More is more.

Abstract

During the past two decades, antibiotic resistance among nosocomial pathogens has gone from bad to worse. According to intensive care unit (ICU) data from U.S. hospitals participating in the National Nosocomial Infections Surveillance System of the Centers for Disease Control and Prevention during the year 2000, 55% of nosocomial Staphylococcus aureus isolates were resistant to methicillin, 26% of nosocomial enterococcal isolates were resistant to vancomycin, and 35% of nosocomial Enterobacter species isolates were resistant to third-generation cephalosporins.1 There is also substantial evidence that these organisms are not just confined to the acute care hospital but that they are also being spread and becoming highly prevalent among residents of long-term–care facilities (LTCFs).2-16 Despite these disturbing data, there has been no concerted or consistently applied, evidence-based effort within the U.S. healthcare system to prevent the spread of these pathogens among the millions of patients entrusting us with their health and safety as they enter hospitals and LTCFs each year. In this issue of Infection Control and Hospital Epidemiology, multiple studies provide important new insights into the epidemiology of colonization and infection with several important nosocomial pathogens, including vancomycin-resistant Enterococcus (VRE), methicillin-resistant Staphylococcus aureus (MRSA), and antibiotic-resistant gram-negative bacilli. Antimicrobial-resistant pathogens are often considered individually, with the relative importance assigned to each organism varying from institution to institution. It has been noted, however, that these pathogens often travel together due to similar modes of transmission, similar risk factors for acquisition,17 and sharing of resistance determinants between pathogens. A particularly notable and worrisome example of the sharing of resistance mechanisms between pathogens was the recent identification of the vanA vancomycin resistance gene from VRE in clinical isolates of vancomycin-resistant S. aureus.18,19 Important new data in this area are presented by Donskey et al., who suggest that the benefit of identifying and isolating patients colonized with VRE may extend beyond that of preventing the spread of VRE.20 A pointprevalence survey in a Veterans Affairs acute care facility and its associated nursing facility found that 19% of the study population had stool colonization with VRE. VREcolonized patients were significantly more likely to be colonized with ceftazidime-resistant gram-negative bacilli than were patients who were not colonized with VRE (17% vs 4%; P = .026). During a 6-month follow-up period, VREcolonized patients were also significantly more likely to have Clostridium dif ficile–associated diarrhea (26% vs 2%) and to have antibiotic-resistant gram-negative bacilli isolated from a clinical specimen (39% vs 11%). In addition, 4 (17%) of the 23 VRE-colonized patients were treated for MRSA infection during the follow-up period. Two (9%) of the VRE-colonized patients were colonized or infected with all three of the other pathogens included in the evaluation (ie, C. dif ficile, a resistant gram-negative bacillus, and MRSA). Diarrhea due to C. dif ficile in patients colonized with VRE has important implications for the spread of both pathogens. On a similar note, Pacio et al. examined the relative frequency of colonization and infection and the rate of clearance of colonization with several antibiotic-resistant organisms (VRE, MRSA, and a select group of antibioticresistant gram-negative bacilli) among residents of an LTCF in New York.21 During the 3-month enrollment period, the investigators identified 65 episodes of colo-