Pathogenesis. 239 



also observed that the time of incubation after virulent inoculations is 24 hours 

 shorter in the higher bred animals, and death as a rule follows half a day earlier 

 than in the black Anatolian cattle, and that these latter may be much more readily 

 immunized. In South Africa (Stockman) and in India (Eogers) the cattle of the 

 mountains appear to be much more susceptible than the animals in the lowlands. 



Buffaloes are much less susceptible. During tlie existence 

 of an outbreak they become affected only exceptionally, and even 

 young animals may withstand artificial infection (NicoUe & 

 Adil-Bey; although the disease exists among buffaloes on the 

 East Indian islands in an epizootic form, Van Ecke, Blin & 

 Carrougeau). 



Of other animals camels are susceptible (according to Tar- 

 takowsky the disease is always mild in these animals) ; also 

 sheep, goats and ruminants living wild, especially deer, zebu, 

 gazelle, etc., and these animals bear an important part in the 

 distribution of the disease. Solipeds and carnivora are not sus- 

 ceptible, and the reliability of the observations relative to the 

 occurrence of the affection in hogs (Percari, Driessa, Pinning) 

 has not been proven beyond a doubt (see p. 237). Man is 

 not susceptible to rinderpest. 



One attack of the disease usually abolishes the susceptibility 

 of the animal; and while repeated attacks were observed in 

 exceptional cases the infection was usually of a mild form. (In 

 the Vaccine Institute of Karlowka it was not possible to repro- 

 duce the disease in a steer which had recovered from the affec- 

 tion produced by inoculation six years previously.) Calves 

 from cows which became ill during advanced pregnancy are also 

 resistant against the infection (Gerlach, Semmer, Rogers), or 

 they become affected only with mild symptoms (Yersin). 



Pathogenesis. The first symptoms are apparently produced 

 by the virus which enters the blood and propagates with great 

 rapidity. The virus appears to have a predilection for exerting 

 inflammatory changes on the mucous membranes, producing 

 catarrhal symptoms in the very beginning of the disease. The 

 croupous-diphtheric inflammation which then develops with 

 great rapidity is evidently the result of _ secondary infection by 

 other micro-organisms from the digestive tract attacking the 

 weakened mucous membrane. These bacteria cannot be desig- 

 nated exactly at present (colon and necrophorus bacilli !) in the 

 absence of accurate bacteriological and histological examina- 

 tions. The tissue changes consist principally in that the ep- 

 ithelial layer of the hyperemic and swollen mucous membrane 

 changes together with the exudate which comes from the blood 

 vessels into an easily detachable and friable pseudo-membrane. 

 Sometimes the tissue of the mucous membrane proper becomes 

 necrotic to a certain depth, forming thicker membranes that are 

 more adherent. The mucous glands, especially those of the intes- 

 tinal mucous membrane swell as a result of cellular infiltration, 

 and later become necrotic. The inflammatory process is some- 



