A Molecular Study of Toxic Shock Syndrome Toxin gene (tsst-1) in β-lactam Resistant Staphylococcus aureus Clinical Isolates

Omar, Nariman Nidhal; Mohammed, Rana Kadhim

doi:10.24996/ijs.2021.62.3.13

Cited by 6 publications

(1 citation statement)

References 25 publications

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“…Bacteria can penetrate the bloodstream and cause organ infections, such as pneumonia, endocarditis, arthritis, osteomyelitis, and severe symptoms of sepsis (Gorwitz, et al, 2008;Nienaber et al, 2011;Tenover & Tickler, 2022). Additionally, S. aureus is responsible for toxin-mediated diseases such as food poisoning (Baba et al, 2002), toxic shock syndrome (Imanishi et al, 2019;Omar & Mohammed, 2021), and scalded skin syndrome (Kuroda et al, 2001;Yamaguchi et al, 2002).…”

Section: Plasmid and Bacterial Strains Used In This Studymentioning

confidence: 99%

Convergent Replication and Mobilization Mechanism of Staphylococcus Pathogenicity Islands (SaPIbov5) by Interfering with Bacteriophage 12 Production Models

et al. 2023

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TAPHYLOCOCCUS aureus can enter the bloodstream, leading to health complications such as sepsis, arthritis, endocarditis, and pneumonia. This study screened for the impact of six replication genes of cos phage 12 (φ12) on the evolution and transfer of cos S. aureus pathogenicity islands (SaPIbov5). An overnight culture of the S. aureus strain RN4220 diluted with fresh TSB was used in the bacteriophage φ12 titering assay. Phage-point mutagenesis was achieved using the pMAD vector, which facilitates homologous recombination in a two-step process. Finally, the transduction SaPI titering assays also utilized the S. aureus strain RN4220, which was then mixed with CaCl 2 and fresh TSB. The study showed that ORF11, ORF12, and VirE mutants did not lyse or produce phage particles after titering into the recipient RN4220 strains. While ORF26, ORF10, and ORF04 mutants generated detectable plaques, the mutations may have an effect on phage replication or packaging after tittering. For instance, complemented φ12 ORF26, ORF10, and ORF04 mutant strains had fully restored phage titers. The experiment found that cos phages facilitate inter and intra-generically transfer of cosSaPIs. It was also established that φ12 transduces SaPIbov5. However, φ12 mutants in VirE, ORF12, and ORF11 did not show SaPI mobilization because of their effects on infective phage particles and lack of replication. The complemented φ12 VirE, ORF12, and ORF11 mutants had partly restored phage titers when they were expressed in the recipient and donor strains. Mutations in ORF26, 0RF10, and ORFO4 decrease the φ12's ability to transfer SaPIbov5. Generally, this study found a new mechanism that facilitates the transfer of SaPI and cos genes. While the VirE, ORF12, and ORF11 affect packaging and are necessary for replication and phage biology

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Section: Plasmid and Bacterial Strains Used In This Studymentioning

confidence: 99%

Convergent Replication and Mobilization Mechanism of Staphylococcus Pathogenicity Islands (SaPIbov5) by Interfering with Bacteriophage 12 Production Models

et al. 2023

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Synergistic Antimicrobial Activity of Eugenol in Combination with Fosfomycin to Combat Escherichia coli and Potential Effect on Plasmid‐Mediated Fosfomycin Resistance Genes

Attaallah Ibrahim,

Kadhim Mohammed

2023

Chemistry & Biodiversity

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The presence of multidrug‐resistant pathogenic microorganisms makes it challenging to cure bacterial illnesses. Syzygium aromaticum has been used for medicinal purposes since ancient times. The objective of this study was to investigate the potential synergistic effect of the combination of Eugenol and Fosfomycin against clinically Uropathogenic Escherichia coli (UPEC) and their possible co‐treatment as well as their contribution to plasmid‐mediated Fosfomycin resistance (fosA3 and fosA4) genes using molecular assays. Eugenol was extracted from clove (Syzygium aromaticum) plants using steam distillation by Clevenger and analyzed by high‐performance liquid chromatography (HPLC). UPEC accounted for 63.6% of all isolates. Specifically, 99.3% of the UPEC isolates exhibited resistance to multiple types of antibiotics [multidrug‐resistant (MDR)]. The MIC for Eugenol was 1.25‐5 µg/mL, and Fosfomycin was 512‐1024 µg/mL, while the MBC for Eugenol was 5‐10 µg/mL and Fosfomycin was 2048 µg/mL. The synergistic effects were considerable, with 1/4 MIC of Eugenol resulting in 1/8 MIC Fosfomycin. Eugenol inhibited most of the UPEC isolates at 4‐8 hours, Fosfomycin at 8‐12 hours, and co‐treatment at 4‐8 hours. The fosA3 and fosA4 genes were detected in 5.7% and 2.9% of the isolates, respectively. The results showed variable gene expression changes in response to the different treatments.

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A Molecular Study of Toxic Shock Syndrome Toxin gene (tsst-1) in β-lactam Resistant Staphylococcus aureus Clinical Isolates

Cited by 6 publications

References 25 publications

Convergent Replication and Mobilization Mechanism of Staphylococcus Pathogenicity Islands (SaPIbov5) by Interfering with Bacteriophage 12 Production Models

Convergent Replication and Mobilization Mechanism of Staphylococcus Pathogenicity Islands (SaPIbov5) by Interfering with Bacteriophage 12 Production Models

Synergistic Antimicrobial Activity of Eugenol in Combination with Fosfomycin to Combat Escherichia coli and Potential Effect on Plasmid‐Mediated Fosfomycin Resistance Genes

Molecular study of glpT and uhpT genes as fosfomycin transport systems in uropathogenic Staphylococcus aureus

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