326 THE AMERICAN MONTHLY [Oct. 



The virus should be injected iuto a vein. The morbid 

 process that results manifests itself almost immediately, 

 with a violence of symptoms and an assemblage of les- 

 ions which recall the picture, clinical and anatomical, of 

 human yellow fever. 



The lesions found after death are extremely interest- 

 in'^ as they are almost identical with those observed in 

 the human cadaver. 



Attention is called before everything to the intense 

 fatty degeneration of the liver. The hepatic cell, exam- 

 ined in a fresh state with a little osmic acid, appears 

 completely turned into fat, as it is in human victims of 

 yellow fever; the yellow-fever toxin, as we shall see 

 later is a true specific poison to the hepatic cell, as are 

 phosphorus and arsenic. A complete fatty degeneration 

 of the liver may be affected by injecting directly iuto it, 

 through the abdominal parietes, a fresh culture of the 

 sjtecitic bacillus. 



The kidney shows a severe fatty degeneration, accom- 

 pained by lesions of acute parenchymatous nephritis, 

 which may be considered the direct causes of the anuria 

 and the ura^mic intoxication. 



The digestive apparatus shows lesions of hemorrhagic 

 gastro-enteritis as intense as those caused by poisoning 

 with cyanide of potassium. They are completely analog- 

 ous to those in man, though more grave. 



A bacteriological fact of great interest in the yellow 

 fever of the dog is that in the majority of cases the 

 "bacillus icteroides" is found in the blood and the organs 

 in variable quantity and in a state uf absolute purity; at 

 times, it is found associated, as in man, with the coli bac- 

 illus and the streptococcus. 



As the tendency to secondary niicrobic infc^ctions has 

 been proved even in the yellow fever intoxication of the 

 dog, provoi<ed with a pure culture, filtered, it must be 

 concluded that the yellow fever poison, whether by itself 



