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Several strains of group B Streptococcus agalactiae were found to be lethal for young adult rats. When bacteria were heat killed and then injected intraperitoneally into rats, rapid death (14 to 18 h) of the rats occurred, characterized by labored breathing, hemolyzed serum, hemoglobinuria, and subungual hemorrhages. Sections of tissues from these rats failed to reveal the cause of death. Rats injected with toxic or nontoxic strains of group B S. agalactiae had reduced numbers of circulating leukocytes and low serum C3 levels in comparison with those in control rats. The toxic strains of group B S. agalactiae induced dramatic decreases in platelet numbers, and in plasma fibrinogen levels as well, suggesting that the toxicity was due to disruption of the coagulation system. Rapid death in the absence of infection suggests that group B S. agalactiae may have a cell-associated toxin that induces these changes. Such a toxin may be a contributory factor in the high mortality rate associated with group B streptococcal infections of the human neonate.

A patient was transfused with a unit of red blood cells that had been frozen accidentally prior to transfusion. Although he had received approximately 60 gm of free hemoglobin intravenously, the patient's only clinical reaction was massive hemoglobinuria. The benign clinical response, in the presence of massive hemoglobinuria, is attributed to the absence of immunologic imcompatibility and, thus, failure to activate vasoactive mediators and disseminated intravascular coagulation. The case illustrates revised concepts of the pathophysiology of acute renal failure associated with hemolytic blood transfusion reactions.

Twenty-six patients with delayed hemolytic transfusion reactions ( DHTR ) were investigated. The reaction of hemolysis often was concealed by other disorders that were usually associated with signs of hemolysis or blood loss. Coating of red cells was analyzed with regard to IgG and/or complement bound in vivo. Although many of the alloantibodies involved (K [8]; E [5]; Fya [2]; Fyb [2]; D [1]; c [1]; multiple [7]) are usually thought to be incapable of complement activation, a strongly positive direct antiglobulin test (DAT) due to C3d was found in all cases. On first examination after transfusion, C3d was present on circulating red cells in large amounts and remained discernible for weeks and even months. IgG on red cells was detected by the DAT in only 10 out of 26 cases. By means of a sensitive radioimmunoassay, IgG was demonstrated in 16 out of 17 cases, but usually in small quantities. Despite the low IgG concentrations, the causative alloantibodies could be eluted in 25 of 26 cases, and, as shown by sequential investigations, in six cases were recoverable from circulating red cells for over 100 days posttransfusion. Since the antiglobulin reactions due to anti-complement were usually strong, not of the "mixed-field" type, and in some cases remained detectable on circulating red cells for months, we conclude that complement is regularly activated in DHTR and binds not only to donated but probably also to autologous red cells.

This paper reports about the occurrence of hemoglobinuria in a herd of grazing dairy cows. Laboratory findings of serum, liver, pasture and soil showed hypocuprosis in this herd. Copper supplementation results in clinical recovery. Possible pathogenetic relations between copper deficiency and hemolytic anaemia are discussed.

A new case of march haemoglobinuria seen in a 21-year-old man is reported. A deficiency in two erythrocytic enzymes (glutathione reductase and glutathione peroxydase) was observed. Treatment with riboflavin corrected the glutathione reductase deficiency. The march haemoglobinuria and glutathione peroxydase deficiency persisted. Several months after resolution of the march haemoglobinuria, a new estimation of glutathione peroxydase showed that the deficiency had disappeared. The possible role of a transient deficiency in erythrocyte glutathione peroxydase in the pathogenesis of march haemoglobinuria is discussed.