Standing order programs (SOPs), which allow for vaccination without an individual physician order, are the most effective mechanism to achieve high vaccination rates. Among the suggested settings for the utilization of SOPs are hospital inpatient units, because they provide care for those most likely to benefit from vaccination. The cost-effectiveness of this approach for elderly hospitalized persons is unknown. The purpose of this study was to estimate the cost-effectiveness of SOPs for pneumococcal polysaccharide vaccine (PPV) vaccination for patients 65 years of age or older in 2 types of hospital.

In 2004, a 1,094-bed tertiary care hospital implemented a pharmacy-based SOP for PPV, and a 225-bed community hospital implemented a nursing-based SOP for PPV. Newly admitted patients 65 years of age or older were screened for PPV eligibility and then offered PPV. Vaccination rates before and after initiation of SOPs in the United States, incidence rates of invasive pneumococcal disease in the United States, and US economic data were the bases of the cost-effectiveness analyses. One-way and multivariate sensitivity analyses were conducted.

PPV vaccination rates increased 30.5% in the tertiary care hospital and 15.3% in the community hospital. In the base-case cost-effectiveness analysis, using a societal perspective, we found that both pharmacy-based and nursing-based SOPs cost less than $10,000 per quality-adjusted life-year gained, with program costs (pharmacy-based SOPs cost $4.16 per patient screened, and nursing-based SOPs cost $4.60 per patient screened) and vaccine costs ($18.33 per dose) partially offset by potential savings from cases of invasive pneumococcal disease avoided ($12,436 per case). Sensitivity analyses showed SOPs for PPV vaccination to be cost-effective, compared with PPV vaccination without SOPs, unless the improvement in vaccination rate was less than 8%.

SOPs do increase PPV vaccination rates in hospitalized elderly patients and are economically favorable, compared with PPV vaccination rates without SOPs.

Most nosocomial acquistion of vancomycin-resistant enterococci (VRE) is due to cross-transmission. We sought to identify risk factors for acquisition of VRE by roommates of patients colonized or infected with VRE.

Retrospective cohort study.

A 472-bed tertiary care teaching hospital.

All patients who shared a room with a patient colonized or infected with VRE at our hospital between January 1, 1999 and December 31, 2006 were identified. These roommates of VRE-positive patients were screened by rectal swab culture on days 2, 5, and 7 after the last exposure to the index patient. Chart reviews were performed to identify risk factors for VRE colonization in these roommates.

Eighty-eight roommates of patients colonized or infected with VRE were identified. Of the 38 roommates with complete follow-up, 8 (21%) became colonized with VRE. These 8 roommates were older (median, 87.5 vs 62.5 years of age; P = .001), had longer duration of room exposure (median, 8.5 vs 4 days; P = .002), and were more likely to have a urinary catheter (odds ratio [OR], 16 [95% confidence interval {CI}, 1.7-152]; P = .005), an elevated serum creatinine level (OR, 17 [95% CI, 1.4-196]; P = .02), low serum albumin level (OR, 9.9 [95% CI, 1.3-113]; P = .01), and recent third-generation cephalosporin use (OR, 8.3 [95% CI, 1.5-47]; P = .02).

Roommates of patients identified as colonized or infected with VRE are at substantial risk of becoming colonized, with the degree of risk increasing in older and more frail patients. VRE control programs should pay particular attention to such patients.

Colonization with vancomycin-resistant Enterococcus (VRE) is a risk factor for subsequent VRE bloodstream infection (BSI); however, risk factors for BSI among colonized patients have not been adequately described. We sought to determine the proportion of VRE-colonized patients who subsequently develop VRE BSI and to identify risk factors for VRE BSI among these patients.

Records of 768 patients colonized with VRE from January 2002 through June 2005 were reviewed. The proportion of patients who developed VRE BSI was calculated, and the characteristics of these patients were compared, in a 2 : 1 ratio, with those of patients who did not develop VRE BSI. To identify risk factors for VRE BSI and for death, we used univariate logistic regression analysis and then multivariate logistic regression analysis. Using pulsed-field gel electrophoresis (PFGE), we compared the isolate recovered when the patient was colonized and the isolate recovered when the patient developed VRE BSI.

Of the 768 patients colonized with VRE, 31 (4.0%) developed VRE BSI. Multivariate analysis identified the following idependent risk factors for developing VRE BSI: infection of an additional body site other than blood (adjusted odds ratio [aOR], 3.9; P = .04), admission to the hospital from a long-term care facility (aOR, 12.6; P = .04), and receipt of vancomycin (aOR, 10.6; P < .001). The independent risk factors for death among patients colonized with VRE were immunosuppression (aOR, 12.9; P = .001 ) and VRE BSI (aOR, 9.1; P = .002). Of the 31 patients who developed VRE BSI, 23 (74%) had a pair of isolates representing VRE colonization and VRE BSI. For 19 (83%) of these 23 patients, the isolate representing BSI was genetically related to the isolate representing VRE colonization: 12 pairs of isolates (52%) had identical banding patterns, 5 had closely related patterns, and 2 had possibly related patterns.

Of the 768 patients colonized with VRE, 31 (4.0%) usually developed VRE BSI due to a related strain. Independent risk factors for BSI among colonized patients were admission from a long-term care facility, infection of an additional body site, and exposure to vancomycin. Independent risk factors for death were immunosuppression and VRE BSI.

To investigate the mode of transmission of imipenem-resistant Acinetobacter baumannii strains causing episodes of sepsis.

A 7-bed trauma intensive care unit (ICU) in an orthopedic hospital in Greece.

During a 14-week period (from January 10 to April 16, 2006), clinical specimens, along with samples taken on a weekly basis from the ICU environment and from the hands of health care workers (HCWs), were prospectively tested for imipenem-resistant A. baumannii. Pulsed-field gel electrophoresis was used to study the genetic relatedness of the isolates recovered from these specimens and samples.

During the survey, imipenem-resistant A. baumannii was identified in 14 hospitalized patients, from whom 40 multidrug-resistant and imipenem-resistant A. baumanii isolates were recovered. These pathogens caused episodes of bacteremia and sepsis in all but one of the patients and contributed to the death of 3 patients. Samples for culture were obtained from the environment and from the hands of HCWs; 29 imipenem-resistant A. baumannii isolates were recovered from the environment, and 12 from HCWs. One predominant genotype and 2 less predominant genotypes were detected among the 81 imipenem-resistant A. baumannii isolates. All 3 of these genotypes were found among patients and HCWs and were recovered from environmental samples.

Control measures consisted of the closure of the ICU and the transfer of the patients to other units. The ICU was disinfected, and adherence to proper hand hygiene protocol was reinforced. These same clonal isolates were not recovered from clinical or environmental samples during the month after the reopening of the ICU.

The extensive dissemination of imipenem-resistant A. baumannii clonal strains causing episodes of bacteremia and/or sepsis resulted from modes of transmission via multiple contaminated surfaces and objects and transiently colonized HCWs' hands. Closure of the ICU and its meticulous environmental decontamination led to the successful control of the outbreak.

Serratia marcescens causes healthcare-associated infections and significant morbidity and mortality in neonatal intensive care units (NICUs). We report the investigation and control of an outbreak of multidrug-resistant (MDR) S. marcescens infection at an NICU.

An outbreak investigation and a case-control study were undertaken at a 36-bed NICU in a tertiary care hospital in Baltimore, Maryland, for the period from October 2004 through February 2005. The outbreak investigation included case identification, review of medical records, environmental cultures, patient surveillance cultures, personnel hand cultures, and pulsed-field gel electrophoresis (PFGE). The case-control study included case identification and review of medical records. Infection control measures were implemented. Eighteen NICU neonates had cultures that grew MDR S. marcescens during the study period. The case-control study included 16 patients with the outbreak strain or an unidentified strain of MDR S. marcescens and 32 control patients not infected and/or colonized with MDR S. marcescens, treated in the NICU for at least 48 hours during the study period.

PFGE analysis identified a single strain of MDR S. marcescens that infected or colonized 15 patients. Two patients had unique strains, and 1 patient's isolate could not be subtyped. An unrelated MDR S. marcescens isolate was recovered from a sink drain. Exposure to inhalational therapy was an independent risk factor for MDR S. marcescens acquisition after adjusting for birth weight. Extensive investigation failed to reveal a point source for the outbreak.

A single epidemic strain of MDR S. marcescens spread rapidly and threatened to become endemic in this NICU. Transient carriage on the hands of healthcare personnel or on respiratory care equipment was the likely mode of transmission. Cohorting patients and staff, at the cost of bed closures and additional personnel, interrupted transmission and halted the outbreak.

To characterize infection control experience during a 6.5-year period in a cooperative care center for transplant patients.

Descriptive analysis.

A cooperative care center for transplanted patients, in which patients and care partners are housed in a homelike environment, and care partners assume responsibility for patient care duties.

Nine hundred ninety one transplant patients.

Infection control definitions from the Centers for Disease Control and Prevention were used to ascertain infection rates. Environmental cultures were used to detect methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Enterococcus (VRE), Clostridium difficile, and fungi during the first 18 months. Surveillance cultures were performed for a subset of patients and care partners.

From June 1999 through December 2005, there were 19,365 patient-days observed. The most common healthcare-associated infection encountered was intravascular catheter-related bloodstream infection, with infection rates of 5.74 and 4.94 cases per 1,000 patient-days for hematopoietic stem cell transplant (HSCT) and solid organ transplant (SOT) patients, respectively. G difficile-associated diarrhea was observed more frequentiy in HSCT patients than in SOT patients (3.97 vs 0.57 cases per 1000 patient-days; P< .0001 ). There was no evidence of environmental contamination with MRSA, VRE, or C. difficile. Acquisition of MRSA was not observed. Acquisition of VRE was documented.

This study documented that cooperative care was associated with some risk of healthcare-associated infection, most notably intravascular catheter-associated bloodstream infection and C. difficile-associated diarrhea, it appears the incidences of these infections were roughly commensurate with those in other care settings.

To determine the range and the mode of germicidal activity of sterilants generated by a nonthermal plasma sterilization system for microorganisms.

Representative bacteria, spores, viruses, bacteriophages, and fungi were exposed to the plasma cycle and the residual viability was measured in vitro. To assess the mode of lethal injury, Escherichia coli, Staphylococcus aureus, Bacillus atrophaeus, and bacteriophages were exposed to the plasma cycle, and the effects of the plasma-generated sterilants on the biological parameters were determined.

There were at least 4-6 log reductions in viability for all microorganisms after 10 minutes of exposure to the plasma cycle. Electron micrographs and studies of the inhibition of bacteriophage infectivity suggested that the primary injury is to the organisms' cell envelopes. The plasma cycle also denatured isolated bacterial proteins and inactivated bacteriophages, but it had no effect on isolated DNA and bacterial proteins within exposed bacteria.

Nonthermal plasma, which is produced at atmospheric temperature and pressure, generates sterilants that kill high concentrations of microorganisms and inactivate viruses during a 10-minute exposure. The primary injury appears to be at the surface structures of the organisms. This suggests that nonthermal plasma has utility for sterilization of heat-sensitive medical materials and devices.