# Genomic and epidemiological insights into the emergence and dominance of MRSA clones in Riyadh’s healthcare facilities

**Authors:** Dalal M. Alkuraythi, Manal M. Alkhulaifi, Dina A. Altwiley, Mohammed Alarwi, Mohammed I. Mujallad, Mohammad K. Alshomrani, Takashi Gojobori, Sulaiman M. Alajel

PMC · DOI: 10.1038/s41598-025-34001-7 · 2026-01-06

## TL;DR

This study analyzes MRSA clones in Riyadh healthcare facilities, identifying dominant strains and their resistance patterns to guide infection control.

## Contribution

The study provides new insights into the genomic and epidemiological dynamics of MRSA clones in Saudi Arabia.

## Key findings

- ST5 and ST6 were the most prevalent MRSA clones, accounting for 45.6% of infections.
- ST5 showed broader multidrug resistance, while ST6 exhibited variable resistance, suggesting a community origin.
- Phylogenetic analysis identified novel variants like ST8111 within Clonal Complex 5.

## Abstract

The emergence and expansion of methicillin-resistant Staphylococcus aureus (MRSA) clones in healthcare facilities pose a significant public health concern due to their adaptability and resistance to commonly used antibiotics. In this study, the genomic and epidemiological characteristics of 81 MRSA isolates collected between February and June 2022 were analyzed. ST5 (25.9%) and ST6 (19.7%) emerged as the dominant sequence types, collectively accounting for 45.6% of infections. Whole-genome sequencing and phenotypic analyses revealed that ST5 clone exhibited a broader multidrug-resistant profile compared to ST6 clone, with higher prevalence of β-lactam, tetracycline, and trimethoprim resistance. ST6 clone showed more variable resistance, including aminoglycoside and macrolide genes, suggesting a possible community origin before adaptation to hospital settings. Phylogenetic analysis demonstrated ongoing microevolution within Clonal Complex 5 (CC5), including the identification of novel single-locus variants such as ST8111. Correlation analyses highlighted significant associations between key resistance genes and their phenotypic profiles, reflecting complex co-resistance mechanisms. Additionally, virulence profiling revealed that ST5 uniquely carried tsst-1, whereas PVL genes were absent in both ST5 and ST6 and appeared only in a small subset of other MRSA clones. The emergence of highly resistant clones like ST672 underscores the potential concern for sustained genomic surveillance. The observed clonal shift from ST239 to ST5 and ST6 signals a dynamic MRSA landscape in Saudi Arabia, emphasizing the need for integrated molecular epidemiology and targeted infection control strategies.

## Linked entities

- **Chemicals:** tetracycline (PubChem CID 54675776), trimethoprim (PubChem CID 5578)
- **Diseases:** MRSA (MONDO:0100073)
- **Species:** Staphylococcus aureus (taxon 1280)

## Full-text entities

- **Genes:** DENND2B (DENN domain containing 2B) [NCBI Gene 6764] {aka HTS1, ST5, p126}, SETBP1 (SET binding protein 1) [NCBI Gene 26040] {aka MRD29, SEB}, SEA (S13 erythroblastosis (avian) oncogene homolog) [NCBI Gene 6395], FOSB (FosB proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 2354] {aka AP-1, G0S3, GOS3, GOSB}, SFTPA2 (surfactant protein A2) [NCBI Gene 729238] {aka COLEC5, ILD2, PSAP, PSP-A, PSPA, SFTP1}, CAT (catalase) [NCBI Gene 847], HLA-A (major histocompatibility complex, class I, A) [NCBI Gene 3105] {aka HLAA}, SAA [NCBI Gene 6287], APEH (acylaminoacyl-peptide hydrolase) [NCBI Gene 327] {aka AARE, ACPH, APH, D3F15S2, D3S48E, DNF15S2}, MSRA (methionine sulfoxide reductase A) [NCBI Gene 4482] {aka PMSR}
- **Diseases:** MRSA (MESH:D013203), hemolysis (MESH:D006461), HA (MESH:C537629), PV (MESH:D011087), infection (MESH:D007239), SCCmec type V (MESH:D011023), toxic shock syndrome (MESH:D012772), systemic shock (MESH:D012769), food poisoning (MESH:D005517), multidrug (MESH:D018088), HAIs (MESH:D003428), COVID-19 (MESH:D000086382), respiratory and wound infections (MESH:D012141)
- **Chemicals:** tetracycline (MESH:D013752), CLI (MESH:D002981), Columbia blood agar (-), ERY (MESH:D004917), aminoglycoside (MESH:D000617), trimethoprim (MESH:D014295), fosfomycin (MESH:D005578), trimethoprim-sulfamethoxazole (MESH:D015662), agarose (MESH:D012685), macrolide (MESH:D018942), beta-lactam (MESH:D047090), cefoxitin (MESH:D002440), ethidium (MESH:D004996), OXA (MESH:D010068), GEN (MESH:D005839), lincosamide (MESH:D055231), PEN (MESH:D010406), MSA (MESH:D015080), Methicillin (MESH:D008712)
- **Species:** Staphylococcus aureus (species) [taxon 1280], Homo sapiens (human, species) [taxon 9606], Phaeobacter inhibens (species) [taxon 221822]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12852192/full.md

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Source: https://tomesphere.com/paper/PMC12852192