Intraerythrocytic crystalloid bodies in cats.

SEVERAL HEMOGLOBINOPATHIES of man are known to produce striking morphologic changes in erythrocytes. In vivo sickling, occurring under low oxygen tension, is well documented in hemoglobin 5 (1-lb S) disease. Osmotic dehydration produced by incubation in hypertonic salt solutions fosters sickling in these cells.’ This phenomenon is explained on the basis of a single amino acid substitution, valine for glutamic acid, at the beta-six position of the hemoglobin molecule. Erythrocytes from most species of deer will also sickle but, in contrast with the behavior of Hb S in man, deer erythrocytes sickle in vitro upon incubation under high oxygen tension and elevated pH.2 This potential to form sickle cells has no apparent pathologic consequences in deer. Amino acid analyses of the various chains of the deer hemoglobin molecules do not permit an explanation of the sickling phenomenon on the basis of a single amino acid substitution as in Hb S disease of man.3 Disordered molecular configuration of the hemoglobin molecule has also been documented in individuals with hemoglobin C (Hb C) disease. In this disorder lysine is substituted for glutamic acid at the same locus in the B chain as in Hb S. Occasional rectangular crystals can be found in blood smears from patients with Hb C disorders.4 Incubation of erythrocytes from these patients in hypertonic salt solution fosters crystal formation, perhaps by a combination of osmotic dehydration and “salting out” of a relatively insoluble protein.5 Crystalloid inclusions resembling those seen in Hb C disease have not previously been described in an animal model. In the present study, squareand rectangular-shaped crystalloid bodies (C.B.) have now been observed within the circulating erythrocytes of cats.