Stephen J. Hernandez-Divers, BVetMed, CBiol, MIBiol, DZooMed, MRCVS, DACZM, RCVS
Specialist in Zoo & Wildlife Medicine, Exotic Animal, Wildlife & Zoological Medicine, Department of Small Animal Medicine & Surgery, College of Veterinary Medicine, University of Georgia
Athens, GA, USA
In general, reptiles are a resilient class of animals that are not inherently predisposed to disease. However, poor husbandry and malnutrition are very common and often predispose to a number of commonly encountered non-infectious diseases. Metabolic derangements, malnutrition, reproductive diseases, and burns are most common. While sound clinical diagnostics and therapy will help resolve many cases, only by understanding and correcting deficient husbandry and nutritional practices can these cases be properly and permanently resolved.
Secondary Nutritional Hyperparathyroidism
Clinical Signs: Anorexia, depression, ileus and constipation, cloacal prolapse, swollen compressible mandible, lethargy and inability to support body weight, muscle fasciculations due to hypocalcemia, and rarely seizures.
Diagnostics: History and complete physical exam are extremely important. Total plasma calcium is usually normal until the terminal stages of the disease. Ionized calcium may be more useful than total calcium. True hypocalcemia is often the cause of muscle tremors, but hyperphosphatemia can cause neurologic signs. Radiography is useful to assess ileus, retained eggs or follicles, bone mineralization, renomegaly (secondary renal hyperparathyroidism).
Treatment: Fluid administration to resolve dehydration and hyperphosphataemia. Warm water soaks to encourage defecation and also promote cloacal fluid uptake. Nutritional support is seldom required as part of emergency assessment and stabilization but long term nutritional management will be essential, and usually involves correction of dietary calcium and phosphorus imbalances and improvements in environmental light for cutaneous vitamin D3 production. It is preferable not to administer bolus injections of calcium to a hyperphosphatemic reptile due to the dangers of inducing mineralization. In cases of severe hypocalcemia and tetany place the reptile on intravenous or intraosseous fluid therapy and add calcium gluconate (100-200 mg/kg) to fluids. If the animal is able to eat, administer oral calcium (200 mg/kg q24h) with a dilute enteral feeding formula. Oral calcium glubionate (Neocalglucon® 23 mg/mL), calcium carbonate (100 mg/mL) or calcium citrate (Tums®). After one week of both calcium and vit D3 supplementation (exposure to UV-B light, preferably unfiltered sunlight), recheck calcium levels. If the reptile is not hypocalcemic, calcitonin can be administered (50 IU/kg IM q 1 week x 2-3 doses) to increase bone mineralization. Warm water enemas may be required in cases of severe ileus and obstipation, but beware of infusing into the bladder. An ovariosalpingectomy is generally recommended in cases of egg or follicle retention once the reptile is stable. If hyperphosphatemic, administer phosphate binder (e.g., Amphogel® 1ml/kg PO q 12 h, in between meals).
Prevention: Correct husbandry e.g., UV lighting, nutrition, heat, cage design, etc. UV-B light exposure 12-14 hours daily, unfiltered sunlight best, Active UV heat (mercury halide) lamps and ZooMed Reptisun 5.0 fluorescent tubes are secondary options. Environmental (vivarium) temperature at species-specific preferred optimum temperature zone.
Clinical Signs: Common in herbivorous chelonians with accompanying clinical signs of chemosis, aural abscesses (manifesting as swelling on the sides of the head), nasal and/or ocular discharge.
Diagnostics: Lesions should be biopsied for confirmation of characteristic metaplastic lesions.
Treatment: Improve diet and husbandry. Use injectable vitamin A very cautiously (500-1000 iu/kg) as iatrogenic hypervitaminosis A causes skin sloughing and moist erythematous dermatitis.
Clinical Signs: Anorexia, depression, ileus with dry, palpable retained feces, cloacal prolapse, swollen compressible mandible, lethargy, inability to support body weight, muscle fasciculations with true hypocalcemia/hyperphosphataemia, seizures rare.
Diagnostics: History and complete physical exam are extremely important. Common in older iguanas, especially with high protein diets (e.g., dog/cat foods) or over-supplementation with vit D3. Complete blood count and plasma chemistry may reveal hyperphosphatemia which is often the first chemistry abnormality seen with renal failure. Advanced cases may show an increase in plasma uric acid. Ca:P ratio normally >1, in advanced disease ratio <1. True hypocalcemia is often the cause of muscle tremors, but hyperphosphatemia can cause neurologic signs. Hyperkalemia (>7mmol/L) and hyperuricemia (>400μmol/L, >6.5mg/dL) may also be seen. Radiography/ultrasonography can be used to assess bone quality, mineralized gout, renomegaly and constipation. Endoscopic renal biopsy for definitive diagnosis.
Treatment: Intraosseous (IO) or intravenous (IV) fluid administration (20-30ml/kg/day). Calcium supplementation but do not give bolus injections of calcium to a hyperphosphatemic reptile. The massive increase in solubility index may predispose to soft tissue mineralization. When hypocalcemia is severe place the reptile on fluid therapy and add calcium gluconate (100-200 mg/kg) to fluids, give IV, IO or intracoelomic (ICe). Give by slow infusion and titrate dose accurately based upon blood calcium levels. Oral phosphate binders such as aluminium hydroxide (Amphogel) can be used between meals to help reduce plasma phosphorus levels. If the animal is able to eat, administer oral calcium (200 mg/kg q24h) with dilute stomach tubing formula. Oral calcium competes with phosphorus for intestinal absorption sites, and so calcium can be used with meals to reduce the absorption of dietary phosphorus. Use calcium glubionate (Neocalglucon) or calcium carbonate. Warm water soaks encourage defecation and promote fluid uptake (fluid can be absorbed via the cloaca and colon in many reptiles). Warm water enemas may be required in cases of severe ileus and obstipation. Nutritional support--not required as part of emergency assessment and stabilization--only instigate once the reptile is rehydrated. An esophageal feeding tube should be placed when prolonged nutritional support is anticipated (especially chelonians). Correct husbandry e.g., UV lighting, heat, nutrition, humidity, cage design, etc.
Clinical Signs: Anorexia, depression, discolored/foul urine/urates, stranguria.
Diagnostics: History and complete physical exam are extremely important; may have been fed high-protein diets or chronically deprived of water. Can palpate large bladder stones in lizards, often possible in chelonians as well. Radiography is generally definitive.
Treatment: General supportive care; fluid administration, route depending upon medical status (PO, ICe, IO, IV); surgical cystotomy.
Clinical Signs: Anorexia, depression, icterus, biliverdinuria (green discolored urates).
Diagnostics: History and complete physical exam are extremely important; hepatic lipidosis--common in obese animals; infectious liver diseases--wild imports, new additions to collection, poor quarantine. Complete blood counts and plasma chemistry; hepatitis--elevations of AST, LDH, GGT, ALT, ALKP, bile acids may be > 60mg/L; hepatosis--enzymes may remain normal, bile acids >60mg/L. Radiography and ultrasonography used to assess liver size and shape. Endoscopic evaluation and biopsy for definitive histologic diagnosis.
Treatment: General supportive care; fluid administration, route depending upon medical status (PO, ICe, IO, IV); nutritional support; improved husbandry; methionine supplementation; anabolic steroids and multivitamins (controversial?). Specific therapy based upon diagnosis; bacterial hepatitis-systemic antibiotics based upon culture and sensitivity; fungal hepatitis--systemic antifungals (e.g., itraconazole); verminous hepatitis--appropriate antiparasitic agents; neoplasia--surgical resection.
Gastro-Intestinal Diseases (Enteritis, Foreign Bodies, Impaction & Constipation)
Clinical Signs: Anorexia, regurgitation, vomiting, diarrhea, depression, asymmetrical swimming in aquatic turtles, intestinal obstruction--especially with ingestion of particulate substrate, ileus secondary to hypocalcemia (SNHP), prolapse through the vent.
Diagnostics: History and complete physical exam are extremely important; quarantine, new arrivals, etc. Complete blood count and plasma chemistry; protein losing enteropathies. Fecal/gastric cytology, culture and sensitivity. Fecal wet mount and flotation; parasitic overgrowth (i) a certain number of flagellates are commensal flora in reptiles, (ii) parasitic overgrowth is most common in imported or stressed animals especially in chelonians; (iii) cryptosporidiosis in snakes and lizards, may be accompanied by regurgitation. Fecal (or gastric wash) for microscopy; bacterial (usually gram-negative), fungal (especially if immunocompromised or secondary to antibiotic administration), Cryptosporidium spp (acid-fast stain). Radiography to assess ileus, bone quality, foreign bodies. Upper and lower gastro-intestinal endoscopy, and biopsy, e.g., for Cryptosporidium spp.
Treatment: Fluid administration if dehydrated. Identification, debridement, resection or replacement of prolapsed tissue. Parasiticide treatment (e.g., oxfendazole 66mg/kg, fenbendazole 100mg/kg, metronidazole 50-100mg/kg, praziquantel 5-8mg/kg) is especially important with an animal recently purchased from an unknown background. Keep on newspaper to maintain high level of hygiene and prevent re-infection during treatment. Do not use ivermectin in any chelonians. Antimicrobial treatment for bacterial enteritis. Calcium therapy for SNHP and hypocalcemic ileus. Warm water soaks encourage defecation and promote fluid uptake (fluid can be absorbed via the cloaca and colon in many reptiles). Nutritional support--not required as part of emergency assessment and stabilization. Only instigate once rehydrated. An esophageal or pharyngeal feeding tube should be placed for prolonged periods of assisted feeding. Warm water enemas may be required in cases of severe ileus and obstipation. Correct husbandry e.g., UV lighting, heat, cage design, hygiene, diet etc.
Clinical Signs: Gravid females only (i.e., must be able to differentiate between males and females). Most lizards are usually oviparous (produce eggs), some are viviparous (produce live young); iguanas are most often seen clinically (early fall through summer); snakes--boas are viviparous; pythons are oviparous; chelonia all produce eggs.
Diagnostics: History and complete physical exam are extremely important; anorexia, depression, mating or nest excavation behavior; gravid lizards and snakes have a distended abdomen, eggs or ovarian follicles are often palpable, chelonia--may palpate eggs per cloaca. Complete blood count and plasma chemistry--dystocia often complicated by secondary hyperparathyroidism. Radiography and ultrasonography; shelled eggs--post-ovulatory egg binding (dystocia); unshelled eggs--pre-ovulatory ova stasis or severe hyperparathyroidism causing poorly mineralized egg shells.
Treatment: If medically stable and not critical; correct husbandry e.g., UV lighting, heat, cage design, nesting sites, and consider subcutaneous oxytocin or topical prostaglandin therapy. If medically unstable or unresponsive to conservative therapy; fluid administration if dehydrated followed by surgical correction (ovariosalpingectomy or salpingotomy)--antimicrobials and analgesics as required. Nutritional support--not required as part of emergency assessment and stabilization, but instigate once rehydrated.
Burns & Trauma
Clinical Signs: Thermal burns--most often seen in snakes or lizards kept in a cage with a hot rock or other high surface temperature heater. Advise clients not to use any unscreened heat source inside the cage. Heat sources should (where possible) be located outside the vivarium. Prey wounds--most often seen in snakes fed live animals, but also seen in lethargic or aestivating lizards fed crickets.
Treatment: Wound debridement--initially under anesthesia but followed up with daily wound care including antiseptic soaks. Topical antibiotic--silver sulphadiazine (Silvadene®). Keep snakes in unlined tanks so ointment is "self-reapplied", or consider the "condom" bandage. Broad-spectrum antibiotics (e.g., Ticarcillin [50-100 mg/kg IM q24h] or ceftazidime [20-30 mg/kg IM q48-72h]). Supportive care--warm environment, fluid therapy, syringe feeding once rehydrated. Wounds heal very slowly in reptiles, so the prognosis may not be readily apparent for some time.
Clinical Signs: Persistent bathing or reclusion in humidity box, poor shedding, retained skin, retained spectacles, dull coloration. Skin disease; trauma (incl surgery), infection (parasitic e.g., mites, bacterial, fungal). Systemic disease (e.g., boid inclusion body disease in snakes, SNHP in lizards) may produce skin lesions.
Diagnostics: History--environmental causes (inappropriate temperature, inappropriate humidity, inappropriate ventilation, lack of bathing facilities or humidity box, insufficient cage furnishings on which to rub). Microscopic examination of skin scrapes, stained impression smears. Debridement and deep swab for culture and sensitivity. Biopsy for histology and culture and sensitivity--often possible under local anesthesia, a single scale contains both epidermal and dermal elements.
Treatment: Correct husbandry issues; bathe snakes for prolonged periods before attempting to remove retained spectacles with cotton-tipped applicators. Ivermectin--mites (e.g., Hirstiella in lizards and Ophionyssus in snakes). Do not use ivermectin in chelonians. Bacterial and fungal dermatitis; debride under general anesthesia, systemic antimicrobials based upon culture and sensitivity, daily povidone-iodine baths and topical antimicrobials (e.g., silver sulphadiazine), analgesics (e.g., meloxicam). Treat any underlying systemic disease (e.g., liver disease).
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2. Raiti, P and Girling, S (2004). Manual of Reptiles, Second edition. British Small Animal Veterinary Association, Cheltenham, England.
3. Mader, DR (2005) Reptile Medicine and Surgery. Second edition. WB Saunders, Philadelphia.