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Pathophysiology of Anthrax
The disease syndromes produced by both Bacillus anthyacis organisms and by sterile in vitro toxins are orderly and predictable. Most of the signs and changes in the blood cellular, chemical, and gaseous elements occur late in the septicemic phase of disease, whereas similar changes occur earlier aft...
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Published in: | The Journal of infectious diseases 1966-04, Vol.116 (2), p.123-138 |
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container_end_page | 138 |
container_issue | 2 |
container_start_page | 123 |
container_title | The Journal of infectious diseases |
container_volume | 116 |
creator | Klein, Frederick Walker, Jerry S. Fitzpatrick, David F. Lincoln, Ralph E. Mahlandt, Bill G. Jones, William J. Dobbs, James P. Hendrix, Kenneth J. |
description | The disease syndromes produced by both Bacillus anthyacis organisms and by sterile in vitro toxins are orderly and predictable. Most of the signs and changes in the blood cellular, chemical, and gaseous elements occur late in the septicemic phase of disease, whereas similar changes occur earlier after administration of toxins. The only pathophysiological response peculiar to any of the 3 species of animals used in this study (rhesus monkey, chimpanzee, and rabbit) was the presence of nucleated red blood cells in the rabbit and the absence of these cells in the 2 primates. All effects appeared to be nonspecific and included elevation of white blood cells with a marked shift to the left, decreased calcium, sodium, and cholinesterase, and increased potassium, chloride, and phosphate. Hyperesthesia frequently was observed, and late in the course of disease a terminal hypoglycemia with alkalosis and hypoxia occurred. One of the most significant observations was failure of the body to respond to the organisms per se but rather to the toxins of B. anthyacis. |
doi_str_mv | 10.1093/infdis/116.2.123 |
format | article |
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Most of the signs and changes in the blood cellular, chemical, and gaseous elements occur late in the septicemic phase of disease, whereas similar changes occur earlier after administration of toxins. The only pathophysiological response peculiar to any of the 3 species of animals used in this study (rhesus monkey, chimpanzee, and rabbit) was the presence of nucleated red blood cells in the rabbit and the absence of these cells in the 2 primates. All effects appeared to be nonspecific and included elevation of white blood cells with a marked shift to the left, decreased calcium, sodium, and cholinesterase, and increased potassium, chloride, and phosphate. Hyperesthesia frequently was observed, and late in the course of disease a terminal hypoglycemia with alkalosis and hypoxia occurred. 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Most of the signs and changes in the blood cellular, chemical, and gaseous elements occur late in the septicemic phase of disease, whereas similar changes occur earlier after administration of toxins. The only pathophysiological response peculiar to any of the 3 species of animals used in this study (rhesus monkey, chimpanzee, and rabbit) was the presence of nucleated red blood cells in the rabbit and the absence of these cells in the 2 primates. All effects appeared to be nonspecific and included elevation of white blood cells with a marked shift to the left, decreased calcium, sodium, and cholinesterase, and increased potassium, chloride, and phosphate. Hyperesthesia frequently was observed, and late in the course of disease a terminal hypoglycemia with alkalosis and hypoxia occurred. 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Most of the signs and changes in the blood cellular, chemical, and gaseous elements occur late in the septicemic phase of disease, whereas similar changes occur earlier after administration of toxins. The only pathophysiological response peculiar to any of the 3 species of animals used in this study (rhesus monkey, chimpanzee, and rabbit) was the presence of nucleated red blood cells in the rabbit and the absence of these cells in the 2 primates. All effects appeared to be nonspecific and included elevation of white blood cells with a marked shift to the left, decreased calcium, sodium, and cholinesterase, and increased potassium, chloride, and phosphate. Hyperesthesia frequently was observed, and late in the course of disease a terminal hypoglycemia with alkalosis and hypoxia occurred. One of the most significant observations was failure of the body to respond to the organisms per se but rather to the toxins of B. anthyacis.</abstract><cop>United States</cop><pub>The University of Chicago Press</pub><pmid>4956203</pmid><doi>10.1093/infdis/116.2.123</doi><tpages>16</tpages></addata></record> |
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source | JSTOR Archival Journals and Primary Sources Collection; Oxford University Press:Jisc Collections:Oxford Journal Archive: Access period 2024-2025 |
subjects | Animals Anthrax Anthrax - physiopathology Bacillus anthracis Blood Blood Cell Count Blood Chemical Analysis Blood Gas Analysis Calcium Chimpanzees Chlorides Cholinesterases Diet Disease course Glucose Haplorhini Hematocrit Hominidae Hyperglycemia - etiology In Vitro Techniques Monkeys Phosphates Proteins Rabbits Sepsis Spores Toxins Toxins, Biological - pharmacology |
title | Pathophysiology of Anthrax |
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