1Wildlife Health Center, School of Veterinary Medicine, University of California, Davis, CA, USA; 2Harbor Branch Oceanographic Institution, Fort Pierce, FL, USA; 3Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA, USA; 4Department of Environmental Science and Policy, University of California, Davis, CA, USA; 5Cardiopet Veterinary Referral Centre, Little Falls, NJ, USA; 6Florida Marine Research Institute, St. Petersburg, FL, USA
Epidemics of morbidity and mortality in double-crested cormorants (Phalacrocorax auritus) along Florida’s Gulf Coast have been known to occur sporadically for at least 30 years. During these epidemics, the Clinic for the Rehabilitation of Wildlife (C.R.O.W.), located on Sanibel Island in Lee County, has admitted a substantial number of cormorants with a consistent presentation of clinical signs. Blooms of the marine dinoflagellate, Gymnodinium breve, are often called red tides and have long been associated with marine animal mortality in the Gulf of Mexico.1-4 In order to correlate epidemics in cormorants to exposure to brevetoxin, we compared the timing of admittance of cormorants to C.R.O.W. with epidemic-specific clinical signs to G. breve blooms around Sanibel Island from 1995 through 1999. We also report the common clinical and pathologic features found in cormorants admitted to the clinic from six epidemics occurring during this period.
The clinic admitted 360 out of 613 cormorants with the common clinical sign of severe cerebellar ataxia. The ataxia was characterized by a broad-based stance, truncal incoordination, hypermetric gait, and intention tremors of the head. Stimuli, such as patient handling, often resulted in exaggerated responses and hyperactivity. Positional vertical nystagmus was also noted in the majority of ataxic cormorants. The ataxia typically resolved after two to four days. Histopathologic findings in 10 cormorants from an epidemic in 1997 were generally non-specific and insignificant.
Admittance of cormorants with epidemic-specific clinical signs was significantly positively correlated with increased concentrations of G. breve (cells per litre) in local water (p<0.05). The cross-correlation coefficient was also significant when G. breve levels lagged cormorant admittances by two, four, six, and eight weeks. The time delay between G. breve blooms and cormorant admittance is consistent with the clinicopathologic features of this disease, which suggest that cormorants most likely experience a chronic and cumulative detrimental effect from exposure. Overall, from 1995 through 1999 there were six major blooms of G. breve around Sanibel Island and six major epidemics in cormorants. The high proportion of cormorants presenting with brevetoxicosis-specific clinical signs to this one rehabilitation center suggests that brevetoxin exposure is a substantial cause of morbidity and mortality in cormorants in this area of southwest Florida.
We thank Dr. P.J. Deitschel, Anita Pinder, David Allen, and Margot White for their assistance with sample collection at the Clinic for the Rehabilitation of Wildlife. We also thank Dr. Karen Steidinger and Dr. Earnest Truby at the Florida Marine Research Institute for sharing the data on the temporal distribution of local G. breve concentration and Dr. Kim Miller, Dr. Rebecca Cole, and Dr. David Jessup for their guidance in clinically evaluating these epidemics in cormorants.
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