Abstract
Staphylococcus epidermidis is frequently implicated in medical device-related infections. As a result of this, novel approaches for control of this opportunistic pathogen are required. We examined the ability of the natural peptide nisin A, produced by Lactococcus lactis, to inhibit S. epidermidis. In addition, a bank of 29 rationally selected bioengineered L. lactis strains were examined with the aim of identifying a nisin derivative with enhanced antimicrobial activity. Agar-based deferred antagonism assays revealed that wild type nisin A inhibited all 18 S. epidermidis strains tested. Larger zones of inhibition than those obtained from the nisin A producing L. lactis strain were observed for each derivative producer against at least one S. epidermidis strain tested. Six derivative producing strains, (VGA, VGT, SGK, M21A, M17Q, AAA), gave larger zones against all 18 strains compared to the wildtype producing strain. The enhanced bioactivity of M17Q was confirmed using well diffusion, minimum inhibitory concentration (MIC) and a broth-based survival assays. Biofilm assays were performed with plastic microtiter plates and medical device substrates (stainless-steel coupons and three catheter materials). The presence of nisin A significantly reduce the amount of biofilm formed on all surfaces. M17Q was significantly better at reducing biofilm production than nisin A on plastic and stainless-steel. Finally, M17Q was significantly better than nisin A at reducing bacterial numbers in a simulated wound fluid. The findings of this study suggest that nisin and bioengineered derivatives warrant further investigation as potential strategies for the control of S. epidermidis.
Highlights
Staphylococcus epidermidis is a habitual member of the human commensal microbiota [1,2]
The ability of a wildtype nisin A-producing L. lactis strain and a bank of 29 L. lactis strains each producing a different variant of nisin A were examined for their ability to inhibit a collection of 18 S. epidermidis strains by performing agar based deferred antagonism assays (Figure 1)
Zones of inhibition were observed for the wildtype nisin A producer against all of the 18 S. epidermidis strains with representative zone sizes ranging from 9.8 to 16.3 mm (Table 1)
Summary
Staphylococcus epidermidis is a habitual member of the human commensal microbiota [1,2]. Benign when present on the skin of healthy individuals, S. epidermidis has been classed as an opportunistic pathogen [1,3]. Have described it as a “formidable nosocomial pathogen,” due to its rapid spread, the development of resistance, its threat to immunocompromised individuals [1,3]. The ability of S. epidermidis to form biofilms on both biotic and abiotic surfaces and invade the body via postoperative skin wounds, complicates the recovery process and increases patient suffering. Once the organism has invaded or been implanted into the body of the patient, development of a slime layer establishes a persistent source of infection within the body, where the most viable treatment option is the complete
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