Pathophysiological changes in the rat associated with anthrax toxin

DC Fish, F Klein, RE Lincoln, JS Walker… - The Journal of infectious …, 1968 - JSTOR
DC Fish, F Klein, RE Lincoln, JS Walker, JP Dobbs
The Journal of infectious diseases, 1968JSTOR
The pathophysiological response following anthrax spore or toxin challenge was studied in
rats. After challenge withanthrax toxin the EEG pattern showed cycles of depression in the
normal activity and was grossly abnormal several minutes before death, with all electrical
activity ceasing prior to death. The respiration rate also cycled from periods of normal rate to
double the normal rate. However, at death when the respiration rate dropped to zero the
EKG and heart rate were essentially normal. Liver and muscle glycogen were utilized in an …
The pathophysiological response following anthrax spore or toxin challenge was studied in rats. After challenge withanthrax toxin the EEG pattern showed cycles of depression in the normal activity and was grossly abnormal several minutes before death, with all electrical activity ceasing prior to death. The respiration rate also cycled from periods of normal rate to double the normal rate. However, at death when the respiration rate dropped to zero the EKG and heart rate were essentially normal. Liver and muscle glycogen were utilized in an attempt to maintain serum glucose at a normal level. Alkaline phosphatase activity increased in the serum and decreased in the kidney. Massive pulmonary edema was seen after toxin challenge, and peritoneal fluid was found after spore challenge. Hematocrit values increased markedly and white blood cell numbers increased because of an increase in the number of polymorphonuclear leukocytes. The ability of the synergistic combination of the toxin components (protective antigen and lethal factor) to cause hemoconcentration and significant changes in the liver glycogen level is discussed. Since the cardiovascular system appears to function normally until respiration ceases, death from anthrax is not attributable to shock even in the Fischer rat. The exact mechanism of death is most likely a combination of several factors, but there is little doubt that the toxin affects the central nervous system and causes respiratory failure by some unknown mechanism.
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