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The VU University Medical Center, a tertiary-care hospital in the Netherlands, has adopted a dress code based on national guidelines. It includes uniforms provided by the hospital and a ‘bare-below-the-elbow’ policy for all healthcare workers (HCWs) in direct patient care. Because compliance was poor, we sought to improve adherence by interventions targeted at the main causes of noncompliance.
To measure compliance with the dress code, to assess causes of noncompliance and to assess whether a behavioral approach (combing a nominal group technique with participatory action) is effective in improving compliance
Between March 2014 and June 2016, a total of 1,920 HCWs were observed in hospital hallways for adherence to the policy, at baseline, and at follow-up measurements. Based on the outcome of the baseline measurement, a nominal group technique was applied to assess causes of noncompliance. The causes revealed served as input for interventions that were developed, prioritized, and tailored to specific groups of HCWs and specific departments through participatory action.
We identified lack of knowledge, lack of facilities, and negative attitudes as the main causes of noncompliance. The importance of each cause varied for different groups of HCWs. Tailored interventions targeted at these causes increased overall compliance by 39.6% (95% CI, 31.7–47.5).
The combination of a nominal group technique and participatory action approach is an effective method to increase and sustain compliance with hospital dress code. This combined approach may also be useful to improve adherence to other guidelines.
To study the presence of bacterial factors in clinical isolates of Acinetobacter species in order to identify markers of epidemic potential.
Forty-six isolates of Acinetobacter species, including 23 epidemic and 23 sporadic strains from different outbreaks in nine European countries, were compared for the presence of the following factors: hemagglutination, presence of capsules and fimbriae, binding to salivary mucins, resistance to drying, and antibiogram typing. Genotyping of all strains was performed by amplified fragment-length polymorphism (AFLP).
All outbreak strains except two (91%) were identified as Acinetobacter baumannii. Binding to salivary mucins and resistance to antibiotics were significantly associated with epidemic behavior. Antibiogram typing showed clustering of predominantly A baumannii strains within one group, and these strains were significantly more resistant to antibiotics than sporadic strains. AFLP genotyping revealed a great heterogeneity among the different European Acinetobacter strains. Cluster analysis of AFLP fingerprints showed several small clusters of different A baumannii outbreak strains. AFLP genotyping could not identify a common epidemic marker within the strains studied.
Antibiogram typing can be used in routine clinical laboratories as a screening method to recognize potentially epidemic A baumannii strains. Several other factors were found, both in different outbreaks as well as in sporadic Acinetobacter isolates. These characteristics were unable to predict epidemic behavior and therefore cannot be used as discriminative epidemic markers. AFLP genotyping demonstrated no common clonal origin of European epidemic A baumannii strains. This indicates that any clinical A baumannii isolate with resistance to multiple antibiotics can be a potential nosocomial outbreak strain.
To determine the prevalence and determinants of fecal carriage of vancomycin-resistant enterococci (VRE) in intensive care unit (ICU), hematology-oncology, and hemodialysis patients in The Netherlands.
Descriptive, multicenter study, with yearly 1-week point-prevalence assessments between 1995 and 1998.
All patients hospitalized on the testing days in ICUs and hematology-oncology wards in nine hospitals in The Netherlands were included.
Rectal swabs obtained from 1,112 patients were screened for enterococci in a selective broth and subcultured on selective media with and without 6 mg/L vancomycin. Resistance genotypes were determined by polymerase chain reaction. Further characterization of VRE strains was done by pulsed-field gel electrophoresis (PFGE). We studied possible determinants of VRE colonization with a logistic regression analysis model. Determinants analyzed included gender, age, and log-transformed length of prior hospital stay.
The results showed that 614 (55%) of 1,112 patients were colonized with vancomycin-sensitive enterococci, and 15 (1.4%) of 1,112 carried VRE. No increase in VRE colonization was observed from 1995 to 1998. Eleven strains were identified as Enterococcus faecium and four as Enterococcus faecalis. All E faecium and one E faecalis carried the vanA gene; the other E faecalis strains harbored the vanB gene. PFGE revealed that three vanB VRE isolated from patients hospitalized in one single ICU were related, suggesting nosocomial transmission. Though higher age seemed associated with VRE colonization, exclusion of patients with the nosocomial strain from the regression analysis decreased this relation to nonsignificant. Duration of hospital stay was not associated with VRE colonization.
VRE colonization in Dutch hospitals is an infrequent phenomenon. Although nosocomial spread occurs, most observed cases were unrelated, which suggests the possibility of VRE acquisition from outside the hospital. Prolonged hospital stay, age, and gender proved unrelated to VRE colonization.
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