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Defense Mechanism Found In Infected Ticks May Protect Against Harmful Parasite

July 17, 2007 — A defense molecule isolated in ticks infected with the Babesia sp. parasite may protect animals and humans against infection. Researchers from the U.S. and abroad report their findings in the July 2007 issue of the journal Infection and Immunity.


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Babesiosis is a well-recognized disease worldwide and recently gained increased attention as an emerging zoonosis. Transmitted to animals and humans by ticks infected with the Bebesia sp. parasite, symptoms may include fever, fatigue and hemolytic anemia. Antimcrobial peptides are defensive molecules found in the innate immune system of animals. Less toxic and more effective against multi-drug resistant bacteria, they are showing promise as a better choice for treatment of some bacterial and fungal infectious diseases.

In the study researchers identified a novel parasiticidal peptide named longicin from the tick species Haemaphysalis longicornis and tested its ability to inhibit infection. It showed a remarkable ability to inhibit the blood stage of equine Babesia equi by killing the parasites and resulted in reduction of parasitemia in animals with the zoonotic and murine Babesia microti. RNA analysis also demonstrated that longicin is capable of killing the canine strain, Babesia gibsoni.

“Here we report a defensin peptide, longicin, from the tick H. longicornis that exerts a babesiacidal effect,” say the researchers. “Theoretically, longicin may serve as a model for the development of chemotherapeutic compounds against tick-borne disease organisms.”

Reference: N. Tsuji, B. Battsetseg, D. Boldbaatar, T. Miyoshi, X. Xuan, J.H. Oliver, Jr., K. Fujisaki. 2007. Babesial vector tick defensin against Babesia sp. Parasites. Infection and Immunity, 75. 7: 3633-3640

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The above story is reprinted from materials provided by American Society for Microbiology, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


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