Diclofenac Contamination In Vulture

letters to nature
24. Hasenfuss, I. A possible evolutionary pathway to insect flight starting from lepismatid organization. J. Zool. Syst. Evol. Res. 40, 65–81 (2002). 25. Chiappe, L. The first 85 million years of avian evolution. Nature 378, 349–355 (1995). 26. Novacek, M. J. Fossils, topologies, missing data, and the higher level phylogeny of eutherian mammals. Syst. Biol. 41, 58–73 (1992). 27.Edwards, D., Selden, P. A., Richardson, J. B. & Axe, L. Coprolites as evidence for plant–animal interactions in Siluro-Devonian terrestrial ecosystems. Nature 377, 329–331 (1995). 28. Gensel, P. G. & Andrews, H. N. Plant Life in the Devonian (Praeger, New York, 1984). 29. Alego, T. J., Scheckler, S. E. & Maynard, J. B. in Plants Invade the Land (eds Gensel, P. G. & Edwards, D.) 213–236 (ColumbiaUniv. Press, New York, 2001). 30. Wellman, C. H., Osterloff, P. L. & Mohiuddin, U. Fragments of the earliest land plants. Nature 425, 282–285 (2003).

Acknowledgements We thank A. J. Ross for loan of the material discussed herein and M. G. Rightmyer for comments on and support of the study. Competing interests statement The authors declare that they have no competing financial interests.Correspondence and requests for materials should be addressed to M.S.E. (msengel@ku.edu).

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Diclofenac residues as the cause of vulture population decline in Pakistan
J. Lindsay Oaks1, Martin Gilbert2, Munir Z. Virani2, Richard T. Watson2, Carol U. Meteyer3, Bruce A. Rideout4, H. L. Shivaprasad5, Shakeel Ahmed6, Muhammad Jamshed IqbalChaudhry6, Muhammad Arshad6, Shahid Mahmood6, Ahmad Ali6 & Aleem Ahmed Khan6
Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington 99164-7040, USA 2 The Peregrine Fund, 5668 West Flying Hawk Lane, Boise, Idaho 83709, USA 3 USGS–National Wildlife Health Center, 6006 Schroeder Road, Madison, Wisconsin 53711-6223, USA 4 Center for Reproduction ofEndangered Species, Zoological Society of San Diego, PO Box 120551, San Diego, California 92112, USA 5 California Animal Health and Food Safety Laboratory System–Fresno Branch, University of California at Davis, 2789 S. Orange Avenue, Fresno, California 93725, USA 6 Zoology Division, Institute of Pure and Applied Biology, Bahauddin Zakariya University, Multan, Pakistan.............................................................................................................................................................................
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Between 2000 and 2002 we performed gross post-mortem examinations on 259 adult and subadult OWBVs, of which 219 (85%) had grossly apparent urate deposits, characteristic of visceral gout, on the surface of internal organs (Fig. 1). Visceral gout in birdsis most commonly the result of renal failure leading to hyperuricaemia and the deposition of uric acid on and within the internal organs, and can be caused by degenerative, metabolic, infectious, or toxic diseases6. To verify renal disease, and to determine the cause, detailed necropsies and diagnostic testing were performed on a subset of 42 OWBVs (33 adults and 9 juveniles; 28 with visceral goutand 14 without visceral gout) that were found within approximately 24 h of death. The remaining OWBVs were significantly decomposed and thus were unsuitable for diagnostic evaluation, although the grossly apparent and characteristic lesions of visceral gout allowed the presence or absence of the disease to be determined. Of the 14 OWBVs without visceral gout, we determined the cause of death in 8(57%), which included trauma, intestinal foreign bodies, lead poisoning, organophosphate poisoning and gun-shot (Supplementary Information). We were unable to determine the cause of death in the remaining six vultures. Among the 28 OWBVs with visceral gout, only one (4%) had an identifiable disease (infection with Mycobacterium avium) in addition to visceral gout. All but two of the visceral gout...