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Humans are an accidental, dead-end host for avian and bovine Schistosomes. Cercariae are not very particular about which host to invade. They usually tend to be in a resting posture at the surface of the water. When they sense a shadow, they begin to swim. Furthermore, light (darkness), temperature (warmth) and chemical stimuli mediate penetration. Hence, innocent swimmers or rice farmers become the inadvertent targets of the cercarial response to environmental stimuli. Once the cercaria penetrates human skin, it is unable to migrate to other sites to complete its development. In a manner of hours they die, leaving their antigens to further stimulate an immune response. Recent animal studies suggest that perhaps in a naive host avian schistosomes survive long enough to migrate to other locations. In the skin, cercariae rapidly develop into schitosomula. It is at this stage that the developing fluke disseminates to the organs of the body. These schistosomula have been found in the lungs, liver, kidneys, heart and intestine of mammalian animal models such as mice and guinea pigs. May suggest that during a priamary infection, there actually is migration to other sites in humans. However, this migration is not productive since the schistosomula die within 2-3 days.


Although not necessarily a vector, since it does not actively spread the disease by biting hosts, crustaceans, mostly snails, are the intermediate host. It spreads the infection basically by releasing the developed cercaria into the water.


Most cercarial dermatitis is caused by avian schistosomiasis. Hence the largest are reservoir are aquatic birds such as ducks. However, mammals and reptiles, such as elephants and crocodiles, also carry their own schistosomiasis that inadvertently infect human. The most common type of animal fluke that causes cercarial dermatitis are those from the genus Trichobilharzia, which infects primarily birds.