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Correlation between biofilm production, antibiotic susceptibility and exopolysaccharide composition in Burkholderia pseudomallei bps I, ppk , and rpo S mutant strains
Author(s) -
Mongkolrob Rungrawee,
Taweechaisupapong Suwimol,
Tungpradabkul Sumalee
Publication year - 2015
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12331
Subject(s) - burkholderia pseudomallei , biofilm , microbiology and biotechnology , melioidosis , biology , rhamnose , antibiotics , mutant , multidrug tolerance , bacteria , antibiotic resistance , mannose , gene , biochemistry , genetics
Burkholderia pseudomallei is the cause of melioidosis, a fatal tropical infectious disease, which has been reported to have a high rate of recurrence, even when an intensive dose of antibiotics is used. Biofilm formation is believed to be one of the possible causes of relapse because of its ability to increase drug resistance. EPS in biofilms have been reported to be related to the limitation of antibiotic penetration in B . pseudomallei . However, the mechanisms by which biofilms restrict the diffusion of antibiotics remain unclear. The present study presents a correlation between exopolysaccharide production in biofilm matrix and antibiotic resistance in B. pseudomallei using bps I, ppk , and rpo S mutant strains. CLSM revealed a reduction in exopolysaccharide production and disabled micro‐colony formation in B. pseudomallei mutants, which paralleled the antibiotic resistance. Different ratios of carbohydrate contents in the exopolysaccharides of the mutants were detected, although they have the same components, including glucose, galactose, mannose, and rhamnose, with the exception being that no detectable rhamnose peak was observed in the bps I mutant. These results indicate that the correlation between these phenomena in the B. pseudomallei biofilm at least results from the exopolysaccharide, which may be under the regulation of bps I, ppk , or rpo S genes.