Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2026
Clonal outbreak of mecC-MRSA carriage linked to phage-mediated acquisition of immune evasion cluster genes.
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Yin Nicolas, Verbelen Valérie, Roussel Gatien, Mairesse Célestin, Vandendriessche Stien, Wautier Magali, Prevost Benoit, Martiny Delphine, Denis Olivier
Аннотация
OBJECTIVES: mecC-carrying methicillin-resistant Staphylococcus aureus (mecC-MRSA) are predominantly animal-associated pathogens that rarely cause human infections and have not been linked to hospital outbreaks. We investigated a suspected cluster of mecC-MRSA in a Belgian hospital and contextualised the outbreak isolates within the global mecC-MRSA population using whole-genome sequencing.
METHODS: Seven mecC-MRSA isolates from screening samples from patients hospitalised in a single unit between September 2024 and January 2025 underwent whole genome sequencing alongside 16 unrelated human and 3 bovine mecC-MRSA from Belgium. Core-genome MLST (cgMLST) was performed to assess clonality. These were compared with 571 publicly available mecC-MRSA genome assemblies from NCBI. Immune evasion cluster (IEC) genes were sought. Associated prophage regions were characterised using PHASTEST.
RESULTS: All seven outbreak isolates belonged to ST599, shared the same complex type (CT47051), and differed by a maximum of 4 cgMLST allelic differences, confirming clonal transmission. Six of seven were detected within 48 hours of admission; all patients resided in a semi-rural area within a 23 km radius. The outbreak isolates harboured IEC genes sak and sea on a ΦSa3-like prophage, a novel IEC variant lacking scn and chp, while an unrelated CC599 Belgian human isolate harboured sak and scn. Among publicly available mecC-MRSA assemblies, CC599 represented only 16 isolates (2.8%), and IEC genes were carried only by 6 isolates (0.9%)- none within CC599. The outbreak cluster was most closely related to an unrelated historical Belgian bovine ST599 isolate (75 allelic differences).
CONCLUSIONS: This first documented clonal mecC-MRSA outbreak was caused by a rare ST599 clone that acquired IEC genes through phage-mediated horizontal transfer, a feature associated with human adaptation and enhanced transmissibility in other S. aureus lineages. These findings highlight the need for mecC-capable diagnostic assays and One Health genomic surveillance to detect emerging human-adaptive mecC-MRSA clones.
METHODS: Seven mecC-MRSA isolates from screening samples from patients hospitalised in a single unit between September 2024 and January 2025 underwent whole genome sequencing alongside 16 unrelated human and 3 bovine mecC-MRSA from Belgium. Core-genome MLST (cgMLST) was performed to assess clonality. These were compared with 571 publicly available mecC-MRSA genome assemblies from NCBI. Immune evasion cluster (IEC) genes were sought. Associated prophage regions were characterised using PHASTEST.
RESULTS: All seven outbreak isolates belonged to ST599, shared the same complex type (CT47051), and differed by a maximum of 4 cgMLST allelic differences, confirming clonal transmission. Six of seven were detected within 48 hours of admission; all patients resided in a semi-rural area within a 23 km radius. The outbreak isolates harboured IEC genes sak and sea on a ΦSa3-like prophage, a novel IEC variant lacking scn and chp, while an unrelated CC599 Belgian human isolate harboured sak and scn. Among publicly available mecC-MRSA assemblies, CC599 represented only 16 isolates (2.8%), and IEC genes were carried only by 6 isolates (0.9%)- none within CC599. The outbreak cluster was most closely related to an unrelated historical Belgian bovine ST599 isolate (75 allelic differences).
CONCLUSIONS: This first documented clonal mecC-MRSA outbreak was caused by a rare ST599 clone that acquired IEC genes through phage-mediated horizontal transfer, a feature associated with human adaptation and enhanced transmissibility in other S. aureus lineages. These findings highlight the need for mecC-capable diagnostic assays and One Health genomic surveillance to detect emerging human-adaptive mecC-MRSA clones.