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Ducklings receiving 9.0 ml or 0.2 ml of filtered malarious plasma underwent comparable anemic responses. Recipients of the larger injection demonstrated a reduction in the level of polychromatophil erythroblasts whereas the recipients of the smaller injection did not. Two tenths milliliter of whole blood or filtered plasma from these ducklings also produced and continued to produce anemia during 24 successive passages in ducklings without any apparent reduction of its efficacy. The anemia-producing agent resides on or in erythrocytes and occurs in the plasma. Transfer of the agent in conjunction with a Plasmodium lophurae infection maintained by transfer of infected blood every four days was demonstrated. Preliminary attempts to characterize the agent beyond being filterable and proliferating met with no success. From consideration of our results we believe that we are observing the effect of a virus that can be transferred either with or without the malaria parasite and is responsible for at least part of the anemia observed in infections of P. lophurae in ducklings.

Adult NZB mice were found to be more susceptible to infection with P. berghei than young mice of the same strain. This enhanced susceptibility was probably related to the presence of reticulocytosis in adult Coombs positive NZB mice and to the defective powers of cell mediated immunity occurring in adult mice of this strain. Over a short period of observation P. berghei infection did not have any effect on an established positive Coombs test. Infection of B/W mice with P. berghei at the age of 5–6 months had some protective effect on the development of their spontaneous autoimmune renal disease but this effect was less marked than when infection was induced at the age of 1 month.