An episodic outbreak of genetically related Burkholderia cepacia among non-cystic fibrosis patients at a university hospital.

OBJECTIVE: To investigate an outbreak of Burkholderia cepacia. DESIGN: Observational study and chart review. PATIENTS: Adult non-cystic fibrosis (CF) patients. SETTING: Intensive care units (ICUs) at a university-affiliated teaching hospital. METHODS: As part of the epidemiological investigation, we conducted a chart review and collected environmental samples. A review of work schedules of healthcare workers also was performed. We used B. cepacia selective agar for preliminary screening for all isolates, which subsequently were confirmed as members of the B. cepacia complex by polyphasic analysis employing conventional biochemical reactions and genus- and species-specific polymerase chain reaction assays. Pulsed-field gel electrophoresis, randomly amplified polymorphic DNA typing, and automated ribotyping were used to genotype the isolates. As part of the intervention, contact isolation precautions were initiated for all patients identified as having had a culture positive for B. cepacia. RESULTS: Between September 1997 and September 1999, B. cepacia was isolated from 31 adult patients without CF in ICUs at a university-affiliated teaching hospital. Based on geographic clustering and genotypic analysis, three distinct clusters were observed involving 20 patients. Isolates from 17 of these patients were available for testing and were found to be of the same strain (outbreak strain). Further taxonomic analysis indicated that the outbreak strain was B. cepacia complex genomovar III. Twelve (71%) of the 17 patients were judged to be infected, and 5 (29%) were colonized with this strain. Six of 200 environmental cultures from multiple sources in the hospital's ICUs yielded B. cepacia. Two of these isolates, both recovered from rooms of colonized patients, were the same genotype as the outbreak strain recovered from patients. CONCLUSION: Despite an extensive investigation, the source of the B. cepacia clone involved in this outbreak remains unknown. The spatial and temporal pattern of cases suggests that cross-transmission of a genetically related strain contributed to clustering among patients. The initiation of contact isolation may have limited the extent of this transmission. Additional studies are needed to elucidate better the epidemiology of nosocomial B. cepacia infection among non-CF adult patients.

Clostridium difficile infection is a risk factor for bacteremia due to vancomycin-resistant enterococci (VRE) in VRE-colonized patients with acute leukemia.

A cohort study was conducted in a cancer center to identify risk factors for bacteremia with vancomycin-resistant enterococci (VRE) in neutropenic cancer patients colonized with VRE. There were 10 patients with VRE bacteremia among 56 colonized with VRE, of whose charts 51 were available for review. One hundred percent of patients with VRE bacteremia (10 of 10) vs. 56% of patients without VRE bacteremia (23 of 41) had acute leukemia (P = .01, Fisher's exact test). Four of the 10 patients with VRE bacteremia had a positive Clostridium difficile toxin assay within 6 days of their first positive VRE blood culture. Both C. difficile infection and antimicrobial (vancomycin and ciprofloxacin) use during VRE colonization were significant risk factors for VRE bacteremia in univariate analysis. When a Cox proportional hazards model was used to account for differences in follow-up time, C. difficile infection was the only statistically significant risk factor (risk ratio, 8.2; P = .007) for VRE bacteremia in VRE-colonized patients with acute leukemia.

Colonization with vancomycin-resistant enterococci in chronic hemodialysis patients.

Vancomycin-resistant enterococcus (VRE) has been identified with increased frequency in dialysis populations, but the risk factors for VRE colonization are not well defined in hemodialysis patients. Patients from a university-affiliated outpatient dialysis center had surveillance stool or rectal cultures for VRE during April 1994 and January 1996. The combined cohort of 168 patients was followed-up for all-cause mortality, subsequent hospitalization, and VRE infection. Demographic and risk factor information, including age, gender, race, diabetes, coronary artery disease (CAD), and human immunodeficiency virus (HIV) infection, were collected on all patients. Sixteen patients had surveillance cultures grow vancomycin-resistant Enterococcus faecium or E faecalis (VREF), and nine additional patients had clinical cultures positive for VREF. The median follow-up time for patients with positive surveillance or clinical cultures for VREF was 421 days versus 423 days for those without VREF. Patients with positive surveillance cultures for VREF had less time on hemodialysis before screening (median = 207 days v 822 days; P < 0.01), and more hospitalization in the year before screening (median = 19 days v 3 days, P < 0.01) compared with those without VREF. Patients with VREF colonization were more likely to develop infection with VREF (25% v 1%, P < 0.01) than those without VREF colonization. However, adjusting for age, diabetes, coronary artery disease, and acquired immune deficiency syndrome (AIDS) using Cox-proportional hazards models, the presence of VREF on screening culture was not associated with increased risk of death (RR = 1.1, P = 0.86). Thus after adjusting for other comorbidities, VREF colonization was not associated with increased mortality. Patients with end-stage renal disease (ESRD) on hemodialysis who are hospitalized are more likely to have VREF, but longer duration on hemodialysis was not associated with presence of this organism. This suggests that VRE transmission occurs predominantly in the inpatient setting.