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The prevalence of patients colonized with extended-spectrum beta-lactamase (ESBL)-producing bacteria increases, especially in long-term-care facilities (LTCFs). Identification of ESBL carriers at hospital admission is relevant for infection control measures and antibiotic therapy for nosocomial infections. We aimed to develop a prediction rule for ESBL carriage at hospital admission for patients admitted from home and LTCFs, and to quantify incidences of nosocomial infections caused by ESBL-producing bacteria. The ESBL-carrier status was determined of patients admitted from LTCFs and from home settings in four hospitals in the Netherlands using perianal swabs obtained within 48 hours of admission. Risk factors for ESBL carriage were assessed. Infections caused by ESBL-producing bacteria were identified retrospectively. Among 1351 patients, 111 (8.2%) were ESBL carriers at admission: 50/579 (8.6%) admitted from LTCFs and 61/772 (7.9%) from home settings (p 0.63). Previous ESBL carriage and previous hospital admission were risk factors for ESBL carriage in multivariable analysis. The area under the curve of the receiver operating characteristic curve of the model was 0.64 (95% CI 0.58-0.71). Presence of ≥1 risk factor (n = 803; 59%) had sensitivity of 72%. Incidences of nosocomial infections caused by ESBL-producing bacteria were 45.5/10,000 and 2.1/10,000 admission days for ESBL carriers and non-carriers, respectively (p <0.05). In conclusion, prevalence of ESBL carriage at hospital admission was 8.2%, and was comparable among patients admitted from LTCF and home. A clinically useful prediction rule for ESBL carriage at admission could not be developed. The absolute incidence of nosocomial infections by ESBL-producing bacteria was low, but higher among patients carrying ESBL-producing bacteria at the time of hospital admission., (Copyright © 2014 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved.)

An increase in the number of outbreaks of Acinetobacter infection was notified in The Netherlands during 1999-2001. The present study compared the outbreaks at the species and strain levels, and analysed the epidemiology and control measures at the different locations. For each institute, three representative isolates from three patients were identified to the species and strain levels by genotyping methods. A questionnaire investigated the impact of the outbreak, the control measures that were taken, and the possible effects of the measures. Seven outbreaks were associated with Acinetobacter baumannii (three outbreaks with a strain designated strain A, two outbreaks with a strain designated strain B, and one outbreak each with strains designated C and D). An additional outbreak was caused by genomic species 13TU, which is related closely to A. baumannii. Strains B and D were identified as European clones III and II, respectively. Except for two hospitals with outbreaks caused by strain A, there was no known epidemiological link between the participating hospitals. In all hospitals the outbreak occurred on one or several intensive care units, and spread to other departments was noted in two hospitals. The number of patients affected ranged from six to 66 over a period of 2-22 months. In most outbreaks, patients were the likely reservoir from which spread occurred. In all hospitals, a large panel of measures was required to bring the outbreak to an end. Extensive environmental sampling yielded numerous positive samples in most but not all hospitals.

Vancomycin-resistant enterococci (VRE) have emerged as important nosocomial pathogens, initially in the USA, but now also in Europe, where hospital outbreaks are being reported with increasing frequency, although the incidence of VRE infections remains extremely low in most European countries. The recently demonstrated in-human transmission of vancomycin resistance from VRE to methicillin-resistant Staphylococcus aureus (MRSA) in two American patients underscores the potential danger of a coexisting reservoir of both pathogens. As MRSA is already endemic in many European hospital settings, prevention of endemicity with VRE seems relevant, but should be balanced against the costs associated with the implementation of effective strategies. The presence of a large community reservoir of VRE in Europe could hamper the feasibility of infection control strategies. Although the prevalence of colonisation amongst healthy subjects has apparently decreased after the ban on avoparcin use in the agricultural industry, a large proportion of admitted patients are still potential sources of VRE transmission. With no risk profile available to identify these carriers, effective screening, followed by barrier precautions for carriers, seems to be impossible. Recent studies, however, have suggested that hospital outbreaks are almost exclusively caused by specific genogroups of VRE that can be characterised phenotypically and genotypically (e.g., co-resistance to ampicillin and the presence of the variant esp gene). Based on our own experience, we propose that VRE infection control programmes should be restricted to patients colonised with these VRE strains. If such a strain is cultured from a clinical sample, surveillance amongst contact patients is recommended and barrier precautions should be implemented in the case of documented spread.

A nationwide laboratory-based surveillance study of invasive group A streptococcal (GAS) infections was conducted in The Netherlands from May 1994 until December 2003 (average population during this period was 15 729 704). Microbiologically invasive isolates were obtained from 1504 patients, with most (70%) isolates cultured from blood. There was a clear seasonal pattern in invasive streptococcal infections, with an estimated annual incidence that peaked in 1996 (4.0 cases/100 000 individuals/year) and was at its lowest in 1999 (2.0 cases/100 000 individuals/year). Twenty-eight different M-types were identified, of which the most frequent were M1 (339/1504, 23%), M3 (187/1504, 12%), M89 (174/1504, 12%), M28 (164/1504, 11%), M12 (109/1504, 7%) and M6 (55/1504, 4%). There was a high degree of variation in the relative annual contributions of the predominant M-types, but variations in M1 and M3 combined correlated with overall changes in the annual incidence. The contribution of the patient group aged > or = 56 years to all cases of invasive GAS disease increased during the study period, whereas that of the group aged 0-20 years decreased. A peak in the incidence of invasive GAS disease among the patient group aged 30-34 years did not vary during the study period, indicating that the high incidence of invasive GAS disease in this age group was age-specific rather than cohort-related.