Experimental concurrent infection with two or more parasite species in mammalian host models may result in heterologous antagonistic and synergistic interactions ranging in magnitude from reduced/enhanced growth and fecundity to blockage/enhancement of establishment/expulsion. With some exceptions only, there is a reasonable correlation between the levels of interaction monitored by parasitological and by clinico-pathological parameters. Heterologous antagonistic interactions mediated by functional and specific immunological cross-reactivity occur between closely related parasite species exhibiting a marked immunobiological similarity. In contrast, antagonistic interactions between antigenetically more remote species of helminths, protozoan-induced resistance to helminth infection and helminth-induced suppression of concurrent protozoan infection generally appear mediated by immunologically non-specific factors like macrophage activation and inflammatory reactions. Synergistic heterologous interactions between helminths, helminth-induced enhancement of concurrent protozoan infection and interference with the development and maintenance of resistance to helminth infection in response to concurrent protozoan infection are generally thought to be mediated by non-specific parasite-induced immunosuppression. Concurrent experimental infection is very complex. There are problems and limitations in extrapolating from experimental studies on concurrent infection in laboratory animals to natural polyparasitism. This fact, coupled with the complex influence of ecological factors on the pattern and frequency of concurrent natural infection means that major consequences of natural concurrent parasite infection have not been definitively demonstrated. Appropriately planned and controlled field studies and further laboratory experiments on primate and domestic animal models are imperative for elucidation of the importance of heterologous interactions in concurrent parasite infection for the disease pattern in man and domestic stock. Experimental studies hitherto conducted on concurrent parasite infection pointing to natural heterologous interactions may be a valuable starting point for further studies.

Objectives:To assess the effect of zinc supplementation on growth and body composition among schoolchildren. Design: Randomized, double-blind, placebo-controlled trial. Setting and Subjects: 313 rural Zimbabwean schoolchildren (144 boys and 169 girls), 11-17 y). Interventions: Supplementation with zinc (30 or 50 mg) or placebo on schooldays for 12 months. Due to drought, a food programme was in operation during the last eight months of the study. Variables: Weight, height, upper arm circumference, triceps skinfold thickness, and weight-for-age, height-forage, weight-for-height, arm muscle-area-for-age and arm fat-area-for-age Z-scores. Results: Significant effects on weight gain (0.51 vs 0.14 kg, P 0.01), weight-for-age Z (70.08 vs 7 0.14, P 0.01) and arm muscle area-for-age Z-score (0.10 vs 0.01, P 0.03) were seen over the first three months, whereas no effects were seen over the full 12 months. Conclusions: Zinc deficiency impairing lean body mass and weight gain was documented. However, the effect of zinc seen over the first three months vanished during the last nine months when the food programme was in operation. Zinc deficiency may have persisted, but another nutrient may have become growth limiting during the last nine months.

The rationale for empirical antischistosoma treatment of adolescents and younger adults in areas where S. haematobium is endemic, with praziquantel alone or in combination with existing anti-STI regimens, is discussed.

Antibody responses to soluble Schistosoma haematobium egg (SEA) and worm (SWA) antigens in a rural Zimbabwean study population were examined by ELISA. One hundred and sixteen S. haematobium infected and 124 non-infected individuals representing individuals greater than five years old, were included. Non-endemic control sera were obtained from a schistosomiasis non-endemic part of Zimbabwe and from Norwegian blood donors. A possible association between IgE antibody responses and resistance to S. haematobium infection was indicated by a negative correlation between IgE anti-SEA levels and intensity of S. haematobium infection, and by a positive correlation between IgE responses to SEA and SWA and age. Similarly, an association between IgA and anti-SWA and resistance to S. haematobium was suggested by a negative correlation to intensity of infection and a positive correlation with age. A probably association between IgM and IgG4 with susceptibility to S. haematobium infection was described; intensity of S. haematobium infection correlated positively with IgG, IgG4 and IgM responses to SEA and with IgG4 and IgM responses to SWA, also age correlated negatively with IgG4 and IgM responses to SEA and with IgG4 responses to SWA. These findings support the concept of IgG4 and IgM as blocking antibodies. Significant positive correlations between antibody responses to SEA and SWA suggests cross-reactivity between eggs and adult worms. In addition, the recognition by IgE and IgG4 of the same schistosomulum antigens in immunoblotting suggests competitions for the same antigens.

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