Objective: Effective infection prevention and control (IPC) measures are key for protecting patients from nosocomial infections and require knowledge of transmission mechanisms in different settings. We performed a detailed outbreak analysis of the transmission and outcome of coronavirus disease 2019 (COVID-19) in a geriatric ward by combining whole-genome sequencing (WGS) with epidemiological data. Design: Retrospective cohort study. Setting: Tertiary care hospital. Participants: Patients and healthcare workers (HCWs) from the ward with a nasopharyngeal sample (NPS) positive for SARS-CoV-2 RNA during the outbreak period. Methods: Patient data regarding clinical characteristics, exposure and outcome were collected retrospectively from medical records. Stored NPS from 32 patients and 15 HCWs were selected for WGS and phylogenetic analysis. Results: Median patient age was 84 years and 17/32 (53%) were male. Fourteen patients (44%) died within 30 days after sampling. Viral load was significantly higher among the deceased. WGS was successful in 28/32 (88%) patient samples and 14/15 (93%) HCW samples. Three separate viral clades were identified, whereof one clade and two subclades among both patient and HCW samples. Integrated epidemiological and genetic analysis revealed six probable transmission events between patients and supported hospital-acquired COVID-19 in 25/32 patients. Conclusion: WGS provided a deep insight into the outbreak dynamics and true extent of nosocomial COVID-19. The extensive transmission between patients and HCWs indicated that current IPC measures were insufficient. We suggest increased use of WGS in outbreak investigations for identification of otherwise unknown transmission links and evaluation of IPC measures.

In 2015, an outbreak caused by OXA-48-producing Enterobacteriaceae affected a neonatal intensive care unit at a Swedish University Hospital. The aim was to explore the transmission of OXA-48-producing strains between infants and the transfer of resistance plasmids between strains during the outbreak. Twenty-four outbreak isolates from ten suspected cases were whole-genome sequenced. A complete assembly was created for the index isolate (Enterobacter cloacae) and used as a mapping reference to detect its plasmids in the remaining isolates (17 Klebsiella pneumoniae, 4 Klebsiella aerogenes, and 2 Escherichia coli). Strain typing was performed using core genome MLST and SNP analysis. As judged from sequencing and clinical epidemiological data, the outbreak involved nine cases (two developed sepsis) and four OXA-48-producing strains: E. cloacae ST1584 (index case), K. pneumoniae ST25 (eight cases), K. aerogenes ST93 (two cases), and E. coli ST453 (2 cases). Two plasmids from the index strain, pEclA2 and pEclA4, carrying blaOXA48 and blaCMY-4, respectively, were traced to all K. pneumoniae ST25 isolates. Klebsiella aerogenes ST93 and E. coli ST453 harboured either only pEclA2, or both pEclA2 and pEclA4. One suspected case harbouring OXA-162-producing K. pneumoniae ST37 could be excluded from the outbreak. Once initiated by an E. cloacae strain, the outbreak was caused by the dissemination of a K. pneumoniae ST25 strain and involved inter-species horizontal transfer of two resistance plasmids, one of which carried blaOXA-48. To our knowledge, this is the first description of an outbreak of OXA-48-producing Enterobacteriaceae in a neonatal setting in northern Europe.