The diagnosis of human infection by Toxocara canis relies heavily upon serological tests, the specificity of which can be inadequate in regions of endemic helminthiasis. When different population groups of tropical Venezuela were evaluated using ELISA based upon Toxocara excretory-secretory antigen (TcESA), solid-phase adsorption of the sera with extracts of a wide variety of non-homologous parasites revealed the existence of significant cross-reactivity. This was effectively and conveniently overcome when the test sera were incubated in the presence of the soluble parasite extracts in a competitive inhibition ELISA. The mean reduction of ELISA values caused by pre-adsorption of the sera tested was 32.2%, and that caused by competitive inhibition was 42.3%, the effects of these two procedures being strongly correlated (r = 0.83). The magnitude of the reduction was inversely proportional to the actual ELISA value (r = -0.55), and ranged from a mean of 68.0% in sera from apparently healthy individuals of medium-high socio-economic level, down to 28.1% in heavily parasitized Amazon indians. Ascaris showed the greatest degree of cross-reactivity in these tests, although under conditions of competitive inhibition even sera with high levels of antibody against this parasite could be negative in Toxocara ELISA. Western blotting revealed a major 81,400 D component that was shared between Ascaris and TcESA. Our results indicate that the competitive inhibition of cross-reactivity by soluble non-homologous parasite extracts provides a convenient and economical means of increasing the specificity of ELISA for the determination of the seroprevalence of toxocariasis in tropical populations.

Repeated exposure of immunocompetent adult rats to aerosolised allergen stimulates persistent IgG responses to the allergen, the magnitude of which varies as a function of genetic background. In contrast, exposed adult animals develop immunological tolerance in the IgE isotype, and are unable to produce allergen‐specific IgE antibody in response to subsequent parenteral immunization. Infant rats appear anergic to challenge with inhaled allergen either in relation to IgG synthesis or expression of tolerance in the IgE antibody class, and both these functions were subsequently acquired during the first week after weaning. Systemic immune responses were essentially normal in the infant animals, suggesting that the failure to ‘recognise’ inhaled antigen in the early postnatal period was due to a selective maturational defect in local respiratory mucosal immune function.