We have developed an enzyme immunoassay (ELISA) for the quantification of the schistosome circulating cathodic antigen (CCA), a glycoprotein associated with the syncitium lining the gut of the parasite. A mouse monoclonal antibody of IgG3 isotype was used as coating (antigen-capture) antibody, while a biotinylated mouse monoclonal IgM was used as second (antigen-detecting) antibody. Streptavidin-alkaline phosphatase was used as enzyme label. The lower detection limit of the assay was 1.0 ng of the trichloroacetic acid soluble fraction of adult worm antigen (AWA-TCA) per ml, which corresponds to approximately 0.2 ng CCA per ml. The ELISA showed a linear range from 1.0 to 62.5 ng AWA-TCA per ml. Serum and urine samples of 16 individuals infected with Schistosoma mansoni (egg counts ranging from 5 to 4820 eggs per gram of faeces) were tested in the assay. Antigen titres ranged from less than 4-8192. This assay represents a considerable advantage in diagnosis of Schistosoma infections as it allows the detection and quantification of CCA in serum and urine in even lightly infected individuals.

This study examines the ability of an assay which measures the amount of a schistosome specific antigen (CAA) in the host circulation to reliably reflect relative worm burden. Mice were infected with 5 species of schistosome with a range of infection dose. The levels of serum CAA increased during schistosome maturation. In all species tested CAA levels correlated well with adult worm burden once the parasites achieved sexual maturity and remained relatively stable during the establishment of egg production. The amount of CAA produced varied between species but within each species CAA levels were proportional to worm numbers: no density-dependent effects on CAA levels were observed even when mice carried worm burdens that were very large relative to host size. T-cell deprivation of the host had no effect on the CAA/worm burden relationship in either Schistosoma mansoni or S. haematobium infections and the CAA equilibrium was unaltered in intact mice when reduction of worm fecundity occurred. These data support the use of the CAA as an accurate and robust estimate of relative schistosome burden in man.

Levels of IgE, IgM, and IgG subclasses against Schistosoma haematobium adult worm antigen (AWA) and soluble egg antigen (SEA) in a cohort of 148 S. haematobium-infected schoolchildren were determined before and up to 12 months after chemotherapy. Infection intensities were determined as concentrations of circulating anodic antigen (CAA) in serum. One month posttreatment, the antibody levels of all isotypes against AWA were increased, but 1 year after treatment they returned to pretreatment levels. CAA concentrations were positively associated with levels of IgG4 against AWA and SEA but not with levels of IgE. Age correlated negatively with CAA concentrations and positively with levels of IgE to AWA. The balance of anti-AWA IgG4 and IgE was significantly correlated to the CAA concentration, in particular in the older age group (11-13 years). This may suggest that protective immune mechanisms in S. haematobium infections become effective around the age of 12 years.

The kinetics of serum levels of circulating anodic antigen (CAA) of Schistosoma mansoni were studied in patients with intestinal schistosomiasis before and after treatment with praziquantel. Day to day fluctuation in faecal egg excretion was compared with fluctuation in antigen level in 20 patients by serum and stool examination on 3 consecutive days before treatment. Antigen levels - calculated either as absorbance value of undiluted serum or as titre - showed less fluctuation than the number of eggs per gram of faeces determined by stool examinations based on single or duplicate 25 mg Kato smears. Compared with a placebo control group of 11 individuals, there was a significant reduction in CAA level in serum of 10 patients treated with praziquantel (40 mg/kg), 10 weeks after treatment. A similar decrease in serum CAA level was observed in a group of 46 patients treated with praziquantel, 6 weeks after treatment. In both groups, patients who remained seropositive after treatment still excreted eggs in their faeces. The kinetics of the antigen decrease were studied in more detail in 20 patients in hospital. Within 10 d after treatment with a double dose of 40 mg praziquantel per kg body weight, the antigen level fell to less than 10% of the original serum level, with a CAA half-life of approximately 2 d.

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