TY - JOUR
T1 - Phenotypic analysis reveals that the 2010 haiti cholera epidemic is linked to a hypervirulent strain
AU - Satchell, Karla J.F.
AU - Jones, Christopher J.
AU - Wong, Jennifer
AU - Queen, Jessica
AU - Agarwal, Shivani
AU - Yildiz, Fitnat H.
N1 - Funding Information:
c-di-GMP quantification was performed at the UCSC Mass Spectrometry Facility, which is funded by NIH grant S10-RR20939. Northwestern Medicine Catalyst Fund provided funding to Karla J. F. Satchell. This work, including the efforts of Karla J. F. Satchell, was funded by HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) (R01AI092825 and R01AI098369). This work, including the efforts of Fitnat H. Yildiz, was funded by HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) (R01AI102584). This work, including the efforts of Jessica Queen, was funded by HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (1F30 DK084623).
PY - 2016
Y1 - 2016
N2 - Vibrio cholerae O1 El Tor strains have been responsible for pandemic cholera since 1961. These strains have evolved over time, spreading globally in three separate waves. Wave 3 is caused by altered El Tor (AET) variant strains, which include the strain with the signature ctxB7 allele that was introduced in 2010 into Haiti, where it caused a devastating epidemic. In this study, we used phenotypic analysis to compare an early isolate from the Haiti epidemic to wave 1 El Tor isolates commonly used for research. It is demonstrated that the Haiti isolate has increased production of cholera toxin (CT) and hemolysin, increased motility, and a reduced ability to form biofilms. This strain also outcompetes common wave 1 El Tor isolates for colonization of infant mice, indicating that it has increased virulence. Monitoring of CT production and motility in additional wave 3 isolates revealed that this phenotypic variation likely evolved over time rather than in a single genetic event. Analysis of available whole-genome sequences and phylogenetic analyses suggested that increased virulence arose from positive selection for mutations found in known and putative regulatory genes, including hns and vieA, diguanylate cyclase genes, and genes belonging to the lysR and gntR regulatory families. Overall, the studies presented here revealed that V. cholerae virulence potential can evolve and that the currently prevalent wave 3 AET strains are both phenotypically distinct from and more virulent than many El Tor isolates.
AB - Vibrio cholerae O1 El Tor strains have been responsible for pandemic cholera since 1961. These strains have evolved over time, spreading globally in three separate waves. Wave 3 is caused by altered El Tor (AET) variant strains, which include the strain with the signature ctxB7 allele that was introduced in 2010 into Haiti, where it caused a devastating epidemic. In this study, we used phenotypic analysis to compare an early isolate from the Haiti epidemic to wave 1 El Tor isolates commonly used for research. It is demonstrated that the Haiti isolate has increased production of cholera toxin (CT) and hemolysin, increased motility, and a reduced ability to form biofilms. This strain also outcompetes common wave 1 El Tor isolates for colonization of infant mice, indicating that it has increased virulence. Monitoring of CT production and motility in additional wave 3 isolates revealed that this phenotypic variation likely evolved over time rather than in a single genetic event. Analysis of available whole-genome sequences and phylogenetic analyses suggested that increased virulence arose from positive selection for mutations found in known and putative regulatory genes, including hns and vieA, diguanylate cyclase genes, and genes belonging to the lysR and gntR regulatory families. Overall, the studies presented here revealed that V. cholerae virulence potential can evolve and that the currently prevalent wave 3 AET strains are both phenotypically distinct from and more virulent than many El Tor isolates.
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U2 - 10.1128/IAI.00189-16
DO - 10.1128/IAI.00189-16
M3 - Article
C2 - 27297393
AN - SCOPUS:84984799730
VL - 84
SP - 2473
EP - 2481
JO - Infection and Immunity
JF - Infection and Immunity
SN - 0019-9567
IS - 9
ER -