Virulence Mechanisms of Bacterial Pathogens 2016
DOI: 10.1128/9781555819286.ch21
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Staying Alive: Vibrio cholerae's Cycle of Environmental Survival, Transmission, and Dissemination

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Cited by 26 publications
(28 citation statements)
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“…Current cholera cases are mainly due to the O1 biotype El Tor (both Inaba and Ogawa), while classical strains are rarely isolated [1][2][3]. Cholera transmission is primarily mediated by either free-living planktonic cells, biofilm-associated cells, or dormant V. cholerae O1 [25,[30][31][32]. Some phenotypic variants, such as rugose cells, also confer increased resistance to antimicrobial compounds and environmental stress conditions during interepidemic periods [33].…”
Section: Vibrio Choleraementioning
confidence: 99%
“…Current cholera cases are mainly due to the O1 biotype El Tor (both Inaba and Ogawa), while classical strains are rarely isolated [1][2][3]. Cholera transmission is primarily mediated by either free-living planktonic cells, biofilm-associated cells, or dormant V. cholerae O1 [25,[30][31][32]. Some phenotypic variants, such as rugose cells, also confer increased resistance to antimicrobial compounds and environmental stress conditions during interepidemic periods [33].…”
Section: Vibrio Choleraementioning
confidence: 99%
“…Importantly, both newly engineered rpoS mutants produced copious amounts of HapR at high cell densities (Fig. 3C), challenging the general notion that RpoS positively regulates HapR production (Yildiz et al ., 2004; Conner et al ., 2016). At this point, we cannot distinguish whether the GOF luxO mutation was introduced into the rpoS::cm mutant strain when it was initially generated (Yildiz and Schoolnik, 1998) or whether it appeared through extended lab domestication while the strain was transferred between group members in the Schoolnik laboratory (we confirmed the luxO mutation in three independent aliquots that were transferred from the Schoolnik laboratory to the Blokesch laboratory in 2009).…”
Section: Resultsmentioning
confidence: 99%
“…The expression of these two virulence factors is regulated by a transcription activator ToxT. [ 85 ] During the infectious process, ToxT undergoes conformational changes depending on signals encountered in the small intestine that promotes production of CT. [ 86 ] In this perspective, a number of compounds were evaluated, designed or synthesized to attack this important route of virulence. These compounds reduce virulence gene expression, like the CT, by binding ToxT and inhibiting ToxT‐DNA binding interactions.…”
Section: Inhibitors Of Expression Of Virulence Factorsmentioning
confidence: 99%