Epidemiology of enecocci

Epidemiology

VRE has become a public health problem on the global perspective. It is clear that the epidemiology of glycopeptide resistance in enterococci is complex, with multiple factors contributing to its evolution and global dissemination. There are contrasting differences between continents and sometimes even between individual countries, depending on the resistance phenotype and genotype studied. Factors associated with these contrasting findings are associated with differences in the use of antimicrobial agents among humans and animals as well as differences associated with spread and colonization of individuals in different countries. Current studies have demonstrated the existence of major differences in the epidemiology of the spread of vancomycin resistance between the United States and Europe.

 United States

VRE in the United States seems to be a nosocomial problem, probably attributable to the extensive use of vancomycin and other broad-spectrum antibiotics. VRE were first reported in France in 1986, their occurrence has been reported from the U.S. in 1987. Since that time, VRE have been isolated from patients in Asia, Australia, and Africa. There is an epidemiological difference between the occurrences of VRE in the United States and in Europe. In the U.S. clones of VRE have spread within and between hospitals, but VRE among non-hospitalized humans have so far not been reported. Thus, VRE are thought to have evolved and spread due to the heavy antibiotic use in hospitals. In the United States, the percentage of nosocomial infections caused by VRE increased more than 20-fold (from 0.3% to 7.9%) between 1989 and 1993, indicating rapid dissemination.  From 1989-1993, the National Nosocomial Infection Surveillance (NNIS) surveys reported that the percentage of enterococcal isolates exhibiting vancomycin resistance increased from 0.3% to 7.9%, with a 34-fold rise seen in intensive care units (ICUs).  According to the NNIS System of the Centers for Diseases Control and Prevention (CDC), the proportion of VRE of the total number of enterococcal blood isolates increased from 13% to 26% between 1995 and 2000. Collecting information from more than 100 clinical U.S. laboratories, showed resistance to ampicillin and the glycopeptides to be rare in E. faecalis but very common in E. faecium, 83% and 52%, respectively. In 2003, the percentage of nosocomial enterococcal isolates exhibiting vancomycin resistance in ICU patients increased to more than 28%, an increase of 12% compared with 1998-2002.

 NNIS data reveal the pooled mean for vancomycin-resistant Enterococcus species from all ICUs, non-ICU inpatient areas, and outpatient areas were 13.9%, 12%, and 4.6%, respectively, from 1998 through June 2004. VRE was initially isolated mainly in large university hospitals, but subsequent reports demonstrate the presence of significant VRE epidemics in community hospitals and chronic care facilities, whereby a single clone can easily spread. VRE is isolated almost exclusively from hospitalized (or recently hospitalized) individuals.

In summary, the heavy increase of VRE in U.S. hospitals seems to be due to serious problems with both antibiotic overuse and infection control practices but there were no indications of input of VRE to hospitals from reservoirs in the community.

 Europe

Studies from European countries report a high prevalence of VRE, mainly E. faecium of the vanA genotype, among non hospitalized individuals, farmers, farm animals, in meat products, and in sewage treatment plants. There is now evidence to support the transmission of VRE to persons in contact with these sources, resulting in increased human reservoirs of VRE colonization. It was soon suspected that the widespread use of avoparcin for growth promoting purposes in farm animals might select for VRE among farm animals. Avoparcin confers cross-resistance to vancomycin of the vanA resistance genotype and this genotype has been dominant among both human and animal VRE isolates in Europe, whereas vanA and vanB have been equally prevalent in U.S. hospitals. Moreover, strains with identical transposons Tn1546 have been found in Europe among both animals and humans. Thus, there are several strong indications of the spread not only of resistant bacterial strains, but also of glycopeptide resistance genes from animals and via the food-chain to humans in European countries.

Southeastern Mediterranean

Despite the increasing reports of VRE in different countries, the reports of the   prevalence of VRE in Egypt, Jordan, Lebanon, are scarce. VRE in Israel seems to be a nosocomial problem.

In a prospective surveillance conducted to monitor the prevalence and dynamics of antimicrobial resistance among enterococci isolated from blood cultures in southern Israel. A total of 242 organisms isolated between 1993 and 1996 were studied. The prevalence of E. faecalis significantly decreased during the study period, whereas that of E. faecium doubled. Antimicrobial drug resistance increased steadily among E. faecium isolates: resistance to ampicillin increased from 19% in 1993–1994 to 53% in 1995, and to 67% in 1996. During the same period, resistance to vancomycin increased from 0% to 20%, and to 50%, and combined resistance to ampicillin and vancomycin and high-level resistance to gentamicin from 0% to 20% and to 38%.

 Other countries

 Saudi Arabia

A prospective study to determine the prevalence of its fecal carriage in patients at a tertiary care center in Saudi Arabia was conducted. During the period from March 1, 1995, to February 29, 1996, stool specimens examined from 4276 patients for the presence of VRE. VRE were found in six patients and all were identified as E. faecium. High resistance to vancomycin (MIC >256 µg/L) was found in all the six isolates, and to gentamicin in five isolates .

 Kuwait

A study conducted to investigate the prevalence of antibacterial resistance in enterococci isolated from clinical samples in five hospitals in Kuwait. This study investigated the species prevalence and antibacterial resistance among enterococci isolated in Kuwait hospitals. They consisted of 415 isolates of E. faecalis (85.3 %), E. faecium (7.7 %), E. casseliflavus (4.0 %), E.avium (1.2 %), E. durans (1.0 %), E. gallinarium (0.5 %) and E. bovis (0.2 %) isolated from urine (36.6 %), blood (10.4 %), wound swabs (11.0 %), stool samples (12.0 %), high vaginal swabs (9.0 %), endocervical swabs (3.0 %) and miscellaneous sources (18.0 %). All of them were susceptible to linezolid. Fifty-two (12.5 %) isolates were ampicillin resistant but none of them produced ß-lactamase. The resistance to vancomycin was 2.6 %. All of the vancomycin-resistant strains carried the vanA phenotype and genotype. There was no evidence of clonal spread of the vancomycin-resistant isolates