VRE in hospitalized patients and non-hospitalized individuals.

This study documents the incidence of intestinal colonization of 100 patients from AL-Shifa hospital (ICU, hemato-oncology and renal unit) and AL-Naser hospital (hemato-oncology, ICU, and general pediatrics unit) in Gaza City and 100 non-hospitalized individuals living in the community.

In this study enterococci were found in 94% of the patients and 89% of the non-hospitalized individuals. This proportion of hospitalized patients who carry enterococci is approximately similar to that found in previous studies, in which 75 to 90% of the patients carried these microorganisms.

There were no apparent differences in the carriage of enterococcal species between hospitalized patients and non-hospitalized individuals. We isolated E. faecium from 37% of the inpatients and 27% of the non-hospitalized individuals. This is in agreement with other findings, where in E. faecium was found in 20 to 40% of stool cultures.

In the present study, among hospitalized patients (Table 4.4), E. faecium had the highest resistance rate to vancomycin (86.5 %), the same distribution pattern is observed in the United States, which has a predominance of E. faecium isolates. This high resistance rate was observed for all E. faecium regardless of the isolation site. Among non-hospitalized individuals E. faecium had the highest resistance rate to Vancomycin, while E. durans had the lowest resistance rate (33.3%).

E. faecalis is more common in nosocomial infections than E. faecium, but E. faecium has a greater ability to acquire drug resistance. This has enabled multiresistant E. faecium to emerge as a severe nosocomial pathogen worldwide, while E. faecalis has remained sensitive to at least one effective antibiotic. According to our data, E. faecalis constituted 67.9% of all entercoccal isolates from hospitalized patients. This could imply a greater risk for nosocomial infections with VRE. No other investigation has reported such high prevalence of vancomycin-resistant E.  faecalis.

In this study (Table 4.4). E. gallinarum contributed to 66.7% of VRE among hospitalized patients and 36.4% among non-hospitalized individuals.

E. gallinarum is a species with intrinsic resistance to vancomycin and rarely recovered from clinical specimens in the United States. A few European studies reported variable isolation rates ranging from 5.9 to 13.6%.

In the United States, the number of E. gallinarum strains among VRE is very low, from 0.5 to 1%. These species are not always taken into account because their resistance to glycopeptides is intrinsic and their pathogenicities are very low. In a Brazilian study, E. gallinarum was very frequently found in contrast with other studies. In a Brazilian ICU, it was found that 84% of VRE species recovered from fecal specimens of critical patients were E. gallinarum. These findings are in contrast with clinical disease due to Enterococci, since it is estimated that 80–90% of the human enterococcal infections are caused by E. faecalis, 10–15% by E. faecium and less than 5% by other species. On the other hand, E. gallinarum have recently been reported as causative agents of clinical disease. Reid et al recently described 20 cases of bacteremia caused by E. gallinarum which were observed in the Mayo Clinic United States between 1992 and 1998.

VRE were isolated from 65% of the 100 hospitalized patients and 39% of the 100 individuals living in the community. Such high rates among non- hospitalized individuals may be explained by the presence of risk factors for VRE acquisition, such as indiscriminate antimicrobial use, frequent and prolonged hospitalization and severity of underlying diseases. This finding is in disagreement with a study in Hong Kong in which VRE were not isolated from either healthy or hospitalized patients. This suggests that colonization rates remain low in Hong Kong. Several European studies have reported lower frequencies in the community.

Although outbreaks of VRE have been reported in Europe, carriage rates are generally lower, with most workers reporting rates between 0.8% and 2%. Even though many patients had received antibiotics, it did not result in carriage of VRE, although receipt of antibiotics has been shown to be a risk factor by other workers.

In the United States, the nosocomial spread of VRE is a serious problem, and enteric carriage of VRE has been reported in 16%–19% of samples from CDC patients. However, a much higher frequency has been reported in United States, hospitals. In a Belgian study, 11 (28%) of 40 volunteers living in the community who were healthy, who were not health care workers, and who had not received antibiotics for at least 1 year were colonized with VRE. The results of North American studies performed in the Houston, Texas, metropolitan area, however, are in contrast with the European data, since VRE appeared to be absent from healthy people in Houston.

The level of colonization with VRE in people in the community in Europe parallels the level of colonization of animals with these resistant organisms. Several studies have reported the absence of VRE from animals and people in the community in the United States, in contrast to the high frequencies in hospitals. Some investigators, however, have cautioned against comparing the results of the studies mentioned above, since differences in methodology could, at least in part, explain the observed differences in isolation rates.

The investigations of Jordens et al. have suggested that VRE can be part of the intestinal microflora of patients inside and outside of the hospital. The latter investigator also demonstrated vancomycin resistant enterococci from animal reservoirs . However, those studies investigated colonization in areas where nosocomial VRE infections and epidemics were ongoing. Therefore, contamination of the environment from the hospital could not be excluded.

In this study the presence of VRE in the stools of non-hospitalized individuals suggests that VRE form part of the normal human fecal flora or can be acquired in the community, as confirmed by several other studies. A possible source of VRE could be the food chain, since VRE has been reported in the feces of farm animals and in animal product-based foodstuffs. The origin of the contamination of meat remains unknown, but it might occur during processing and packaging or through the intestinal flora of slaughtered animals.

Some European investigators have raised the possibility that the glycopeptide avoparcin, which has been used as a feed additive for growth enhancement in animals for nearly 20 years, might have selected VRE strains in animals. The gastrointestinal tract is probably the major reservoir in humans, from which subsequent infection can eventually develop. This is in agreement with a recent report from New York City.  Food has been proposed as a source. Others have put forward pets and other domestic animals. Furthermore, the use of antibiotics as feed additives for growth enhancement in animals may be associated with the emergence of VRE.