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.