In 1952, Bruton,1 introduced the term ``agammaglobulinemia'' to describe a new syndrome in an 8-year-old boy, who from the age of 3½ years had had multiple attacks of respiratory and blood-stream infections, often with the same micro-organism. This patient was found to be unable to develop circulating antibodies to a series of injected antigens, and electrophoretic analysis of his plasma disclosed an almost complete absence of γ-globulin. Since that time more than 30 comparable cases have been observed in children here and abroad. Inasmuch as these patients were all boys, the defect has been considered to be genetically determined as a sex-linked recessive. These children characteristically suffer from an early age with recurrent severe infections due to the common pyogenic bacteria. Such infections include pyoderma, purulent conjunctivitis, otitis media, purulent sinusitis, pneumonia, meningitis, and purulent arthritis. Administration of appropriate antibiotics often controls these infections,