Nosocomial transmission and risk factors

Spread in hospitals

Several studies have demonstrated the ability of resistant strains of enterococci to prevail and spread in hospitals. Enterococci are able to colonize not only the gut but also the skin, oral cavity and lungs of hospitalized patients. 

The intrinsic robustness of E. faecalis may allow members of this species to survive for extended periods of time, leading to its persistence and nosocomial spread. E. faecalis can grow at 10 to 45 ºC, in 6.5 % NaCl, in the presence of 40 % bile salts and over a broad range of pH. 

Originally, enterococcal infections were thought to arise from a patient’s own endogenous microbiota or to be introduced into the abdomen during transplant surgery or its complications . 

However, molecular epidemiological studies provided evidence for epidemic spread of enterococci in a hospital setting and nosocomial acquisition of enterococci. Long duration of stay in hospitals, stay in units with high proportions of colonized patients, use of electronic thermometers, and diarrhea have all been factors associated with spread of resistant strains. All these experiences make obvious the importance of having efficient infection-control routines in hospitals. Use of surveillance, isolation and barrier precautions has been successful in controlling minor outbreaks in non-endemic situations. 

Livornese et al. were the first to document an inanimate object, in this case rectal thermometer probes, as the mode of transmission of a vancomycin resistant E. faecium. Removal of the rectal thermometer probes resulted in termination of the outbreak. These reports were followed by many reports on nosocomial outbreaks and transmission of antibiotic resistant enterococci. The hands of health care workers are efficient tools for spreading microorganisms between patients in hospitals, this is true also for resistant enterococci. The impact of hand-washing has not been uniformly positive in US studies, possibly because use of gloves sometimes seems to have replaced hand-washing. Half a minute of wash with 60% alcohol solutions was more effective in eradicating VRE from the hands than was soap and water. E. faecium isolates survive for 7 days on counter tops, 24 hours on bedrails, 60 minutes on telephones and 30 minutes on stethoscopes. Rectal thermometers and even blood pressure cuffs have been involved in the spread of VRE. One recent study showed the environment to be contaminated around VRE colonized patients, another that the hands of medical staff may be equally easy contaminated with VRE by environmental contacts and colonized patients.

These findings illustrate the importance of proper cleaning of devices shared between patients and the use of hand disinfectants both before and after patient contact when trying to control spread of resistant bacteria in hospitals. Recently it was demonstrated that VRE could be controlled in a large region with 32 health care facilities, provided that consequent and active infection control measures including surveillance cultures and isolation of all infected and colonized patients were carried out. In that region, the overall prevalence of VRE decreased from 2.2% to 0.5% within 2 years.

On the other hand, if smaller outbreaks are not controlled the situation may become complex and even endemic. Bonten and coworkers studied VRE epidemiology in an ICU and introduced the term “colonization pressure” meaning the proportion of colonized patients in a setting during a given period. They found that if the colonization pressure was >50% all other measures had only little impact on the time to acquisition of VRE. In endemic setting measures such as protection of high risk groups, reduction of the total antibiotic pressure and education of staff may be more important than surveillance and isolation of every patient.

Risk factors for the nosocomial acquisition of enterococci that are described in the majority of studies are: previous antimicrobial therapy, duration of hospitalization, severe underlying disease, or invasive procedures. Nosocomial enterococcal acquisition and infection are often due to superinfection after the use of antibiotics with little or no anti-enterococcal activity like cephalosporins or quinolones.

Prevention and control of transmission include the controlled use of antibiotics, active surveillance cultures to identify the reservoir for spread and stringent application of recommended contact precautions. A variant of the esp gene was detected in all epidemic vancomycin-resistant E. faecium in hospitals, but not in non-epidemic animal isolates. This indicates that the surface protein Esp is associated with enterococcal colonization and spread. Analysis of the mechanism underlying the influence of this surface protein on enterococcal transmission might lead to new ways to prevent colonization and transmission.