2004 Denver Annual Meeting (November 7–10, 2004)

Paper No. 15
Presentation Time: 11:45 AM

EVALUATING THE HYPERDISEASE HYPOTHESIS FOR THE END-PLEISTOCENE MEGAFAUNAL EXTINCTION USING WEST NILE VIRUS


LYONS, S. Kathleen1, SMITH, Felisa A.2, WAGNER, Peter J.3, WHITE, Ethan P.2 and BROWN, James H.2, (1)National Center for Ecological Analysis and Synthesis, Univ of California, Santa Barbara, 735 State St., Suite 300, Santa Barbara, CA 93101, (2)Department of Biology, Univ of New Mexico, 167 Castetter Hall, Albuquerque, NM 87131, (3)Department of Geology, Field Museum of Nat History, 1400 S. Lake Shore Dr, Chicago, IL 60605, lyons@nceas.ucsb.edu

Numerous hypotheses have been proposed to explain the end Pleistocene extinction of large bodied mammals. The disease hypothesis attributes the extinction to the arrival of a novel hyperdisease brought by immigrating aboriginal humans. However, until West Nile virus invaded the United States, no known disease met the criteria of a hyperdisease. We evaluate the disease hypothesis using West Nile virus in the United States as a model system. A disease can result in a size-biased extinction if there is size-bias in either infection or mortality rates. We show that West Nile virus is size-biased in its infection of North America birds, but is unlikely to result in an extinction similar to that of the end Pleistocene. West Nile virus infects birds more uniformly across the body size spectrum than extinctions did across mammals and is not size-biased within orders. Our study explores the potential impact of West Nile virus on bird populations and provides no support for disease as a causal mechanism for the end Pleistocene megafaunal extinction.