Epizootics in the double-crested cormorant (Phalacrocorax auritus) population have been documented along southern Florida’s gulf coast for the past 20 years. Affected animals exhibited ataxia and disorientation and were frequently captured and brought to local wildlife rehabilitation centers for treatment. C.R.O.W., a rehabilitation center on Sanibel Island, received 227 affected cormorants in 1995 and 161 affected cormorants in 1996. In both years, the majority of debilitated birds were admitted during a period of only a few months. Histopathology on tissues collected postmortem failed to reveal a common etiology or an explanation of clinical signs. Multi-organ bacterial cultures were non-specific and virus isolation was unproductive.
Between October and December of 1997, C.R.O.W. admitted 55 cormorants. Severe ataxia was the predominant clinical finding in 50 cormorants. The five cormorants in which ataxia was not noted presented for other reasons (hit by car, unknown trauma, and fish hook ingestion). All affected cormorants suffered from cerebellar ataxia characterized by a broad-based stance, truncal incoordination, hypermetric gait, and intention tremors of the head. Normal limb strength was preserved. Stimuli often resulted in exaggerated responses and hyperactivity. Neurologic signs were worsened by patient handling. Eighty-four percent of affected cormorants were markedly underweight (<1.3 kg). All of the ataxic cormorants had melena and watery diarrhea. Severe anemia (PCV less than 20%) was present in 28% of affected birds and hypoproteinemia (TS less than 2.0 g/dl) was present in 40% of affected birds. Endoparasitism was a common clinical feature. Contracaecum spp. and Tetramera spp. were frequently identified. Renal trematodiasis was observed in all samples that were examined with light microscopy. Thirty-two percent of affected cormorants responded to supportive care and were released 4–8 weeks later.
As in previous years, the histopathologic findings from the 1997 epizootic were non-specific. Pulmonary hemorrhage and congestion were commonly noted but were thought to be associated with acute agonal cardiovascular collapse. Other consistent findings included hepatic and splenic hemosiderosis as well as chronic mild cholangitis and nephritis. None of these lesions were interpreted as severe enough to be the primary cause of death. Acute bacterial septicemia and intravascular coagulation were noted in several cases. No brain or brainstem lesions were found.
A brevetoxin immunohistochemical staining technique was used to detect brevetoxin in samples from four affected cormorants. Brevetoxin, produced by the marine dinoflagellate Gymnodinium breve, is a neurotoxin known to affect marine animals. Furthermore, blooms of this dinoflagellate, called red tide, are often associated with fish kills. The immunohistochemical test documented uptake of brevetoxin in lymphoid cells of the spleen and macrophages of the spleen and lung in all four cormorants. Coincident with the 1996 and 1997 epizootics in cormorants, West Indian manatees (Trichechus manatus latirostris) in this area experienced a mortality event attributed to brevetoxicosis.1 Local red tide blooms were documented during these time periods also. The cormorant immunohistochemical results showed a pattern of immunostaining similar to the pattern seen in samples taken from the manatees. A controlled study is currently in progress to validate the use of the brevetoxin immunohistochemical test in the double-crested cormorant.
The authors would like to thank Dr. Kim Miller and the staff at the National Wildlife Health Center for graciously providing the double crested cormorant samples necessary to validate the immunohistochemical test.
1. Bossart GD, Baden DG, Ewing RV, Roberts B, Wright SD. Brevetoxicosis in manatees (Trichechus manatus latirostris) from the 1996 epizootic: gross histologic and immunohistochemical features. Toxicol Pathol. 1998;26:276–282.