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Parasitic Flatworms
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Biology Laboratory Manual, 6/e
Darrell S. Vodopich, Baylor University
Randy Moore, University of Minnesota--Minneapolis

Parasitic Flatworms

Student Research Project
Immunological studies in schistosomiasis

Morgan W. Richie
Major: Zoology
Future Plans: Graduate school, research, and/or teaching career

Paul J. Hyler
Major: Genetics
Future Plans: Graduate school, research career

Raymond T. Damian, Professor and Head, Department of Cellular Biology, University of Georgia, Athens

Schistosomiasis is a disease of humans caused by parasitic flatworms called schistosomes, or blood flukes. The disease affects over 200 million persons worldwide, mostly in developing countries. The intermediate hosts of schistosomes are certain aquatic or amphibious snails, whose distribution basically defines the geographical range of endemic schistosomiasis. People acquire the infection by entering fresh water in which infected snails have shed schistosome larvae (cercaria) that can actively penetrate human skin. The cycle is completed when infected people pass eggs of the parasite in feces or urine and these eggs reach the water to hatch and liberate a second larval type, the miracidium, which is capable of finding and penetrating vector snails. Thus, the schistosome's life cycle and transmission is tied to snail vectors, human water contact, and unsanitary conditions.

Although effective schistosomicida drugs exist, there is a definite need for vaccines to confer long-term protection. Our laboratory is focused on vaccines as an ultimate goal, but we realize that much more needs to be learned about the relationship of the parasite with its mammalian host and the host immune response before effective vaccines can be designed. For example, one can ask how this parasite coexists for many years with a host's immune response, which is exactly what it does. It is clear from our research and that of others that the schistosome has evolved special adaptations that enable it to avoid, evade, and perhaps even exploit the host's immune response. One such mechanism suggested by our previous research is that the worm can actively repair its outer membrane after or even during immune attack. These repair mechanisms probably involve cytoskeletal proteins like actin and actin-binding proteins. Morgan Richie, originally hired as an undergraduate "glassware processor" in the lab, has had her interest stimulated by the ongoing research, so has volunteered to become involved in this project. She is working closely with Research Associate Dr. Roger W. Stich in an effort to immunolocalize actin isoforms and actin-binding proteins in worms undergoing immune attack.

Another project in our lab has to do with the early or acute phase of schistosomiasis, which can be very dangerous, even fatal. We have found that the baboon reproduces the acute schistosomiasis syndrome very faithfully, and that most of the symptoms of acute schistosomiasis including fever and wasting (cachexia) are associated with egg production by newly matured, mated worms in a primary infection. We have hypothesized that the parasite's eggs stimulate a florid immune response that leads to the overproduction of certain immune cell products called inflammatory cytokines that can cause these symptoms. Earlier results have also shown that anti-egg antibodies may be able to ameliorate the symptoms of acute schistosomiasis. Undergraduate student volunteer Paul Hyler is learning how to assay the sera of infected baboon for these antibodies, using techniques like the enzyme-linked immunosorbent assay (ELISA) and immunofluorescence. He is being taught these techniques by Dr. Herminia Kanamura, a faculty member at the University of São Paulo, Brazil, who is in our lab as a U.S. Public Health Service Fogarty International Research Fellow.