Evidence map›Paper›PMID 39732629›Full record

ArticleBMC microbiology2024

Antimicrobial resistance, virulence gene profiling, and genetic diversity of multidrug-resistant Pseudomonas aeruginosa isolates in Mazandaran, Iran.

Ghazaleh Elahi, Hamid Reza Goli, Morvarid Shafiei, Vajihe Sadat Nikbin, Mehrdad Gholami

Erratum issuedAbstract read
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Article in BMC microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Occurrence of Virulence and Antibiotic Resistance inAntibiotics (Basel, Switzerland) · 2025
    Article
  6. Sub-inhibitory tobramycin concentration suppresses ToxA and LipA in single- and dual-species biofilms.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025
    Article
  7. Article
  8. Prevalence of Antibiotic Resistance Determinants in Carbapenem-ResistantInternational journal of molecular and cellular medicine · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Ghazaleh ElahiDepartment of Microbiology and Virology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Hamid Reza GoliDepartment of Microbiology and Virology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Morvarid ShafieiDepartment of Bacteriology, Pasteur Institute of Iran, Tehran, Iran.
Vajihe Sadat NikbinDepartment of Bacteriology, Pasteur Institute of Iran, Tehran, Iran.
Mehrdad GholamiDepartment of Microbiology and Virology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. mehrdad_gholami90@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPseudomonas aeruginosa is a major cause of healthcare-associated infections (HAIs), particularly in immunocompromised patients, leading to high morbidity and mortality rates. This study aimed to investigate the antimicrobial resistance patterns, virulence gene profiles, and genetic diversity among P. aeruginosa isolates from hospitalized patients in Mazandaran, Iran.

methodsFrom September 2021 to April 2022, 82 non-duplicate P. aeruginosa isolates were collected from diverse clinical sources. Identification was confirmed using API 20 NE (bioMérieux, Marcy l'Etoile, France). Antimicrobial susceptibility testing was conducted using the Kirby-Bauer disk diffusion method according to CLSI guidelines to assess resistance to a range of antibiotics. The virulence profile (exoT, exoY, exoU, toxA, plcH, plcN, algD, aprA, lasB and exoS) of each P. aeruginosa isolate was determined by PCR. The genetic diversity among the strains was evaluated using the random amplification of polymorphic DNA (RAPD) technique. Clustering was based on a Dice similarity coefficient of ≥ 85%.

resultsOf the 82 total strains, P. aeruginosa exhibited the highest and lowest resistance toward ticarcillin-clavulanate (98.78%) and colistin (0%), respectively. Moreover, 100% of the P. aeruginosa isolates were MDR. The following prevalence of virulence factor genes was observed: aprA, lasB, algD, toxA, plcH, exoY, and exoT in 100% of isolates. The plcN, exoS, and exoU were identified 98.78%, 67.07%, and 45.12%, respectively. The RAPD patterns obtained with primers 272 and 208 had respectively 2-19 and 6-17 bands. According to the Dice similarity coefficient of higher than 85%, 56 and 39 clusters were recognized.

conclusionThe high rate of multidrug resistance combined with the widespread presence of virulence genes in P. aeruginosa isolates highlights the potential for increased infection severity, morbidity, and mortality in hospitalized patients. The substantial genetic diversity observed among isolates suggests that P. aeruginosa in this region may rapidly evolve, necessitating ongoing surveillance and more targeted antimicrobial strategies. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

Anti-Bacterial AgentsDrug Resistance, Multiple, BacterialGenetic VariationMicrobial Sensitivity TestsPseudomonas aeruginosaPseudomonas InfectionsVirulence FactorsAdultCross InfectionFemaleHumansIranMaleMiddle AgedRandom Amplified Polymorphic DNA TechniqueVirulenceAnti-Bacterial AgentsVirulence FactorsAntibiotic resistanceMultidrug-resistantP. aeruginosaRAPDVirulence gene

Identifiers

PMID39732629
PMCPMC11681713

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.