An investigation of the acid-soluble phosphorus compounds in the muscle of guinea pigs injected with diphtheria toxin was undertaken in the hope of finding a clue to the nature of the metabolic disorders which must underlie the manifestations of such a toxemia. Although a good deal has been written about the changes in carbohydrate metabolism produced in animals by Corynebacterium diphtheriae or its toxin (1, 2), as yet there has been no demonstration of a primary metabolic defect adequate to

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... plain death. Pappenheimer has collected evidence indicating that the diphtheria toxin is the protein part of bacterial cytochrome b, and he has suggested that the primary defect produced by the toxin in the host is inhibition of synthesis of a comparable host enzyme (3-6). Since weakness is a major symptom of this and other infectious diseases, and since death may be looked upon as a failure either to utilize or produce energy adequately, the high energy bond organic phosphorus compounds seemed a logical place to look for a fundamental metabolic defect leading to death. It is well recognized that peripheral circulatory collapse or shock is a frequent finding in terminal infectious states, and it has been shown by Bollman and Flock (7) that shock decreases the muscle stores of high energy phosphate bonds. Studies of arterial and venous blood oxygen content were, therefore, included so that if a change was found in the energy reserves it might be possible to determine whether this was caused by a failure of oxygen transport to the tissues, or by inability of the tissues to utilize adequately the oxygen transported t,o them because of a defect such as that postulated by Pappenheimer. Materials and Afethods Guinea pigs, weighing between 360 and 450 gm., before fasting, and fed a diet of Purina rabbit chow supplemented with daily inje&ions of 20 mg.