Intestinal fluid accumulation induced by oral challenge with Vibrio cholerae or cholera toxin in infant mice

Baselski, Vickie S.; Briggs, R. E.; Parker, C D

doi:10.1128/iai.15.3.704-712.1977

Cited by 82 publications

(47 citation statements)

References 27 publications

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“…It is interesting that other pathogens, such as V. cholerae , which do not colonize the intestine of adult mice, are able to colonize the small intestine of suckling mice and cause deadly infection (Pitkin and Actor, 1972; Baselski et al ., 1977; Attridge and Rowley, 1983; Klose, 2000; Wu et al ., 2001). The mechanisms responsible for this susceptibility have not been elucidated, but it seems reasonable to assume that immature host defences play a role.…”

Section: Discussionmentioning

confidence: 99%

“…The newborn mouse is susceptible to several pathogens, such as Vibrio cholerae , that are not able to colonize the small intestine of adult animals (Pitkin and Actor, 1972; Baselski et al ., 1977; Attridge and Rowley, 1983; Klose, 2000; Wu et al ., 2001). The susceptibility of these animals is likely to reflect the immaturity of their innate antibacterial defence mechanisms or of the mechanisms that regulate inflammation.…”

Section: Introductionmentioning

confidence: 99%

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A newborn mouse model for the study of intestinal pathogenesis of shigellosis

et al. 2003

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SummaryShigella infection is characterized by the induction of acute inflammation, which is responsible for the massive tissue destruction of the intestinal mucosa. A murine model would be a valuable tool for gaining a better understanding of the physiopathology of shigellosis and the host immune response to Shigella infection, but adult mice do not develop disease upon oral inoculation. We therefore attempted to develop a model of infection in newborn mice. Four-day-old mice inoculated with 50 m m m m l of 5 ¥ ¥ ¥ ¥ 10 9 invasive wild-type Shigella flexneri 5a were susceptible to bacterial infection, but mice inoculated with the non-invasive strain BS176 were not. Histologically, 4-day-old mice infected with the invasive strain presented intestinal lesions and inflammation similar to those described in patients with shigellosis. Moreover, cytokine and chemokine responses consistent with inflammation were observed. Lower bacterial inocula induced less severe intestinal damage. In contrast, 5-day-old mice inoculated with either the invasive or the non-invasive strain were not infected. We have thus established a mouse model that is suitable for the study of the pathogenesis of intestinal Shigella infection.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A newborn mouse model for the study of intestinal pathogenesis of shigellosis

et al. 2003

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“…Another model with an occluded intestinal tract is the sealed adult mouse model of Richardson et al (372), in which the ano-rectal canal is sealed with cyanoacrylate ester glue. Unoccluded infant mice have also been used to study diarrhea induced by V. cholerae strains or CT (18) and are particularly useful in studying the colonization potential of strains in competitive colonization assays (123). The infant mouse model, like the infant rabbit model of Dutta et al (91), is limited by the fact that the animals are susceptible to infection only for a relatively short time after birth.…”

Section: Models Of Pathogenesismentioning

confidence: 99%

Cholera

1995

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Despite more than a century of study, cholera still presents challenges and surprises to us. Throughout most of the 20th century, cholera was caused by Vibrio cholerae of the O1 serogroup and the disease was largely confined to Asia and Africa. However, the last decade of the 20th century has witnessed two major developments in the history of this disease. In 1991, a massive outbreak of cholera started in South America, the one continent previously untouched by cholera in this century. In 1992, an apparently new pandemic caused by a previously unknown serogroup of V. cholerae (O139) began in India and Bangladesh. The O139 epidemic has been occurring in populations assumed to be largely immune to V. cholerae O1 and has rapidly spread to many countries including the United States. In this review, we discuss all aspects of cholera, including the clinical microbiology, epidemiology, pathogenesis, and clinical features of the disease. Special attention will be paid to the extraordinary advances that have been made in recent years in unravelling the molecular pathogenesis of this infection and in the development of new generations of vaccines to prevent it.

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“…Virulence testing of V. cholerae mutants. The virulence of CA401, CA40130, and the heme utilization mutants was tested by the fluid accumulation assay of Baselski et al (1). Fourto six-day-old CFW or BALB/c mice (3 to 10 mice per bacterial strain) were orally inoculated with 106 or 107 cells.…”

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confidence: 99%

Vibrio cholerae iron transport systems: roles of heme and siderophore iron transport in virulence and identification of a gene associated with multiple iron transport systems

1994

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Vibrio cholerae iron transport mutants were tested for their ability to cause disease in an infant mouse model.The mice were challenged with either the wild-type strain, a vibriobactin synthesis mutant, a heme utilization mutant, or double mutants containing both the vibriobactin synthesis defect and the heme utilization defect.When mice were challenged with 107 bacteria, the ability of the double mutant to survive in the intestines was greatly reduced and that of the heme utilization mutant was slightly reduced compared with that of the wild type or the vibriobactin synthesis mutant. When the inoculum size was reduced 10-fold, all of the iron transport mutants failed to colonize the intestines and failed to cause diarrhea in the mice, whereas the wild-type strain was not cleared and elicited a diarrheal response. These data indicate that disruption of either the heme utilization or the vibriobactin uptake system reduces the ability of V. cholerae to cause disease. One of the heme utilization mutants, DHH1, was found to be defective also in utilization of vibriobactin and ferrichrome, mimicking the Escherichia coli TonB-phenotype. This mutant was the least virulent of the iron transport mutants tested. Transformation of DHH1 with the recombinant plasmid pHUT4 restored the abilities to use hemin, vibriobactin, and ferrichrome as iron sources, suggesting that pHUT4 encodes a gene(s) involved globally in the iron transport systems. Hybridization of Vibrio DNA with the V. cholerae heme utilization genes demonstrated the presence of DNA homologous to the genes encoding the outer membrane protein HutA and the inner membrane protein HutB in all the V. cholerae strains tested. The probe containing hutA, but not that containing hutB, also hybridized to DNA from Vibrio parahaemolyticus.

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Intestinal fluid accumulation induced by oral challenge with Vibrio cholerae or cholera toxin in infant mice

Cited by 82 publications

References 27 publications

A newborn mouse model for the study of intestinal pathogenesis of shigellosis

A newborn mouse model for the study of intestinal pathogenesis of shigellosis

Cholera

Vibrio cholerae iron transport systems: roles of heme and siderophore iron transport in virulence and identification of a gene associated with multiple iron transport systems

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