Letters to Nature

Nature 427, 630-633 (12 February 2004) | doi:10.1038/nature02317; Received 14 September 2003; Accepted 23 December 2003; Published online 28 January 2004

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 Iqbal Chaudhry6, Muhammad Arshad6, Shahid Mahmood6, Ahmad Ali6 & Aleem Ahmed Khan6

  1. 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 of Endangered 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

Correspondence to: J. Lindsay Oaks1 Email: loaks@vetmed.wsu.edu

The Oriental white-backed vulture (OWBV; Gyps bengalensis) was once one of the most common raptors in the Indian subcontinent1. A population decline of >95%, starting in the 1990s, was first noted at Keoladeo National Park, India2. Since then, catastrophic declines, also involving Gyps indicus and Gyps tenuirostris, have continued to be reported across the subcontinent3. Consequently these vultures are now listed as critically endangered by BirdLife International4. In 2000, the Peregrine Fund initiated its Asian Vulture Crisis Project with the Ornithological Society of Pakistan, establishing study sites at 16 OWBV colonies in the Kasur, Khanewal and Muzaffargarh–Layyah Districts of Pakistan to measure mortality at over 2,400 active nest sites5. Between 2000 and 2003, high annual adult and subadult mortality (5–86%) and resulting population declines (34–95%) (ref. 5 and M.G., manuscript in preparation) were associated with renal failure and visceral gout. Here, we provide results that directly correlate residues of the anti-inflammatory drug diclofenac with renal failure. Diclofenac residues and renal disease were reproduced experimentally in OWBVs by direct oral exposure and through feeding vultures diclofenac-treated livestock. We propose that residues of veterinary diclofenac are responsible for the OWBV decline.

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