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RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION : II. FACTORS RESPONSIBIE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT
Determinations of pH, Eh, and concentrations of acetic, butyric and lactic acids were made on the content of cecum and transverse colon of groups of mice killed 1, 3, and 5 days after oral administration of 50 mg streptomycin. Control observations on untreated mice are reported in the preceding comm...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
1964
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137859/ https://www.ncbi.nlm.nih.gov/pubmed/14247722 |
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author | Bohnhoff, Marjorie Miller, C. Phillip Martin, William R. |
author_facet | Bohnhoff, Marjorie Miller, C. Phillip Martin, William R. |
author_sort | Bohnhoff, Marjorie |
collection | PubMed |
description | Determinations of pH, Eh, and concentrations of acetic, butyric and lactic acids were made on the content of cecum and transverse colon of groups of mice killed 1, 3, and 5 days after oral administration of 50 mg streptomycin. Control observations on untreated mice are reported in the preceding communication. Heat-killed supenatants of suspensions of bowel content were tested in vitro for their ability to inhibit multiplication of our standard streptomycin-resistant strain of Salmonella enteritidis during aerobic and anaerobic incubation. Also tested in like fashion were series of cultures in broth buffered at various pH levels and containing acetic, butyric, and lactic acids in varying concentrations. In colon content of mice on the 1st day after streptomycin treatment, the pH had risen and the concentrations of the fatty acids fallen, a combination of effects which adequately accounts for its inability to inhibit multiplication of Salmonella in vitro and in vivo. By the 3rd day after streptomycin treatment, pH and fatty acid concentrations had returned to normal levels. The susceptibility of mice to oral challenge on the 3rd day was explained by the finding that lactic acid had accumulated in colon content to levels which, in broth, effectively counteracted the activity of inhibitory concentrations of the fatty acids. Other cocarboxylic acids also antagonized the inhibitory activity of the fatty acids; glucose did not. |
format | Text |
id | pubmed-2137859 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1964 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21378592008-04-17 RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION : II. FACTORS RESPONSIBIE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT Bohnhoff, Marjorie Miller, C. Phillip Martin, William R. J Exp Med Article Determinations of pH, Eh, and concentrations of acetic, butyric and lactic acids were made on the content of cecum and transverse colon of groups of mice killed 1, 3, and 5 days after oral administration of 50 mg streptomycin. Control observations on untreated mice are reported in the preceding communication. Heat-killed supenatants of suspensions of bowel content were tested in vitro for their ability to inhibit multiplication of our standard streptomycin-resistant strain of Salmonella enteritidis during aerobic and anaerobic incubation. Also tested in like fashion were series of cultures in broth buffered at various pH levels and containing acetic, butyric, and lactic acids in varying concentrations. In colon content of mice on the 1st day after streptomycin treatment, the pH had risen and the concentrations of the fatty acids fallen, a combination of effects which adequately accounts for its inability to inhibit multiplication of Salmonella in vitro and in vivo. By the 3rd day after streptomycin treatment, pH and fatty acid concentrations had returned to normal levels. The susceptibility of mice to oral challenge on the 3rd day was explained by the finding that lactic acid had accumulated in colon content to levels which, in broth, effectively counteracted the activity of inhibitory concentrations of the fatty acids. Other cocarboxylic acids also antagonized the inhibitory activity of the fatty acids; glucose did not. The Rockefeller University Press 1964-10-31 /pmc/articles/PMC2137859/ /pubmed/14247722 Text en Copyright © 1964 by The Rockefeller Institute This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Bohnhoff, Marjorie Miller, C. Phillip Martin, William R. RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION : II. FACTORS RESPONSIBIE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT |
title | RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION : II. FACTORS RESPONSIBIE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT |
title_full | RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION : II. FACTORS RESPONSIBIE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT |
title_fullStr | RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION : II. FACTORS RESPONSIBIE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT |
title_full_unstemmed | RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION : II. FACTORS RESPONSIBIE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT |
title_short | RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION : II. FACTORS RESPONSIBIE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT |
title_sort | resistance of the mouse's intestinal tract to experimental salmonella infection : ii. factors responsibie for its loss following streptomycin treatment |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137859/ https://www.ncbi.nlm.nih.gov/pubmed/14247722 |
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