STUDIES ON THE MECHANISM OF VOMITING PRODUCED BY STAPHYLOCOCCUS ENTEROTOXIN

THE EMETIC ACTION OF STAPHYLOCOCCUS ENTEROTOXIN WAS TESTED ON YOUNG AND ADULT CATS UNDER VARIOUS EXPERIMENTAL CONDITIONS WITH THE FOLLOWING RESULTS: 1. No direct action on isolated intestinal strips was observed. 2. Emesis resulted following intravenous, intracardial, and intraperitoneal injections, but failed to appear subsequent to oral, subcutaneous, or intramuscular administration. 3. Emesis occurred following (a) celiac ganglionectomy, (b) gastrectomy, (c) spinal cord transection at T(2) or caudad, and (d) unilateral vagotomy. 4. Mild retching movements and rarely emesis resulted subsequent to enterotoxin injection following (a) double vagotomy, (b) abdominal evisceration, and (c) spinal cord transection at C(7). 5. Emesis never occurred following (a) destruction of the vomiting center, (b) injection of enterotoxin into the fourth ventricle over the vomiting center, and (c) transection of the central nervous system between the anterior border of the pons and the posterior border of the hypothalamus. 6. Morphine inhibited, ergotoxine inhibited or delayed, while atropine and pentobarbital had little or no effect on emesis due to enterotoxin injection. These experiments indicate that the action of staphylococcus enterotoxin on peripheral sensory structures is of greater importance in the initiation of emesis than direct action of the enterotoxin on the vomiting center. The principal pathways of the afferent and efferent impulses are described.