Increasing resistance to beta-lactam antibiotics among clinical isolates of Enterococcus faecium: a 22-year review at one institution

Abstract

To identify any change in the antibiotic resistance of Enterococcus faecium, we examined the antibiotic susceptibilities of clinical strains (n = 84) isolated at one institution during the 22 years since 1968. A significant increase in resistance to penicillin was observed during the study period: the MICs of penicillin for 50 and 90% of isolates tested were 16 and 64 ,ug/ml, respectively, from 1969 to 1988 (n = 48; geometric mean MIC, 14 yLg/ml), whereas they were 256 and 512'Ig/ml, respectively, from 1989 to 1990 (n = 36; geometric mean MIC, 123 tig/ml) (P < 0.001). A comparable increase in resistance to ampicillin was also noted (P < 0.001). No straing produced detectable 3-lactamase. In contrast, susceptibilities to vancomycin, teicoplanin, and ciprofloxacin remained stable. High-level resistance to gentamicin was observed in none of 48 isolates from 1969 to 1988, but was present in 22 of 36 strains (61%) from 1989to 1990 (P < 0.001) and was significantly associated with resistance (MIC, .128 ,ug/ml) to penicillin (P < 0.001). 'To assess the potential evolution of antibiotic resistance in this species, clinical isolates (n = 24) were compared with strains isolated in 1968 from a human population in the Solomon Islands that was never exposed to antibiotics. Solomon Island isolates were significantly more susceptible than all clinical strains to penicillin, ampicillin, and vancomycin (P < 0.001 for each), but they exhibited no differences in susceptibility to teicoplanin or ciprofioxacin. The penicillip-binding affinit of penicillin-binding protein 5 (PBP 5) in penicillin-resistant clinical strains (MIC, 512 ILg/ml) was notably lower than that in strains with more typical susceptibilities, suggesting an alteration in this PBP as a possible mechanism for increased penicillin resistance. Solomon Island strains most susceptible to penicillin demonstrated a prominent PBP 5* and the absence of PBP 5. These changes in the antibiotic resistance of E. faecium emphasize the importance of identifying this species in patients with serious enterococcal infections and the necessity of assessing its susceptibility to both beta-lactams and aminoglycosides if effective therapy is to be identified.

Nosocomial Infections and their Surveillance in Veterinary Hospitals

“…In a study conducted in veterinary teaching hospital in Switzerland, two multiresistant E. faecium isolates with similar antibiotic resistant and PFGE profiles was recovered from two different cats with less than one month interval suggesting the persistence in hospital environment and nosocomial transmission (Boerlin et al, 2001). In the early 1980's the emergence of Hospital associated Ampicillin resistant Enterococci (ARE) in USA preceded rise of vancomycin resistance in enterococci, which happend in the 1990s, is the reason why virtually all VRE of nosocomial infections in humans are also ampicillin resistant (Grayson et al, 1991) but ARE associated with human infections remain vancomycin susceptible (Tremblay et al, 2013). The hospital associated ARE have been recovered from dogs suffering from urinary tract infections in US (Simjee et al, 2002), Denmark (Damborg et al, 2009), Korea (Kwon et al, 2012) and also from the faeces of dogs departing the intensive care unit of an American veterinary medicine teaching hospital (Ghosh et al, 2011).…”

Genetic modifications to temperate Enterococcus faecalis phage ϕEf11 that abolish the establishment of lysogeny and sensitivity to repressor, and increase host range and productivity of lytic infection

“…In terms of oral disease, E. faecalis is the most commonly isolated species from infected root canals of teeth that fail to heal following root canal therapy (Sundqvist et al, 1998;Peciuliene et al, 2000;Pinheiro et al, 2003 Complicating management of these infections is the development of resistance among many enterococcal strains against many of the available, previously effective antibiotics, including vancomycin (Havard et al, 1959;Murray & Mederski-Samaroj, 1983;Uttley et al, 1988;Grayson et al, 1991;Bonten et al, 2001;Tenover & McDonald, 2005). Although a modest number of new antibiotics, such as linezolid and daptomycin, have been developed to provide treatment alternatives in cases of infection by organisms that are resistant to all previously available antibiotics, there have been numerous reports of resistance by E. faecalis and E. faecium strains to these antibiotics as well (Eliopoulos et al, 1998;Prystowsky et al, 2001;Gonzales et al, 2001;Herrero et al, 2002;Johnson et al, 2004;Munoz-Price et al, 2005;Kanafani et al, 2007;Hidron et al, 2008;Marshall et al, 2009;Kelesidis et al, 2011;Ross et al, 2011;Ntokou et al, 2012).…”

Emergence of Clonal Complex 17 Enterococcus faecium in The Netherlands

“…Genotyping revealed that 86% of AREF isolates belonged to CC17, including four dominant MLVA types found in >3 hospitals, accounting for 64% of the AREF isolates. Infections caused by CC17 E. faecium has increased nationwide, especially in university hospitals due to the clonal spread of four MLVA types, and seems associated with acquisition of the esp gene.The emergence of vancomycin-resistant Enterococcus faecium (VREF) in the United States in the 1990s was preceded by the emergence of ampicillin-resistant Enterococcus faecium (AREF) in the 1980s (8,11,27,28). Molecular epidemiological studies of human-and animal-derived E. faecium since then, revealed the existence of a genetic lineage, labeled clonal complex 17 (CC17), associated with nosocomial E. faecium outbreaks and infections in five continents.…”

“…The emergence of vancomycin-resistant Enterococcus faecium (VREF) in the United States in the 1990s was preceded by the emergence of ampicillin-resistant Enterococcus faecium (AREF) in the 1980s (8,11,27,28). Molecular epidemiological studies of human-and animal-derived E. faecium since then, revealed the existence of a genetic lineage, labeled clonal complex 17 (CC17), associated with nosocomial E. faecium outbreaks and infections in five continents.…”