RESUMO
PURPOSE: According to the WHO vancomycin-resistant Enterococcus faecium (VRE) belongs to the microorganisms for which new antibiotics are urgently needed. Depending on the type of vancomycin resistance vanA gene VRE is differentiated from vanB VRE and other types. In this retrospective analysis the results of VRE surveillance performed at a German tertiary hospital with approximately 1,200 beds between 2013 and 2017 are shown. PATIENTS AND METHODS: Rectal screening swabs were taken at admission and once per week on the early rehabilitation ward of Ingolstadt Hospital (ERWIN) but not at other wards. The number of VRE colonized patients was evaluated by using appropriate computer software (LabCentre, Hybase). The Hybase program was also used to find out the number of Saccharomyces boulardii and multi-susceptible Escherichia coli Nissle in blood cultures of patients at ERWIN. The mechanism of vancomycin resistance was examined by PCR and clonality of VRE strains was analyzed by pulsed-field gel electrophoresis. RESULTS: Between 2013 and 2015 the number of VRE increased from 30 to 78 per year whereas in 2016 and 2017 the number declined to 51. Systematic analysis of the laboratory data revealed that this increase was driven by oligoclonal transmission of vanB VRE on ERWIN until August 2016 despite performing intensified infection control measures. However, afterward the number of VRE decreased at ERWIN and subsequently at the other wards. While searching for the reason behind this beneficial development we noticed that at ERWIN, patients treated with antibiotics received two probiotic medications simultaneously (S. boulardii, E. coli Nissle) for the duration of the antibiotic therapy plus an additional 2 days. There was no indication of side effects caused by these microorganisms, particularly no infections. CONCLUSION: Application of S. boulardii and E. coli Nissle was safe and associated with reduced transmission of VRE from patient to patient at ERWIN. Therefore, in our setting, probiotic treatment of patients receiving antibiotics contributed to the increase of patients' safety.
RESUMO
PURPOSE: In January 2015, we noticed by rectal swab analyses that seven of 23 patients at an early rehabilitation ward had been colonized with carbapenem-resistant Klebsiella pneumoniae (CKP). Here, we describe risk factors for CKP acquisition. METHODS: In the present study, the outbreak is described and risk factors for CKP acquisition are examined, e.g., antibiotic treatment. Microbiological analyses including corresponding results were examined to study when colonization with CKP occurred and whether patients had suffered from diarrhea. To examine whether spread of bacteria was clonal, multi-locus sequence typing as well as Xbal macrorestriction and pulsed-field gel electrophoresis was performed. The presence of carbapenmase was examined by PCR analysis. Through univariate analysis of risk factors in the small study sample, the role of antibiotic consumption, isolation procedures, patient's age, gender, and Barthel index on colonization was elucidated. RESULTS: Clonal spread of the novel sequence type (ST)2255 was identified. Additionally, one patient was colonized with Escherichia coli and Serratia marcescens, both resistant to carbapenems, while a further patient carried another carbapenem-resistant E. coli strain. In all isolates, carbapenemase gene bla OXA-48 was found to be located on a conjugative plasmid (60 kb), suggesting in vivo transmission from CKP to E. coli and S. marcescens. Univariate tests indicated that antibiotic treatment was the only risk factor showing a significant association with being colonized by CKP. In addition, the likelihood of diarrhea appeared to be higher in this group. Antibiotic treatment was associated with CKP colonization, whereas patients´ age, gender, Barthel index at admission, and residence with a CKP-colonized roommate were not. Diarrhea also seemed to support to distribution of CKP. CONCLUSIONS: In this small outbreak, antibiotic treatment seemed to be the predominant risk factor for monoclonal transmission of bla OXA-48 positive CKP.
