Occurrence. Etiology. 331 



disease reappeared in the States of New York, Pennsylvania, Michigan and Mary- 

 land. (See p. 353.) 



Argentina was severely affected in 1900. 



In Asia and Africa the disease prevails from time to time over large areas, 

 while Australia is free from the infection. 



At certain times, and in certain localities the disease shows a deviation from 

 the normal course, by exhibiting a very severe character, and in such instances 

 many animals are destroyed by it. Thus according to Bychener 2,000 cattle died 

 in 1839, in the Swiss Kantons Bern and Freiburg, while in 1872 in the District 

 of Nievre in Prance 20.3% of calves and 22.2% of hogs succumbed to the disease 

 inside of two months. During the summer of 1892 more than 3,000 animals died 

 in Bavaria; in the course of 1896, 1,500 in Wiirttemberg, two years later 1,300. 

 In 1901 the disease appeared in Spain with such a malignant character, that in 

 Barcelona 50-70% of the young stock succumbed, and these heavy losses caused 

 a suspicion that the disease in question was the oriental rinderpest. In Hungary 

 the disease raged in a severe form in 1893 in certain parts of the counties of Gomor 

 and Pest, in 1899 in Siebenbiirgen (in the counties of Csik, Maros-Torda and 

 Udvarhely of 7,498 cattle, 711 died, amounting to 9.4%). 



Etiology. Lofifler & Frosch, also Hecker, and later Nocard 

 & Eoux proved that the virus of foot-and-mouth disease in dilu- 

 tion will pass the porous (Chamberland, Berkefeld) porcelain 

 filters, while it is partially retained by the denser Kitasato 

 filter. It has not yet been possible to demonstrate the organisms 

 either by methods of staining or cultivation. The virus is there- 

 fore an extremely minute, ultra-microscopic micro-organism. 



Eecently Ferni claimed that the causative agent is a protozoon 0.5 /* in size 

 (Cytoryctes Jeuneri), which he succeeded in demonstrating in the lymph of the 

 cysts, and also in the internal organs of 472 affected cattle, arranged like the 

 pavement of a street, or radiating like the spokes of a wheel. A confirmation of 

 this finding has not yet been made. 



The virus is contained in the purest state in the contents 

 of the vesicles which develop in the course of the disease, and 

 greatly diluted also in the blood though only during the begin- 

 ning of the fever. The saliva, the tears, the nasal discharge, the 

 milk, and the other secretions become infectious only after being 

 contaminated with the contents of the ruptured vesicles. In 

 the later course of the disease the virulence of the serous fluid 

 of the vesicles diminishes, and after ten days the saliva of 

 infected cattle is no longer infectious for other animals (Schiitz). 



Tenacity. Virus dried at room temperature and in daylight, loses its virulence 

 inside of 24 hours, diluted in proportion of 1:10 and kept in glass tubes closed 

 at both ends by melting, it remains infective for 3 to 4 months. A temperature of 

 37.5 degrees destroys it in 12 to 24 hours, one of 50 degrees in 15 minutes, and 

 70 degrees in 10 minutes. Heating to lOO degrees destroys its virulence immediately 

 (Lofaer & Frosch). The action of a temperature of — 8-9 degrees destroys it in 

 several hours (Perroncito). Of the disinfectants, milk of lime, a 1% carbolic acid, 

 2% formalinj»3% soda, and 1% hydrochloric acid destroy its virulence in one 

 -. hour (LofBer & Frosch). Infectious milk which has stood for 3 to 4 days, becoming 

 soured and coagulated, is no longer infectious (Ebert?). In fresh cow and hog 

 manure the virus is destroyed at a depth of more than 20 cm. within a short 

 time (Hecker). 



Pathogenicity. Intravenous injection of fresh pure lymph 

 will sometimes, even in a quantity of 1/5000 cc, produce the 

 disease in susceptible cattle. Depending upon the quantity 

 and the virulence of the virus, typical vesicles develop in from 



