Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/149842
Title: Genomic insights into Vibrio cholerae O1 responsible for cholera epidemics in Tanzania between 1993 and 2017
Authors: Hounmanou, Yaovi Mahuton Gildas
Leekitcharoenphon, Pimlapas
Kudirkiene, Egle
Mdegela, Robinson H.
Hendriksen, Rene S.
Olsen, John Elmerdahl
Dalsgaard, Anders
Keywords: Engineering::Bioengineering
Issue Date: 2019
Source: Hounmanou, Y. M. G., Leekitcharoenphon, P., Kudirkiene, E., Mdegela, R. H., Hendriksen, R. S., Olsen, J. E. & Dalsgaard, A. (2019). Genomic insights into Vibrio cholerae O1 responsible for cholera epidemics in Tanzania between 1993 and 2017. PLoS Neglected Tropical Diseases, 13(12). https://dx.doi.org/10.1371/JOURNAL.PNTD.0007934
Journal: PLoS Neglected Tropical Diseases
Abstract: Background: Tanzania is one of seven countries with the highest disease burden caused by cholera in Africa. We studied the evolution of Vibrio cholerae O1 isolated in Tanzania during the past three decades. Methodology / Principal findings: Genome-wide analysis was performed to characterize V. cholerae O1 responsible for the Tanzanian 2015-2017 outbreak along with strains causing outbreaks in the country for the past three decades. The genomes were further analyzed in a global context of 590 strains of the seventh cholera pandemic (7PET), as well as environmental isolates from Lake Victoria. All Tanzanian cholera outbreaks were caused by the 7PET lineage. The T5 sub-lineage (ctxB3) dominated outbreaks until 1997, followed by the T10 atypical El Tor (ctxB1) up to 2015, which were replaced by the T13 atypical El Tor of the current third wave (ctxB7) causing most cholera outbreaks until 2017 with T13 being phylogenetically related to strains from East African countries, Yemen and Lake Victoria. The strains were less drug resistant with approximate 10-kb deletions found in the SXT element, which encodes resistance to sulfamethoxazole and trimethoprim. Nucleotide deletions were observed in the CTX prophage of some strains, which warrants further virulence studies. Outbreak strains share 90% of core genes with V. cholerae O1 from Lake Victoria with as low as three SNPs difference and a significantly similar accessory genome, composed of genomic islands namely the CTX prophage, Vibrio Pathogenicity Islands; toxin co-regulated pilus biosynthesis proteins and the SXT-ICE element. Conclusion / Significance: Characterization of V. cholerae O1 from Tanzania reveals genetic diversity of the 7PET lineage composed of T5, T10 and T13 sub-lineages with introductions of new sequence types from neighboring countries. The presence of these sub-lineages in environmental isolates suggests that the African Great Lakes may serve as aquatic reservoirs for survival of V. cholerae O1 favoring continuous human exposure.
URI: https://hdl.handle.net/10356/149842
ISSN: 1935-2727
DOI: 10.1371/JOURNAL.PNTD.0007934
Rights: © 2019 The Author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SCBE Journal Articles

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