Outbreak of Acinetobacter spp. bloodstream infections in a nursery associated with contaminated aerosols and air conditioners.

BACKGROUND: Acinetobacter spp. are multidrug-resistant bacteria that grow well in water and cause infections with unexplained, increased summer prevalence. In August, 1996, eight infants acquired Acinetobacter spp. bloodstream infection (A-BSI) while in a nursery in the Bahamas; three infants died and an investigation was initiated. METHODS: A case patient was defined as any newborn in the nursery during August 6 to 13, 1996, with A-BSI. To identify risk factors for A-BSI we conducted a retrospective cohort study and performed environmental cultures and air sampling using settle plates. The genetic relatedness of environmental isolates was assessed by pulsed field gel electrophoresis. RESULTS: Of 33 patients in the nursery 8 (24%) met the case definition. Patients with peripheral iv catheters were more likely to develop A-BSI (8 of 21 vs. O of 10, P < 0.05). Multivariate analysis among patients with iv catheters indicated that only exposure to one nurse was an independent risk factor for developing A-BSI (P < 0.005). Nursery settle plates were more likely to grow Acinetobacter spp. than were settle plates from other hospital areas (8 of 9 vs. 0 of 5, P < 0.005); cultures from nursery air conditioners also grew Acinetobacter spp. Environmental isolates were genetically diverse. After installation of a new air conditioner in May, 1995, A-BSIs occurred more frequently during months of increased absolute humidity or environmental dew point. CONCLUSIONS: Acinetobacter spp. may cause nosocomial BSI and death among infants during periods of polyclonal airborne dissemination; breaks in aseptic technique during i.v. medication administration may facilitate transmission from the environment to the patient. Environmental conditions that increase air conditioner condensate may predispose to airborne dissemination via contaminated aerosols and increase the risk of nosocomial A-BSI.

Acquisition of Pseudomonas cepacia at summer camps for patients with cystic fibrosis. Summer Camp Study Group.

To assess the risk of acquisition of Pseudomonas cepacia by person-to-person transmission at cystic fibrosis summer camps, we conducted in 1990 a study at three camps attended by patients with cystic fibrosis who had P. cepacia infection and patients without P. cepacia infection but who were considered susceptible to infection. We obtained sputum or throat cultures from campers on their arrival at, weekly during, at the end of, and 14 to 30 days after camp. We compared the incidence of sputum conversion of patients at camp with that of patients outside camp by culturing specimens from noncamper control subjects with cystic fibrosis who were known not to be infected < or = 2 weeks before and 4 to 6 weeks after camp. We also determined the risk factors for P. cepacia acquisition by determining the relative risk of acquisition between campers who were exposed versus campers who were not exposed to campers known to be infected or to potential environmental sources of P. cepacia at camp. The ribotype of P. cepacia isolates from campers with sputum conversion was compared with that of isolates from other campers and from an environmental source. The cumulative incidence of sputum conversion during the study period was 6.1% (11/181) among campers compared with no incidence (0/92) among noncampers (p = 0.02, Fisher Exact Test). The incidence of sputum conversion at camp varied according to the prevalence of campers with known infection (p < 0.001, chi-square test for trend). The rate of sputum conversion was higher in the camp with longer duration (relative risk = 12.0; 95% confidence interval = 2.7 to 53.5). Ribotyping showed that P. cepacia isolates from all 11 campers with sputum conversion were identical or similar (1 to 2 band difference) to isolates of other P. cepacia-infected campers including co-converters. These results suggest that P. cepacia can be acquired by patients with cystic fibrosis who are attending summer camp for such patients, possibly through person-to-person transmission, and that the risk increases with the prevalence of P. cepacia-infected campers and the duration of camp.

Pseudomonas cepacia colonization in patients with cystic fibrosis: risk factors and clinical outcome.

During the period of 1979 to 1983, 38 patients with cystic fibrosis (CF) at the CF center of St. Christopher's Hospital for Children in Pennsylvania developed respiratory tract colonization with Pseudomonas cepacia. Seventeen (45%) of the patients with colonization died. Yearly incidence rates of P. cepacia colonization fluctuated between 1.3% and 6.1%, suggesting an endemic phenomenon. Case-control studies showed that severe underlying CF, use of aminoglycosides, and having a sibling with CF and P. cepacia colonization were significant risk factors for P. cepacia colonization. Once colonized with P. cepacia, patients with CF were likely to be hospitalized longer (P = 0.008) and to die sooner (P = 0.0001) than control patients with CF. Environmental and microbiologic studies did not identify a common source or mode of transmission of P. cepacia among patients. The results of this investigation suggest that P. cepacia colonization of patients with CF was endemic in the hospital, occurred more frequently in those with severe disease, and was associated with adverse clinical outcome.