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      Antibiotic resistance: The challenges and some emerging strategies for tackling a global menace

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          Abstract

          Background

          Antibiotic resistance is currently the most serious global threat to the effective treatment of bacterial infections. Antibiotic resistance has been established to adversely affect both clinical and therapeutic outcomes, with consequences ranging from treatment failures and the need for expensive and safer alternative drugs to the cost of higher rates of morbidity and mortality, longer hospitalization, and high‐healthcare costs. The search for new antibiotics and other antimicrobials continues to be a pressing need in humanity's battle against bacterial infections. Antibiotic resistance appears inevitable, and there is a continuous lack of interest in investing in new antibiotic research by pharmaceutical industries. This review summarized some new strategies for tackling antibiotic resistance in bacteria.

          Methods

          To provide an overview of the recent research, we look at some new strategies for preventing resistance and/or reviving bacteria's susceptibility to already existing antibiotics.

          Results

          Substantial pieces of evidence suggest that antimicrobials interact with host immunity, leading to potent indirect effects that improve antibacterial activities and may result in more swift and complete bactericidal effects. A new class of antibiotics referred to as immuno‐antibiotics and the targeting of some biochemical resistance pathway components including inhibition of SOS response and hydrogen sulfide as biochemical underlying networks of bacteria can be considered as new emerging strategies to combat antibiotic resistance in bacteria.

          Conclusion

          This review highlighted and discussed immuno‐antibiotics and inhibition of SOS response and hydrogen sulfide as biochemical underlying networks of bacteria as new weapons against antibiotic resistance in bacteria.

          Abstract

          Immuno‐antibiotics inhibit the non‐mevalonate or methyl‐D‐erythritol phosphate (MEP) pathway of isoprenoid biosynthesis and riboflavin biosynthesis pathway in bacteria. This image was created with BioRender ( https://biorender.com/).

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          Most cited references71

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          Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis

          (2022)
          Summary Background Antimicrobial resistance (AMR) poses a major threat to human health around the world. Previous publications have estimated the effect of AMR on incidence, deaths, hospital length of stay, and health-care costs for specific pathogen–drug combinations in select locations. To our knowledge, this study presents the most comprehensive estimates of AMR burden to date. Methods We estimated deaths and disability-adjusted life-years (DALYs) attributable to and associated with bacterial AMR for 23 pathogens and 88 pathogen–drug combinations in 204 countries and territories in 2019. We obtained data from systematic literature reviews, hospital systems, surveillance systems, and other sources, covering 471 million individual records or isolates and 7585 study-location-years. We used predictive statistical modelling to produce estimates of AMR burden for all locations, including for locations with no data. Our approach can be divided into five broad components: number of deaths where infection played a role, proportion of infectious deaths attributable to a given infectious syndrome, proportion of infectious syndrome deaths attributable to a given pathogen, the percentage of a given pathogen resistant to an antibiotic of interest, and the excess risk of death or duration of an infection associated with this resistance. Using these components, we estimated disease burden based on two counterfactuals: deaths attributable to AMR (based on an alternative scenario in which all drug-resistant infections were replaced by drug-susceptible infections), and deaths associated with AMR (based on an alternative scenario in which all drug-resistant infections were replaced by no infection). We generated 95% uncertainty intervals (UIs) for final estimates as the 25th and 975th ordered values across 1000 posterior draws, and models were cross-validated for out-of-sample predictive validity. We present final estimates aggregated to the global and regional level. Findings On the basis of our predictive statistical models, there were an estimated 4·95 million (3·62–6·57) deaths associated with bacterial AMR in 2019, including 1·27 million (95% UI 0·911–1·71) deaths attributable to bacterial AMR. At the regional level, we estimated the all-age death rate attributable to resistance to be highest in western sub-Saharan Africa, at 27·3 deaths per 100 000 (20·9–35·3), and lowest in Australasia, at 6·5 deaths (4·3–9·4) per 100 000. Lower respiratory infections accounted for more than 1·5 million deaths associated with resistance in 2019, making it the most burdensome infectious syndrome. The six leading pathogens for deaths associated with resistance (Escherichia coli, followed by Staphylococcus aureus, Klebsiella pneumoniae, Streptococcus pneumoniae, Acinetobacter baumannii, and Pseudomonas aeruginosa) were responsible for 929 000 (660 000–1 270 000) deaths attributable to AMR and 3·57 million (2·62–4·78) deaths associated with AMR in 2019. One pathogen–drug combination, meticillin-resistant S aureus, caused more than 100 000 deaths attributable to AMR in 2019, while six more each caused 50 000–100 000 deaths: multidrug-resistant excluding extensively drug-resistant tuberculosis, third-generation cephalosporin-resistant E coli, carbapenem-resistant A baumannii, fluoroquinolone-resistant E coli, carbapenem-resistant K pneumoniae, and third-generation cephalosporin-resistant K pneumoniae. Interpretation To our knowledge, this study provides the first comprehensive assessment of the global burden of AMR, as well as an evaluation of the availability of data. AMR is a leading cause of death around the world, with the highest burdens in low-resource settings. Understanding the burden of AMR and the leading pathogen–drug combinations contributing to it is crucial to making informed and location-specific policy decisions, particularly about infection prevention and control programmes, access to essential antibiotics, and research and development of new vaccines and antibiotics. There are serious data gaps in many low-income settings, emphasising the need to expand microbiology laboratory capacity and data collection systems to improve our understanding of this important human health threat. Funding Bill & Melinda Gates Foundation, Wellcome Trust, and Department of Health and Social Care using UK aid funding managed by the Fleming Fund.
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            Discovery, research, and development of new antibiotics: the WHO priority list of antibiotic-resistant bacteria and tuberculosis

            Lawrence D. Kerr, Souha Kanj, Timothy Jinks … (2018)
            The spread of antibiotic-resistant bacteria poses a substantial threat to morbidity and mortality worldwide. Due to its large public health and societal implications, multidrug-resistant tuberculosis has been long regarded by WHO as a global priority for investment in new drugs. In 2016, WHO was requested by member states to create a priority list of other antibiotic-resistant bacteria to support research and development of effective drugs.
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              A common mechanism of cellular death induced by bactericidal antibiotics.

              Michael A Kohanski, Daniel Dwyer, Boris Hayete … (2007)
              Antibiotic mode-of-action classification is based upon drug-target interaction and whether the resultant inhibition of cellular function is lethal to bacteria. Here we show that the three major classes of bactericidal antibiotics, regardless of drug-target interaction, stimulate the production of highly deleterious hydroxyl radicals in Gram-negative and Gram-positive bacteria, which ultimately contribute to cell death. We also show, in contrast, that bacteriostatic drugs do not produce hydroxyl radicals. We demonstrate that the mechanism of hydroxyl radical formation induced by bactericidal antibiotics is the end product of an oxidative damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH, destabilization of iron-sulfur clusters, and stimulation of the Fenton reaction. Our results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.
              Article 0 comments Cited 856 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                David Chinemerem Nwobodo: nwobododave@gmail.com
                Morteza Saki:
                ORCID: https://orcid.org/0000-0001-7419-0116
                mortezasaki1981@gmail.com
                Journal
                Journal ID (nlm-ta): J Clin Lab Anal
                Journal ID (iso-abbrev): J Clin Lab Anal
                Journal ID (doi): 10.1002/(ISSN)1098-2825
                Journal ID (publisher-id): JCLA
                Title: Journal of Clinical Laboratory Analysis
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0887-8013
                ISSN (Electronic): 1098-2825
                Publication date (Electronic): 10 August 2022
                Publication date Collection: September 2022
                Volume: 36
                Issue: 9 ( doiID: 10.1002/jcla.v36.9 )
                Electronic Location Identifier: e24655
                Affiliations
                [ 1 ] Department of Microbiology Renaissance University Enugu Nigeria
                [ 2 ] Department of Pharmaceutical Microbiology and Biotechnology Nnamdi Azikiwe University Awka Nigeria
                [ 3 ] Department of Pharmaceutical Microbiology Faculty of Pharmacy Delta State University Abraka Abraka Nigeria
                [ 4 ] Department of Microbiology College of Medicine University of Anbar Ramadi Iraq
                [ 5 ] Department of Pharmaceutical Microbiology and Biotechnology Madonna University Elele Nigeria
                [ 6 ] Department of Microbiology Faculty of Medicine Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran
                [ 7 ] Infectious Ophthalmologic Research Center Imam Khomeini Hospital Clinical Research Development Unit Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran
                Author notes
                [*] [* ] Correspondence

                Morteza Saki, Department of Microbiology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

                Email: mortezasaki1981@ 123456gmail.com

                David Chinemerem Nwobodo, Department of Pharmaceutical Microbiology and Biotechnology, Nnamdi Azikiwe University, Awka, Nigeria.

                Email: nwobododave@ 123456gmail.com

                Author information
                https://orcid.org/0000-0001-7419-0116
                Article
                Publisher ID: JCLA24655 Other ID: JCLA-22-1816.R1
                DOI: 10.1002/jcla.24655
                PMC ID: 9459344
                PubMed ID: 35949048
                SO-VID: b4bf6bc3-50fd-4c9f-8283-5ce8c0a68014
                Copyright © © 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                Date revision received : 22 July 2022
                Date received : 22 June 2022
                Date accepted : 01 August 2022
                Page count
                Figures: 3, Tables: 0, Pages: 10, Words: 7803
                Categories
                Subject: Review Article
                Subject: Review Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date September 2022
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.1.8 mode:remove_FC converted:09.09.2022

                ScienceOpen disciplines: Clinical chemistry
                Keywords: antibiotic resistance,hydrogen sulfide,immuno‐antibiotics,sos response
                Data availability:
                ScienceOpen disciplines: Clinical chemistry
                Keywords: antibiotic resistance, hydrogen sulfide, immuno‐antibiotics, sos response

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