Ten adult captive Chilean flamingos (Phoenicopterus chilensis) died acutely in late October of 2001. Concurrently, an algal bloom was noted in the exhibit pond in which the flock of over 100 birds resided. The ten affected flamingos presented dead or moribund with clinical signs of extreme weakness, lethargy, recumbency, and dyspnea. Bleeding from injection sites was noted in the five birds in which venipuncture and treatment were attempted. Blood abnormalities included severe hypoglycemia and marked elevations in aspartate transaminase (AST), creatine kinase (CK), lactic dehydrogenase (LDH), and iron. Therapeutic efforts focused on controlling shock, hypoglycemia, dehydration, and delayed hemostasis. Despite treatment attempts with fluids (10–15 ml/kg 5% dextrose IV and/or 25–40 ml/kg 2.5% dextrose/0.45% NaCl SC, Abbott Laboratories, North Chicago, IL, USA), 50% dextrose (1 ml/kg IV, Dextrose, Phoenix Scientific, Inc., St. Joseph, MO, USA), vitamin K (2.5–5 mg/kg IM, K-Ject, Phoenix Scientific, Inc., St. Joseph, MO, USA), oxygen, vitamin E/Se (0.06–0.09 mg/kg IM, E-SE® injection, Schering-Plough Animal Health Corporation, Union, NJ, USA), dexamethasone (0.5–2 mg/kg IM, DexaJect, Phoenix Scientific, Inc., St. Joseph, MO, USA), and piperacillin (100 mg/kg IM, Pipracil, Lederle, Carolina, Puerto Rico), all birds died within 8 hours of presentation. Initial differential diagnoses included toxicosis (anticoagulants, blue-green algae toxins), trauma, sepsis, or capture myopathy. Necropsies were performed on seven birds. Cultures from the liver, kidney, lung, and brain of three birds showed mixed bacterial growth, but no sole causative etiologic agent for the epornitic. Consistent gross and histopathologic lesions included multifocal areas of hemorrhage in the muscle, gastrointestinal, and respiratory tracts, severe hepatocellular dissociation and necrosis with hemorrhage, and splenic congestion. High-performance liquid chromatography (HPLC) was used to determine the presence of toxicologic agents in pond water samples and internal organs of two birds. Livers were negative for seven different anticoagulant rodenticides, while gastrointestinal contents and pond samples contained microcystins. With a detection limit of 0.25 µg/g, HPLC analysis showed gastrointestinal contents containing microcystin-LR concentrations of 0.4 µg/g and 5.5 µg/g, and microcystin-LA, of 2.3 µg/g and 3.0 µg/g. Concentrations of microcystin-LR in water samples ranged from 1.7 µg/g to 13.3 µg/g, while levels of microcystin-LA ranged between 0.3 µg/g and 13.4 µg/g. Under light microscopy, pond water samples also contained non-filamentous granular clumps of cells surrounded by a clear calyx, consistent with the morphology of organisms of the genus Microcystis. Microcystins are hepatotoxic cyclopeptides produced by some Microcystis spp. and other genera of cyanobacteria. Based on our clinical and diagnostic findings, we determined that blue-green algae toxicosis caused the acute deaths seen in this flamingo flock. Further flamingo access to the exhibit pond was prohibited and no further mortalities occurred.
We thank Sea World Orlando’s aviculture staff and Kimberly Engle for their assistance with case management and data collection. We thank the California Animal Health and Food Safety Laboratory System at Davis for their help with toxicologic analysis and interpretation, and the Kissimmee Diagnostic Laboratory for their contributions to histologic and toxicologic analysis. We also thank Dr. Genny Dumonceaux and Dr. Michael Carmichael for sharing their expertise in algae toxicosis.