Accession Number : AD0818342

Title :   PATHOPHYSIOLOGICAL CHANGES IN THE RAT ASSOCIATED WITH ANTHRAX TOXIN,

Corporate Author : FORT DETRICK FREDERICK MD

Personal Author(s) : Fish, Donald C. ; Klein, Frederick ; Lincoln, Ralph E. ; Walker, Jerry S.

Report Date : JUN 1967

Pagination or Media Count : 22

Abstract : The pathophysiological response following spore or toxin challenge was studied in rats. After challenge with anthrax toxin the electroencephalogram pattern showed cycles of depression in their normal activity, but just prior to death all electrical activity ceased. 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. Following both spore and toxin challenge, the hematocrit values increased markedly. Massive pulmonary edema was seen after toxin challenge, and peritoneal fluid was found after spore challenge. The white blood cell level increased because of an increase in the number of polymorphonuclear leukocytes. The over-all picture is of central nervous system involvement and respiratory failure. The cardiovascular system appeared to function normally until respiration ceased. 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. (Author)

Descriptors :   *TOXINS AND ANTITOXINS), (*BACILLUS ANTHRACIS, PATHOLOGY, PHYSIOLOGY, RATS, ELECTROENCEPHALOGRAPHY, ELECTROPHYSIOLOGY, RESPONSE(BIOLOGY), RESPIRATION, MEDICAL RESEARCH, NONLETHAL AGENTS, HYPOGLYCEMIA, BLOOD ANALYSIS, LETHAL DOSAGE, HYPERGLYCEMIA, NERVOUS SYSTEM, EDEMA, GLYCOGEN, CARDIOVASCULAR SYSTEM, HEMATOCRIT.

Subject Categories : Anatomy and Physiology
      Medicine and Medical Research

Distribution Statement : APPROVED FOR PUBLIC RELEASE