Abstract
The sandhill crane is one of 14 crane species in the world. Two subspecies of sandhill crane reside in Florida: the Florida sandhill crane (Grus canadensis pratensis) and the greater sandhill crane (Grus canadensis tabida). The Florida subspecies is considered threatened due to its low reproductive potential, specialized habitat requirements and habitat destruction. The Florida sandhill crane is nonmigratory and nests in Florida, whereas the greater sandhill crane is a migratory species, spending winters in Florida and the remainder of the year in the Great Lakes states. The U.S. Fish and Wildlife Service and Canadian Wildlife Service have established a nonmigratory population of whooping crane (Grus americana), a critically endangered species, in Florida.
From 1981 to 1991, numerous injured and ill sandhill cranes were presented to the University of Florida Veterinary Medical Teaching Hospital (VMTH) by the Florida Freshwater Fish and Game Commission for a variety of problems.2 Cholangiocarcinoma, hepatic disease, and a “neck paresis syndrome” were seen with unusual frequency.1,2 Mycotoxins are the most likely underlying etiology in two of these conditions (cholangiocarcinoma and the “neck paresis syndrome”). This presentation will focus on the neck paresis syndrome. This syndrome was first noted in 1985 in sandhill cranes in Florida when wildlife officials began monitoring the birds in areas near peanut fields. The peanut harvest in Florida occurs in late October. The syndrome is triggered by the onset of cold weather, usually in late December or early January, and continues for approximately 3 months. Approximately 5–10% of the flocks (up to 300 birds) in Alachua, Levy, and Marion counties are affected annually by this syndrome. An estimated 9,500 sandhill cranes died in Gaines County, Texas and Roosevelt County, New Mexico between 1982 and 1987 from this syndrome. Trichothecene and other mycotoxins produced by Fusarium spp. were isolated from waste peanuts that the birds were feeding on and were considered to be the most likely cause of the clinical signs the cranes were showing.2,4
In the past in Florida, predators focused on roosts with affected birds or the birds would die of starvation or dehydration. Now birds are taken by wildlife officials before they die of the syndrome. Numerous cranes have been admitted to the VMTH with drooping necks and severe, dependent cervical edema. A thorough diagnostic evaluation was performed on all cases prior to instituting therapy. This included a physical examination, complete blood count, plasma biochemical profile, and plasma bile acid level. An equine encephalitis viral screen, fecal direct and flotation, whole body and cervical radiographs, electromyogram, muscle biopsy, and a liver biopsy were performed on selected cases. Birds with this condition that died received a complete postmortem examination. Consistent abnormalities included elevation of aspartate aminotransferase (AST), creatine phosphokinase (CPK), fibrinogen, and white blood cell count. Similar changes have been noted in previous reports on this condition.3 Most birds had histologic changes to the liver including chronic lymphocytic hepatitis, biliary hyperplasia, hemosiderosis, and hepatic necrosis. Cholangiocarcinoma was observed in one bird with this syndrome. No histologic changes were noted in cervical muscle biopsies performed on several birds. However, an electromyogram in one bird revealed changes consistent with a peripheral neuropathy. Pesticide screens on gizzard contents and selected tissues on three cranes were negative. Mycotoxin analysis on peanut stubble samples collected from November to February from peanut fields used by the cranes in Alachua county were inconclusive.
Upon arrival to the VMTH, most of these birds were moderately to severely dehydrated and in shock. Blood samples were obtained and then the birds were treated for shock and dehydration. The cranes were unable to eat or drink in this condition; thus, force feeding and parenteral fluid therapy were instituted until the head could be held up in a normal position. For the first several cases, the crane’s head would be manually held in a normal position for 5 to 10 minutes four times daily. With this technique, recovery times would be approximately 3 to 4 weeks. Some of these birds died from secondary diseases such as disseminated visceral coccidiosis (DVC) and aspergillosis. In order to decrease recovery time and stress of handling, a pulley system was developed. A piece of roll gauze was placed through the external nares of the bird, then the roll gauze was extended over to the next enclosure and a 1-kg weight was attached to the other end. This elevated the head of the bird and allowed it to move back and forth in the enclosure. Recovery time with this technique was 24 to 48 hours. The most important parts of the therapy appear to be elevating the head long enough for the cervical edema to subside and isolating the birds from further toxin exposure.
Eleven sandhill cranes were successfully rehabilitated and released using this technique from 1987 to 1991. Six of these were sighted for 1 year post-release and one for 3 years post-release. This treatment regimen continues to be successful and could be utilized by other institutions encountering this problem in sandhill cranes and potentially other crane species.
Rendering moldy peanuts inaccessible to cranes by conventional tillage as soon after harvest as possible has resulted in reduced crane mortality in Florida and other areas where cranes feed on peanuts.4 There are plans to establish a second migratory flock of whooping cranes which will nest in Wisconsin and winter in Florida. If this project proceeds, the resultant population will have the potential to be exposed to waste peanuts in the same areas and at the same rates as the sandhill cranes described above. This increases the importance of a quick diagnosis and initiating the treatment procedure.
Acknowledgments
We would like to thank all the clinicians, residents, students, technicians, and wildlife officials who assisted with these cases.
Literature Cited
1. Allen, J. L., H. D. Martin, and A. M. Crowley. 1985. Metastatic cholangiocarcinoma in a Florida sandhill crane. J. Am. Vet. Med. Assoc. 21(2):111–119.
2. Norton, T.M. and S. Nesbitt. 1988. Diseases of free ranging sandhill cranes (Grus canadensis pratensis). Am. Assoc. Zoo Vet. and Am. Assoc. Wildl. Vet. Joint Conference Proceedings. p. 10.
3. Roffe, T.J., R.K. Stroud, and R.M. Windingstad. 1989. Suspected fusariomycotoxicosis in sandhill cranes (Grus canadensis): clinical and pathological findings. Avian Dis. 33(3):451–457.
4. Windingstad, R. M., J.C. Richard, P.E. Nelson, T.J. Roffe, R.R. George, and J.W. Dorner. 1989. Fusarium mycotoxin from peanuts suspected as a cause of sandhill crane mortality. J. Wildl. Dis. 25(1):38–46.