Deja vu: nosocomial hepatitis B virus transmission and fingerstick monitoring.

PURPOSE: Three patients with acute hepatitis B virus infection were identified who had been hospitalized on the same medical ward during a 19-day period several months earlier. An investigation was undertaken to determine if nosocomial transmission had occurred. SUBJECTS AND METHODS: A cohort study of patients admitted to the medical ward during the 19-day period in 1995 was conducted. In addition, we reviewed medical charts and laboratory records of all patients with acute hepatitis B virus infection who had been admitted to the hospital from 1992 through October 1996 to identify other cases with possible nosocomial acquisition. RESULTS: The 3 patients who had developed acute hepatitis B infection 2 to 5 months after hospitalization on the same medical ward had diabetes mellitus but no identified risk factors for hepatitis B infection. A source patient with diabetes mellitus and hepatitis B "e" antigenemia also was present on the same medical ward at the same time; all 4 patients were infected with the same viral subtype (adw2). Diabetes mellitus and fingerstick monitoring were associated with illness (P <0.001). Through the review of medical charts and laboratory records, 11 additional cases of suspected nosocomial acquisition via fingersticks were identified in 1996, including two clusters involving an unusual subtype of hepatitis B virus (adw4). The fingerstick device employed had a reusable base onto which disposable lancet caps were inserted. There was ample opportunity for cross-contamination among patients because deficiencies in infection control practices, particularly failure to change gloves between patients, were reported by nurses and patients with diabetes mellitus. CONCLUSION: Transmission during fingerstick procedures was the most likely cause of these cases of nosocomial hepatitis B infection. Contamination probably occurred when healthcare workers failed to change gloves between patients undergoing fingerstick monitoring, although other means of contamination cannot be ruled out.

Manipulation of a hospital antimicrobial formulary to control an outbreak of vancomycin-resistant enterococci.

Infection control practices are not uniformly successful in limiting outbreaks of vancomycin-resistant enterococci (VRE). Despite the implementation of barrier precautions for VRE-infected patients, nearly one-half of the inpatients at our center were found to have gastrointestinal colonization by VRE. In an attempt to control the outbreak, we altered the antibiotic formulary by restricting the use of cefotaxime and vancomycin and adding beta-lactamase inhibitors to replace third-generation cephalosporins. The use of clindamycin was also restricted because of a concomitant outbreak of Clostridium difficile colitis. After 6 months, the average monthly use of cefotaxime, ceftazidime, vancomycin, and clindamycin had decreased by 84%, 55%, 34%, and 80%, respectively (P < .02). The point prevalence of fecal colonization with VRE decreased from 47% to 15% (P < .001), and the number of patients whose clinical specimens were culture positive also gradually decreased. A change in antibiotic use appears to have significantly affected our VRE outbreak when previous measures failed.

Experience with a hospital-wide outbreak of vancomycin-resistant enterococci.

BACKGROUND: Vancomycin-resistant enterococci (VRE) were first detected in our institution in 1991. An outbreak was recognized in late 1992 when there was a sudden rise in the number of patients per month with VRE. Little information exists concerning the natural history of infection with these pathogens, and the effect of antimicrobial therapy is unclear. Recent guidelines emphasize prudent use of vancomycin and prompt institution of barrier precautions to limit the spread of vancomycin resistance. METHODS: Data were obtained by review of microbiologic and clinical records. Patients were categorized according to site of infection, and outcome of therapy was assessed. Hospital antibiotic usage was analyzed to determine any correlation with the outbreak. Infection control measures instituted in 1993 included patient isolation, environmental cleaning, and a reemphasis of barrier precautions. Surveillance cultures were performed to assess the extent of the outbreak in January 1995. RESULTS: VRE were detected in clinical cultures from 159 patients from 1991 through 1994. Mortality rate was 48%, but in most cases death could not be attributed to enterococcal infection. Patients with wound infections healed without specific therapy. Many patients with bacteremia had resolution with ampicillin or without specific therapy. Patients were widely scattered throughout the hospital from the beginning of the outbreak. Hospital usage of cefotaxime correlated with the number of cases. Infection control measures were not successful. Surveillance culture results in January 1995 revealed that 53% of all medical and surgical inpatients had fecal colonization with VRE. Genetic analysis of selected isolates revealed that one strain predominated, but at least seven distinct strains were identified. CONCLUSIONS: Our data suggest that many infections with VRE resolve without specific therapy. The infection control measures we used were ineffective, possibly because of the multiple strains present in our hospital. Isolation of all patients with VRE is impractical when there is widespread fecal carriage.

Comparison of five selective media for identifying fecal carriage of vancomycin-resistant enterococci.

There is no uniformly accepted method for detecting colonization with vancomycin-resistant enterococci (VRE). The sensitivities of five culture methods were determined for patients known to harbor VRE. Of 189 inpatients, 101 were found to harbor VRE by at least one method. Three methods detected fewer than half of the cultures. Campylobacter agar identified 70% of patients. Enterococcosel broth (containing vancomycin and aztreonam) identified 88% and may be preferred over other media for routine surveillance.