Their findings are published online in PNAS Early Edition.
The resistant strain E. faecalis V583 has numerous mobile genetic elements in its genome that could hinder its ability to compete with native bacteria in the absence of antibiotics. Michael S. Gilmore, Ph.D., senior scientist at Mass. Eye and Ear and Sir William Osler Professor of Ophthalmology, Department of Ophthalmology and Director, Infectious Disease Institute at Harvard Medical School, and colleagues found that native gut bacteria killed V583 when the bacteria were cultured together.
Harmless strains of E. faecalis were responsible for killing the resistant strain, but the harmless strains lost this ability when pheromone production was disrupted. The authors identified the pheromone cOB1, produced by the native strains, as the cause of the killing, and identified the mobile genetic elements in the resistant strain that confer vulnerability to the pheromone.
These results suggest that the mobile genetic elements in multidrug resistant E. faecalis prevent it from coexisting with native strains, and that maintaining healthy populations of native gut bacteria may aid in preventing hospital infections.
Antibiotic resistant superbugs, called “enterococci,” emerged as a leading healthcare problem in the mid 1980s when they became resistant to the last line antibiotic, vancomycin. Dr. Gilmore was part of the team that discovered the first vancomycin resistant enterococcus in the US. Since this initial discovery, enterococci have been leading causes of multidrug resistant infection. In 2013, CDC estimated that there are 66,000 enterococcal infections in the US each year, about 20,000 of those being drug resistant resulting in 1,300 deaths.
“Antibiotic-resistant infections are a risk for all body sites, especially the delicate tissues of the eye,” Dr. Gilmore said.
Article # 15-00553: “Pheromone killing of multidrug resistant Enterococcus faecalis by native commensal strains” by Michael S. Gilmore et al.
(Information for this release provided by PNAS)
Contact: Mary Leach