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To test the hypothesis that methicillin-susceptible Staphylococcus aureus (MSSA) carriage may protect against nosocomial methicillin-resistant S. aureus (MRSA) acquisition by competing for colonization of the anterior nares.
Prospective cohort and nested case-control study.
Swiss university hospital.
All adult patients admitted to 14 wards of the general medicine division between April 1 and October 31, 2007.
Patients were screened for MRSA and MSSA carriage at admission to and discharge from the division. Associations between nosocomial MRSA acquisition and MSSA colonization at admission and other confounders were analyzed by univariable and multivariable analysis.
Of 898 patients included, 183 (20%) were treated with antibiotics. Nosocomial MRSA acquisition occurred in 70 (8%) of the patients (case patients); 828 (92%) of the patients (control subjects) were free of MRSA colonization at discharge. MSSA carriage at admission was 20% and 21% for case patients and control subjects, respectively. After adjustment by multivariate logistic regression, no association was observed between MSSA colonization at admission and nosocomial MRSA acquisition (adjusted odds ratio [aOR], 1.2 [95% confidence interval (CI), 0.6–2.3]). By contrast, 4 independent predictors of nosocomial MRSA acquisition were identified: older age (aOR per 1-year increment, 1.05 [95% CI, 1.02–1.08]); increased length of stay (aOR per 1-day increment, 1.05 [95% CI, 1.02–1.09]); increased nursing workload index (aOR per 1-point increment, 1.02 [95% CI, 1.01–1.04]); and previous treatment with macrolides (aOR, 5.6 [95% CI, 1.8–17.7]).
Endogenous MSSA colonization does not appear to protect against nosocomial MRSA acquisition in a population of medical patients without frequent antibiotic exposure.
To describe the course and management of a protracted outbreak after intercontinental transfer of 2 patients colonized with multidrug-resistant Acinetobacter baumannii (MDRAB).
An 18-month outbreak investigation.
An 860-bed university hospital in France.
Case patients (ie, carriers) were those colonized or infected with an MDRAB isolate.
During the epidemic period, all intensive care unit (ICU) patients and contacts of carriers who were transferred to wards were screened for MDRAB carriage. Contact precautions, environmental screening, and auditing of healthcare worker (HCW) practices were implemented; rooms were cleaned with hydrogen peroxide mist disinfection. One ICU, in which most of the cases occurred, was closed on 4 occasions for thorough cleaning and disinfection.
The 2 index case patients were identified as 2 patients who carried the same MDRAB strain and who were admitted to the hospital after repatriation from Tahiti 5 months apart. During an 18-month period, a total of 84 secondary cases occurred. Reintroduction of MDRAB into the ICUs occurred from patients previously colonized or from healthcare personnel. Termination of the outbreak was only achieved when all carriers from wards or the ICU were cohorted to an isolation unit with dedicated healthcare personnel.
Intercontinental transfer of carriers of MDRAB can result in extensive outbreaks and serious disruption of the hospital's organization. Transmission from carriers most likely occurred via the hands of HCWs, poor cleaning protocols, airborne spread, and contaminated water from sink traps. This protracted outbreak was controlled only after implementation of an extensive control program and eventual cohorting of all carriers in an isolation unit with dedicated healthcare personnel.
To measure the incidence of nosocomial infection (NI) among patients with septic shock according to the place of septic shock acquisition and to evaluate the increase in the risk of pulmonary infection associated with septic shock.
Prospective cohort study.
TWO intensive care units (ICUs) of a French university hospital.
Patients and Methods.
The study included a total of 209 septic shock patients during the period December 1, 2001 through April 30, 2005. The place of septic shock acquisition for 108 patients was the community; for 87, the hospital; and for 14, the ICU. To evaluate the impact of septic shock on the development of pulmonary infection, a competitive and adjusted hazard ratio (aHR) model was applied to nontrauma ICU patients.
Among the 209 study patients, 48 (23%) experienced 66 NIs after septic shock. There was no significant difference in the NI attack rates according to place of acquisition: for the community acquisition group, 24 cases per 100 patients (95% confidence interval [CI], 16-32); for the hospital acquisition group, 20 cases per 100 patients (95% CI, 11-28); and for the ICU acquisition group, 36 cases per 100 patients (95% CI, 11-61) (P = .3). For nontrauma ICU patients, the presence of community-acquired septic shock was found to be independently associated with a higher incidence of pulmonary infection, compared with the absence of septic shock (aHR, 2.12 [95% CI, 1.08-4.16]; P = .03).
The risk of NI did not differ by the place of septic shock acquisition. The risk of pulmonary infection was higher for ICU patients with community-acquired septic shock who were admitted for underlying nontrauma disease. Studies are needed to investigate the pathogenic mechanisms that facilitate pulmonary infection in this population, taking into account exposure to invasive devices and immunosuppression after the initial phase of septic shock.
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