Evidence map›Paper›PMID 35400326›Full record

ArticleInfectious disorders drug targets2022

Molecular Study of Integrase Gene I and Integrase Gene II in Clinical Isolates of

Maysaa El Sayed Zaki, Noha Mostafa Mahmoud, Mohamed Anies Rizk

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Article in Infectious disorders drug targets, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 53% of its field
1 · What the graph read from it

What it found

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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

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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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Maysaa El Sayed ZakiClinical Pathology Department, Mansoura University, Mansoura, Egypt.
Noha Mostafa MahmoudMedical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Mohamed Anies RizkClinical Pathology Department, Mansoura University, Mansoura, Egypt.
Mansoura University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe presence of the class I integron gene is associated with the emergence of multiple drug resistance (MDR) phenotype in Pseudomonas aeruginosa (P. aeruginosa) isolates.

aimThe objectives of this research were to study the prevalence of integrase genes I (Intel I) and integrase genes II (Intel II) in clinical isolates of P. aeruginosa and its association with antibiotic resistance in these isolates.

methodsThe study was a retrograde cross-sectional study that was carried out on 150 clinical isolates of P. aeruginosa isolated from patients with healthcare-associated infections. The isolates were subjected to biochemical identification and antibiotic sensitivity study by discs diffusion test. Intel I & Intel II genes were detected by polymerase chain reaction (PCR).

resultsIntel I gene was present in 48% of the isolates, and Intel II was present in 1.3% of the isolates. Intel I gene was detected at a statistically significant high rate in MDR- P. aeruginosa (76.9%, P=0.001) compared to non-MDR- P. aeruginosa (3.4%), while intel II had a statistically insignificant increase in MDR- P. aeruginosa (1.1%, P=1.00) compared to non-MDR-P. aeruginosa (1.7%). Both Intl I/Intl II genes were detected in 2.2% of MDR-P. aeruginosa isolates and were absent in non- MDR-P. aeruginosa isolates with statistically insignificant difference (P=1.00). P. aeruginosa isolates with Intel I gene had an increase in antibiotic resistance pattern to the used antibiotics discs. However, this increase had statistically significant rates only for gentamicin (63.9%, P≤0.001), meropenem (47.2%, P=0.009), trimethoprim/sulfamethoxazole (37.5%, P=0.013) and imipenem (44.4%, P=0.025).

conclusionThe present study highlights the high prevalence of the Intel I gene in clinical isolates of P. aeruginosa, while the Intel II gene was less prevalent in these isolates. There was a significant association between the prevalence of the Intel I gene and the MDR phenotype of P. aeruginosa and resistance to gentamicin, meropenem, trimethoprim/sulfamethoxazole, and imipenem. These findings need future evaluation in a higher number of clinical isolates of P. aeruginosa.

Indexed as

gentamicinintegrase I geneintegrase II geneintegronsmultiple drug resistanceP. aeruginosa

Identifiers

PMID35400326
OpenAlexW4223432513

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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.