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Evaluation of the impact of adaptation of Klebsiella pneumoniae clinical isolates to benzalkonium chloride on biofilm formation

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DOI: 10.1186/s43042-021-00170-z

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Adaptation; Benzalkonium chloride; Biofilm; Cell surface hydrophobicity; Klebsiella pneumoniae

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The study suggests that adaptation to sublethal concentrations of biocides like benzalkonium chloride (BAC) could lead to increased cell surface hydrophobicity and enhanced biofilm formation in Klebsiella pneumoniae isolates, potentially resulting in treatment failure of infections generated by this pathogen.
Background The percentage of the multidrug resistant Klebsiella pneumoniae clinical isolates is increasing worldwide. The excessive exposure of K. pneumoniae isolates to sublethal concentrations of biocides like benzalkonium chloride (BAC) in health care settings and communities could be one of the causes contributing in the global spread of antibiotic resistance. Results We collected 50 K. pneumoniae isolates and these isolates were daily exposed to gradually increasing sublethal concentrations of BAC. The consequence of adaptation to BAC on the cell surface hydrophobicity (CSH) and biofilm formation of K. pneumoniae isolates was explored. Remarkably, 16% of the tested isolates showed an increase in the cell surface hydrophobicity and 26% displayed an enhanced biofilm formation. To evaluate whether the influence of BAC adaptation on the biofilm formation was demonstrated at the transcriptional level, the RT-PCR was employed. Noteworthy, we found that 60% of the tested isolates exhibited an overexpression of the biofilm gene (bssS). After sequencing of this gene in K. pneumoniae isolates before and after BAC adaptation and performing pairwise alignment, 100% identity was detected; a finding that means the absence of mutation after adaptation to BAC. Conclusion This study suggests that the widespread and increased use of biocides like BAC at sublethal concentrations has led to an increase biofilm formation by K. pneumoniae isolates. Enhanced biofilm formation could result in treatment failure of the infections generated by this pathogen.

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