Dataset Information

Multiple-locus VNTR Analyses of Methicillin-resistant Staphylococcus aureus from Jamaica.

ABSTRACT:

Background

This study assessed the antimicrobial susceptibilities and the presence of inducible macrolide-lincosamide-streptogramin B (iMLSB) resistance in methicillin-resistant Staphylococcus aureus (MRSA) of Jamaica as well as the relatedness using polymerase chain reaction-based staphylococcal cassette chromosome mec (SCCmec) and multiple-locus variable numbers of tandem repeat analyses (MLVAs).

Materials and methods

Antimicrobial susceptibility, the presence of MLSB resistance, and SCCmec and MLVA patterns were assessed for 61 nonduplicate isolates of MRSA from hospitalized patients.

Results

While no isolate was resistant to vancomycin, 53 (86.9%) isolates were resistant to ciprofloxacin, 52 (85.3%) to erythromycin, 49 (80%) to lincomycin, and 45 (74%) to clindamycin. Of the 52 erythromycin-resistant isolates, 48% exhibited constitutive resistance and 8% showed inducible MLSB (iMLSB) resistance. Most (85%) of typable isolates were SCCmec type IV, and among these, 16 MLVA patterns were identified.

Conclusion

Multidrug resistance continues to characterize MRSA. Among the erythromycin-resistant isolates, constitutive resistance and iMLSB resistance are common. These facts will complicate the treatment of MRSA infections and warrant continued surveillance and judicial use of antimicrobial agents.

SUBMITTER: Brown PD

PROVIDER: S-EPMC4583095 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Methicillin resistant Staphylococcus aureus (MRSA) infection is becoming refractory to existing antibiotic therapy owing to the inherent ability of S. aureus to develop rapid resistance and is considered a major threat to public health. We found that a natural isolate of Bacillus pumilus from the Columbia River Estuary produces a strong anti-MRSA compound, amicoumacin A. As amicoumacin A has been reported to exhibit anti-microbial, anti-inflammatory, and anti-ulcer activities, we sought to uncover its mechanism of action. Genome-wide transcriptome analysis of S. aureus COL in response to amicoumacin A showed alteration in the expression of genes involved in several cellular processes including cell envelope turnover, cross-membrane transport, virulence, metabolism, and general stress response. The most highly induced gene was lrgA, encoding an antiholin-like product, which has been shown to be induced in response to a collapse of membrane potential. In order to gain further insight into the mechanism of action of amicoumacin A, a whole genome comparison of wild-type COL and amicoumacin A-resistant mutants isolated by serial passage method was carried out. Single point mutations resulting in codon substitutions were uncovered in several distinct genes: ksgA, RNA dimethyltranferase; fusA, elongation factor G; dnaG, primase, ; lacD, tagatose 1,6-bisphosphate aldolase, ; and SACOL0611, encoding a putative glycosyl transferase gene. Based on these results, a candidate approach was undertaken to recreate the same amino acid substitution individually in FusA and KsgA, each of which resulted in two-fold resistance towards amicoumacin A. The fusA gene is known as the site for fusidic acid- resistant mutations; however the codon substitutions in EF-G that cause amicoumacin A resistance and fusidic acid resistance occur in separate domains and do not bring about cross resistance. Taken together, these results suggest that amicoumacin A might cause perturbation of the cell membrane and lead to energy dissipation. Decreased rates of cellular metabolism including protein synthesis and DNA replication in resistant strains might allow cells to compensate for membrane dysfunction and thus increase cell survivability.