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Characterizing Multidrug Efflux Systems in Acinetobacter baumannii Using an Efflux-Deficient Bacterial Strain and a Single-Copy Gene Expression System

Characterizing Multidrug Efflux Systems in Acinetobacter baumannii Using an Efflux-Deficient Bacterial Strain and a Single-Copy Gene Expression System

Published on: January 5, 2024

Multidrug-resistant enterococci lack CRISPR-cas.

Kelli L Palmer¹, Michael S Gilmore

¹Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA.

|November 10, 2010

Summary

This summary is machine-generated.

Clustered regularly interspaced short palindromic repeats (CRISPR) systems defend against mobile genetic elements. Antibiotic use in Enterococcus strains inversely correlates with CRISPR-cas presence, suggesting compromised genome defense.

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Area of Science:

Microbiology
Genetics
Bacterial Defense Mechanisms

Background:

Mobile genetic elements, including plasmids and phages, are prevalent in multidrug-resistant (MDR) enterococci.
Clustered regularly interspaced short palindromic repeats (CRISPR) systems confer sequence-specific immunity in prokaryotes.

Purpose of the Study:

To investigate the codistribution of CRISPR and acquired antibiotic resistance in enterococcal lineages.
To understand the role of CRISPR in regulating mobile element flux within Enterococcus faecalis.

Main Methods:

Construction of a database from 16 Enterococcus faecalis draft genome sequences.
Identification and analysis of CRISPR loci, spacers, and associated genes (CRISPR3-cas).
Screening of additional E. faecalis strains, including historical isolates, and eight E. faecium genomes.

Main Results:

CRISPR spacers showed sequence identities with mobile elements like plasmids and phages in E. faecalis.
A significant inverse correlation was observed between the presence of a CRISPR-cas locus and acquired antibiotic resistance in E. faecalis and E. faecium.
A mechanism for CRISPR-cas loss in E. faecalis was identified.

Conclusions:

CRISPR-cas systems play a role in defending enterococci against mobile genetic elements.
Antibiotic use appears to inadvertently select for enterococcal strains with diminished genome defense mechanisms due to CRISPR-cas loss.