SYNOPSIS
Aboriginal school children with elevated erythrocyte sedimentation rates were selected, and associated features of growth retardation, hyperimmunoglobulinaemia, high streptococcal carrier rates and antibody levels, and high loads of bowel parasite infestation, noted previously, were confirmed. Medical records showed these children to have had significant growth retardation in infancy, which suggested an association with previous protein‐calorie malnutrition. Antibody responses of these children to influenza vaccine were significantly poorer than controls, both in the magnitude of antibody rise and the proportion of children showing significant rises in titre. Some improvement in antibody response followed treatment of chronic streptococcal infection, or of bowel parasites. Cell‐mediated immune responses, as measured by lymphocyte transformation in vitro in response to specific antigens streptolysin O, tetanus toxoid, non‐specific mitogens PHA and streptolysin S, and also by delayed hypersensitivity reactions to monilia antigen on skin testing, were diminished in children with high ESR, relative to controls. However, enhanced cellular responses in the abnormal children occurred to influenza A2 antigen, and to streptococcal group A polysaccharide, the latter possibly explaining chronic low‐grade tissue damage noted previously in these children. These findings are discussed in relation to resistance to infection and the pathogenesis of rheumatic fever, and a possible basis suggested in acquired change in function of the thymus, perhaps related to protein‐calorie malnutrition in infancy.