Antimicrobial resistance-attributable mortality: a patient-level analysis

Ioannis Baltas; Timothy Miles Rawson; Hamish Houston; Louis Grandjean; Gabriele Pollara

doi:10.1093/jacamr/dlae202

Antimicrobial resistance-attributable mortality: a patient-level analysis

JAC Antimicrob Resist. 2024 Dec 19;6(6):dlae202. doi: 10.1093/jacamr/dlae202. eCollection 2024 Dec.

Authors

Ioannis Baltas^{1

2}, Timothy Miles Rawson^{3

4

5}, Hamish Houston², Louis Grandjean¹, Gabriele Pollara^{2

6}

Affiliations

¹ Infection, Immunity & Inflammation Department, UCL Institute of Child Health, London, UK.
² Department of Clinical Microbiology, University College London Hospitals NHS Foundation Trust, London, UK.
³ National Institute for Health Research Health Protection Research Unit in Healthcare Associated Infections and Antimicrobial Resistance, Imperial College London, London, UK.
⁴ Centre for Antimicrobial Optimisation, Imperial College London, London, UK.
⁵ David Price Evans Infectious Diseases & Global Health Group, The University of Liverpool, Liverpool, UK.
⁶ Division of Infection & Immunity, University College London, London, UK.

Abstract

Background: The impact of antimicrobial resistance (AMR) on death at the patient level is challenging to estimate. We aimed to characterize AMR-attributable deaths in a large UK teaching hospital.

Methods: This retrospective study investigated all deceased patients in 2022. Records of participants were independently reviewed by two investigators for cases of AMR-attributable deaths using a newly proposed patient-level definition.

Results: In total, 758 patients met inclusion criteria. Infection was the underlying cause of death for 11.7% (89/758) and was implicated in the pathway that led to death in 41.1% (357/758) of participants. In total, 4.2% (32/758) of all deaths were AMR-attributable. Median time from index sample collection to death was 4.5 days (IQR 2-10.5 days). The majority of AMR-attributable deaths (56.3%, 18/32) were associated with intrinsic resistance mechanisms, primarily by Enterococcus faecium (20.7%), Enterobacterales carrying repressed chromosomal ampicillinase Cs (AmpCs) (14.7%) and Pseudomonas aeruginosa (11.8%), whereas a minority (43.7%, 14/32) had acquired resistance mechanisms, primarily derepressed chromosomal AmpCs (11.8%) and ESBLs (8.8%). The median time to effective treatment was 32 h 15 min (no difference between subgroups). Only 62.5% (20/32) of AMR-attributable deaths had infection recorded on the death certificate. AMR was not recorded as a cause of death in any of the patients.

Conclusions: Infection and AMR were important causes of death in our cohort, yet they were significantly underreported during death certification. In a low-incidence setting for AMR, pathogen-antimicrobial mismatch due to intrinsic resistance was an equally important contributor to AMR-attributable mortality as acquired resistance mechanisms.