COS 88-10 - Managing multiple pathogens: A case study of Lyme disease and anaplasmosis

Thursday, August 6, 2009: 11:10 AM
Galisteo, Albuquerque Convention Center
Felicia Keesing, Program in Biology, Bard College, Annandale-On-Hudson, NY, Michael Tibbetts, Biology, Bard College, Annandale-On-Hudson, NY, Jesse Brunner, School of Biological Sciences, Washington State University, Pullman, WA, Mary Killilea, Biology, New York University, New York, NY, Kathleen LoGiudice, Biological Sciences, Union College, Schenectady, NY, Laura Cheney, Department of Biology, Bard College, Annandale-On-Hudson, NY, Shannon T. Duerr, Cary Institue of Ecosystem Studies, Millbrook, NY, Kenneth A. Schmidt, Department of Biological Sciences, Texas Tech University, Lubbock, TX and Richard S. Ostfeld, Cary Institute of Ecosystem Studies, Millbrook, NY
Background/Question/Methods

Human granulocytic anaplasmosis (HGA) is an emerging tick-borne disease in North America, Europe, and Asia. Patients with HGA suffer flu-like symptoms that can be acute, and approximately 1-4% of patients die, though many less severe cases probably go unreported. HGA is caused by infection with a rickettsial bacterium, Anaplasma phagocytophilum (Ap), that is passed from host to host by ixodid ticks. In North America, Ap is carried by the same ticks that transmit the bacterium that causes Lyme disease (LD), and ticks are frequently co-infected with both pathogens. These ticks feed on a wide variety of hosts and, as with LD, hosts vary in the probability that they will transmit Ap to feeding ticks.

Results/Conclusions

We are determining the probability with which particular host species transmit Ap to feeding ticks. Hosts were captured in the field and brought into the lab, where feeding ticks finished their blood meals, dropped off, and were collected. Ticks were then assayed for infection using PCR. Hosts vary in reservoir competence for Ap, but not as much as they vary for the Lyme bacterium. We have combined this information with extensive data on tick burdens on hosts to produce a model of how host community composition influences risk for both LD and HGA. Understanding the differences between HGA and LD will allow the development of appropriate management to reduce overall disease transmission to humans.

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