The Increasing Issue of Vancomycin-Resistant Enterococci and the Bacteriocin Solution
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The Increasing Issue of Vancomycin-Resistant Enterococci and the Bacteriocin Solution Ingvild S. Reinseth 1 & Kirill V. Ovchinnikov 1 & Hanne H. Tønnesen 2 & Harald Carlsen 1 & Dzung B. Diep 1
# Springer Science+Business Media, LLC, part of Springer Nature 2019
Abstract Enterococci are commensals of human and other animals’ gastrointestinal tracts. Only making up a small part of the microbiota, they have not played a significant role in research, until the 1980s. Although the exact year is variable according to different geographical areas, this was the decade when vancomycin-resistant enterococci (VRE) were discovered and since then their role as causative agents of human infections has increased. Enterococcus faecium is on the WHO’s list of “bacteria for which new antibiotics are urgently needed,” and with no new antibiotics in development, the situation is desperate. In this review, different aspects of VRE are outlined, including the mortality caused by VRE, antibiotic resistance profiles, animal-modeling efforts, and virulence. In addition, the limitations of current antibiotic treatments for VRE and prospective new treatments, such as bacteriocins, are reviewed. Keywords Enterococcus faecium . Enterococcus faecalis . VRE . Antibiotic resistance . Virulence . Bacteriocin
Introduction Vancomycin-resistant enterococci (VRE) emerged from the commensal enterococci in the 1980s and have developed from “generally regarded as safe” bacteria to significant nosocomial pathogens [2, 3, 21, 23, 45, 53, 68, 93, 109]. The World Health Organization (WHO) still considers VRE a pathogen with high priority on its global priority list [116]. VRE exist in the gastrointestinal tract of healthy humans and other animals, but may colonize and disseminate if conditions are suitable [1, 15, 57, 71, 97, 111]. Suitable conditions for colonization include treatment with anti-anaerobic antibiotics including vancomycin, which remove colonization resistance and provide a vacant niche for the VRE to invade [15, 84, 116]. In this context, colonization is the establishment of vancomycinresistant enterococcal populations in the gastrointestinal
* Dzung B. Diep [email protected] 1
Department of Chemistry, Biotechnology and Food Science, Norwegian University of Life Sciences, P.O. Box 5003, 1432 Ås, Norway
2
Section of Pharmaceutics and Social Pharmacy, Department of Pharmacy, University of Oslo, P.O. Box 1068 Blindern, 0316 Oslo, Norway
tract due to displacement of the non-resistant enterococcal counterparts. Dissemination is the spread from the gastrointestinal tract and thereby start of an infection. Enterococci are innately resistant to many classes of antibiotics, but when they acquire additional resistance through, for example, mobile genetic elements, they become increasingly difficult to treat [54, 67, 101]. The factors that contribute to virulence in VRE are not completely characterized, but factors such as enterococcal surface protein, aggregation substance, gelatinase, and collagen adhesin molecule Acm have been implicated in
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