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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Infectious Bacterial Diseases Research » Research » Publications at this Location » Publication #117713
Title: [1N,12N]BIS(ETHYL)-CIS-6,7-DEHYDROSPERMINE: A NEW DRUG FOR TREATMENT AND PREVENTION OF CRYPTOSPORIDIUM PARVUM INFECTION OF MICE DEFICIENT IN T-CELL RECEPTOR ALPHA

Author
item Waters, Wade
item FRYDMAN, B - SLIL BIOMED, MADISON, WI
item MARTON, L - UNIV. WISCONSIN, MADISON
item VALASINAS, A - SLIL BIOMED, MADISON, WI
item REDDY, V - SLIL BIOMED, MADISON, WI
item Harp, James
item WANNEMUEHLER, M - IOWA STATE UNIV., AMES
item YARLETT, N - HASKINS LABS, NEW YORK,NY

Submitted to: Antimicrobial Agents and Chemotherapy
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/6/2000
Publication Date: N/A
Citation: 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 biochemical pathways during its growth and development. In the present study, we treated mice with a synthetic analog of a compound important in one of these pathways, and then exposed them to Cryptosporidium. Mice treated with this compound were protected from infection with Cryptosporidium. Treatment with the compound was also able to cure mice already infected with Cryptosporidium. Further study of this and similar compounds may lead to ways to treat 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 infection of TCR-alpha-deficient mice results in a persistent infection. In this study, treatment of suckling TCR-alpha- deficient mice with a polyamine analogue (SL-11047) prevented C. parvum infection and cleared an existing infection in older mice. Treatment with putrescine, while capable of preventing infection, did not clear C. parvum from previously infected mice. These findings provide further evidence that polyamine metabolic pathways are targets for new anti-cryptosporidial chemotherapeutic agents.