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  ¿î¿µÀÚ 2005-05-23 23:26:23 | Hit : 18950 | Vote : 8160
Subject   [ÀÚ·á] Increased Infectious Disease Susceptibility Resulting from Outbreeding Depression
Conservation Biology
Volume 19 Issue 2 Page 455  - April 2005
doi:10.1111/j.1523-1739.2005.00091.x
  

Increased Infectious Disease Susceptibility Resulting from Outbreeding Depression


TONY L. GOLDBERG*¡×, EMILY C. GRANT, KATE R. INENDINO, TODD W. KASSLER**, JULIE E. CLAUSSEN, AND DAVID P. PHILIPP¡×*Department of Veterinary Pathobiology, University of Illinois at Urbana-Champaign, 2001 South Lincoln Avenue, Urbana, IL 61802, U.S.A., email tlgoldbe@uiuc.eduDepartment of Natural Resources and Environmental Sciences, University of Illinois at Urbana-Champaign, 1102 South Goodwin Avenue, Urbana, IL 61801, U.S.A.Illinois Natural History Survey, Center for Aquatic Ecology, 607 East Peabody Drive Champaign, IL 61820, U.S.A.¡×Program in Ecology and Evolutionary Biology, University of Illinois at Urbana-Champaign, 286 Morrill Hall, 505 South Goodwin Avenue, Urbana, IL 61801, U.S.A.**Washington Department of Fish and Wildlife, 600 Capitol Way North, Olympia, WA 98501-1091, U.S.A.
Abstract: The mechanisms by which outbreeding depression leads to reduced fitness are poorly understood. We considered the hypothesis that outbreeding can depress fitness by increasing the susceptibility of hybrid individuals and populations to infectious disease. Competitive breeding trials in experimental ponds indicated that outbred largemouth bass ( Micropterus salmoides) crossed from two geographically and genetically distinct populations suffered a reduction in fitness of approximately 14% relative to parental stocks. We measured the comparative susceptibility of these same outbred stocks to a novel viral pathogen, largemouth bass virus. Following experimental inoculation, F2 generation hybrids suffered mortality at a rate 3.6 times higher than either F1 generation hybrids or wild-type parental fish. Analysis of viral loads indicated that viral replication was more rapid in F2 fish than in F1 hybrids or wild-type parental fish. We attribute these results to the disruption of coadapted gene complexes in the immune systems of outbred fish in the F2 generation. Increased susceptibility to infectious disease may be an important but underappreciated mechanism by which outbreeding reduces the fitness of individuals and populations and by which novel infectious diseases emerge in populations of hybrid organisms.

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