Previous studies in school children have demonstrated the slow development with age of resistance to reinfection after chemotherapy of Schistosoma mansoni infections, and have indicated that inappropriate ("blocking") antibody responses prevent the expression of immunity in young children. The present study was designed to investigate further the nature of the protective responses, by serological studies on a group of 151 S. mansoni-infected individuals resident in an endemic area in Machakos District, Kenya. Antibody levels against various antigens in blood samples before treatment were related to intensity of previous infections; antibodies in blood samples taken 6 months after treatment were related to cumulative reinfection rates over the following 30 months. IgE against an adult-worm antigen preparation correlated positively with age and negatively with reinfection. In contrast, IgE antibodies against other life-cycle stages showed either no relationship or the reverse correlation. Furthermore, antibodies of other isotypes against adult-worm antigens showed no correlations with reinfection. The correlation with IgE could be demonstrated for different preparations of adult worms, including a periodate-treated preparation presumptively depleted of carbohydrate epitopes. For both the intact and the periodate-treated preparations, multiple regression analysis of the results for children less than or equal to 16 years old demonstrated an IgE effect after allowing for age, although this effect was not observed in a previously studied group of school children. Western blot analysis of the adult-worm preparation revealed a limited set of antigens recognized by IgE, among which an antigen of 22 kDa was prominent. The qualitative presence of IgE against this antigen could also be shown to be related to a lack of subsequent reinfection.

In schistosomiasis endemic areas, intensities of reinfection after treatment are greater amongst young children than amongst adults, and high levels of parasite-specific IgE are associated with resistance to reinfection in an age-dependent manner. Previously we have reported that, in Western blots, a 22 kDa band was recognized by human IgE and that the incidence and intensity of S. mansoni reinfection were significantly lower amongst individuals who had IgE against this band, compared with those who did not (Dunne et al. 1992). Here we report the isolation of a 22 kDa SDS-PAGE band, its incorporation into ELISA and the demonstration that levels of human anti-22 kDa IgE had a significant negative correlation with intensities of subsequent reinfection. Rabbit anti-22 kDa band serum recognized the outer tegument, gut tegument, and the collecting ducts and flame cells of adult worms. The 22 kDa band antigen(s) was also present in "lung'- and "post-lung' schistosomula stages of S. mansoni, and in S. haematobium, S. bovis and S. japonicum adult worms. Metabolic labelling of schistosomula and worms demonstrated the in vitro synthesis and release of 22 kDa antigens.

In schistosomiasis mansoni, soluble egg antigens of the worm induce chronic T-cell-mediated granulomatous tissue responses. Since the first preparation of crude soluble egg antigen extract, a dearth of highly purified antigens has hampered the identification of granuloma inducer molecules. Here we report that a cloned 38-kDa egg polypeptide (r38) with homologies to small heat shock proteins is a strong immunogen. The recombinant and the sodium dodecyl sulfate-polyacrylamide gel electrophoresis separated and eluted native 38-kDa (p38) polypeptides, used in microgram amounts and unaided by adjuvant, sensitized mice for a Th1-type immune response, with strong interleukin-2 (IL-2) and gamma interferon secretion but no IL-4 and IL-10 secretion. Extensive cross-reactivity between these two polypeptides was evident. This pattern was confirmed by reverse transcription-PCR that showed strong IL-2 and gamma interferon message expression but trace amounts of IL-4 message expression in r38-sensitized splenocytes. In mice, the polypeptide induced pulmonary mononuclear granuloma formation around antigen-coupled beads or worm eggs. We propose that the superior immunogenicity of r38 is linked to its relatedness to small heat shock proteins and that the 38-kDa polypeptide may induce the Th1 cytokine responses observed during the early development phase of the egg-induced granuloma.

Changes in the surface antigenicity and susceptibility to eosinophil-dependent killing during in vitro development of schistosomula of Schistosoma mansoni, were examined using sera from rabbits and mice immunized with antigens that are shed from the schistosomulum in vitro (shed antigen), a carbohydrate extract of shed antigen (SAg/CHO) or a periodate-insensitive fraction of shed antigen (SAg/PEP). Anti-SAg/CHO antisera recognised mainly carbohydrate epitopes on the parasite surface, whilst anti-SAg/PEP antisera bound to periodate-insensitive, putative peptide, surface epitopes. Anti-SAg/PEP antibodies failed to recognise the surface of newly transformed schistosomula unless the parasite was first treated with sodium periodate, suggesting that these epitopes may be masked by periodate sensitive (i.e., carbohydrate) epitopes. There was an increase in anti-SAg/PEP antibody binding to the larval surface with age of the parasite in vitro; five-day-old lung schistosomula were also recognised by anti-SAg/PEP antisera. In contrast, anti-SAg/CHO antibody binding declined with parasite age, and failed totally to recognise lung schistosomula. This change in epitope expression was reflected in eosinophil-dependent cytotoxicity assays, with anti-SAg/CHO antisera killing young larvae and anti-SAg/PEP antisera only killing older larvae. Lung worms were not killed by either antisera. The difference in epitopes recognised by the antisera was also reflected in the antigens identified by immunoprecipitation and SDS-PAGE.

SUMMARY It has been suggested that high zinc concentrations found in men may prevent Trichomonas vaginalis from being established in the male reproductive tract. In this investigation T vaginalis was readily killed at concentrations of zinc that occur in the prostatic fluid of healthy men (minimum trichomonacidal concentration (MTC) of 6.4 mmol/l). T vaginalis was also shown to be killed by human prostatic extracts as well as by human seminal fluid, even when the zinc content was much lower than the MTC for T vaginalis. It seems likely, therefore, that there are at least two antitrichomonal mechanisms in the male reproductive tract, one being zinc dependent and the other not relating to zinc content. Tritrichomonasfoetus, which causes venereal trichomoniasis in cattle, was unaffected by bovine seminal fluid and was killed by zinc only at concentrations far higher than those found in the prostatic fluid in the bull (MTC 200 mmol/l).Venereal trichomoniasis may be caused by two flagellates, Trichomonas vaginalis in man' and Tritrichomonas foetus, which infects cattle.2 In man, women have long been recognised as the reservoir of T vaginalis, 1 3whereas men are seen to serve merely as the short term vector of the organism.4 In symptomatic women the disease is often characterised by severe inflammation and a malodourous seropurulent vaginal discharge. 1 35 Men suffering from T vaginalis infections most often exhibit no symptoms, although mild cases of urethritis, prostatitis, and epididymitis have been associated with venereal trichomoniasis.The role of the male in bovine trichomoniasis appears to be far more important than it is in human venereal trichomonad infections. The bull serves as both the reservoir and the vector of T foetus, the organism tending to be localised in secretions in the prepuce and around the penis.89 Unlike men, who often seem to be only transiently infected, the bull, if untreated, usually remains infected and infective for long periods, if not for life.9 The cow, however, tends to suffer from short term trichomonad infections, which are often fairly mild. They can occur as fulminant infections if the cow is pregnant, however, in which case early abortion of a poorly developed foetus often results.8 '-' Most of the trichomonads are Address for reprints: Miss J G Langley,