SummarySeveral studies have shown that the characteristic hepatic abnormalities induced by Schistosoma mansoni detectable by ultrasound correlate with the degree of oesophageal varices. So far the value of ultrasound for predicting variceal haemorrhage has not been assessed. Fifty Brazilian patients with schistosomal periportal fibrosis from Alagoas State, 18 of whom had already bled from oesophageal varices, were enrolled in a combined cross-sectional and longitudinal study and investigated clinically, by endoscopy and by ultrasound. Twenty-seven of the patients were monitored until another bleeding episode, death or for a minimum of 28 months. Eight of these patients could be followed up for a further three years. A sonographic score, which accounts for the degree of echogenic periportal thickening and of portal vein dilatation, was calculated for all patients. A highly significant correlation (P Ͻ 0.0001) existed between the sonographic score and the occurrence of previous variceal haemorrhage, paralleled by a similar correlation between the sonographic score and the degree of oesophageal varices (P Ͻ 0.001). In the 27 patients monitored longitudinally, the sonographic score indicated the risk of future variceal bleeding (P Ͻ 0.0001). The sonographic score reliably predicts the risk of variceal bleeding in individual patients with periportal fibrosis. Hence, the application of endoscopy, if available at all in endemic areas, may be restricted to the patients at risk of future variceal bleeding, as determined by ultrasound. Since portable devices can be carried even to remote areas, the application of the proposed score in community surveys could provide a new means for the identification of high-risk patients in S. mansoni-infected populations.keywords S. mansoni, hepatic abnormalities, oesophageal varices, ultrasound correspondence Joachim Richter,

Sera of individuals from Burundi excreting eggs of Schistosoma mansoni (prevalence 35%; 178 subjects) and of similar individuals from Maniema, Zaire (prevalence 95%; 99 subjects), and of 159 Dutch and 81 Zairean non-infected controls, were screened by enzyme-linked immunosorbent assay for the presence of schistosome circulating anodic antigen (CAA). No false positive results were obtained. The sensitivity of the test was 75% in Burundi and 93% in Zaire, a significant difference (P less than 0.05). However, in matched egg output classes the test results did not differ significantly; 60% and 67%, respectively, of those excreting 1-100 eggs per gram of faeces (epg), 86% and 100% of those excreting 101-400 epg, and 100% of those excreting over 400 epg were detected. The efficiency of the assay was 91% in Burundi and 93% in Zaire. The Spearman rank coefficient of correlation between antigen titre and egg output (determined by 3 consecutive Kato egg counts) was 0.61 in Burundi and 0.82 in Zaire. The sensitivity of the test compared well with a single egg count. In addition, preliminary data showed that occasionally CAA was detectable in serum of individuals not excreting schistosome eggs. As CAA is found only in the presence of living worms, such cases reflect active infections.

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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Abstract. Surprisingly low cure rates were repeatedly observed after treatment with a standard dosage of praziquantel in a recently established Schistosoma mansoni focus in northern Senegal. In 4 discrete cohorts from the same population, cure rates were 18-36% and egg count reduction rates were 77-88%. Data and material of 920 compliant subjects from all 4 cohorts were further analyzed to identify possible host-related factors associated with low cure rates. The lowest cure rates were found in the highest egg count groups. However, in low and moderate egg count groups, drug efficacy was also below normal values. Cure rates were similar in males and females, showed no seasonal variation, and were independent of previous praziquantel treatment. They were significantly higher in adults than in children, also after allowing for intensity of infection. Individual water contact behavior and specific humoral immune responses were examined in 2 extreme subgroups, either without significant egg count reduction or showing complete parasitologic cure. There was no significant difference in frequency and duration of water contact between those individuals with complete cure and those that showed little effect of praziquantel treatment. Levels of IgG, IgG1, IgG3, IgG4, IgM, and IgE against adult worm antigen were not different between the 2 subgroups. Thus, the abnormally frequent failure of treatment observed in this focus could not be associated with any host-related factor, other than age and pretreatment egg counts.In a recently established focus of Schistosoma mansoni in the Senegal River Basin, praziquantel treatment apparently showed a lower efficacy and induced more side effects than usually reported. 1,2 In an initial cohort of 400 subjects, only 18% was found to be parasitologically negative 12 weeks after treatment with the standard single oral dosage of 40 mg/kg. However, egg reduction rates were substantial (86%) in those remaining positive. Results were confirmed by determination of circulating antigens excreted by metabolically active adult worms.2 Similar low cure rates were found in 3 subsequent cohorts from the same focus (Stelma FF, unpublished data). An increased dosage of praziquantel, given at the same day, showed no significant improvement, 3 while normal cure rates were found after treatment with oxamniquine, 4 or after repeated treatment with praziquantel within a period of 40 days. 5Possible explanations for these findings can be divided into 3 main categories: 1) parasite-related, including reduced strain susceptibility to praziquantel, 2) drug-related, including drug quality or bioavailability, and 3) host-related, including high initial intensity of infection, prepatent infections, rapid reinfection, and still under-developed pharmacosynergistic humoral immune responses. 2 This paper focuses on the third category of hypotheses. We use data from all four cohorts to analyze the contribution of host-related factors on the efficacy of praziquantel treatment in this area, with emphasis on the variabl...