Browsing by Author "Isawumi, A."
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Item The burden of hospital acquired infections and antimicrobial resistance(Heliyon, 2023) Abban, M.K.; Ayerakwa, E.A.; Mosi, L.; Isawumi, A.The burden of Hospital care-associated infections (HCAIs) is becoming a global concern. This is compounded by the emergence of virulent and high-risk bacterial strains such as “ESKAPE” pathogens – (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter species), especially within Intensive care units (ICUs) that house high-risk and immunocompromised patients. In this review, we discuss the contributions of AMR pathogens to the increasing burden of HCAIs and provide insights into AMR mechanisms, with a particular focus on last-resort antibiotics like polymyxins. We exten sively discuss how structural modifications of surface-membrane lipopolysaccharides and cationic interactions influence and inform AMR, and subsequent severity of HCAIs. We highlight some bacterial phenotypic survival mechanisms against polymyxins. Lastly, we discuss the emergence of plasmid-mediated resistance as a phenomenon making mitigation of AMR difficult, especially within the ICUs. This review provides a balanced perspective on the burden of HCAIs, associated pathogens, implication of AMR and factors influencing emerging AMR mechanisms.Item Profiling Mycobacterium ulcerans: sporulation, survival strategy and response to environmental factors(Future Science OA, 2023) Ayerakwa, E.A.; Abban, M.K.; Isawumi, A.; Mosi, L.Mycobacterium ulcerans is the causative agent of Buruli ulcer – a necrotizing skin infection. As an environmental pathogen, it has developed stress response mechanisms for survival. Similar to endospore formation in M. marinum, it is likely that M. ulcerans employs sporulation mechanisms for its survival and transmission. In this review, we modeled possible transmission routes and patterns of M. ulcerans from the environment to its host. We provided insights into the evolution of M. ulcerans and its genomic profiles. We discuss reservoirs of M. ulcerans as an environmental pathogen and its environmental survival. We comprehensively discuss sporulation as a possible stress response mechanism and modelled endospore formation in M. ulcerans. At last, we highlighted sporulation associated markers, which upon expression trigger endospore formation.Item Pseudogenomic Insights Into The Evolution Of Mycobacterium Ulcerans(BMC Genomics, 2024) Kyei-Baffour, E.S.; Owusu-Boateng, K.; Isawumi, A.; et al.Background: Buruli ulcer (BU) disease, caused by Mycobacterium ulcerans (MU) and characterized by necrotic ulcers is still a health problem in Africa and Australia. The genome of the bacterium has several pseudogenes due to recent evolutionary events and environmental pressures. Pseudogenes are genetic elements regarded as non-essential in bacteria, however, are less studied due to limited available tools to provide understanding of their evolution and roles in MU pathogenicity. Results This study developed a bioinformatic pipeline to profile the pseudogenomes of sequenced MU clinical isolates from different countries. One hundred and seventy-two MU genomes analyzed revealed that The pseudogenomes of African strains corresponded to the two African lineages 1 and 2. Pseudogenomes were lineages and location-specific, and African lineage 1 was further divided into A and B. Lineage 2 had less relaxation in positive selection than lineage 1, which may signify different evolutionary points. Based on the Gil-Latorre model, African strains may be in the latter stages of evolutionary adaptation and are adapting to an environment rich in metabolic resources with a lower temperature and decreased UV radiation. The environment fosters oxidative metabolism and MU may be less reliant on some secondary metabolites. In-house pseudogenomes from Ghana and Cote d’Ivoire were different from other African strains; however, they were identified as African strains. Conclusion Our bioinformatic pipeline provides pseudogenomic insights to complement other whole genome analyses, providing a better view of the evolution of the genome of MU and suggesting an adaptation model which is important in understanding transmission. MU pseudogene profiles vary based on lineage and country, and an apparent reduction in insertion sequences used for the detection of MU, which may adversely affect the sensitivity of diagnosis. Significance Prevention and treatment of Buruli ulcer is still a problem but large whole genome datasets on M. ulcerans are readily available. However, genomic studies fail to thoroughly investigate pseudogenes to probe evolutionary changes in the bacteria, and this can be attributed to the lack of bioinformatic tools. This work studied pseudogenes in Mycobacterium ulcerans (MU) to understand its adapted niche and evolutionary differences across African strains. Our results suggest that an MU niche-adapted model is important in understanding transmission. Also, MU pseudogene profiles vary based on lineage and country, suggesting their influence on pseudogenization patternsItem Pseudogenomic Insights Into The Evolution Of Mycobacterium Ulcerans(BMC Genomics, 2024) Kyei-Baffour, E.S.; Owusu-Boateng, K.; Isawumi, A.; et al.Background: Buruli ulcer (BU) disease, caused by Mycobacterium ulcerans (MU) and characterized by necrotic ulcers is still a health problem in Africa and Australia. The genome of the bacterium has several pseudogenes due to recent evolutionary events and environmental pressures. Pseudogenes are genetic elements regarded as non-essential in bacteria, however, are less studied due to limited available tools to provide understanding of their evolution and roles in MU pathogenicity. Results This study developed a bioinformatic pipeline to profile the pseudogenomes of sequenced MU clinical isolates from different countries. One hundred and seventy-two MU genomes analyzed revealed that The pseudogenomes of African strains corresponded to the two African lineages 1 and 2. Pseudogenomes were lineages and location-specific, and African lineage 1 was further divided into A and B. Lineage 2 had less relaxation in positive selection than lineage 1, which may signify different evolutionary points. Based on the Gil-Latorre model, African strains may be in the latter stages of evolutionary adaptation and are adapting to an environment rich in metabolic resources with a lower temperature and decreased UV radiation. The environment fosters oxidative metabolism and MU may be less reliant on some secondary metabolites. In-house pseudogenomes from Ghana and Cote d’Ivoire were different from other African strains; however, they were identified as African strains. Conclusion Our bioinformatic pipeline provides pseudogenomic insights to complement other whole genome analyses, providing a better view of the evolution of the genome of MU and suggesting an adaptation model which is important in understanding transmission. MU pseudogene profiles vary based on lineage and country, and an apparent reduction in insertion sequences used for the detection of MU, which may adversely affect the sensitivity of diagnosis. Significance Prevention and treatment of Buruli ulcer is still a problem but large whole genome datasets on M. ulcerans are readily available. However, genomic studies fail to thoroughly investigate pseudogenes to probe evolutionary changes in the bacteria, and this can be attributed to the lack of bioinformatic tools. This work studied pseudogenes in Mycobacterium ulcerans (MU) to understand its adapted niche and evolutionary differences across African strains. Our results suggest that an MU niche-adapted model is important in understanding transmission. Also, MU pseudogene profiles vary based on lineage and country, suggesting their influence on pseudogenization patternsItem Suboptimal antimicrobial stewardship in the COVID-19 era: is humanity staring at a postantibiotic future?(FUTURE MICROBIOLOGY, 2021) Owoicho, O.; Tapela, K.; Zune, A.L.D.; Nghochuzie, N.N.; Isawumi, A.; Mosi, L.In the absence of potent antimicrobial agents, it is estimated that bacterial infections could cause millions of deaths. The emergence of COVID-19, its complex pathophysiology and the high propensity of patients to coinfections has resulted in therapeutic regimes that use a cocktail of antibiotics for disease management. Suboptimal antimicrobial stewardship in this era and the slow pace of drug discovery could result in large-scale drug resistance, narrowing future antimicrobial therapeutics. Thus, judicious use of current antimicrobials is imperative to keep up with existing and emerging infectious pathogens. Here, we provide insights into the potential implications of suboptimal antimicrobial stewardship, resulting from the emergence of COVID-19, on the spread of antimicrobial resistance