BACTERIAL POISONS 41 



tern. In such instances as the injury of the motor areas by tetanus 

 poison, that of certain peripheral nerves by diphtheria toxin, or even 

 the characteristic lesions of post-syphilitic maladies like tabes, we 

 can be reasonably sure that we are dealing with the specific action 

 of the poisons, independent of actual localized growth of the infec- 

 tious agents. 



Diphtheria toxin, after distribution through the body, may act 

 upon many different tissues, as is evident by degenerations in the 

 heart muscle, liver, and kidney, and the petechial hemorrhages in 

 serous surfaces. In addition to this general action, however, there is 

 a very marked selection of certain nerve centers. By Meyer and 

 Gottlieb 34 diphtheria toxin is classed as a specific vascular poison. 

 Its action results in a rapid sinking of the blood pressure with final 

 cardiac death in spite of artificial respiration. These manifestations 

 seem to have a central origin, with particular action upon the vagi 

 and the phrenic nerves. Apparently also the localization of the 

 diphtheritic lesion may influence the selection of individual nerves, 

 the most concentrated action taking place upon the nerves whose 

 endings are distributed in this particular region, for, as Meyer and 

 Ransom 35 have shown, this poison, like tetanus toxin, may be ab- 

 sorbed into the nerves directly through the nerve endings. An in- 

 teresting selective action also of diphtheria poison is the apparently 

 specific alteration of the suprarenal glands which is regularly no- 

 ticed, as enlargement and congestion, in diphtheria-infected guinea 

 pigs, and which has been associated by many workers with the char- 

 acteristic drop in blood pressure which accompanies all severe cases 

 of the disease. Abramow 36 has studied this lesion particularly, and 

 believes that it consists in a degeneration and final disappearance of 

 the chromaffin substance and of the medullary cells. He believes 

 that this, together with degeneration of the heart muscle itself, is of 

 great importance in causing the characteristic vascular failure. 



In botulinus poisoning there is, as Marinesco 3T and Kempner 

 and Pollack 38 have shown, a direct effect upon the cells of the an- 

 terior horns with degenerative changes in the Nissl granules. 



Tetanus poison, which has been studied extensively by pharma- 

 cologists, shows a very marked affinity for the nervous system, as, in 

 fact, the symptoms of tetanus indicate. Indeed, while many of the 

 bacterial poisons are distributed by the blood stream to the point of 

 final attack, in tetanus the absorption of the toxin from the lesion or 



34 Meyer and Gottlieb. "Pharmacology Trans. Halsey," Lippincott, 1914, 

 p. 556. 



35 Meyer and Ransom. Arch, de pharmacodyn,, Vol. 15, 1905, also Meyer, 

 Berl. klin. Woch., 25 and 26, 1909, also Arch. f. exp. Path. u. Ther., Vol. 

 60, 1909. 



36 Abramow. Zeitschr. f. Imm., Vol. 15, 1912. 



37 Marinesco. Compt. rend, de la soc. de biol., Vol. 3, 1896. 



38 Kempner and Pollack. Deutsche med. Woch., 32, 1897. 



