Epidemiology of Glycopeptide-Resistant Enterococci Colonizing High-Risk Patients in Hospitals in Johannesburg, Republic of South Africa

Gottberg, Anne von; Nierop, W van; Dusé, Adriano; Kassel, Merel N van; McCarthy, Kerrigan; Brink, Adrian; Meyers, Marvin J.; Smego, Raymond A.; Koornhof, H. J.

doi:10.1128/jcm.38.2.905-909.2000

Cited by 22 publications

(20 citation statements)

References 25 publications

(25 reference statements)

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“…Using classical methods, isolates of this clone were initially identified as E. avium ; however, the VITEK 2 system and the MLSA molecular approach [17] both classified the isolates unequivocally as E. raffinosus . Since E. avium has been associated more often with human infection, and has been reported to be vancomycin‐resistant more frequently than has E. raffinosus [28–33], there was a possibility of misidentification of these two species. Wilke et al .…”

Section: Discussionmentioning

confidence: 99%

Hospital outbreak of vancomycin-resistant enterococci caused by a single clone of Enterococcus raffinosus and several clones of Enterococcus faecium

Kawalec

Kędzierska

Gajda

et al. 2007

Clinical Microbiology and Infection

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A mixed outbreak caused by vancomycin-resistant Enterococcus raffinosus and Enterococcus faecium carrying the vanA gene was analysed. The outbreak occurred in a large hospital in Poland and affected 27 patients, most of whom were colonised, in three wards, including the haematology unit. The E. raffinosus isolates had a high-level multiresistant phenotype and were initially misidentified as Enterococcus avium; their unambiguous identification was provided by multilocus sequence analysis. The molecular investigation demonstrated the clonal character of the E. raffinosus outbreak and the polyclonal structure of the E. faecium isolates. All of the isolates carried the same Tn1546-like element containing an IS1251-like insertion sequence, located on a c. 50-kb conjugative plasmid. One of the E. faecium clones, found previously to be endemic in the hospital, was probably the source of the plasmid. The results of the study suggest that difficulties in identification may have led to an underestimate of the importance of E. raffinosus in vancomycin-resistant enterococci (VRE) control strategies.

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Section: Discussionmentioning

confidence: 99%

Hospital outbreak of vancomycin-resistant enterococci caused by a single clone of Enterococcus raffinosus and several clones of Enterococcus faecium

Kawalec

Kędzierska

Gajda

et al. 2007

Clinical Microbiology and Infection

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“…While to date approximately 90% of E. faecium from healthcare-associated infections in the United States are resistant to ampicillin and 80% to vancomycin, these resistance percentages are significantly lower in E. faecalis ($4% resistance to ampicillin and 7% resistance to vancomycin) (Hidron et al, 2008). Also, globally, the epidemiology of VRE is dominated by E. faecium with vancomycin-resistant E. faecium being isolated from all continents (von Gottberg et al, 2000;Padiglione et al, 2003;Lee et al, 2004;Tenover & McDonald, 2005;Camargo et al, 2006;Dahl et al, 2007;Zheng et al, 2007;Hoshuyama et al, 2008;Werner et al, 2008).…”

Section: Vancomycin Resistance: a Serious Threatmentioning

confidence: 99%

Population biology of Gram-positive pathogens: high-risk clones for dissemination of antibiotic resistance

et al. 2011

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Infections caused by multi-resistant Gram positive bacteria represent a major health burden in the community as well as in hospitalized patients. Staphylococcus aureus, Enterococcus faecalis and Enterococcus faecium are well-known pathogens of hospitalized patients, frequently linked with resistance against multiple antibiotics, compromising effective therapy. Streptococcus pneumoniae and Streptococcus pyogenes are important pathogens in the community and S. aureus has recently emerged as an important community-acquired pathogen. Population genetic studies reveal that recombination prevails as a driving force of genetic diversity in E. faecium, E. faecalis, S. pneumoniae, and S. pyogenes and thus, these species are weakly clonal. Although recombination has a relatively modest role driving the genetic variation of the core genome of S. aureus, the horizontal acquistion of resistance and virulence genes plays a key role in the emergence of new clinically relevant clones in this species. In this review we discuss the population genetics of E. faecium, E. faecalis, S. pneumoniae, S. pyogenes, and S. aureus. Knowledge of the population structure of these pathogens is not only highly relevant for (molecular) epidemiological research but also for identifying the genetic variation that underlies changes in clinical behaviour, to improve our understanding of the pathogenic behaviour of particular clones and to identify novel targets for vaccines or immunotherapy.

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“…Since the initial descriptions, VRE (predominantly the vanA phenotype) have emerged as important nosocomial pathogens worldwide [1,12–23]. The first VRE outbreaks in US hospitals often resulted from dissemination of a single strain, especially in ICUs and nephrology wards [24–26].…”

Section: Introductionmentioning

confidence: 99%

Vancomycin-resistant enterococci: consequences for therapy and infection control

Mascini

Bonten

2005

Clinical Microbiology and Infection

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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.

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Epidemiology of Glycopeptide-Resistant Enterococci Colonizing High-Risk Patients in Hospitals in Johannesburg, Republic of South Africa

Cited by 22 publications

References 25 publications

Hospital outbreak of vancomycin-resistant enterococci caused by a single clone of Enterococcus raffinosus and several clones of Enterococcus faecium

Hospital outbreak of vancomycin-resistant enterococci caused by a single clone of Enterococcus raffinosus and several clones of Enterococcus faecium

Population biology of Gram-positive pathogens: high-risk clones for dissemination of antibiotic resistance

Vancomycin-resistant enterococci: consequences for therapy and infection control

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