 85.76% in CoNS isolates, RR 2.57 (CI 95% 0.97-6.80, p = 0.05). Although none S. aureus was positive for IS256-A + IS256-D, therapeutic failure was observed in 35.8%. CONCLUSIONS: The presence of icaA/D genes along with the sequence element IS256 was associated with therapeutic failure in most CoNS infections, even though its absence in S. aureus isolates does not ensure therapeutic success.

SUBMITTER: Diemond-Hernandez B

PROVIDER: S-EPMC2848661 | biostudies-literature | 2010

REPOSITORIES: biostudies-literature

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Production of icaADBC-encoded polysaccharide intercellular adhesin and therapeutic failure in pediatric patients with Staphylococcal device-related infections.

Diemond-Hernández Bernardo B Solórzano-Santos Fortino F Leaños-Miranda Blanca B Peregrino-Bejarano Leoncio L Miranda-Novales Guadalupe G

BMC infectious diseases 20100315

<h4>Background</h4>Biofilm production has been established as a virulence factor which allows Staphylococcus to adhere and persist in medical devices. The objective was to determine whether therapeutic failure in patients infected with Staphylococcus spp. is linked to biofilm production, the presence of the ica operon, and the bacterial insertion sequence element IS256.<h4>Methods</h4>Staphylococcus spp. isolates from patients with device-related infections were collected. Therapeutic failure wi ...[more]

PMID: 20230642

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Project description:Staphylococcus epidermidis is a common bacterial colonizer of human skin and mucous membranes, yet it has emerged as an important nosocomial pathogen largely due to its ability to form biofilms. Tobacco smoke has been demonstrated as a contributor to various infection diseases by improving the biofilm formation of multiple bacterial species; however, the association between tobacco smoke and S. epidermidis biofilm is still unclear. In this study, we tested the effect of nicotine, one of the most active components of tobacco, on S. epidermidis biofilm formation, and we studied the underlying mechanisms. Our results showed that nicotine promoted the biofilm formation of S. epidermidis 1457 strain (SE1457) and enhanced its initial attachment to a polyethylene surface as well as polysaccharide intercellular adhesin (PIA) production. In addition, an increased extracellular DNA release and a higher autolysis rate of SE1457 was detected after nicotine treatment, which was consistent with the increased ratio of dead cells in nicotine-treated SE1457 biofilm observed with confocal laser-scanning microscopy. Furthermore, the effect of nicotine on several autolysis-related and biofilm-related gene knockout mutants of SE1457 was tested. It showed that in ?saeRS, ?lytSR, and ?sceD, nicotine induced increase in biofilm formation was similar to that in SE1457; but in ?arlRS, ?atlE, and ?icaC, the effect was obviously impaired. Consistently, the increase of the bacterial autolysis rate in ?arlRS and ?atlE induced by nicotine was not as significant as that in SE1457. Meanwhile, the growth inhibition of nicotine on SE1457 was observed, and it was much less on ?arlRS and restored by the arlRS complementation. The arlRS transcription in SE1457 was inhibited by nicotine during cultivation as indicated by a promoter reporter assay using green fluoresent protein. Taken together, our study indicates that nicotine improves S. epidermidis biofilm formation by promoting its initial attachment and intercellular accumulation; the arlRS, atlE, and ica genes mediating bacterial autolysis and PIA production play an important role in this process.

Dataset Information

Production of icaADBC-encoded polysaccharide intercellular adhesin and therapeutic failure in pediatric patients with Staphylococcal device-related infections.

Publications

Production of icaADBC-encoded polysaccharide intercellular adhesin and therapeutic failure in pediatric patients with Staphylococcal device-related infections.

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