Cholera

Harris, Jason B.; LaRocque, Regina C.; Qadri, Firdausi; Ryan, Edward T.; Calderwood, Stephen B.

doi:10.1016/s0140-6736(12)60436-x

Cited by 535 publications

(557 citation statements)

References 141 publications

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“…Classical strains were responsible for the six cholera pandemics that occurred during the 19th century and the first half of the 20th century and are noted for their severe clinical presentation. In 1961, the El Tor strains emerged as the cause of the ongoing seventh pandemic, completely displacing the classical strains from the environment and as a cause of cholera in humans (1). These strains colonize the intestine more effectively and spread between hosts more efficiently but cause fewer deaths and significantly more asymptomatic colonization (2).…”

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confidence: 99%

Mechanisms of Inflammasome Activation by Vibrio cholerae Secreted Toxins Vary with Strain Biotype

et al. 2015

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Activation of inflammasomes is an important aspect of innate immune responses to bacterial infection. Recent studies have linked Vibrio cholerae secreted toxins to inflammasome activation by using murine macrophages. To increase relevance to human infection, studies of inflammasome-dependent cytokine secretion were conducted with the human THP-1 monocytic cell line and corroborated in primary human peripheral blood mononuclear cells (PBMCs). Both El Tor and classical strains of V. cholerae activated ASC (apoptosis-associated speck-like protein-containing a CARD domain)-dependent release of interleukin-1␤ (IL-1␤) when cultured with human THP-1 cells, but the pattern of induction was distinct, depending on the repertoire of toxins the strains produced. El Tor biotype strains induced release of IL-1␤ dependent on NOD-like receptor family pyrin domain-containing 3 (NLRP3) and ASC due to the secreted pore-forming toxin hemolysin. Unlike in studies with mouse macrophages, the MARTX toxin did not contribute to IL-1␤ release from human monocytic cells. Classical biotype strains, which do not produce either hemolysin or the MARTX toxin, activated low-level IL-1␤ release that was induced by cholera toxin (CT) and dependent on ASC but independent of NLRP3 and pyroptosis. El Tor strains likewise showed increased IL-1␤ production dependent on CT when the hemolysin gene was deleted. In contrast to studies with murine macrophages, this phenotype was dependent on a catalytically active CT A subunit capable of inducing production of cyclic AMP and not on the B subunit. These studies demonstrate that the induction of the inflammasome in human THP-1 monocytes and in PBMCs by V. cholerae varies with the biotype and is mediated by both NLRP3-dependent and -independent pathways. V ibrio cholerae is the causative agent of the diarrheal disease cholera. The O1 serogroup, which is most associated with disease, is divided into two biotypes, classical and El Tor. Classical strains were responsible for the six cholera pandemics that occurred during the 19th century and the first half of the 20th century and are noted for their severe clinical presentation. In 1961, the El Tor strains emerged as the cause of the ongoing seventh pandemic, completely displacing the classical strains from the environment and as a cause of cholera in humans (1). These strains colonize the intestine more effectively and spread between hosts more efficiently but cause fewer deaths and significantly more asymptomatic colonization (2).The primary virulence factor for pandemic cholera strains is cholera toxin (CT), an ADP-ribosylating toxin that disables the G␣ s subunit, resulting in increased cyclic AMP (cAMP) production and secretion of fluid from enterocytes due to the opening of chloride channels. The toxin is composed of the catalytically active A (CTA) subunit associated with five CTB subunits that bind to surface GM 1 gangliosides, facilitating toxin endocytosis (3). In addition to enterotoxigenic activity, CT has also been demonstrated to have immunomodulat...

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confidence: 99%

Mechanisms of Inflammasome Activation by Vibrio cholerae Secreted Toxins Vary with Strain Biotype

et al. 2015

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“…Most V. cholerae O1 infections are asymptomatic, and moderate diarrhea may be indistinguishable from other causes of gastroenteritis [13]. Approximately 5% of infected patients develop a severe form of cholera [14].…”

Section: Introductionmentioning

confidence: 99%

Clinical and Epidemiological Characterization of Cholera, Mexico 2013-2014

Pedroza¹,

Vázquez²,

Monroy³

et al. 2018

J Infect Dis Preve Med

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“…It is one of the most prevalent infectious diseases in regions where there is limited access to clean water. There have been seven pandemics of cholera since 1817 (Harris et al, 2012). The current and seventh pandemic began in 1961; although it was initially caused by the V. cholerae O1 El Tor biotype, the V. cholerae O139 type was detected in 1993 (Chongsa-nguan et al, 1993;Garg et al, 1993;Albert et al, 1993;Ramamurthy et al, 1993) and variants of V. cholerae O1 El Tor emerged in the 1990s (Ansaruzzaman et al, 2004;Nair et al, 2006;Raychoudhuri et al, 2008;Safa et al, 2008;Morita et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Molecular epidemiology of Vibrio cholerae O1 in northern Vietnam (2007–2009), using multilocus variable-number tandem repeat analysis

Nguyen

Ngo

et al. 2016

Journal of Medical Microbiology

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Cholera is an infectious disease of major concern in Vietnam and other Asian countries. In 2009, there was a large outbreak of cholera in northern Vietnam. To investigate relationships among isolates of the causative pathogen Vibrio cholerae in this region since 2007, we carried out a multilocus variable-number tandem repeat analysis (MLVA) of 170 isolates collected between 2007 and 2009. A total of 24 MLVA types were identified using seven loci. Five clones (1-5) were identified using five loci of the large V. cholerae chromosome; clones 1 and 2 were major, and the others were minor. Clone 1 isolates were responsible for the 2009 outbreak. A shift in the predominant clone occurred between 2007 and 2009, with clone 1 likely derived from clone 2. Moreover, the former was less diverse than the latter, suggesting a single source of cholera dissemination. Epidemiological data indicated a wavelet prior to the large outbreak, suggesting that drinking water source or food chain became contaminated during dissemination. Our results reveal the utility of MLVA for analysis of V. cholerae isolates within a relatively short period and broaden our understanding of its transmission and response to cholera.

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Cholera

Cited by 535 publications

References 141 publications

Mechanisms of Inflammasome Activation by Vibrio cholerae Secreted Toxins Vary with Strain Biotype

Mechanisms of Inflammasome Activation by Vibrio cholerae Secreted Toxins Vary with Strain Biotype

Clinical and Epidemiological Characterization of Cholera, Mexico 2013-2014

Molecular epidemiology of Vibrio cholerae O1 in northern Vietnam (2007–2009), using multilocus variable-number tandem repeat analysis

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