Gout in Reptiles
Gout is observed in all orders of reptiles; visceral and articular forms have been reported. Radiographs often reveal mineralized or radiolucent tophi in affected organs and joints (see images of gout in a chameleon). Primary visceral gout is the accumulation of urate microcrystals in organs secondary to a chronic hyperuricemia and is generally caused by excessive protein in the diet. Secondary visceral gout is due to chronic hyperuricemia from such causes as dehydration and renal insufficiency. Gout can be very debilitating, causing discomfort to the point that some reptiles refuse to move, eat, or drink.
Courtesy of Dr. Stephen Divers.
Primary visceral gout is treated by correcting the diet. Secondary visceral gout is treated by attempting to correct the underlying problem, be it dehydration or renal disease. The prognosis is typically poor in advanced cases. Allopurinol is effective at decreasing blood uric acid levels. Drug administration usually must be long-term, because clinical signs typically recur if treatment is discontinued. Euthanasia must be considered in reptiles in which movement is painful and appetite becomes suppressed.
Metabolic Bone Diseases of Reptiles
Secondary nutritional hyperparathyroidism is the most common bone disease encountered in reptile practice. It is caused by poor diet (low calcium:phosphorus ratio, vitamin D3 deficiency) or poor husbandry (lack of UVB light, inadequate thermal provision) (see secondary nutritional hyperparathyroidism photograph and radiograph).
Courtesy of Dr. Stephen Divers.
Courtesy of Stephen J. Divers.
Affected reptiles are generally rapidly growing herbivorous and insectivorous lizards and chelonians. Clinical signs include the following:
anorexia
lethargy
inability to walk normally
swollen/distorted mandible, maxilla, and/or long bones
limb and spinal pathologic fractures
cloacal prolapse
muscle fasciculations
tetany
Diagnosis requires radiographic examination to document generalized demineralization of the skeleton and low plasma levels of 25-dihydroxycholecalciferol. Findings in the late stages include hyperphosphatemia and low total and ionized calcium.
Treatment of critical cases requires fluid therapy, nutritional support, parenteral calcium therapy if hypocalcemic, and phosphate binders if hyperphosphatemic. Correction of the diet and husbandry are the mainstays of successful therapy, and the prognosis is favorable, particularly if the animal is still eating.
Secondary renal hyperparathyroidism occurs in adult reptiles and is associated with hyperphosphatemia, soft tissue calcification, osteodystrophy, and hypocalcemia secondary to a primary nephrosis. Provisional diagnosis generally rests on history, radiographic examination, and plasma biochemical analysis, although a definitive diagnosis requires demonstration of decreased renal function(eg, iohexol clearance) and renal pathology (eg, renal biopsy).
Reports of hypertrophic osteopathy are uncommon and currently appear to be limited to lizards with extensive periosteal proliferation beginning in the distal long bones and progressing proximally. The pathogenesis is unknown, but theories include chronic anoxia, toxins, and vagal neurological pathways. Many cases appear to be chronic bacterial infections of the spine.
Nutritional Disorders of Reptiles
Hypovitaminosis A in Nutritional Disorders of Reptiles
Hypovitaminosis A is common in aquatic turtles and insectivorous lizards fed a diet deficient in preformed vitamin A. The commonly used nutritional supplement beta carotene cannot be metabolized by many reptiles.
Lack of vitamin A leads to squamous cell metaplasia and hyperkeratosis and may affect cartilage development and growth and oral and ocular tissues. Affected animals may show poor growth, anorexia, stomatitis, and blepharedema due to squamous metaplasia. Secondary respiratory infections, aural abscesses, and edema secondary to nephropathy can ensue. Treatment includes dietary improvement and the use of a dietary supplement containing preformed vitamin A. Injectable vitamin A is best avoided, as hypervitaminosis A can cause skin erythema and sloughing
Hypovitaminosis B (Thiamine) in Nutritional Disorders of Reptiles
Hypovitaminosis B1 is common in piscivorous snakes (eg, garter and water snakes, turtles) that are fed frozen/thawed fish high in thiaminases and/or deficient in thiamine. Neurological signs (eg, ataxia, opisthotonos, torticollis, apparent blindness), muscle tremors, and death are common. Initial treatment with injectable thiamine may be effective. Dietary improvement is critical and centers on increased thiamine supplementation and transition to more nutritional fish prey or nonfish food items (eg, small amphibians, rodents).
Obesity in Nutritional Disorders of Reptiles
Restricted opportunities for exercise, reproduction, and hibernation (in those species for which it is appropriate), combined with excessive caloric intake, can quickly result in morbid obesity and hepatic lipidosis. Treatment involves increased exercise and dietary modification to slowly decrease caloric intake over many months.
Starvation in Nutritional Disorders of Reptiles
Inappropriate husbandry and nutrition can result in chronic debilitation, starvation, and death. Maladaption syndrome, once commonly associated with wild-caught reptiles that refused to eat in captivity, has become less of an issue with the reliance on captive-bred animals for the pet trade.
Miscellaneous Endocrine Disorders of Reptiles
Endocrine diseases are not often documented in reptiles. Diabetes mellitus has been reported in chelonians; glucosuria and hyperglycemia are the primary findings, and polyphagia may or may not be apparent. The etiology is often undetermined but in bearded dragons has been associated with gastric neuroendocrine carcinomas. Pancreatectomy in lizards may result in hypoglycemia, implying that hormones other than just insulin, such as glucagon or somatotropin, may play a role in the pathogenesis of diabetes mellitus in reptiles.
Hyperthyroidism has been reported in a female green iguana that developed polyphagia, loss of the dorsal spines, hyperactivity, increased aggression, tachycardia, and a bilobate mass palpable anterior to the thoracic inlet. Surgical thyroidectomy returned the lizard to a euthyroid state.
For More Information
Divers SJ, Stahl SJ. Mader's Reptile and Amphibian Medicine and Surgery. 3rd ed. Elsevier; 2019.
