26th Annual Meeting and Symposium of the
Desert Tortoise Council, March 16-18, 2001
Abstracts

Results of Necropsy Findings of Desert Tortoises from the Chemehuevi Valley Study Site in 1999 and from the Goffs Study Site in 2000

Bruce L. Homer¹ and Kristin H. Berry^2
1Dept. of Pathobiology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32611
²USGS, Western Ecological Research Center, Box Springs Field Station, 6221 Box Springs Blvd., Riverside, CA 92507

Three ill desert tortoises were received for complete health and necropsy examinations from each of two long-term desert tortoise study sites in San Bernardino County, California: Chemehuevi Valley in 1999 and Goffs study site in 2000. Examinations included identification of gross and microscopic lesions; hematologic and biochemical profiles, Mycoplasma and herpesvirus serology, and thyroxine (T4) analysis on blood collected prior to necropsy; urinalysis of urine collected at necropsy; bacterial culture and isolation from the nasopharynx and colon; fungal culture of shell; Mycoplasma culture of nasal cavity; polymerase chain reaction analysis of nasal cavity and lung for Mycoplasma; and analysis of liver, kidney, scute and plasma for metals, minerals and organic compounds. In addition, one millimeter cubed sections of shell and thyroid were submitted for electron microscopic analysis from representative tortoises. Several essential elements, minerals and vitamins were low or low normal, including plasma vitamin E (1.18 - 1.53 µg/ml Chemehuevi; 0.78 - 1.06 µg/ml Goffs), selenium (0.035 - 0.04 ppm Chemehuevi; non-detectable - 0.03 ppm Goffs), and vitamin A (as low as 0.36 µg/ml in Goffs). Packed cell volume (21.8 - 24.5% Chemehuevi; 19 - 28% Goffs), albumin (1.2 g/dl Chemehuevi; 0.9 - 1.2 g/dl Goffs) and total protein (2.1 - 2.3 g/dl Chemehuevi; 2.4 - 3.0 g/dl Goffs) were low or at the low end of the normal range. Other abnormalities in the plasma biochemical profiles included elevated total iron (487 - 1024 µg/dl Chemehuevi; 459 - 973 µg/dl Goffs) in both populations, elevated bile acids (4.1 - 7.7 µmol/L) in Goffs and low calcium (8.7 - 8.8 mg/dl males; 9.2 mg/dl female) in Goffs. In the Chemehuevi tortoises, abnormal tissue concentrations of metals and minerals in one or more tortoises included high hepatic iron (1000 ppm), selenium (2.1 - 3.5 ppm), and boron 7.09 ppm); low hepatic calcium (52 - 83 ppm); high renal cobalt (0.69 - 1.2 ppm); low renal iron (16 - 21 ppm), calcium (120 - 135 ppm), and molybdenum (0.34 - 0.43 ppm); high scute barium (5.1 - 7.9 ppm), cadmium (0.41 - 0.45 ppm), selenium (1.6 - 1.8 ppm), and copper (1.8 - 1.9 ppm); and low scute zinc (19 - 32 ppm). In the Goffs tortoises, abnormal tissue concentrations of metals and minerals in one or more tortoises included high hepatic iron (1100 - 1200 ppm), copper (21 - 40 ppm), mercury (0.79 ppm), zinc (53 -62 ppm) , selenium (1.5 - 2.1 ppm), molybdenum (2.0 - 2.1 ppm), cadmium (0.88 - 0.9 ppm), boron (15.4 ppm) and phosphorus (2500 - 2900 ppm); low hepatic calcium (58 - 85 ppm) in all tortoises; elevated renal phosphorus (3000 ppm) in one tortoise and low phosphorus (1800 ppm) in another tortoise; elevated renal mercury (0.76 - 1.15 ppm), cobalt (0.72 ppm), and cadmium (2.1 - 3.8 ppm); low renal calcium (91 -105 ppm) and iron (14 - 23 ppm); high scute copper (1.9 - 2.1 ppm), zinc (67 ppm), cadmium (0.36 - 0.53 ppm), iron (160 - 180 ppm), selenium (2.4 ppm) and nickel (200 ppm in one tortoise only); and low scute calcium (560 - 690 ppm). Mycoplasma titers were negative in all tortoises, but one tortoise from each site had a positive titer to herpesvirus. The T4 range for nine tortoises from different study sites was 1.1 - 10.2 ng/ml. The range for Chemehuevi tortoises was 2.6 - 10.2 ng/ml and the range for Goffs tortoises was 1.1 - 5.2 ng/ml suggesting an elevated T4 for one tortoise from each site and low T4 for two tortoises from Goffs. Primary lesions in tortoises from Chemehuevi Valley study site included thyroid dysplasia or atrophy; osteopenia of dermal bone in shell; shell necrosis with fungal colonization; testicular degeneration; mild inflammation of the nasal cavity; dermal necrosis and inflammation; hepatocellular degeneration; and cutaneous dyskeratosis. Primary lesions in tortoises from Goffs study site included cutaneous dyskeratosis with fungal colonization; advanced shell disease with necrosis and fungal colonization; atrophy and/or degeneration of the liver, skeletal muscle, myocardium, pancreas, testicles, spleen and thyroid; and osteopenia. There was mild multifocal chronic inflammation of the nasal cavity of two tortoises, including one with a positive ELISA test for herpesvirus. However, no specific herpesvirus lesions were seen in either of the two seropositive tortoises. Electron microscopic examination of shell revealed fragmentation of the horny material, consistent with cutaneous dyskeratosis. Thyroid follicular epithelium were in various stages of necrosis. No infectious agent was identified, suggesting that the thyroid lesion was toxic in origin. Fungal species isolated from scute were individual colonies of Alternarium sp., Penicillium sp., Cladosporium sp., Trichophyton sp., and Dematiaceous mold. Lesions in tortoises from both populations were indicative of metabolic disease and loss of body condition, possibly increasing the susceptibility of the shell to colonization by fungi. Mineral imbalances were suggestive of nutritional imbalances. Although elevated metal concentrations (e.g., cadmium and mercury) were not considered to be at toxic levels, the presence of these metals in liver and scute may have tied up selenium in these locations, resulting in selenium deficiency in other organs as suggested by the low plasma selenium. Several of the degenerative tissue lesions could be associated with a selenium deficiency.