|Moore, Danielle - VMRI, IA STATE UNIV, AMES|
|Wannemuehler, Michael - VMRI, IA STATE UNIV, AMES|
Submitted to: Journal of Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 14, 2000
Publication Date: N/A
Interpretive Summary: Cryptosporidium parvum is an intestinal parasite that causes diarrheal disease in calves. This disease is costly to dairy and beef producers, and the disease can also spread to humans. There are no effective vaccines or drug treatments available for this parasite. Cryptosporidium has been shown to use some unusual chemical compounds during its growth and development. One of these, agmatine, is an important part of parasite development, but is not used by calves or humans in this way. In the present study, we treated mice with agmatine, and then exposed them to Cryptosporidium. Mice treated with agmatine were protected from infection with Cryptosporidium. This indicates that the excess agmatine disrupted growth and development of the parasite. Use of agmatine, or similar compounds, may be a useful way to reduce Cryptosporidium infection in calves, thus reducing economic losses to producers and reducing the risk of human disease through exposure to sick calves.
Technical Abstract: Cryptosporidium parvum is an intracellular protozoan parasite that causes enteric infection and diarrhea in a wide range of mammalian hosts, including humans and economically important livestock species. There are no effective vaccines or drug treatments available for this parasite. C. parvum has been shown to utilize a unique metabolic pathway for the synthesis of polyamines, forming agmatine as an intermediary metabolite. In the present study, we treated infant mice with oral doses of agmatine for 2 days before, the day of, and 5 days following experimental infection with C. parvum. Mice treated with agmatine were significantly less infected with C. parvum than were control mice receiving phosphate- buffered saline. Mice treated with agmatine only on the day of experimental infection with C. parvum were also significantly less infected than were control mice. These data suggest that exogenous agmatine alters the metabolism of C. parvum sufficient to interfere with its ability to colonize the mammalian intestine.