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To evaluate the efficacy of contact and droplet precautions in reducing the incidence of hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) infections.
A 439-bed, university-affiliated community hospital.
To identify inpatients infected or colonized with MRSA, we conducted surveillance of S. aureus isolates recovered from clinical culture and processed by the hospital's clinical microbiology laboratory. We then reviewed patient records for all individuals from whom MRSA was recovered. The rates of hospital-acquired MRSA infection were tabulated for each area where patients received nursing care. After a baseline period, contact and droplet precautions were implemented in all intensive care units (ICUs). Reductions in the incidence of hospital-acquired MRSA infection in ICUs led to the implementation of contact precautions in non-ICU patient care areas (hereafter, “non-ICU areas”), as well. Droplet precautions were discontinued. An analysis comparing the rates of hospital-acquired MRSA infection during different intervention periods was performed.
The combined baseline rate of hospital-acquired MRSA infection was 10.0 infections per 1,000 patient-days in the medical ICU (MICU) and surgical ICU (SICU) and 0.7 infections per 1,000 patient-days in other ICUs. Following the implementation of contact and droplet precautions, combined rates of hospital-acquired MRSA infection in the MICU and SICU decreased to 4.3 infections per 1,000 patient-days (95% confidence interval [CI], 0.17-0.97; P = .03). There was no significant change in hospital-acquired MRSA infection rates in other ICUs. After the discontinuation of droplet precautions, the combined rate in the MICU and SICU decreased further to 2.5 infections per 1,000 patient-days. This finding was not significant (P = .43). In the non-ICU areas that had a high incidence of hospital-acquired MRSA infection, the rate prior to implementation of contact precautions was 1.3 infections per 1,000 patient-days. After the implementation of contact precautions, the rate in these areas decreased to 0.9 infections per 1,000 patient-days (95% CI, 0.47-0.94; P = .02).
The implementation of contact precautions significantly decreased the rate of hospital-acquired MRSA infection, and discontinuation of droplet precautions in the ICUs led to a further reduction. Additional studies evaluating specific infection control strategies are needed.
To determine risk factors for ceftazidime-resistant Klebsiella pneumoniae infection and the effect of cef-tazidime-resistant K. pneumoniae infection on mortality during an isolated outbreak.
Case–control investigation using clinical and molecular epidemiology and prospective analysis of infection control interventions.
Surgical intensive care unit of a university-affiliated community hospital.
Fourteen case-patients infected with ceftazidime-resistant K. pneumoniae and 14 control-patients.
Ten of 14 case-patients had identical strains by pulsed-field gel electrophoresis. Broad-spectrum antibiotic therapy before admission to the unit was strongly predictive of subsequent ceftazidime-resistant K. pneumoniae infection. In addition, patients with ceftazidime-resistant K. pneumoniae infection experienced increased mortality (odds ratio, 3.77).
Cephalosporin restriction has been shown to decrease the incidence of nosocomial ceftazidime-resistant K. pneumoniae. However, isolated clonal outbreaks may occur due to lapses in infection control practices. Reinstatement of strict handwashing, thorough environmental cleaning, and repeat education led to termination of the outbreak. A distinct correlation between ceftazidime-resistant K. pneumoniae infection and mortality supports the important influence of antibiotic resistance on the outcome of serious bacterial infections.
To assess nosocomial transmission of imipenem-resistant Pseudomonas aeruginosa (IRPA) following bronchoscopy during August through October 1998.
Traditional and molecular epidemiological investigation of a case series.
University-affiliated community hospital.
18 patients with IRPA bronchial-wash isolates.
We reviewed clinical data, performed environmental cultures and molecular analysis of all IRPA isolates, and observed disinfection of bronchoscopes.
Of 18 patients who had IRPA isolated from bronchoscopic or postbronchoscopic specimens, 13 underwent bronchoscopy for possible malignancy or undiagnosed pulmonary infiltrates. Following bronchoscopy, 3 patients continued to have IRPA isolated from sputum and demonstrated clinical evidence of infection requiring specific antimicrobial therapy. The remaining 15 patients had no further IRPA isolated and remained clinically well 3 months following bronchoscopy. Pulsed-field gel electrophoresis revealed that all strains except one were >95% related. STERIS SYSTEM 1 had been implemented in July 1998 as an automatic endoscope reprocessor (AER) for all endoscopes and bronchoscopes. Inspection of bronchoscope sterilization cycles revealed incorrect connectors joining the bronchoscope suction channel to the STERIS SYSTEM 1 processor, obstructing peracetic acid flow through the bronchoscope lumen. No malfunction warning was received, and spore strips remained negative.
The similarity of diverse connectors and limited training by the manufacturer regarding AER for bronchoscopes were the two factors responsible for the outbreak. Appropriate connections were implemented, and there was no further bronchoscope contamination. We suggest active surveillance of all bronchoscopy specimen cultures, standardization of connectors of various scopes and automated processors, and systematic education of staff by manufacturers with periodic on-site observation.
To investigate suspected pseudo-outbreaks of Mycobacterium tuberculosis (MTB) during August 1994 and July 1995 among patients who did not have clinical findings consistent with tuberculosis.
Retrospective and prospective surveys of all clinical and laboratory data using standard epidemiological tools and DNA fingerprinting.
A university-affiliated community hospital.
Those with positive MTB cultures during periods when we noted that the number of MTB positive cultures greatly outnumbered the usual monthly average (retrospective analysis, 1994) and patients with positive MTB cultures without clinical findings consistent with tuberculosis (prospective survey, 1995).
Epidemiological and molecular studies revealed specimen cross-contamination in the laboratory due to a faulty exhaust hood. Improvement in laboratory ventilation and change of the implicated hood prevented further specimen contamination.
The identification of positive MTB cultures from patients without clinical evidence of tuberculosis should be a signal to suspect laboratory contamination and implement control measures. These should include a thorough epidemiological investigation, DNA fingerprint analysis, and an environmental inspection.
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