1913] Siceet: Epilhdiiima of llic Coininon Fowl 'M 



help I received from my friend, "Sir. 0. H. Robertsou, who was 

 working in the same laboratory on a somewhat similar problem. 



History of Disease. — An historical review of the disease 

 hardly seems necessarj' since it has already been so well done 

 by Reischauer (1906). Burnet (1906), and others. Only a few 

 of the main points will be mentioned in passing. Rivolta (1865) 

 described cellular inclusions, similar to those already described 

 by Virchow in moUuscum contagiosum of man. These inclusions 

 he interpreted a.s gregarines. This was also the classifieation of 

 Priedberger and Frohner (1908), who described avian diph- 

 theria as (1) croupous diphtheritic mucous membrane inflamma- 

 tion, the familiar diphtheria of fowls, bacterial in origin, and (2) 

 croupous diphtheritic mucous membrane inflammation in which 

 the mucous membranes of the head give the same clinical picture 

 as in the diphtheria of bacterial origin, but in addition epith- 

 elioma contagiosum may appear on the skin of the head, a con- 

 dition ascribed to the presence of gregarines. Bollinger (1873) 

 characterized the disease as an epithelioma. ]\Iarx and Sticker 

 (1902) proved the causative agent of the disease to be filterable 

 through a Berkfeld filter (but not through a Chamberland P 

 filter) and thereby placed it in the great class of di-seases which 

 are supposed to be due to ultra-microseopic organisms. They also 

 demonstrated the very great resistance of the virus to heat and 

 chemical agents, finding the dried virus still virulent after being 

 placed in sealed tubes, within a steam sterilizer at 100° C, for 

 an hour. After thirty minutes' exposure to 2% carbolic acid 

 the virus was no longer active, but was active after very long 

 exposure to the action of 17c carbolic acid. They conclude that 

 the cell inclusions are the products of cell degeneration produced 

 by an ultra-microseopic, very resistant virus. Juliusberg (1904) 

 confirmed the filtration results of Marx and Sticker (1902). 

 Borrel (1904) observed granules within the cell inclusions and 

 thought the inclusions were the organic caiisative agent of the 

 disease. Reischauer (1906) made extensive microscopic studies 

 of the diseased tissue and was of the opinion that the cell inclu- 

 sions contained the causative agent of the disease and represented 

 development stages of a protozoan. However, it does not seem 

 that he was able to demonstrate a complete life cycle, although 



