780 East African Coast Fever. 



tick is similar to that of tlie piroplasma bigemiuum (Koch see 

 p. 766). 



Stockman suoeeeded in producing the disease in cattle in England •with 

 nymphs of the brown ticks sent there from Africa. 



The infection always occurs during pasturing, especially 

 easily after the appearance of the rainy season and during 

 the high grass season when the ticks, which are present in 

 great numbers^, easily jump from the high grass blades to the 

 cattle. As a matter of fact, previously healthy cattle become 

 affected Avith a dangerous form of the disease after they are 

 pastured in the same field with animals from infected localities, 

 or if they are driven over infected pastures. 



In tlie endemicly infected territories on the coast and in 

 lowlands cattle under one year of age usually become affected. 

 In these the loss usually amounts to 60 to 90%, while older 

 animals are imnnme if they have already passed through the 

 disease. The infection in the highlands is less severe, as there 

 hardly more than 15% of the increase in stock die of the disease. 

 For this reason older cattle in these localities are immune only 

 to a slight extent, and a certain number of them fall victims to 

 the disease (Lichtenheld). 



Contrary to the described conception on the etiology of coast fever, Ollwig, 

 as well as Fiilleborn is of the opinion that the cause is possibly ultra-microscopic, 

 as it does not produce anemia, is not directly transmissible, and that the dii^ease 

 leaves an absolute immunity. Piroplasina mutans and Piroplasma pai-vum are, 

 according to their views, not only morphologically but also etiologically identical, 

 and bolh types probably produce the piroplasmosis which extends iu all tropical 

 and sub-tropical localities, and which shows variations only iu its manifestations. 

 This conception is also substantiated by the experience that cattle which have recov- 

 ered from coast fever are no longer infectious for ticks, and thereby they are 

 apparently free of the virus. 



Anatomical Changes. The autopsy reveals lumctiform 

 hemorrhages in tlie subcutis and the subserous comu^ctive 

 tissue, medullary or hemorrhagic swelling of the lym]ih glands, 

 edema of the lungs and of the mediastinum, hyperemia, or 

 ulcerative inflammation of the intestinal mucous membrane and 

 of the abomasum ; further grayish-white spots in the liver sul)- 

 stance, and as a specially striking lesion hazelnut-sized, wedge- 

 shaped infarcts in the cortex of the kidneys. The spleen is 

 not swollen. 



The specific bodies, so-called plasma splieres (Kocli). arc present 

 in the swollen lymph glands, in the spleen, fnrtlier in tlie spots of tlu> 

 liver and in the infarcts of the kidneys, as well as in the borders of the 

 ulcers of the mucous membrane, likewise also in the blood. By Giemsa's 

 stain they appear as sharply circumscribed, blue-colored spheres, con- 

 taining point or comma-shaped chromatin granules, or they are covered 

 by sucli. 



Colland considers the formation of infarcts to be due to an injury of the 

 endothelia of the vessels by endocellular toxins of the piroplasma. Similar toxins 

 are supposed to be also produced by the Piroplasmr. bigcminum, only that they 

 attack the erythrocytes. 



