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• Invasive devices, antibiotics and ICU stay predispose to acquire an Enterobacter bacteremia. • Enterobacter bacteremia increased mortality in patients with comorbidities or a severe infection. • The outcome was not affected by antibiotic resistances of the isolates or the antibiotic therapy. Enterobacter is among the main etiologies of hospital-acquired infections. This study aims to identify the risk factors of acquisition and attributable mortality of Enterobacter bacteremia. Observational, case-control study for risk factors and prospective cohort for outcomes of consecutive cases with Enterobacter bacteremia. This study was conducted in five hospitals in Spain over a three-year period. Matched controls were patients with negative blood cultures and same sex, age, and hospitalization area. The study included 285 cases and 570 controls. E. cloacae was isolated in 198(68.8%) cases and E. aerogenes in 89(31.2%). Invasive procedures (hemodialysis, nasogastric tube, mechanical ventilation, surgical drainage tube) and previous antibiotics or corticosteroids were independently associated with Enterobacter bacteremia. Its attributable mortality was 7.8%(CI95%2.7–13.4%), being dissimilar according to a McCabe index: non-fatal=3.2%, ultimately fatal=12.9% and rapidly fatal=0.12%. Enterobacter bacteremia remained an independent risk factor for mortality among cases with severe sepsis or septic shock (OR 5.75 [CI95%2.57–12.87], p <0.001), with an attributable mortality of 40.3%(CI95%25.7–53.3). Empiric therapy or antibiotic resistances were not related to the outcome among patients with bacteremia. Invasive procedures, previous antibiotics and corticosteroids predispose to acquire Enterobacter bacteremia. This entity increases mortality among fragile patients and those with severe infections. Antibiotic resistances did not affect the outcome. [ABSTRACT FROM AUTHOR]

Background: Enterobacter is among the main etiologies of hospital-acquired infections. This study aims to identify the risk factors of acquisition and attributable mortality of Enterobacter bacteremia.Methods: Observational, case-control study for risk factors and prospective cohort for outcomes of consecutive cases with Enterobacter bacteremia. This study was conducted in five hospitals in Spain over a three-year period. Matched controls were patients with negative blood cultures and same sex, age, and hospitalization area.Results: The study included 285 cases and 570 controls. E. cloacae was isolated in 198(68.8%) cases and E. aerogenes in 89(31.2%). Invasive procedures (hemodialysis, nasogastric tube, mechanical ventilation, surgical drainage tube) and previous antibiotics or corticosteroids were independently associated with Enterobacter bacteremia. Its attributable mortality was 7.8%(CI95%2.7-13.4%), being dissimilar according to a McCabe index: non-fatal=3.2%, ultimately fatal=12.9% and rapidly fatal=0.12%. Enterobacter bacteremia remained an independent risk factor for mortality among cases with severe sepsis or septic shock (OR 5.75 [CI95%2.57-12.87], p<0.001), with an attributable mortality of 40.3%(CI95%25.7-53.3). Empiric therapy or antibiotic resistances were not related to the outcome among patients with bacteremia.Conclusions: Invasive procedures, previous antibiotics and corticosteroids predispose to acquire Enterobacter bacteremia. This entity increases mortality among fragile patients and those with severe infections. Antibiotic resistances did not affect the outcome. [ABSTRACT FROM AUTHOR]

• Outbreak description of an unusual combination specie-carbapenemase type: bla GES-6 S. marcescens. • In vivo emergence of ceftazidime-avibactam resistance and increase of carbapenem susceptibility. • Intra-host evolution of S. marcescens in a relatively short period. To describe the in vivo emergence of ceftazidime-avibactam resistance in GES-type carbapenemases and to characterize an unusual outbreak of GES-6-producing Serratia marcescens during the COVID-19 pandemic in Spain. Retrospective study to describe a GES-CPSM outbreak based on whole genome sequencing and antimicrobial susceptibility testing (AST). Transferability of bla GES -carrying plasmid was assessed by conjugation experiments. In December 2020, we identified a cluster of S. marcescens harbouring bla GES-6 involving 9 patients. Whole-genome sequence analysis revealed a clonal relationship (≤3 SNPs) between the first isolates identified in each of the evolved patients and environmental samples with GES-CPSM detection. Plasmid analysis showed that the bla GES-6 gene was located in an IncQ3-type plasmid. Triparental mating experiments using a helper plasmid demonstrated mobilization of the bla GES-6 -carrying plasmid. Our results also demonstrate within-host evolution in S. marcescens isolates, leading to a transition from bla GES-6 to the new bla GES-55 , caused by the P162S mutation, in a subsequent infection in one of the affected patients. In bla GES-55 we identified emergence of ceftazidime-avibactam resistance along with an increase of carbapenems susceptibility. This patient had been treated with a 14-day course of ceftazidime-avibactam. AST of the transformants bearing bla GES-6 and bla GES-55 plasmids, confirmed susceptibility variation affecting ceftazidime-avibactam and carbapenems. We report an unusual outbreak of GES-6 whose incidence is becoming increasing. Transition from GES-6 to GES-55 may readily occur in vivo leading to ceftazidime-avibactam resistance, which brings to the fore the critical need for developing more accurate diagnosis tools for detection of GES β–lactamases and optimise the use of antimicrobials. [ABSTRACT FROM AUTHOR]