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Defective chemotaxis and phagocytosis of Staphylococcus aureus was identified in a female infant with marked hepatosplenomegaly and recurrent infections. Neutrophil mobilization from the marrow and marginal pool; random mobility; phagocytosis of yeast particles, latex beads and carbon particles; phagocytosis and intracellular killing capacity of Streptococcus pyogenes and E. coli; and NBT dye reduction were normal. Infiltration of neutrophils was depressed in the skin window test. The complement system and cellular immunity were intact. The patient also had a persistent EB virus infection. Defective phagocytosis limited to Staphylococcus aureus seems to be caused by an intrinsic cellular defect, such as congenital defect in neutrophil receptors for Staphylococcus aureus.

The effect of the IgE-mediated reaction on the passive cutaneous anaphylaxis (PCA) reaction was studied at local skin sites of monkeys, and we found that the IgE-mediated reaction appeared to enhance the PCA reaction. Interactions among IgE-mediated reaction, PCA reaction and delayed hypersensitivity reaction were also determined. Contact dermatitis induced with DNCB was utilized as the delayed hypersensitivity reaction. The IgE-mediated reaction or PCA reaction, as well as simple serum irritation, enhanced the delayed hypersensitivity reaction. It is thus assumed that the IgE-mediated reaction enhances the PCA reaction and that this in turn accelerates the delayed hypersensitivity reaction.

To clarify the immunological mechanisms in poststreptococcal acute glomeulonephritis (PSAGN) and anaphylactoid purpura (AP), anti-streptococcal cell membrane (anti-SCM) and anti-human glomerular basement membrane (anti-GBM) titers in the sera of patients with PSAGN and AP were determined by passive hemagglutination with chromic chloride-treated sheep erythrocytes. Sodium lauryl sulfate (SLS) soluble SCM and collagenase soluble GBM were used as soluble antigens. Positive anti-SCM titers (greater than 1:8) were demonstrated in 10 of 14 patients (71.4%) with PSAGN and in 4 of 9 patients (44.4%) with AP with evidence of antecedent streptococcal infection. Two of 4 patients with AP without evidence of antecedent streptococcal infection had positive anti-SCM titers. No correlation was noted between anti-streptolysin O (ASO) titers and anti-SCM titers in patients with PSAGN or AP, but many patients with high ASO titers also had high anti-SCM titers. No positive anti-GBM reactions were detected in patients with PSAGN or AP. No cross-reactions were noted between SLS soluble SCM and collagenase soluble GBM.