This retrospective cohort study analysed Enterococcus isolates collected at a tertiary hospital in Sohar, Oman, over six years (2020–2025). The dataset comprised 1,626 non-duplicate Enterococcus isolates from 1,018 patients. The investigation aimed to characterise the epidemiology of vancomycin-resistant enterococci (VRE), evaluate antimicrobial resistance trends over time, and identify predictors of in-hospital mortality among affected patients. The authors explicitly considered the impact of changing surveillance practices and distinguished colonisation from clinical infection.
VRE was defined using a composite approach: either a vancomycin-resistant result on laboratory susceptibility testing or a laboratory VRE flag. Agreement between the susceptibility-based and flag-based routes was assessed. To control for surveillance artefacts, trend analyses were repeated using a phenotype-only definition restricted to clinical (non-screening) specimens and excluding intrinsically vancomycin-resistant vanC species. Active rectal screening was introduced only in 2024 and was incorporated into the analyses to understand its effect on apparent VRE rates.
Using the composite definition, 395 of 1,626 isolates (24.3%) met VRE criteria. The composite VRE proportion rose from 1.8% in 2020 to 47.4% in 2025 (Cochran–Armitage Z = 16.56, p < 0.001). However, only 196 of these 395 isolates (49.6%) were explicitly vancomycin-resistant on susceptibility testing; 199 (50.4%) were flagged as VRE without a vancomycin susceptibility result, and an additional 66 isolates were vancomycin-resistant but had not been flagged.
Active rectal screening, implemented in 2024, contributed 186 of the 395 composite VRE isolates (47.1%). When analyses were restricted to tested clinical non-vanC isolates, the vancomycin-resistant proportion rose from 0.5% to 21.8% and then plateaued after 2023 (21.8% in 2023, 20.7% in 2024, 21.8% in 2025; Z = 8.32, p < 0.001). The authors emphasise that much of the post-2023 increase in composite VRE is attributable to the new active screening program and to inclusion of intrinsically resistant vanC species.
Among 193 VRE-positive patients described in the abstract, Enterococcus faecium predominated, accounting for 141 patients (73.1%). In terms of clinical significance versus colonisation, 96 of 193 VRE-positive patients (49.7%) were detected by rectal screening alone, indicating colonisation without a clinical specimen. Thirty patients (15.5%) carried vanC species, which are intrinsically resistant to vancomycin. Excluding these, 67 patients (34.7%) had acquired resistance detected in a clinical specimen, and 29 patients (15.0% of VRE-positive patients) had bacteraemia.
According to the abstract, last-line agents retained strong activity against the VRE isolates analysed. Linezolid had a non-susceptibility proportion of 0.9%, and tigecycline had 1.9% non-susceptibility, indicating near-complete activity among tested isolates. The abstract does not provide further breakdowns of susceptibility for other agents or species-specific resistance percentages beyond these values and the vancomycin results described above.
A subset of patients underwent chart review to extract comorbidity, biomarker, and outcome data. The chart-reviewed cohort comprised 213 patients, of whom 163 were microbiologically confirmed as VRE-positive. Among the confirmed patients with available outcome data, in-hospital mortality was 29.5% (44 of 149). The study evaluated routine admission biomarkers, including serum albumin, as potential prognostic factors for mortality.
Mortality models were fitted on complete cases and after multiple imputation by chained equations (m = 20), with Rubin’s rules applied. On complete-case analysis, low serum albumin was an independent predictor of in-hospital mortality (adjusted OR 0.86 per g/L, 95% CI 0.77–0.95, p = 0.004; n = 82, 24 events). After multiple imputation, the association was attenuated and no longer reached conventional statistical significance (OR 0.94, 95% CI 0.87–1.00, p = 0.066).
Admission to the intensive care unit emerged as the most robust predictor of in-hospital mortality in imputed models (OR 3.14, 95% CI 1.36–7.24, p = 0.007). Model performance was modest and unstable: cross-validated discrimination (logistic AUC) averaged 0.775 with a standard deviation of 0.128 and a wide fold range (0.345–1.000). Calibration slope was 0.81. Accuracy at a 0.5 probability threshold was 73.8%, which only marginally exceeded a naive strategy of predicting survival for every patient (70.7%). The authors therefore caution that these prognostic models, based on routinely available admission biomarkers, are insufficiently discriminating and calibrated for clinical use and should be considered hypothesis-generating.
The study documents a substantial increase in composite VRE detection at this centre between 2020 and 2025, concentrated in E. faecium and with preserved activity of key last-line agents (linezolid and tigecycline). However, the authors stress that the marked rise in composite VRE after 2023 largely reflects the introduction of active rectal screening and the inclusion of intrinsically vancomycin-resistant vanC species; nearly half of VRE-positive patients were colonised and identified by screening alone rather than having clinical infection.
Prognostic modelling using routine admission biomarkers yielded limited and unstable predictive performance; intensive-care admission was the most consistent mortality predictor. The abstract notes that these findings should guide interpretation of local surveillance data and inform infection prevention and control practices, while recognising the limits of routine biomarkers for prognostication. Detailed methodological information, full susceptibility tables beyond the summary figures provided, and additional subgroup analyses are reported in the full article; if further specifics are required they were not fully reported in the abstract.