engleski

Antibiotic resistance of Lactobacillus brevis L62

Fluoroquinolones induce double-strand breaks in bacterial DNA by trapping DNA gyrase and topoisomerase IV onto DNA. In Gram-positive bacteria fluoroquinolone resistance is mediated by alteration of the target enzymes, and/or by overexpression of efflux pumps in order to decrease intracellular accumulation of this drug. Quinolones such as nalidixic acid are extensively used antibiotic in both human and veterinary medicine. Furthermore, microorganisms in food as vehicles of antibiotic resistance genes have been given increased focus recently. Lactic acid bacteria Lactobacillus brevis widely used as probiotics or in starter cultures have the potential to serve as hosts of antibiotic resistance genes with the risk of transferring the antibiotic resistance genes in many lactic acid bacteria and other pathogenic bacteria. The purpose of this study was to determine antibiotic susceptibility of L. brevis L62 and to estimate its antibiotic resistance mechanism as well as its genome stability during prolonged stationary phase. Using the disc diffusion method and the quantitative broth microdilution method, antibiotic resistance of L. brevis against nalidixic acid and vancomycin was detected. In L. brevis L62 three individual plasmids in size 5, 7 and 25 kb were determined. Plasmids presence has no influence on nalidixic acid resistance of L. brevis L62. High performance liquid chromatography was used to determine nalidixic acid level in L. brevis L62. Extracellular concentration of nalidixic acid was ten fold higher then intracellular concentrations in L. brevis. The genome of L. brevis was altered in the isolates taken after 10 days starvation period. With regard to human health, additional attention should be paid to the antibiotic-resistance profiles of novel lactic acid bacteria strains used as starters or probiotics in dairy products.

Lactobacillus brevis L62; nalidixic acid resistance; genome stability

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