Evidence map›Paper›PMID 42064214›Full record

ArticleFrontiers in cellular and infection microbiology2026

Comparative phenotypic and genotypic analysis of distinct

Nada K Alharbi, Naser A El-Sawy, Naief A Dahran, Banan Atwah, Abdullah G Al-Kushi, Maha Alharbi, Sozan M Abdelkhalig, Rasha A Mosbah, Abdallah Tageldein Mansour, Mahmoud M Bendary

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Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Nada K AlharbiDepartment of Biology, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.
Naser A El-SawyDepartment of Anatomy and Embryology, Faculty of medicine, Zagazig university, Zagazig, Egypt.
Naief A DahranDepartment of Basic Medical Sciences, College of Medicine, University of Jeddah, Jeddah, Saudi Arabia.
Banan AtwahDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Umm Al-Qura University, Makkah, Saudi Arabia.
Abdullah G Al-KushiDepartment of Anatomy, Faculty of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia.
Maha AlharbiDepartment of Biology, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.
Sozan M AbdelkhaligDepartment of Basic Medical Sciences, College of Medicine, AlMaarefa University, Diriyah, Riyadh, Saudi Arabia.
Rasha A MosbahInfection Control Unit, Zagazig University Hospital, Zagazig, Egypt.
Abdallah Tageldein MansourAnimal and Fish Production, College of Agricultural and Food Sciences, King Faisal University, Al-Ahsa, Saudi Arabia.
Mahmoud M BendaryDepartment of Microbiology and Immunology, Faculty of Pharmacy, Port Said University, Port Said, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Methods: Five hundred clinical specimens, sputum, urine, burn, wound, and eye exudates, 100 each, were collected from multiple hospitals for isolation of P. aeruginosa. Phenotypic and genotypic methods identified isolates and characterized T3SS effector genotypes, antimicrobial susceptibility, resistance genes, virulence genes, and serotypes. Clustering, strain typing, and correlation analyses assessed associations among resistance, virulence, epidemiology, and disease severity. Results: Among 125 isolates, exoS+ was the most prevalent T3SS effector, followed by exoU+, while exoT+ and exoY+ were less frequent. The exoU+ isolates were consistently associated with severe clinical manifestations across specimen types and were more often hospital acquired, with enrichment for serotypes O6 and O11. The exoS+ isolates showed broader serotype diversity with balanced hospital and community acquisition, whereas ExoT and ExoY were mainly associated with O6 and O11, with ExoY more common in community-acquired cases but less prevalent overall. Despite widespread antimicrobial resistance and broad distribution of resistance genes, polymyxin remained the most effective agent, with a low resistance rate of 15.2%. Multidrug resistance affected 81.6% of isolates and was observed across all T3SS effector genotypes, with frequent coexistence of resistance and virulence genes within individual isolates. Hierarchical clustering revealed marked intra-group and inter-group heterogeneity, with no evidence of dominant clonal expansion by effector genotype or specimen type, and correlation analysis showed weak associations among resistance, virulence, serotypes, and epidemiological features, except for a consistent link between exoU+ and markers of severe tissue injury. Conclusions:

Indexed as

GenotypePseudomonas aeruginosaPseudomonas InfectionsType III Secretion SystemsVirulence FactorsAnti-Bacterial AgentsBacterial ProteinsDrug Resistance, BacterialHumansMicrobial Sensitivity TestsPhenotypeSerogroupVirulenceAnti-Bacterial AgentsBacterial ProteinsType III Secretion SystemsVirulence Factorsantimicrobial resistancedisease severityexoU+P. aeruginosaT3SS effectorsvirulence

Identifiers

PMID42064214
PMCPMC13126654

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