Abstract
Karenia brevis blooms are common in manatee habitat on the southwestern coast of Florida and produce a group of cyclic polyether toxins collectively referred to as red tide toxins, or brevetoxin. During a mass mortality event related to red tide in southwest Florida in the winter and spring of 2012–2013, 16 manatees were rescued and presented to Tampa's Lowry Park Zoo (TLPZ). All manatees were examined, had blood samples taken for routine complete blood cell counts (CBC), serum biochemistry panels, and coagulation profiles (prothrombin time [PT]), partial thromboplastin time (PTT), fibrinogen, platelet counts, and D-dimers). Serum or plasma was banked for brevetoxin analysis and whole blood was collected in heparinized blood tubes for lymphocyte transformation (LTT) assays when possible. Brevetoxin analysis and LTT were repeated as possible during the convalescent as well as at pre-release health assessments. A complete hematology and biochemistry panel was repeated as the pre-release health assessment as well. One manatee was treated with intravenous steroids at admission and the remaining 15 were given atropine; 0.02 mg/kg with ¼ the dose given IV and the remaining ¾ SQ. All manatees were given a course of injectable tulathromycin at 2.5 mg/kg SQ q7d for 3 treatments. All manatees were fitted with flotation devices at entry and monitored until they could support themselves in the water. Times to the removal of the flotation gear were recorded. Fifteen manatees survived and were subsequently released. All manatees had seizures to various degrees during rescue, transport and at presentation. Five animals presented comatose between seizures, with the nictitating membrane covering at least ¾ of the eye, and no palpebral or vibrissae response. One fatality occurred within this group of 5 about 12 hours after presentation. Gross findings included hemorrhage into the small intestine, lungs and around the brain. Histological findings included acute hemorrhage and necrosis of the intestine, acute intrabronchiolar and intraalveolar hemorrhage, and neuronal necrosis. All of the entry clinical pathology data, recovery time, and serum brevetoxin levels were reviewed retrospectively. Means of CBC, serum biochemistries, and coagulation panels were compared to those of manatees healthy enough for release from TPLZ analyzed by the same reference laboratory. Statistical differences between brevetoxin exposed manatees and the control population included higher white blood cell counts (p = 0.02), higher red blood cell counts (p = 0.013), higher hemoglobin concentration (p = 0.012), higher packed cell volumes (p = 0.039), higher heterophils (p = 0.00003), higher eosinophils (p = 2.07*10-5), higher PTT (p = 0.0465), lower blood urea nitrogen (p = 0.0001), lower calcium (p = 3.9*10-8), lower sodium (p = 6.61*10-5), lower potassium (p = 0.006), lower chloride (p = 0.003), higher globulins (p = 0.038), higher total bilirubin (p = 0.048), lower amylase (p = 0.005), higher creatinine kinase (p = 0.025), and lower gamma glutamase (p = 3.2*106) in the brevetoxin exposed group. There were no statistical differences in any parameter when the conscious to unconscious manatees were compared. Recovery time for all manatees that were conscious averaged 7.6 hrs compared to 17 hrs for unconscious manatees (p = 0.04). Serum brevetoxin levels (PbTx3, ng/ml) were not different between conscious and unconscious manatees (p = 0.18) but all manatees measured tended to have serum brevetoxin levels decrease during the first several weeks of rehabilitation.
Acknowledgements
The authors wish to thank Dr. Nico Maldonado; the Veterinary Clinic Staff of Heather Henry, CVT and Michelle Devlin CVT, and the Manatee Rehabilitation Team led by Virginia Edmonds from Tampa's Lowry Park Zoo.
* Presenting author