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A Clinical Analysis of Thirty-Eight Cases

JOSEPH A. EZZO, M.D.; WILLIAM A. KNIGHT, Jr., M.D.

AMA Arch Intern Med. 1957;99(5):701-707.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The physiological disturbances produced by the blood-stream invasion of bacteria or their products manifested by peripheral vascular collapse has been called bacterial shock. This entity, although it occurs not infrequently and has also been produced in the experimental animal, is poorly understood.^1-5

The experimental syndrome has been produced by the intravenous injection of an endotoxin obtained from certain Gram-negative organisms.^1-5 Thomas² describes this endotoxin as a group of toxic substances which exist as a phosphorus-containing, polysaccharide, protein-lipid complex. The polysaccharide contributes immunological specificity; the protein is closely bound to the polysaccharide and when separated is toxic if in combination with the phosphorus-containing radical. This latter radical also seems to confer toxicity on the otherwise nontoxic polysaccharide.

The physiological changes which occur following the intravenous administration of this endotoxin in animals have been reported by several authors ^2-7 and include profound vasomotor collapse, characterized by alternating arteriolar constriction . . . [Full Text PDF of this Article]

Author Affiliations
St. Louis

From the Department of Internal Medicine, St. Louis University School of Medicine.

Footnotes
Accepted for publication Nov. 1, 1956.

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