In the recent years, various red cell auto-antibodies have been determined in someanimal diseases, including autoimmune hemolytic anemia and systemic lupus erythe-matosus in dogs, ") Aleutian disease in minks, 8) and equine infectious anemia."?">In this report, the red cell auto-antibodies were examined for symptomatiCchanges, serological characteristics, and immunopathological roles in 20 horses infectedwith equine infectious anemia virus (Table l).Pathologic cold hemagglutiuain and warm hemagglutinin were identified in theplasma of artificially infected horses. The direct antiglobulin tests of red cells gavealso positive results, showing an intimate correlation with the appearance of warmhemagglutinin, in infected horses of febrile stage (Chart l and Table l). Red cellsin the portal veins of the liver tissue were always higher in titer in the antiglobulintests than those in the jugular veins. There was an intimate correlation between thistiter and the number of red cells in the jugular vein of the infected horses (Table 2).Both warm and cold hemagglutinins were macroglobulins (IglVI) which were inn-activated with 2-mercaptoethanol, and found in the first peak of the plasma proteinfractions obtained by get filtration using Sephadex G-200 (Chart 2). These auto-hemagglutinins reacted with horse red cells, but did not with red cells of any otheranimal species, such as sheep, rabbit, guinea pig, or chicken. In tl?e pattern ofreaction between warm hemagglutinin and horse red cells, prozones were formed byexcess antigen or antibody (Table 3) . The auto-antibodies, combined with the redcells of the infected horses and correlated with the antiglobulin test, were serologicallydetermined to be composed predominantly of IgM, like warm hemagglutinin, andprobably partially of IgG (Table 4 and Fig. l).Warm hemagglutinin among these red cell auto-antibodies exhibited 2L1l opsonicaction but no hemolytic action, and accelerated phagocytosis of horse red cells bymacrophages (Figs. 3, 4, and 5).It was considered that the presence

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[in Japanese]

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[in Japanese]

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In 1932 and 1938, one of the authors, YAMAGIWA, studied the histopathologicalchanges in the brain autd spinal cords of chickens infected naturally with fowl plaguein Manchuria. Moreover, he and his associates published three papers on experimentalwork with fowl plague passage virus. This paper deals with neurohistopathologicalinvestigation of the brain and spinal cord carried out on experimental cases with thefowl plague passage virus mentioned above.The materials and methods used in this study had been described in the previousreport, part 111.9) The viruses used were the Hoten A (A) and European strains (D).The chickens used were White Leghorn adults. Chicken brain emulsion containingthe virus was used as inoculum for chickens by the intramuscular route. Microscopicalexamination was performed on a total of 13 chickens. The experimental history ofthese birds was shown in Tables 2, 4, and 6 in the previous report, part [119).The basic histological changes were confined consistently to the ectodermal tissue, and composed mainly of focal microglial proliferation, which was occasionally accom-panied by a few oligodendroglial cells. The glial lesions were divided roughly intotwo groups, nodular foci (Fig. 4) and minute foci (Figs. 3, 6, 7, and 8). The formerwas well-defined, spherical in shape, and generally larger than the latter though vari-able in size. The latter was very minute in size and irregular in shape. A large numberof proliferated glial cells were arranged compactly in the former, but a few proliferatedglial cells were presented sparsely in the latter. It was difficult to find out whethertlae nodular foci were related to nerve cells, blood vessels, or non. On the other hand, the minute foci were often closely connectd with blood vessels, chiefly capillaries.There was a relationship between the occurrence of lesions and the inculated doseor virulent materials (Table 1). In cases given 10-2, 10-3, NO-4, and 10-5 g of brainmaterials, the lessions were predominantly large in number, while they were very small noticed. Changes in the mesenchymal tissue were scarcely observed in chicken inocu-lated experimentally with fowl plague passage virus. Some discussion, thereupon, wasmade on histogenesis in microglial reactions to viral infections.

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