Research Article
Characterization of Quinolone Resistance Genes in Gram-Negative Bacilli Isolated from Pus and Vaginal Swabs at Saint Camille Hospital, Ouagadougou (HOSCO), Burkina Faso
Issue:
Volume 13, Issue 5, October 2025
Pages:
90-97
Received:
20 August 2025
Accepted:
29 August 2025
Published:
27 October 2025
DOI:
10.11648/j.ajbls.20251305.11
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Abstract: Introduction: Antibiotic resistance, particularly to quinolones, represents a major public health concern in Burkina Faso. In recent decades, plasmid-mediated quinolone resistance (PMQR) mechanisms have emerged, especially among Gram-negative bacteria. These mechanisms include, among others, qnr genes (qnrA, qnrB, qnrS). This study aimed to investigate the presence of quinolone resistance determinants in Gram-negative bacilli isolated from pus and vaginal samples at Saint Camille Hospital of Ouagadougou (HOSCO). Methodology: A total of 19 strains of Escherichia coli isolated from pus and vaginal swabs were collected for bacteriological and molecular analysis. Four antibiotics, namely ciprofloxacin (CIP), norfloxacin (NOR), ofloxacin (OF) and levofloxacin (LEV) were used for sensitivity testing and molecular analysis focused on the detection of qnrA, qnrB, and qnrS type genes. Results: Resistance rates to CIP, NOR, OF, and LEV were 57.89%, 52.63%, 52.63%, and 31.37%, respectively. Molecular analysis revealed the presence of qnrB, and qnrS genes in 28.47% of the isolates, for each gene. The qnrA gene was not detected in any isolate. The analysis of the genetic support of resistance genes revealed that 50% of the qnrS genes were plasmid-borne, while only 25% of the qnrB genes were associated with plasmids. La Correlation analysis between resistance genes and antibiotics showed a moderate positive correlation between qnrB and NOR/LEV, thereby suggesting the involvement of qnrB in resistance to these antibiotics. Conclusion: These findings highlight the need for continuous surveillance of antibiotic resistance in clinical isolates.
Abstract: Introduction: Antibiotic resistance, particularly to quinolones, represents a major public health concern in Burkina Faso. In recent decades, plasmid-mediated quinolone resistance (PMQR) mechanisms have emerged, especially among Gram-negative bacteria. These mechanisms include, among others, qnr genes (qnrA, qnrB, qnrS). This study aimed to investi...
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Review Article
Molecular Mechanisms of Cellular Senescence and Immuno-Senescence: Insights from Model Organisms and Emerging Pathways
Alebachew Molla*
Issue:
Volume 13, Issue 5, October 2025
Pages:
98-113
Received:
25 September 2025
Accepted:
5 October 2025
Published:
30 October 2025
DOI:
10.11648/j.ajbls.20251305.12
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Abstract: Cellular senescence and immunosenescence encompass critical molecular pathways that govern aging and age-related pathologies. Central to cellular senescence are DNA damage response activation, telomere attrition, chromatin remodeling, metabolic reprogramming, and cytoplasmic DNA sensing via cGAS-STING signaling, which collectively drive cell cycle arrest and the pro-inflammatory senescence-associated secretory phenotype (SASP). Immunosenescence involves progressive deterioration of immune cell function characterized by depleted naive lymphocytes, accumulation of dysfunctional senescent immune cells, and chronic inflammation (inflammaging), creating a feedback loop that exacerbates tissue degeneration and systemic aging. Model organisms such as mice and killifish have been indispensable for unraveling these mechanisms, enabling genetic and functional studies that illuminate senescence dynamics and immune clearance processes. Future research, empowered by multi-omics, single cell sequencing, and artificial intelligence, promises deeper dissection of senescence heterogeneity and tissue-specific pathways, offering biomarkers and therapeutic targets with unprecedented precision. Therapeutic strategies aiming to selectively eliminate or modulate senescent cells through senolytics, senomorphics, and immunomodulatory approaches hold promise to extend health span and ameliorate chronic diseases. However, challenges including senescent cell heterogeneity, context-dependent functions, and biomarker limitations necessitate individualized and careful translation of findings into clinical therapies. Continued interdisciplinary efforts integrating molecular biology, systems medicine, and clinical research will be pivotal in harnessing the full potential of senescence targeting for healthy aging and transformative disease management. This review was conducted to comprehensively compile and discuss the intricate molecular mechanisms underlying cellular senescence and immunosenescence, which are critical processes involved in aging and age-related diseases. The aim of this review article is to comprehensively elucidate the molecular mechanisms underlying cellular senescence and immunosenescence, integrating insights gained from model organism research and emerging signaling pathways.
Abstract: Cellular senescence and immunosenescence encompass critical molecular pathways that govern aging and age-related pathologies. Central to cellular senescence are DNA damage response activation, telomere attrition, chromatin remodeling, metabolic reprogramming, and cytoplasmic DNA sensing via cGAS-STING signaling, which collectively drive cell cycle ...
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