| Summary: | The effect of various factors on the infectivity of the cercariae of S. mansoni and S. haematobium were studied. It has clearly been shown that the infectivity of cercariae of both species is directly influenced by those factors. Almost equal proportions of cercariae of both species died or were severely damaged during penetration of mammalian host. skin: 24-48% died in mouse skin compared with only 11-19% in hamster skin. These differential losses in the skin of different hosts account for the fact that hamsters yield higher adult worm. recoveries than mice. However, adult worm recoveries from animals infected with S. haematobium cercariae were much less, almost one third, than those from S. mansoni infections. Young mice were more susceptible to S. mansoni than old mice and this was mainly due to the low level of mortality of cercariae during penetration of young mouse skin. More cercariae of S. mansoni died, at lest during the early stages of penetration, in the skin of infected animals than in the skin of normal previously non-infected animals. It is very difficult to explain this observation; it could be related to the immune state of the host or to local reaction, provoked by previous exposure to cercariae, at the site of penetration. No difference was found in the susceptibility of male or female mice to S. mansoni but male hamsters were more susceptible to S. haematobium than female hamsters. The percentages of S. mansoni and S. haematobium cercariae which die, during penetration of host skin, steadily increased with increase in the post-emergence age of the cercariae and this accounted for the observed decline in infectivity which accompanied ageing of the cercariae. It has been demonstrated that death of S. mansoni cercariae during penetration of host skin is probably due to the exhaustion of their stored energy reserves. Ultra-violet irradiation affected the infectivity of cercariae of S. mansoni and S. haematobium by increasing the level of mortality of cercariae in the skin and delaying their migration in the lungs beyond days 3-4 postinfection. Gamma irradiation also inhibited the development of S. mansoni cercariae to the adult stage : cercariae were mainly destroyed in the liver although some form of damage occurred in the lungs as well. Maintenance of cercariae of S. mansoni and S. haematobium at low or high temperatures increased their mortality in the skin and consequently resulted in a marked reduction in the worm burdens of animals infected with these cercariae. Treatment of S. mansoni cercariae with sublethal concentrations of niclosamide (Bayluscide) had the same effect as temperature. The in vivo development of S. haeratobium was also studied. It followed the same general pattern as for S. mansoni and S. japonicum: six stages of development, characterized by morphological and histochemical criteria, were distinguished. However, the development of S. haematobium was slower (61-63 days) than S. mansoni (34-35 days) or S. japonicum (23-29 days).
|
|---|
