Ultrastructural changes in the small intestine of suckling mice, caused by Vibrio cholerae hemagglutinin/protease

ABSTRACT Acid adaptation has previously been shown to increase the infectivity of Vibrio cholerae in the infant mouse model. To better understand this phenomenon, we monitored the spatial distribution and temporal changes in the ratios of acid-adapted cells to unadapted V. cholerae cells in the small intestine, as well as the timing of virulence factor expression. We found that the competitive advantage afforded by acid adaptation does not become manifest until greater than 3 h postinfection; thus, acid adaptation does not increase V. cholerae passage through the gastric acid barrier. Additionally, acid-adapted and unadapted V. cholerae cells colonize the same sections of the small intestine and show similar kinetics of transcriptional induction of the virulence genes tcpA and ctxA. These studies suggest that the increased infectivity of acid-adapted V. cholerae is due to a more rapid onset of multiplication and/or to an increased multiplication rate within the infant mouse intestine.

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Ultrastructural Changes in the Small Intestine of Neonatal Calves with Enteric Colibacillosis

Veterinary Pathology ◽

10.1177/030098588201900210 ◽

1982 ◽

Vol 19 (2) ◽

pp. 190-201 ◽

Cited By ~ 4

Author(s):

G. R. Pearson ◽

E. F. Logan

Keyword(s):

Small Intestine ◽

Epithelial Cells ◽

Small Groups ◽

Ultrastructural Changes ◽

Post Inoculation ◽

Cytoplasmic Inclusions ◽

Distal Small Intestine ◽

Enteropathogenic Strain ◽

Neonatal Calves ◽

Small Intestines

The small intestines of calves inoculated orally with the enteropathogenic strain of Escherichia coli 0101:K'B41′, K99 were examined by electron microscopy at 3, 6, 12, 16, 21, 36, 69, 70 and 72 hours after inoculation. The challenge organism adhered to the mucosa of the distal small intestine from six hours post-inoculation. Bacteria were separated from the microvillous brush border by a gap of 200 to 300 nm in which bacterial fimbriae and the microvillous glycocalyx were seen. Bacteria never were found in epithelial cells but were present in macrophages in the lamina propria from 12 hours. At three and six hours, cytopathic changes were not seen in the small intestine, but from 12 hours epithelial cells on affected villi had blunt and thick microvilli and contained cytoplasmic inclusions. Epithelial cells were seen frequently in the process of extrusion from the villi, either singly, in small groups, or as ribbons of cells. Intervillous bridges, characteristic of villous fusion, were seen frequently from 69 hours.

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Niche adaptation limits bacteriophage predation of Vibrio cholerae in a nutrient-poor aquatic environment

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1810138116 ◽

2019 ◽

Vol 116 (5) ◽

pp. 1627-1632 ◽

Cited By ~ 11

Author(s):

Cecilia A. Silva-Valenzuela ◽

Andrew Camilli

Keyword(s):

Small Intestine ◽

Vibrio Cholerae ◽

Strong Evidence ◽

Biological Entity ◽

Aquatic Environments ◽

Estuarine Water ◽

Human Small Intestine ◽

Niche Adaptation ◽

Adaptation Limits ◽

Potential Use

Vibrio cholerae, the causative agent of cholera, has reservoirs in fresh and brackish water where it interacts with virulent bacteriophages. Phages are the most abundant biological entity on earth and coevolve with bacteria. It was reported that concentrations of phage and V. cholerae inversely correlate in aquatic reservoirs and in the human small intestine, and therefore that phages may quench cholera outbreaks. Although there is strong evidence for phage predation in cholera patients, evidence is lacking for phage predation of V. cholerae in aquatic environments. Here, we used three virulent phages, ICP1, ICP2, and ICP3, commonly shed by cholera patients in Bangladesh, as models to understand the predation dynamics in microcosms simulating aquatic environments. None of the phages were capable of predation in fresh water, and only ICP1 was able to prey on V. cholerae in estuarine water due to a requirement for salt. We conclude that ICP2 and ICP3 are better adapted for predation in a nutrient rich environment. Our results point to the evolution of niche-specific predation by V. cholerae-specific virulent phages, which complicates their use in predicting or monitoring cholera outbreaks as well as their potential use in reducing aquatic reservoirs of V. cholerae in endemic areas.

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Disaccharidase Activities in Small Intestine of Rotavirus-Infected Suckling Mice

Journal of Pediatric Gastroenterology and Nutrition ◽

10.1097/00005176-199010000-00020 ◽

1990 ◽

Vol 11 (3) ◽

pp. 395-403 ◽

Cited By ~ 21

Author(s):

J. Collins ◽

D. C. A. Candy ◽

W. G. Starkey ◽

A. J. Spencer ◽

M. P. Osborne ◽

...

Keyword(s):

Small Intestine ◽

Suckling Mice

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EPIDEMIC DIARRHEAL DISEASE OF SUCKLING MICE

Journal of Experimental Medicine ◽

10.1084/jem.88.3.317 ◽

1948 ◽

Vol 88 (3) ◽

pp. 317-324 ◽

Cited By ~ 9

Author(s):

Alwin M. Pappenheimer ◽

F. Sargent Cheever

Keyword(s):

Small Intestine ◽

Epithelial Cells ◽

Inflammatory Reaction ◽

Diarrheal Disease ◽

Gram Positive ◽

Cytoplasmic Inclusions ◽

Suckling Mice ◽

Large Numbers ◽

Intestinal Contents ◽

Frequent Presence

1. Cytoplasmic inclusions were found in the epithelial cells of the small intestine in a major proportion of suckling mice suffering from the spontaneous or experimentally produced diarrheal disease now prevalent in this laboratory. 2. They were not found in healthy stock mice of corresponding age. 3. Feeding of intestinal extract from healthy mice did not produce diarrhea or inclusions. 4. Feeding of boiled extract from diarrheal mice did not lead to the formation of cytoplasmic inclusions, when precautions were taken to prevent accidental infection. 5. The inclusions were regularly present only in the first few days of the disease. The inclusion-bearing cells desquamated. There was no inflammatory reaction. 6. Attention is called to the frequent presence of large numbers of Gram-positive coccoid bodies in the intestinal contents of suckling mice with diarrhea.

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