This study suggests that praziquantel treatment against S. mansoni during pregnancy has similar efficacy as praziquantel treatment in non-pregnant women, despite the presence of lower levels of anti-schistosome antibodies and tendency to reduced boosting of both antibody and cytokine responses observed during pregnancy.
In assessing effects on S. mansoni infection intensity, the chief limitation of this study was the use of a single stool sample to determine prevalence and intensity of S. mansoni after treatment. A single stool sample has low sensitivity in detection of helminth infections [29–31], hence the prevalence will have been underestimated and estimates of intensity will have been imprecise. However, since comparisons were made between randomised groups, these limitations are likely to have applied similarly at follow up in both groups; the proportion apparently "cured" will have been exaggerated in both groups, but the comparison remains valid, suggesting little difference in the effect of treatment during pregnancy or after delivery.
In this study, alterations in the levels of schistosome antigen-specific antibodies during pregnancy, as well as the effect of praziquantel treatment during pregnancy on the antibody levels, were elucidated. Levels of IgG1, IgG2, IgG3, IgG4 and IgE against SWA and SEA, were generally low during pregnancy. These findings accord those of Novato-Silva and colleagues  showing that antibody levels against adult schistosome worm antigens declined with progression of pregnancy. These observations are contrary to other reports on antibodies to non-schistosome antigens showing that humoral immune responses are not affected by progression of pregnancy [19, 33]. There is normally an increase in plasma and blood volume during pregnancy  which is apparent at six weeks, and is maximum (40–50%) between 32–36 weeks, of pregnancy [34, 35]. Although this dilution effect of increased blood volume of pregnancy was not examined in our study, it could potentially explain the low antibody levels during pregnancy rather than a decline in the antibody responses per se.
Praziquantel treatment during pregnancy caused a boost in antibody levels against SWA and to a limited extent SEA; although a significant drop in levels of IgG4 against SEA was observed. These boosts in antibodies at six weeks post-treatment were consistent with those observed at five weeks post-treatment , three months post-treatment  and at six months post-treatment  among S. mansoni infected non-pregnant individuals in endemic areas. Similar increases in antibodies were recently reported following treatment among non-pregnant adults from a new focus of S. mansoni infection . The decline in the level of IgG4 against SEA following praziquantel treatment was also consistent with findings reported among non-pregnant individuals [37, 39]. The boost in IgE against SWA was less marked than for other antibodies against SWA. It is possible that six weeks after treatment could have been too short a follow-up time to observe a significant boost in levels of IgE against SWA. This was consistent with other studies where post-treatment levels of IgE against SWA were not significantly boosted at three weeks  and five weeks , following treatment, suggesting that this particular isotype remains relatively stable over time among adults in S. mansoni endemic areas.
Although boosts in schistosome antigen-specific antibody response were observed during pregnancy, these were generally lower, and post-treatment antibody levels were lower, compared with treatment after delivery. However, in spite of this, the data did not show evidence that pregnancy and having lower boosts in schistosome antigen specific antibody isotypes had any significant impact on the efficacy of praziquantel treatment against S. mansoni. Suppression of the boosts in antibodies during pregnancy may, however, have effects on resistance to reinfection. Due to limited follow-up time and since all the women received praziquantel treatment after delivery, the impact of treatment during pregnancy on susceptibility to reinfection after treatment was not explored. Therefore, further studies might be necessary to examine the long-term implications of the suppression of boosts in some of the antibody isotypes following treatment during pregnancy.