Pathogenesis. 239 



also ohserved 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, an<l that these latter may be much more readily 

 immunized. In South Africa (Stockman) and in India (Rogers) 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 (Nicolle & 

 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 l)ear an important part in the 

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

 ceptible, and the reliabilitv of the ol)servations 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 susceptibihty 

 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 bv 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 (Yersm). 



Pathogenesis. The first symptoms are apparently produced 

 by the virus Avhich enters the l)lood and propagates with great 

 rapidity. The virus appears to have a predilection for exerting 

 inflammatory changes on the mucous membranes, producing 

 catarrhal sjanptoms 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 on the weakened 

 mucous membrane. These bacteria cannot be designated exactly 

 at present (colon and necrophorus bacilli !) in the absence of 

 accurate bacteriological and histological examinations. The tis- 

 sue changes consist principally in that the epithelial layer of the 

 hvperemic and swollen mucous membrane changes together 

 with the exudate which comes from the blood vessels into an 

 easily detachable and frial)le pseudo-membrane. Sometimes tHe 

 tissue of the mucous membrane proper liecomes necrotic to a 

 certain depth, forming thicker membranes that are more adhe- 

 rent. The mucous glands, especially those of the intestinal 

 mucous membrane swell as a result of cellular infiltration and 

 later become necrotic. The inflammatory process is sometimes 



