dc.description.abstract |
Epidemiological studies in different geographical regions of the world have demonstrated similarity in age-related susceptibility to schistosome infection in human populations. Data from these communities provide some strong evidence for an abrupt increase in intensity of human schistosomiasis that coincides with puberty. Many physiological changes that occur (luring puberty are honnonally controlled. In this study, the homional and immunopathological changes in mice infected with Schisrosoma mansoni were examined. Eighty Balb/c mice of pre-pubertal age (24-25 days old) and sixty ofpost-pubertal age (9- l5 weeks old) was acquired. Half the number of these mice from each group was infected with 110 S. mansoni cercariae whereas the rest were controls. Five mice from each group were sampled at weeks 2, 4, 6,8 and 10 post-infection (PI) for spleen and lymph node (LN) cells for in vilro proliferation assays. Plasma taken on the above sampling points was assayed for testosterone and luteinizing hormone (LH). The pathology was examined on livers taken on weeks 7,10 and ll PI and the number of adult wonns recovered on week7Pl. ' Compared with post-puberty infected mice, pre-puberty infected mice displayed signiticantly higher (P<0.05) number of adult worms, larger and more severe granulomas. They also displayed a higher mortality rate (9.75%). LN and spleen cells stimulated with Soluble Wonn Antigen Preparations (SWAP) from pre—puberty infected mice showed significantly higher (P<0.05) proliferative responses compared to the post-puberty infected mice. Both concanavalin A (Con A) stimulated LN and spleen cells from the control and experimental animals showed a substantiative high responses throughout the experiment. Also both plasma levels of testosterone and LH decreased significantly (P<0.05) in infected mice when compared with their controls. Plasma LH levels were positively correlated (R I 0.693) with plasma testosterone levels. The lowered levels of testosterone in the infected mice could be attributed to suppressed production of LH at the pituitary gland. This study shows that the pre-puberty infected mice are more susceptible to S. munsoni infection than the post-puberty infected mice and that both Ll-I and testosterone productions are suppressed in murine sehistosomiasis. |
en_US |