Three clusters of carbapenemase-producing Citrobacter freundii in Finland, 2016–20

• Published in: Journal of antimicrobial chemotherapy 2021-10, Vol.76 (10), p.2697-2701
• Main Authors: Räisänen, Kati, Sarvikivi, Emmi, Arifulla, Dinah, Pietikäinen, Risto, Forsblom-Helander, Benita, Tarkka, Eveliina, Anttila, Veli-Jukka, Grönroos, Juha O, Rintala, Esa, Kauranen, Jari, Ahlsved, Matias, Broas, Markku, Mikkola, Janne, Sieberns, Jennifer, Jalava, Jari, Lyytikäinen, Outi
• Format: Article
• Language: English
• ISSN: 0305-7453; 1460-2091
• DOI: 10.1093/jac/dkab209

Abstract Objectives Carbapenemase-producing Enterobacterales (CPE) have spread widely into health care facilities (HCF) but clusters caused by carbapenemase-producing (CP) Citrobacter freundii have been uncommon until recent years. Here we describe CP C. freundii clusters detected in Finland during 2016–20. Methods As a part of the national CPE surveillance, clinical microbiology laboratories send potential CP C. freundii isolates to the reference laboratory for confirmation and further characterization. Whole genome sequencing (WGS) with Illumina MiSeq sequencer was used to detect clusters. Resistance genes and STs were analysed using SRST2 and typing with core genome (cg) MLST. A case was defined as a patient with a CP C. freundii isolate belonging to one of the detected clusters. Results We detected three CP C. freundii clusters: cluster 1 included 16 cases in five HCFs during 2016–20, cluster 2 had two cases in two HCFs during 2018–19 and cluster 3 had two cases in one HCF in 2020. The isolates (11 clinical and 5 screening) in cluster 1 had KPC-2 carbapenemase and were sequence type (ST)18. Cluster 2 (2 clinical isolates) had OXA-181/GES-5 carbapenemases and were ST604 and cluster 3 (two screening isolates) had KPC-3 carbapenemase and were ST116. None of the cases had a history of recent travel abroad. Conclusions CP C. freundii also causes outbreaks and can be a reservoir of carbapenemase genes. The long intervals between successive cases, mostly found in clinical specimens in two clusters, suggest that besides unknown carriers, environmental contamination may play a role in transmission.