A STUDY OF THE ROLE OF ACUTE INFECTIONS IN PRECIPITATING CRISES IN CHRONIC HEMOLYTIC STATES

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Abstract
We have been impressed by the apparent coincidence of acute hemolytic crises in chronic hemolytic syndromes with the onset of acute infectious states such as the common cold. In an earlier study of the susceptibility of red blood cells to phagocytosis by macrophages, it was noted that individuals serving as controls, on developing acute coryza, showed a marked enhancement of phagocytosis of their red cells. Study of this apparent modification of the red blood cell surface by virus has been pursued on the thesis that this additional insult is the "last straw" in persons whose bone marrow is already struggling to maintain effective erythroid balance. Using the virus treated red cell as the model, the following observations have been made: (1) In vitro and in vivo virus (Newcastle, mumps and influenza) treated red cells are more readily phagocytized by tissue culture macrophages than are normal control cells. (2) In vitro and in vivo virus (Newcastle, mumps and influenza) treatment of red blood cells modifies the antigenicity of the red blood cell from the normal. (3) In vitro virus (influenza) treated red blood cells have a shortened survival in the rabbit when measured with Cr51 labeled cells. Chickens infected with Newcastle disease virus also have short-lived RBC. Clinical observations substantiate this concept. Twenty-two of twenty-three consecutive admissions of patients with sickle cell anemia in acute hemolytic crisis had various infections, with the respiratory tract predominating. Most were in the acute stages or complications of coryza. These data suggest that virus modification of red blood cells may trigger an acute hemolytic crisis in chronic hemolytic states.