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Hip and knee arthroplasty infections are associated with considerable healthcare costs. The merits of reducing the postoperative surveillance period from 1 year to 90 days have been debated.
To report the first pan-Canadian hip and knee periprosthetic joint infection (PJI) rates and to describe the implications of a shorter (90-day) postoperative surveillance period.
Prospective surveillance for infection following hip and knee arthroplasty was conducted by hospitals participating in the Canadian Nosocomial Infection Surveillance Program (CNISP) using standard surveillance definitions.
Overall hip and knee PJI rates were 1.64 and 1.52 per 100 procedures, respectively. Deep incisional and organ-space hip and knee PJI rates were 0.96 and 0.71, respectively. In total, 93% of hip PJIs and 92% of knee PJIs were identified within 90 days, with a median time to detection of 21 days. However, 11%–16% of deep incisional and organ-space infections were not detected within 90 days. This rate was reduced to 3%–4% at 180 days post procedure. Anaerobic and polymicrobial infections had the shortest median time from procedure to detection (17 and 18 days, respectively) compared with infections due to other microorganisms, including Staphylococcus aureus.
PJI rates were similar to those reported elsewhere, although differences in national surveillance systems limit direct comparisons. Our results suggest that a postoperative surveillance period of 90 days will detect the majority of PJIs; however, up to 16% of deep incisional and organ-space infections may be missed. Extending the surveillance period to 180 days could allow for a better estimate of disease burden.
To assess clinically relevant outcomes after complete cessation of control measures for vancomycin-resistant enterococci (VRE).
Quasi-experimental ecological study over 3.5 years.
All VRE screening and isolation practices at 4 large academic hospitals in Ontario, Canada, were stopped on July 1, 2012. In total, 618 anonymized abstracted charts of patients with VRE-positive clinical isolates identified between July 1, 2010, and December 31, 2013, were reviewed to determine whether the case was a true VRE infection, a VRE colonization or contaminant, or a true VRE bacteremia. All deaths within 30 days of the last VRE infection were also reviewed to determine whether the death was fully or partially attributable to VRE. All-cause mortality was evaluated over the study period. Generalized estimating equation methods were used to cluster outcome rates within hospitals, and negative binomial models were created for each outcome.
The incidence rate ratio (IRR) for VRE infections was 0.59 and the associated P value was .34. For VRE bacteremias, the IRR was 0.54 and P=.38; for all-cause mortality the IRR was 0.70 and P=.66; and for VRE attributable death, the IRR was 0.35 and P=.49. VRE control measures were not significantly associated with any of the outcomes. Rates of all outcomes appeared to increase during the 18-month period after cessation of VRE control measures, but none reached statistical significance.
Clinically significant VRE outcomes remain rare. Cessation of all control measures for VRE had no significant attributable adverse clinical impact.
Pseudomonas aeruginosa has been increasingly recognized for its ability to cause significant hospital-associated outbreaks, particularly since the emergence of multidrug-resistant strains. Biofilm formation allows the pathogen to persist in environmental reservoirs. Thus, multiple hospital room design elements, including sink placement and design, can impact nosocomial transmission of P. aeruginosa and other pathogens.
From December 2004 through March 2006, 36 patients exposed to the intensive care unit or transplant units of a tertiary care hospital were infected with a multidrug-resistant strain of P. aeruginosa. All phenotypically similar isolates were examined for genetic relatedness by means of pulsed-field gel electrophoresis. Clinical characteristics of the affected patients were collected, and a detailed epidemiological and environmental investigation of potential sources was carried out.
Seventeen of the infected patients died within 3 months; for 12 (71%) of these patients, infection with the outbreak organism contributed to or directly caused death. The source of the outbreak was traced to hand hygiene sink drains, where biofilms containing viable organisms were found. Testing by use of a commercial fluorescent marker demonstrated that when the sink was used for handwashing, drain contents splashed at least 1 meter from the sink. Various attempts were made to disinfect the drains, but it was only when the sinks were renovated to prevent splashing onto surrounding areas that the outbreak was terminated.
This report highlights the importance of biofilms and of sink and patient room design in the propagation of an outbreak and suggests some strategies to reduce the risks associated with hospital sinks.
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