OBJECTIVE: To reduce transmission of carbapenem-resistant Enterobacteriaceae (CRE) in an intensive care unit with interventions based on simulations by a developed mathematical model.DESIGN: Before-after trial with a 44-week baseline period and 24-week intervention period.SETTING: Medical intensive care unit of a tertiary care teaching hospital.PARTICIPANTS: All patients admitted to the unit.METHODS: We developed a model of transmission of CRE in an intensive care unit and measured all necessary parameters for the model input. Goals of compliance with hand hygiene and with isolation precautions were established on the basis of the simulations and an intervention was focused on reaching those metrics as goals. Weekly auditing and giving feedback were conducted.RESULTS: The goals for compliance with hand hygiene and contact precautions were reached on the third week of the intervention period. During the baseline period, the calculated R0 was 11; the median prevalence of patients colonized by CRE in the unit was 33%, and 3 times it exceeded 50%. In the intervention period, the median prevalence of colonized CRE patients went to 21%, with a median weekly Rn of 0.42 (range, 0–2.1).CONCLUSIONS: The simulations helped establish and achieve specific goals to control the high prevalence rates of CRE and reduce CRE transmission within the unit. The model was able to predict the observed outcomes. To our knowledge, this is the first study in infection control to measure most variables of a model in real life and to apply the model as a decision support tool for intervention.Infect Control Hosp Epidemiol2016;1–8

Health care associated infections (HAIs) are currently among the major challenges to the care of hematopoietic stem cell transplantation (HSCT) patients. The objective of the present study was to evaluate the impact of 2% chlorhexidine (CHG) bathing on the incidence of colonization and infection with vancomycin-resistant Enterococcus (VRE), multidrug-resistant (MDR) gram-negative pathogens, and to evaluate their CHG minimum inhibitory concentration (MIC) after the intervention. A quasi-experimental study with duration of 9 years was conducted. VRE colonization and infection, HAI rates, and MDR gram-negative infection were evaluated by interrupted time series analysis. The antibacterial susceptibility profile and mechanism of resistance to CHG were analyzed in both periods by the agar dilution method in the presence or absence of the efflux pump inhibitor carbonyl cyanide-m-chlorophenyl hydrazone (CCCP) and presence of efflux pumps (qacA/E, qacA, qacE, cepA, AdeA, AdeB, and AdeC) by polymerase chain reaction (PCR). The VRE colonization and infection rates were significantly reduced in the postintervention period (P = 0.001). However, gram-negative MDR rates in the unit increased in the last years of the study. The CHG MICs for VRE increased during the period of exposure to the antiseptic. A higher MIC at baseline period was observed in MDR gram-negative strains. The emergence of a monoclonal Pseudomonas aeruginosa clone was observed in the second period. Concluding, CHG bathing was efficient regarding VRE colonization and infection, whereas no similar results were found with MDR gram-negative bacteria.

Stenotrophomonas maltophilia has emerged as an important opportunistic pathogen in the last decade. Increased resistance to sulfamethoxazole/trimethoprim (SMX/TMP) has been reported in S. maltophilia strains in the past few years, leading to few therapeutic options. We conducted a prospective multicenter study at two Brazilian teaching hospitals that identified S. maltophilia isolates and evaluated their antimicrobial susceptibility profile, SMX/TMP resistance genes and their clonality profile. A total of 106 non-repeated clinical samples of S. maltophilia were evaluated. Resistance to SMX/TMP was identified in 21.6% of the samples, and previous use of SMX/TMP occurred in 19 (82.6%). PCR detected the sul1 gene in 14 of 106 strains (13.2%). Of these isolates, nine displayed resistance to SMX/TMP. The resistant strains presented a polyclonal profile. This opportunistic pathogen has emerged in immunocompromised hosts, with few therapeutic options, which is aggravated by the description of emerging resistance mechanisms, although with a polyclonal distribution profile.