1887

Abstract

There are several β-lactamase genes described for s strains, of which and are specific for and define two genetic divisions. The expression and phenotypic effects of these genes are usually regulated by insertional activation.

Information is lacking about how is regulated for most of the strains and whether there could be a genetic element for it.

We aimed to investigate the molecular background of ampicillin (and other β-lactam) resistance among strains as mediated mainly by and also to find a genetic element for it as known for .

Various PCR methods were used for β-lactamase-resistance gene and insertion sequence (IS) element detection in 42 strains. β-Lactamase activity measurements and antimicrobial-susceptibility testing using agar dilution were also applied. Further molecular experiments involved sequencing, gene targeting, Southern blotting and bioinformatic analyses.

We found that high antibiotic resistance and β-lactamase levels are brought about by insertional activation of the gene or by similar or dissimilar activation of or , or by the newly described genes. Non-activated genes produced low levels of specific β-lactamase activities that did not correlate with ampicillin resistance. We found a genetic element for and another region close to it that are characteristic for division I strains, which are replaced by other sequences in division II strains.

usually is not activated by IS elements and usually produces low β-lactamase activities that do not correlate with the ampicillin MICs; therefore, it probably involves some non-β-lactamase-mediated resistance mechanism(s). is a newly described, effective β-lactamase gene that is located on a plasmid, and resides on a well-defined chromosomal segment that is mutually replaced in division II strains. This latter finding demonstrates the genetic dichotomy of in and requires further investigation.

Funding
This study was supported by the:
  • Szegedi Tudományegyetem, Általános Orvostudományi Kar (HU)
    • Principle Award Recipient: JozsefSoki
  • European Society of Clinical Microbiology and Infectious Diseases
    • Principle Award Recipient: ElisabethNagy
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2021-08-31
2024-05-06
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