The conflicting role of parasitic infections in modulating the prevalence of asthma.

Nothwithstanding difficulties associated with the limitations of survey techniques and methodology employed to define asthma, the evidence accumulated to date suggests that the reported differences in the prevalence rates of this disease from country to country and within local populations of the one country are real. It is accepted that allergy is not the sole cause of asthma but nonetheless hypersensitivity to environmental allergens is a significant triggering factor in most countries of the world. Comparisons between countries might therefore be influenced by the time of the year when the survey is taken since the prevalence of seasonal asthma would be higher in the period of pollinosis. Environmental factors, and in particular the relative atmospheric concentrations of pollens and the density of house dust mite (D. pteronyssinus and D. farinae) in dwellings, must therefore be considered when accumulating prevalence data. The prevalence rate for childhood asthma is high in Australia, United Kingdom, United States of America and New Zealand, and medium to low in the Scandinavian countries and Switzerland. It is not clear what factors contribute toward these differences since several studies indicate that racial characteristics per se are not pre-eminent in defining susceptibility to asthma. Most surveys indicate that the prevalence of childhood asthma is low to very low among low-income populations living in tropical areas. While it is possible to implicate inadequate diagnosis, genetic factors, nutritional status and allergen exposure as factors contributing towards the low prevalence, it has become fashionable to attribute this observation to the influence of certain helminthic infections. Parasites stimulate the production of high levels of serum IgE, the bulk of which has as yet an undetermined specificity. The suggestion that this IgE blocks mast cell receptors leaving insufficient sites available for sensitization by allergen-specific IgE antibody is attractive. However, since the kinetics of binding to mast cell receptors is unlikely to be the same for all IgE molecules, irrespective of their specificity, this hypothesis appears to be an oversimplification of the problem. It is more likely that parasitic infections repress the synthesis of IgE antibody to environmental allergens, although the mechanism for this is unclear. Circumstantial evidence suggests that the time course of exposure to parasites versus sensitization by environmental allergens may be critical. Another possibility is that parasitic infections in some way nullify the effect of allergens at the level of the target organ, perhaps through the modulating role of eosinophils. If it is established that parasitic infections, particularly in early childhood, suppress the capacity of potentially atopic children to develop asthma and other allergic disorders, there would be some justification in attempting to circumvent allergic disorders in susceptible individuals by a harmless preparation of parasite antigens.