Vancomycin-resistant enterococci pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Pathophysiology
Genetics
Enterococci are intrinsically resistant to many antibiotics. Unlike acquired resistance and virulence traits, which are usually transposon or plasmid encoded, intrinsic resistance is based in chromosomal genes, which typically are nontransferrable. Penicillin, ampicillin, piperacillin, imipenem, and vancomycin are among the few antibiotics that show consistent inhibitory, but not bactericidal, activity against E. faecalis. E. faecium are less susceptible to ß-lactam antibiotics than E. faecalis because the penicillin-binding proteins of the former have markedly lower affinities for the antibiotics.
]Enterococci often acquire antibiotic resistance through exchange of resistance-encoding genes carried on conjugative transposons, pheromone-responsive plasmids, and other broad-host-range plasmids. Simultaneously, sporadic outbreaks of nosocomial E. faecalis and E. faecium infection appeared with penicillin resistance due to ß-lactamase production, however, such isolates remain rare.
Among several phenotypes for vancomycin-resistant enterococci, VanA (resistance to vancomycin and teicoplanin) and VanB (resistance to vancomycin alone) are most common. In the United States, VanA and VanB account for approximately 60% and 40% of vancomycin-resistant enterococci (VRE) isolates, respectively. Inducible genes encoding these phenotypes alter cell wall synthesis and render strains resistant to glycopeptides.
VanA and VanB types of resistance are primarily found among enterococci isolated from clinical, veterinary, and food specimens , but not other common intestinal or environmental bacteria. In the laboratory, however, these genes can be transferred from enterococci to other bacteria. For example, Staphylococcus aureus has been rendered vancomycin-resistant through apparent transfer of resistance from E. faecalis on the surface of membrane filters and on the skin of hairless obese mice, which indicates that there is no biologic barrier to the emergence of vancomycin-resistant S. aureus. Clinical isolates of highly vancomycin-resistant S. aureus have yet to be identified, although strains with reduced susceptibility to vancomycin have appeared. The mechanism of resistance for these strains remains undetermined but does not appear to involve genes associated with VanA or VanB phenotypes.
Transmission
VRE is usually passed to others by direct contact with stool, urine, or blood containing VRE. It can also be spread indirectly via the hands of healthcare providers or on contaminated environmental surfaces. VRE usually is not spread through casual contact such as touching or hugging. VRE is not spread through the air by coughing or sneezing.
Although the exact role of human antimicrobial use in the transmission of VRE is not known, observations from an animal model (in which mice were orally administered VRE and became only transiently colonized unless simultaneously exposed to antimicrobials) support an important role for antimicrobial drugs in establishing persistent colonization. Antimicrobial drugs used in health-care settings may alter bowel flora, rendering patients more susceptible to colonization by VRE transmitted from other colonized or infected patients. Epidemiologic evidence of foodborne VRE transmission in the community suggests that antimicrobial drugs may predispose hospitalized patients to colonization with ingested VRE. Contamination of a patient's food may occur during consumption by a variety of mechanisms, including contamination with VRE from the hands of the patient or health-care worker. In areas where VRE is also found in the animal food supply, contamination may also occur during processing by contact with VRE from the bowel flora of the food animal.
Habitat
Enterococci normally inhabit the bowel. They are found in the intestine of nearly all animals, from cockroaches to humans. Enterococci are readily recovered outdoors from vegetation and surface water, probably because of contamination by animal excrement or untreated sewage. In humans, typical concentrations of enterococci in stool are up to 108 CFU per gram. Although the oral cavity and vaginal tract can become colonized, enterococci are recovered from these sites in fewer than 20% of cases. The predominant species inhabiting the intestine varies. In Europe, the United States, and the Far East, Enterococcus faecalis predominates in some instances and E. faecium in others. Ecologic or microbial factors promoting intestinal colonization are obscure. Of 14 or more enterococcal species, only E. faecalis and E. faecium commonly colonize and infect humans in detectable numbers. E. faecalis is isolated from approximately 80% of human infections, and E. faecium from most of the rest. Infections to other enterococcal species are rare.
Enterococci are exceedingly hardy. They tolerate a wide variety of growth conditions, including temperatures of 10°C to 45°C, and hypotonic, hypertonic, acidic, or alkaline environments. Sodium azide and concentrated bile salts, which inhibit or kill most microorganisms, are tolerated by enterococci and used as selective agents in agar-based media. As facultative organisms, enterococci grow under reduced or oxygenated conditions. Enterococci are usually considered strict fermenters because they lack a Kreb's cycle and respiratory chain. E. faecalis is an exception since exogenous hemin can be used to produce d, b, and o type cytochromes. In a survey of 134 enterococci and related streptococci, only E. faecalis and Lactococcus lactis expressed cytochrome-like respiration. Cytochromes provide a growth advantage to E. faecalis during aerobic growth. E. faecalis cytochromes are only expressed under aerobic conditions in the presence of exogenous hemin and, therefore, may promote the colonization of inappropriate sites.