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Eight western osprey (Pandion haliaetus) presented to the Clinic of Rehabilitation of Wildlife (CROW, Sanibel, Florida) over a 2-month period with neurologic signs. Clinical signs included generalized ataxia, head tremors, and depressed mentation. Diagnostics performed included complete blood count, radiographs, and a blood gas point-of-care blood analyzer. Patients were treated supportively with antibiotics and parenteral fluids; however, all patients were euthanized due to declining neurologic status. Three patients were necropsied and fresh frozen tissues (brain, liver, and kidney) were submitted for heavy metal analysis, infectious disease testing, and histopathology through the U.S. Geological Survey National Wildlife Health Center. Tissues from all three of these patients demonstrated elevated mercury:selenium ratios > 1 (1.14, 1.29, 1.37, 1.35, 1.35), suggestive of mercury toxicosis. Brevotoxicosis and infectious disease testing, including for avian influenza, were negative, and tissue concentrations of other heavy metals were within normal limits. Control samples were obtained from three apparently healthy adult osprey that presented to CROW with severe trauma and were humanely euthanized. These tissue samples demonstrated normal mercury:selenium ratios (< 1) in the liver, brain, and kidney, which are supportive of protective levels of selenium. Research has previously demonstrated bioamplification of mercury in fledgling and adult healthy osprey, with the species playing an important sentinel role in water and ecosystem health.1-3 Recent literature has demonstrated that mercury toxicity produces a selenium deficient state and directly inhibits essential oxidative mechanisms of selenium.4,5 We postulate that clinical signs in these neurological osprey resulted from selenium deficiency secondary to mercury toxicity, which broadens horizons for potential treatments and has One Health implications for water ecosystems in Florida. [ABSTRACT FROM AUTHOR]