Anemia and Mechanism of Erythrocyte Destruction in Ducks with Acute Leucocytozoon Infections *

SYNOPSIS. In the anemia which accompanies infection by Leucocytozoon simondi in Pekin ducks there was a far greater loss of erythrocytes than could be accounted for as a result of direct physical rupture by the parasite. Erythrocyte loss began at the same time the 1st parasites appeared in the blood and was severest just prior to maximum parasitemia. Blood replacement and parasite loss occurred simultaneously. Examination of the spleen and bone marrow revealed that erythrophagocytosis was not the cause of anemia as reported for infections of Plasmodium, Babesia and Anaplasma . An anti‐erythrocyte (A‐E) factor was found in the serum of acutely infected ducks which agglutinated and hemolyzed normal untreated duck erythrocytes as well as infected cells. This A‐E factor appeared when the 1st red cell loss was detected and reached its maximum titer just prior to the greatest red cell loss. Titers of the A‐E factor were determined using normal uninfected erythrocytes at temperatures between 4 and 42 C. Cells agglutinated below 25 C and hemolyzed at 37 and 42 C. These results indicated that the A‐E factor could be responsible for loss of cells other than those which were infected and could thus produce an excess loss of red cells. Attempts to implicate the A‐E factor as an autoantibody were all negative. The A‐E factor was present in the gamma fraction of acute serum but no anamnestic response could be detected when recovered ducks were reinfected. Anemia was never as severe in reinfections as in primary infections. The A‐E factor also never reached as high a titer and was removed from the circulation very rapidly in reinfected ducks. It is concluded that red cell loss in ducks with acute Leucocytozoon disease results from intravascular hemolysis rather than erythrophagocytosis. The A‐E factor responsible for hemolysis is more likely a parasite product rather than autoantibody.