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    African Journal of Laboratory Medicine

    On-line version ISSN 2225-2010Print version ISSN 2225-2002

    Abstract

    MOHAMMED, Yahaya; ABODERIN, Aaron O.; OKEKE, Iruka N.  and  OLAYINKA, Adebola T.. Antimicrobial resistance of Vibrio cholerae from sub-Saharan Africa: A systematic review. Afr. J. Lab. Med. [online]. 2018, vol.7, n.2, pp.1-7. ISSN 2225-2010.  https://doi.org/10.4102/ajlm.v7i2.778.

    BACKGROUND: The World Health Assembly adopted the Global Action Plan on Antimicrobial Resistance, which includes improving the knowledge base through surveillance and research. Noteworthily, the World Health Organization has advocated a Global Antimicrobial Resistance Surveillance System to address the plan's surveillance objective, with most African countries enrolling in or after 2017. AIM: The aim of this article was to review prior data on antimicrobial resistance of Vibrio cholerae from sub-Saharan Africa with a view for future control and intervention strategies. METHODS: We used the Preferred Reporting Items for Systematic Review and Meta-Analysis (or 'PRISMA') guidelines to search the PubMed and African Journals Online databases, as well as additional articles provided by the Nigeria Centre for Disease Control, for articles reporting on the antibiotic susceptibility of V. cholerae between January 2000 and December 2017. RESULTS: We identified 340 publications, of which only 25 (reporting from 16 countries within the sub-Saharan African region) were eligible. The majority (20; 80.0%) of the cholera toxigenic V. cholerae isolates were of the serogroup O1 of the El Tor biotype with Ogawa and Inaba serotypes predominating. Resistance was predominantly documented to trimethoprim-sulphamethoxazole (50% of the studies), ampicillin (43.3% of the studies), chloramphenicol (43.3% of the studies) and streptomycin (30% of the studies). Resistance mechanisms were reported in 40% of the studies. CONCLUSION: Our results demonstrate a documented antimicrobial resistance of V. cholerae to multiple antibiotic classes, including cell wall active agents and antimetabolites with evidence of phenotypic/genotypic resistance to fluoroquinolones.

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