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Near absence of VRE but high carriage rates of quinolone-resistant ampicillin-resistant enterococci among hospitalized patients and non-hospitalized individuals in Sweden
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
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1999 (English)In: Journal of Clinical Microbiology, ISSN 0095-1137, E-ISSN 1098-660X, Vol. 37, no 11, 3509-3513 p.Article in journal (Refereed) Published
Abstract [en]

Rates of colonization with enterococci with acquired resistance to vancomycin (vancomycin-resistant enterococci [VRE]) and ampicillin (ampicillin-resistant enterococci [ARE]) were determined by using fecal samples from 670 nonhospitalized individuals and 841 patients in 27 major hospitals. Of the hospitalized patients, 181 (21.5%) were carriers of ARE and 9 (1.1%) were carriers of VRE. In univariate analyses, length of hospital stay (odds ratio [OR], 4.6; 95% confidence interval [CI], 2.5 to 8.9) and antimicrobial therapy (OR, 4.7; 95% CI, 3.3 to 6.7) were associated with ARE colonization, as were prior treatment with penicillins (OR, 3.1; 95% CI, 1.8 to 5. 5), cephalosporins (OR, 2.9; 95% CI, 1.7 to 5.0), or quinolones (OR, 2.7; 95% CI, 1.5 to 4.7). In logistic regression analysis, antimicrobial therapy for at least 5 days was independently associated with ARE carriage (adjusted OR, 3.8; 95% CI, 2.6 to 5.4). Over 90% of the ARE isolates were fluoroquinolone resistant, whereas 14% of the ampicillin-susceptible Enterococcus faecium isolates were fluoroquinolone resistant. ARE carriage rates correlated with the use of fluoroquinolones (P = 0.04) but not with the use of ampicillin (P = 0.68) or cephalosporins (P = 0.40). All nine VRE isolates were E. faecium vanB and were found in one hospital. Seven of these isolates were related according to their types as determined by pulsed-field gel electrophoresis. Among the nonhospitalized individuals, the ARE carriage rate was lower (6%; P < 0.05), and only one person, who had recently returned from Africa, harbored VRE (E. faecium vanA). The absence of VRE colonization in nonhospitalized individuals reflects an epidemiological situation in Sweden radically different from that in countries in continental Europe where glycopeptides have been widely used for nonmedical purposes.

Place, publisher, year, edition, pages
1999. Vol. 37, no 11, 3509-3513 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-90180OAI: oai:DiVA.org:uu-90180DiVA: diva2:162444
Available from: 2003-03-28 Created: 2003-03-28 Last updated: 2017-12-14Bibliographically approved
In thesis
1. Epidemiology of Enterococci with Acquired Resistance to Antibiotics in Sweden: Special emphasis on Ampicillin and Vancomycin
Open this publication in new window or tab >>Epidemiology of Enterococci with Acquired Resistance to Antibiotics in Sweden: Special emphasis on Ampicillin and Vancomycin
2003 (English)Doctoral thesis, comprehensive summary (Other academic)
Alternative title[sv]
Enterokocker med förvärvad resistens mot ampicillin och vancomycin i Sverige
Abstract [en]

The first hospital outbreak of vancomycin-resistant enterococci (VRE) and carriage rates of VRE and ampicillin-resistant enterococci (ARE) in Sweden were investigated. Clonal relationships and mutations in fluoroquinolone resistance determining regions among ARE collected nation-wide were studied. Risk factors for ARE infection, shedding of ARE and the presence of the virulence gene esp in ARE isolates and patients on a hematology unit and other units at Uppsala University Hospital were further investigated.

The first Swedish hospital VRE outbreak was due to clonal spread of E. faecium, vanA. The nation wide carriage rates of ARE and VRE were 21.5% / 1% and 6% / 0%, among hospitalized patients and non-hospitalized individuals respectively. All ARE and VRE were E. faecium and >90% resistant to ciprofloxacin. All VRE carried vanB. Carriage of ARE was independently associated with >5 days of antibiotic treatment. Phenotypic and genetic typing showed a significantly higher homogeneity among ARE compared to matched ASE E. faecium isolates. Mutations conferring high-level ciprofloxacin resistance were found only in ARE. Risk factors for ARE infection included long duration of hospital stay and exposure to antibiotics. Skin carriage was associated with ARE shedding. ARE bacteremia was independently associated with prior ARE colonization and hematopoietic stem cell transplantation. Death was more common in ARE septicemia cases compared to controls. Esp was significantly more common in ARE surveillance compared to ARE blood isolates from patients on the hematology ward.

In conclusion, VRE were rare but clonally related multi-resistant ARE E. faecium were highly prevalent in Swedish hospitals. Spread of ARE in hospitals during the 1990s is suggested to be the main explanation for the emergence of ARE in Sweden. Spread was facilitated by use of antibiotics and probably by the presence of virulence genes in E. faecium isolates.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2003. 80 p.
Series
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1237
Keyword
Communicable diseases, Antimicrobial resistance, enterococci, epidemiology in Sweden, intra-hospital spread, shedding, risk-factors, infection, colonization, virulence factors, ARE, VRE, Php, PFGE, esp, gyrA, parC, Infektionssjukdomar
National Category
Infectious Medicine
Research subject
Infectious Diseases
Identifiers
urn:nbn:se:uu:diva-3344 (URN)91-554-5574-3 (ISBN)
Public defence
2003-04-24, Avdelningen för Klinisk Mikrobiologi, Hörsalen, Dag hammarskölds väg 17, Uppsala, 09:15
Opponent
Available from: 2003-03-28 Created: 2003-03-28Bibliographically approved

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