Enterococci are normal gut flora that are found in most humans. The two major species that live in and effect humans are Enterococcus faecalis and Enterococcus faecium (the species name gives you some idea of where and how they are distributed as well).
A recent report out of Sweden is describing the growing incidence of vancomycin resistant enterococci (VRE) in hospital patients. And by growing, I mean exploding. In the report, they stated that from from all of 2000 until 2006 they saw a total of 197 cases of patients that were colonized or infected with VRE. From July 2007 until February 2009 they saw an astounding total of 760 cases reported.
How does E. facalis gain the ability to resist treatment with vancomycin? It obtains a plasmid that confers high level resistance to this antibiotic. This is a problem because gut bacteria can conjugate and spread the plasmid to other organisms that live in the gut. (E. coli, another gut resident, is gram negative and therefore already innately resistant to treatment with vancomyin).
Additionally? Enterococci are either innately resistant to or have acquired resistance to:
penicillinase-susceptible penicillin (low level), penicillinase-resistant penicillins, cephalosporins, nalidixic acid, aztreonam, macrolides, and low levels of clindamycin and aminoglycosides. They use already-formed folic acid, which allows them to bypass the inhibition of folate synthesis, resulting in resistance to trimethoprim-sulfamethoxazole.
Enterococci also have acquired resistance, which includes resistance to penicillin by beta-lactamases, chloramphenicol, tetracyclines, rifampin, fluoroquinolones, aminoglycosides (high levels)
The presence and increasing incidence of antibiotic resistant bacteria should be making us all much more conscious of how and when we use antibiotics. The problem? We think we know when and how to take antibiotics.
More on this tomorrow…