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Am. J. Trop. Med. Hyg., 24(2), 1975, pp. 206-213
Copyright © 1975 by The American Society of Tropical Medicine and Hygiene

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Pathogenesis of Acute Avian Malaria

II. Anemia Mediated by a Cold-Active Autohemagglutinin from the Blood of Chickens with Acute Plasmodium gallinaceum Infection

Jiya L. Soni* AND Herbert W. Cox
Department of Microbiology and Public Health, Michigan State University, East Lansing, Michigan 48824

A cold-active hemagglutinin for trypsinized human type "O" erythrocytes (CAH) from blood of chickens with acute Plasmodium gallinaceum malaria was found to be associated with the 19 S and 7 S globulin fractions of malarious chicken blood, but cleavage with 2-mercaptoethanol indicated that it was primarily of the IgM class of antibody. In serologic tests CAH reacted with trypsinized erythrocytes, and anti-chicken globulin. It did not react with other of the antigens or antibodies detected in the blood of malarious chickens. When the absorbed and eluted CAH was injected into normal chickens it produced an anaphylacticlike shock and caused a 25% reduction in red blood cell counts within 48 hours. Plasma samples collected during this interval showed signs of hemolysis. Reactions of blood cells from the recipient birds with fluorescein conjugated anti-chicken globulin indicated that CAH reacted with erythrocytes. The absence of fluorescent activity 3 days after injection suggested that these erythrocytes had been removed from the circulation. When normal chickens were injected with trypsinized autologous blood cells, CAH was detected within 3 days. The agglutination test again was active at temperatures below 22°C and was negative when tested at 37°C. In these birds the appearance of CAH was accompanied by reductions in red blood cell counts and by hemolysis. The results of these experiments suggest that CAH was not stimulated by plasmodial parasite antigen, but rather by autoantigens, which appear to be common to heterologous animal species, and which were in some manner expressed by the presence of the intracellular parasites, or by trypsin treatment. The experiments further suggest that this autohemagglutinin was partially causal of malarial anemia. The presence of other anemia factor(s) was indicated by anemia following injection of plasma that had been absorbed free of CAH.

Accepted for publication August 17, 1974.


* U.S. State Department, Agency for International Development, Fellow. Present address: College of Veterinary Science and Animal Husbandry, Jawaharlal Nehru Agricultural University, Jabalpur, Madhaya Pradesh, India.







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Copyright © 1975 by the American Society of Tropical Medicine and Hygiene.