///A BACILLUS AND THE BACTERIOLOGY OF TET.\.\rs 229 



and the milk one-half. Injections of toxin were then given the mare, so 

 that it doubled its original strength in one month. The milk increased 

 eightfold, but the foal's continued to lose in antitoxin, although it w;i> 

 feeding on the antitoxic milk. 



Toxin and Antitoxin in the Living Organism. Animal Experiments. 

 Very recently the studies of H. Meyer and Ransom as well as those 

 of Marie and Morax in Roux's laboratory have thrown considerable 

 light on the much disputed phenomena observed in poisoning by tetanus 

 toxin. The investigations of Gumprecht in 1895 had made it highly 

 probable that all the pathological symptoms were due to a poisoning 

 of the central nervous system. The paths, however, by which the 

 poison reached its central points of attack were still doubtful. The 

 experiments of Meyer and Ransom and of Marie and Morax have 

 practically proved that the poison is transported to the central nervous 

 system by way of the motor nerves and by no other channel. So 

 far as the experiments are concerned, I must refer the reader to the 

 original. These show that the essential element for the absorption 

 and transportation of the toxin is not the nerve sheath or the lymph 

 channels, but the axis-cylinder, the intramuscular endings of which 

 the toxin penetrates. The poison is taken up quite rapidly. Marie 

 and Morax were able to demonstrate the poison in the corresponding 

 nerve trunk (sciatic) one and a half hours after the injection. Absorp- 

 tion, however, and conduction are dependent to a large extent on the 

 nerves being intact. A nerve cut across takes very much longer to 

 take up the poison (about twenty-four hours), and a degenerated nerve 

 takes up no poison whatever. In other words, we see that section of 

 the nerve prevents the absorption of the poison by way of the nerve 

 channels. Similarly section of the spinal cord prevents the poison from 

 ascending to the brain. 



According to Meyer and Ransom the reason why the sensory nerves 

 do not play any role in the conduction of the poison lies in the presence 

 of the spinal ganglion, which places a bar to the advance of the poison. 

 Injections of toxin into the posterior root leads to a tetanus dolorosus, 

 which is characterized by strictly localized sensitiveness to pain. 



Ascending centripetally along the motor paths the poison reaches 

 the motor spinal ganglia on the side of inoculation; then it affects the 

 ganglia of the opposite side, making them hypersensitive. The visible 

 result of this is the highly increased muscle tonus i. e., rigidity. If 

 the supply continues, the toxin next affects the nearest sensory appa- 

 ratus ; there is an increase in the reflexes, but only when the affected 

 portion is irritated. In the further course of the poisoning the toxin 

 as it ascends continues to affect more and more motor centres, and 

 also the neighboring sensory apparatus. This leads to spasm of all the 

 striated muscles and general reflex tetanus. 



If the toxin gets into the blood the only path of absorption to the 

 central nervous system is still by way of the motor-nerve tracts. There 

 seems to be no other direct path, as, for example, by means of the 

 bloodvessels supplying the central nervous system. Even after intro- 



