Vancomycin-resistant Enterococcus faecium (VREfm) is an opportunistic pathogen among the highest global priorities regarding public and environmental health. Following One Health approach, we determined for the first time the antibiotic resistance and virulence genes, and sequence types (STs) affiliation of VREfm recovered simultaneously from marine beach waters, submarine outfall of a wastewater treatment plant and an offshore discharge of untreated sewage, and compared them with the surveillance VREfm from regional university hospital in Croatia to assess the hazard of their transmission and routes of introduction into the natural environment. Importantly, VREfm recovered from wastewater, coastal bathing waters and hospital shared similar virulence, multidrug resistance, and ST profiles, posing a major public health threat. All isolates carried the vanA gene, while one clinical isolate also possessed the vanC2/C3 gene. The hospital strains largely carried the aminoglycoside-resistance genes aac(6\')-Ie-aph(2″)-Ia, and aph(2″)-Ib and aph(2″)-Id, which were also predominant in the environmental isolates. The hyl gene was the most prevalent virulence gene. The isolates belonged to 10 STs of the clonal complex CC17, a major epidemic lineage associated with hospital infections and outbreaks, with ST117 and ST889 common to waterborne and hospital isolates, pointing to their sewage-driven dissemination. To gain better insight into the diversity of accompanying taxons in the surveyed water matrices, microbiome taxonomic profiling was carried out using Illumina-based 16S rDNA sequencing and their resistome features predicted using the PICRUSt2 bioinformatics tool. An additional 60 pathogenic bacterial genera were identified, among which Arcobacter, Acinetobacter, Escherichia-Shigella, Bacteroides and Pseudomonas were the most abundant and associated with a plethora of antibiotic resistance genes and modules, providing further evidence of the hazardous effects of wastewater discharges, including the treated ones, on the natural aquatic environment that should be adequately addressed from a sanitary and technological perspective.

This study investigated the prevalence and antimicrobial susceptibility of enterococci isolated from dogs and cats with urinary tract infections in northwestern Croatia. During this study, the laboratory received 787 urine samples, 651 from dogs and 136 from cats. A total of 260 urine samples (211 from dogs and 49 from cats) were bacteriologically positive. Of these, 29 isolates belonged to Enterococcus spp.; 22 from dogs and seven from cats. Enterococci isolates were identified by PCR method, 12 of which were Enterococcus faecium and 17 were Enterococcus faecalis species. In dogs, 16 E. faecalis and six E. faecium strains were identified, whereas in cats, six E. faecium and only one E. faecalis strain were identified. Antimicrobial susceptibility was determined by the Kirby-Bauer disk diffusion method for nine antimicrobials: penicillin, ampicillin, vancomycin, nitrofurantoin, rifampicin, tetracycline, chloramphenicol, enrofloxacin, ciprofloxacin. The isolates were tested for high-level resistance to streptomycin and gentamicin. The highest resistance of Enterococcus spp. was observed to rifampicin (86%) and enrofloxacin (83%), followed by tetracycline and ciprofloxacin (69%). Resistance to vancomycin was 28%, and the lowest resistance was to chloramphenicol (17%). Multidrug resistance was found in 76% of enterococci isolates. High-level streptomycin resistance was detected in 17% and high-level gentamicin resistance in 10% of the isolated enterococci. When comparing species susceptibility, E. faecium isolates were significantly more resistant to penicillin, ampicillin, nitrofurantoin, and ciprofloxacin (p < 0.05). Eleven E. faecium isolates (92%) and 12 E. faecalis isolates (76%) were multidrug resistant.

High-level aminoglycoside, ampicillin and vancomycin resistance and virulence genes among enterococcal isolates collected from healthy middle-school children in Ardabil, Iran, during 2016 were investigated.
Totally, 305 faecal specimens were collected. Isolates underwent antimicrobial susceptibility testing, virulence gene detection and molecular typing.
Totally, 409 enterococcal isolates were collected, comprising Enterococcus faecium (235; 57.5%), Enterococcus faecalis (56; 13.7%) and other Enterococcus spp. (118; 28.9%). Overall, 71 (17.4%), 11 (2.7%) and 10 (2.4%) isolates were identified as high-level streptomycin-resistant (HLSR), high-level gentamicin-resistant (HLGR) and ampicillin-resistant (AR), respectively. Among HLSR isolates, 40 (56.3%), 5 (7.0%) and 26 (36.6%) were E. faecium, E. faecalis and other Enterococcus spp., respectively. Among HLGR isolates 4 (36.4%) and 7 (63.6%) and among AR isolates 7 (70.0%) and 3 (30.0%) were E. faecium and other Enterococcus spp., respectively. Accordingly, 21.6%, 3.6% and 3.3% of subjects were colonised with HLSR, HLGR and AR Enterococcus spp. Carriage of HLGR, HLSR and AR isolates was associated with prior antibiotic consumption (P≤0.05). Additionally, male sex and antacid consumption were associated with AR enterococcal carriage. Moreover, 69 (97.2%), 10 (90.9%) and 9 (90.0%) of HLSR, HLGR and AR isolates were multidrug-resistant, respectively. No vancomycin-resistant enterococci were detected. ERIC-PCR revealed high genetic diversity among isolates. gelE and asa1 were major virulence genes both in E. faecalis and E. faecium. Presence of gelE was associated with HLSR and HLGR phenotypes (P≤0.05).
Community intestinal carriage of HLSR enterococci was high; however, carriage of HLGR and AR enterococci was low.

The combination of ampicillin plus ceftaroline has been suggested to be more reliably synergistic against Enterococcus faecalis than ampicillin plus ceftriaxone using time-kill methods. The purpose of this study was to determine if this trend persists in a two-compartment model of simulated endocardial vegetations (SEV) using clinically relevant pharmacokinetic exposures of these antimicrobials. Three clinically derived E. faecalis strains were included in the study. The MICs of study antimicrobials were determined by broth microdilution. Simulations of ampicillin (2 g every 4 h [q4h]; maximum concentration of drug in serum [Cmax], 72.4 mg/liter; half-life [t1/2], 1.9 h), ceftaroline-fosamil (600 mg q8h; Cmax, 21.3 mg/liter; t1/2, 2.66 h), ceftriaxone (Cmax, 257 mg/liter; t1/2, 8 h), and ampicillin plus ceftaroline and ampicillin plus ceftriaxone were evaluated against 3 strains of E. faecalis isolated from patients with endocarditis in an in vitro PK/PD SEV model over 72 h, with a starting inoculum of ∼9 log10 CFU/g. All strains were susceptible to ampicillin (MIC, ≤2 mg/liter). Ceftaroline MICs varied from 2 to 16 mg/liter. All strains had ceftriaxone MICs of 256 mg/liter. W04 and W151 exhibited high-level aminoglycoside resistance but W07 did not. Ampicillin plus ceftaroline resulted in significantly greater reductions in CFU per gram by 72 h than ampicillin for all strains (P ≤ 0.025) than ampicillin plus ceftriaxone for W04 (P = 0.019) but not W07 or W151 (P ≥ 0.15). A 4-fold increase in ampicillin MIC was observed for W07 at 72 h, but this was prevented by the addition of ceftaroline or ceftriaxone. The combination of ampicillin plus ceftaroline appears to be at least as efficacious as ampicillin plus ceftriaxone and may lead to improved activity against some strains of E. faecalis, but these differences may be small and the clinical significance should not be overestimated.

The objective of this study was to investigate the genetic basis of high level aminoglycoside resistance in Acinetobacter baumannii clinical isolates from Beijing, China. 173 A. baumannii clinical isolates from hospitals in Beijing from 2006 to 2009 were first subjected to high level aminoglycoside resistance (HLAR, MIC to gentamicin and amikacin>512 µg/mL) phenotype selection by broth microdilution method. The strains were then subjected to genetic basis analysis by PCR detection of the aminoglycoside modifying enzyme genes (aac(3)-I, aac(3)-IIc, aac(6\')-Ib, aac(6\')-II, aph(4)-Ia, aph(3\')-I, aph(3\')-IIb, aph(3\')-IIIa, aph(3\')-VIa, aph(2″)-Ib, aph(2″)-Ic, aph(2″)-Id, ant(2″)-Ia, ant(3″)-I and ant(4\')-Ia) and the 16S rRNA methylase genes (armA, rmtB and rmtC). Correlation analysis between the presence of aminoglycoside resistance gene and HLAR phenotype were performed by SPSS. Totally 102 (58.96%) HLAR isolates were selected. The HLAR rates for year 2006, 2007, 2008 and 2009 were 52.63%, 65.22%, 51.11% and 70.83%, respectively. Five modifying enzyme genes (aac(3)-I, detection rate of 65.69%; aac(6\')-Ib, detection rate of 45.10%; aph(3\')-I, detection rate of 47.06%; aph(3\')-IIb, detection rate of 0.98%; ant(3″)-I, detection rate of 95.10%) and one methylase gene (armA, detection rate of 98.04%) were detected in the 102 A. baumannii with aac(3)-I+aac(6\')-Ib+ant(3″)-I+armA (detection rate of 25.49%), aac(3)-I+aph(3\')-I+ant(3″)-I+armA (detection rate of 21.57%) and ant(3″)-I+armA (detection rate of 12.75%) being the most prevalent gene profiles. The values of chi-square tests showed correlation of armA, ant(3″)-I, aac(3)-I, aph(3\')-I and aac(6\')-Ib with HLAR. armA had significant correlation (contingency coefficient 0.685) and good contingency with HLAR (kappa 0.940). The high rates of HLAR may cause a serious problem for combination therapy of aminoglycoside with β-lactams against A. baumannii infections. As armA was reported to be able to cause high level aminoglycoside resistance to most of the clinical important aminoglycosides (gentamicin, amikacin, tobramycin, etc), the function of aminoglycoside modifying enzyme gene(s) in A. baumannii carrying armA deserves further investigation.

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In the past two decades the members of the genus Enterococcus have emerged as important nosocomial pathogens worldwide. In the present study, we evaluated the antimicrobial resistance and genotypic characteristics of 203 Enterococcus spp. recovered from different clinical sources from two hospitals in Porto Alegre, Rio Grande do Sul, Brazil. The species were identified by conventional biochemical tests and by an automated system. The genetic diversity of E. faecalis presenting high-level aminoglycoside resistance (HLAR) was assessed by pulsed-field gel electrophoresis of chromosomal DNA after SmaI digestion. The E. faecalis was the most frequent specie (93.6%), followed by E. faecium (4.4%). The antimicrobial resistance profile was: 2.5% to ampicillin, 0.5% to vancomycin, 0.5% teicoplanin, 33% to chloramphenicol, 2% to nitrofurantoin, 66.1% to erythromycin, 66.5% to tetracycline, 24.6% to rifampicin, 30% to ciprofloxacin and 87.2% to quinupristin-dalfopristin. A total of 10.3% of the isolates proved to be HLAR to both gentamicin and streptomycin (HLR-ST/GE), with 23.6% resistant only to gentamicin (HLR-GE) and 37.4% only to streptomycin (HLR-ST). One predominant clonal group was found among E. faecalis HLR-GE/ST. The prevalence of resistance among beta-lactam antibiotics and glycopeptides was very low. However, in this study there was an increased number of HLR Enterococcus which may be spreading intra and inter-hospital.

In a developing country like India, where the patients have to bear the cost of their healthcare, the microbiological culture and the sensitivity testing of each and every infection is not feasible. Moreover, there are lacunae in the data storage, management and the sharing of knowledge with respect to the microorganisms which are prevalent in the local geographical area and with respect to the antibiotics which are effective against them. Thus, an empirical therapy for treating infections is imperative in such a setting. The beta lactam antibiotics have been widely used for the empirical treatment of infections since the the discovery of penicillin. Many generations of beta lactams have been launched with, the claims of a higher sensitivity and less resistance, but their sensitivity has drastically decreased over time. Thus, the preference for beta lactams, especially the cephalosporins, as an empirical therapy, among the prescribers was justified initially, but the current sensitivity patterns do not support their empirical use in hospital and community acquired infections. There is a need for increasing the awareness and the attitudinal change among the prescribers, screening of the antibiotic prescriptions, the strict implementation of antibiotic policies in hospital settings, restricting the hospital supplies and avoiding the prescriptions of beta lactams, a regular census of the local sensitivity patterns to formulate and update the antibiotic policies, upgradation of the laboratory facilities for a better and faster detection of the isolates, proper collection, analyses and sharing of the data and the encouragement of the research and development of newer antibiotics with novel mechanisms of action.