Nontoxigenic Vibrio Cholerae O1 Bacteremia: Case Report and Review

Ninin, E.; Caroff, Nathalie; Kouri, D. El; Espaze, E.; Richet, H.; Quilici, M; Fournier, Jean‐Michel

doi:10.1007/s100960000296

Cited by 26 publications

(21 citation statements)

References 5 publications

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“…Neutrophils contribute to host defense by limiting bacterial dissemination and systemic inflammation. Nontoxigenic cholera is linked clinically not only to inflammatory diarrhea but also to extraintestinal infections, including septicemia (37,45). 8 CFU of nontoxigenic V. cholerae El Tor O1 strain P4 or mock inoculated with PBS.…”

Section: Resultsmentioning

confidence: 99%

“…The role of neutrophils here is clinically relevant since nontoxigenic strains lacking the CTX⌽ prophage are often reported as the agents of local outbreaks of mild-to-moderate diarrheal disease, as well as extraintestinal infections and septicemia, particularly in immunocompromised or liver-damaged individuals. Unlike toxigenic cholera, nontoxigenic V. cholerae induces a more inflammatory diarrhea, characterized by fever, chills, abdominal pain, and bloating (5,33,37,45,49,55). Development of these more severe complications of nontoxigenic infection may be occurring in persons with weakened immune systems either from underlying disease or poor nutrition.…”

Section: Discussionmentioning

confidence: 99%

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Neutrophils Are Essential for Containment of Vibrio cholerae to the Intestine during the Proinflammatory Phase of Infection

Queen

Satchell

2012

Infect Immun

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Cholera is classically considered a noninflammatory diarrheal disease, in comparison to invasive enteric organisms, although there is a low-level proinflammatory response during early infection with Vibrio cholerae and a strong proinflammatory reaction to live attenuated vaccine strains. Using an adult mouse intestinal infection model, this study examines the contribution of neutrophils to host defense to infection. Nontoxigenic El Tor O1 V. cholerae infection is characterized by the upregulation of interleukin-6 (IL-6), IL-10, and macrophage inflammatory protein 2 alpha in the intestine, indicating an acute innate immune response. Depletion of neutrophils from mice with anti-Ly6G IA8 monoclonal antibody led to decreased survival of mice. The role of neutrophils in protection of the host is to limit the infection to the intestine and control bacterial spread to extraintestinal organs. In the absence of neutrophils, the infection spread to the spleen and led to increased systemic levels of IL-1␤ and tumor necrosis factor alpha, suggesting the decreased survival in neutropenic mice is due to systemic shock. Neutrophils were found not to contribute to either clearance of colonizing bacteria or to alter the local immune response. However, when genes for secreted accessory toxins were deleted, the colonizing bacteria were cleared from the intestine, and this clearance is dependent upon neutrophils. Thus, the requirement for accessory toxins in virulence is negated in neutropenic mice, which is consistent with a role of accessory toxins in the evasion of innate immune cells in the intestine. Overall, these data support that neutrophils impact disease progression and suggest that neutrophil effectiveness can be manipulated through the deletion of accessory toxins. G lobal pandemics of the diarrheal disease cholera have occurred throughout human history. The disease is caused by ingestion of the Gram-negative bacterium Vibrio cholerae in contaminated water. Cholera is typified by symptoms of severe, watery diarrhea that leads to life-threatening dehydration and loss of electrolytes (48). There have been seven cholera pandemics in recorded history. The first six were caused by V. cholerae O1 of the classical biotype. The seventh and currently ongoing pandemic began in 1961, when V. cholerae O1 strains of the El Tor biotype began to predominate and spread throughout the world (22). Recent whole-genome analysis of single-nucleotide polymorphisms revealed that the seventh pandemic consists of three distinct waves of transmission from the pandemic center in South Asia. Strain diversification has resulted from continuous local evolution punctuated by sporadic long-range transmission to countries where this pathogen is not endemic, such as in the case of Haiti in 2010 (34). It is estimated that 1.4 billion people worldwide are at risk for cholera, with approximately 2.8 million cholera cases occurring in areas of endemicity each year (1).The innate immune response to V. cholerae infection is poorly understood. Recent studies i...

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neutrophils Are Essential for Containment of Vibrio cholerae to the Intestine during the Proinflammatory Phase of Infection

Queen

Satchell

2012

Infect Immun

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“…This inflammatory response possibly becomes excessive in the absence of genes for CT since volunteers given CT-deficient strains have significantly increased titers of lactoferrin and CXCL8, indicative of more severely inflammatory disease typified by symptoms that include vomiting, fever, mild diarrhea, and cramping (25). These symptoms are also typical of nonepidemic strains of V. cholerae that do not produce CT (4,7,10,13,16,17). This increase in the inflammatory nature of V. cholerae infection could be due to the absence of the immunomodulatory activity of the B subunit of CT that blocks the secretion of proinflammatory cytokines by macrophages, dendritic cells, and epithelial cells in response to bacterial lipopolysaccharide (LPS) (24) due to downregulation of mitogen-activated protein kinase pathways (6).…”

mentioning

confidence: 99%

Role of Toll-Like Receptor 4 in the Proinflammatory Response to Vibrio cholerae O1 El Tor Strains Deficient in Production of Cholera Toxin and Accessory Toxins

Haines¹,

Sayed

Rohrer

et al. 2005

Infect Immun

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Following intranasal inoculation, Vibrio cholerae KFV101 (⌬ctxAB ⌬hapA ⌬hlyA ⌬rtxA) colonizes and stimulates tumor necrosis factor alpha and interleukin 1␤ (IL-1␤) in mice, similar to what occurs with isogenic strain P4 (⌬ctxAB), but is less virulent and stimulates reduced levels of IL-6, demonstrating a role for accessory toxins in pathogenesis. Morbidity is enhanced in C3H/HeJ mice, indicating that Toll-like receptor 4 is important for infection containment.Vibrio cholerae is a gram-negative pathogen that induces diarrhea dependent upon the action of the cyclic AMP-stimulating cholera toxin (CT) (11). During cholera disease, patients in the acute phase do not have extensive tissue damage such as might be observed with shigellosis (21, 22). However, low levels of infiltration of neutrophils, mast cells, and eosinophils in infection and the presence of mediators of inflammatory cell regulation on the second day of cholera disease indicate that V. cholerae stimulates a proinflammatory response early during infection (21). This inflammatory response possibly becomes excessive in the absence of genes for CT since volunteers given CT-deficient strains have significantly increased titers of lactoferrin and CXCL8, indicative of more severely inflammatory disease typified by symptoms that include vomiting, fever, mild diarrhea, and cramping (25). These symptoms are also typical of nonepidemic strains of V. cholerae that do not produce CT (4,7,10,13,16,17). This increase in the inflammatory nature of V. cholerae infection could be due to the absence of the immunomodulatory activity of the B subunit of CT that blocks the secretion of proinflammatory cytokines by macrophages, dendritic cells, and epithelial cells in response to bacterial lipopolysaccharide (LPS) (24) due to downregulation of mitogen-activated protein kinase pathways (6).A major problem with this residual disease of non-CT-producing V. cholerae is that these strains are frequently sufficiently virulent to make them unsafe for use as live attenuated vaccines (2,14,26,27). It has been proposed that the actions of accessory toxins of V. cholerae are responsible for this increased inflammation and contribute to the reactogenicity of live attenuated vaccine strains (24). Recently, we developed a murine model that is sensitive to accessory toxins and can be used to investigate early events in the initiation of the host response to non-CT-producing V. cholerae. Although adult mice are resistant to intestinal colonization by V. cholerae (12), we found that acute inflammation develops in the lung tissue after intranasal inoculation with V. cholerae, providing a model for the assessment of the toxic action on inflammation of a mucosal epithelial layer (8). This model is based on experiments using Shigella flexneri dependent on the premise that the bronchial tree is composed of a mucosal lining with relevant characteristics similar to those of the intestine, including simple cubodial-to-columnar epithelial cells, lymphoid aggregates, bronchiole-associated lymphoid ti...

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“…Many other cases of septicemia due to non O1 and non O139 were also reported by various researchers in different underlying disorder [51][52][53][54]. A case of Vibrio cholerae non O1 sepsis in healthy patient was reported in Spain [20] followed by a report on the infection of non O1 Vibrio cholerae in Southern Taiwan with bacteremia with concurrent spontaneous bacterial peritonitis or invasive soft tissue infection occurring solely in cirrhotic patients, self-limited acute febrile gastroenteritis that often resulted from a wound on extremities [55]. The same year another case was reported in Mexico in which a 55 year old man developed acute cholera cystitis.…”

Section: Discussionmentioning

confidence: 94%

Isolation of Vibrio cholerae in Homogenized Tissues of Liver, Gall Bladder and Bile in Rabbit Model

Abdullah

Aamenah³

et al. 2014

Interdiscip J Microinflammation

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Vibrio cholerae O139 is well known as the causative agent of cholera. It is noninvasive but many reports suggested it to cause bacteremia which brings in a little controversy with the previously reported old literature especially after reported histopathological invasion pattern of Vibrio cholerae O139 and Vibrio cholerae O1 ElTor. The rabbits were processes for ileac loops inoculation of Vibrio cholerae O139 followed by biochemical and molecular analysis of the presence of Vibrio cholerae O139 in liver, gall bladder and bile. We concluded the presence of Vibrio cholerae in liver, bile and gall bladder homogenized tissue. Retrograde spreading of bacteria to the liver via the common bile duct was excluded by complete closure of the intestinal lumen distant to the duct in the intestinal lumen. However, the bacteria might traffic, probably via macrophages, to distant area in the body including the liver. Another study in future is a need to identify the lesions of Vibrio cholerae invasions within liver and gall bladder by immunohistochemistry and using GFP visibility for Vibrio cholerae passage.

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Nontoxigenic Vibrio Cholerae O1 Bacteremia: Case Report and Review

Cited by 26 publications

References 5 publications

Neutrophils Are Essential for Containment of Vibrio cholerae to the Intestine during the Proinflammatory Phase of Infection

Neutrophils Are Essential for Containment of Vibrio cholerae to the Intestine during the Proinflammatory Phase of Infection

Role of Toll-Like Receptor 4 in the Proinflammatory Response to Vibrio cholerae O1 El Tor Strains Deficient in Production of Cholera Toxin and Accessory Toxins

Isolation of Vibrio cholerae in Homogenized Tissues of Liver, Gall Bladder and Bile in Rabbit Model

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