Professional Documents
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Exotic Pet
R A C T
VOLUME 3
SCIENTIFIC ARTICLE
ISSUE 5
MAY 1998
Meaningful normal reference leukogram values are difficult to obtain in reptiles because of the variables affecting the hemic cells and the lack of standard methods for assessing the leukocytes. In general, total and differential leukocyte counts must differ greatly from the norm to be considered significant. In some cases, the morphologic features of the leukocytes may be more valuable than the actual cell counts in the assessment of the reptilian patient. The value of hematologic studies is in the assessment of the reptilian patients response to treatment or the examination of the course of the disease. Favorable responses include the resolution of an anemia, leukocytosis, leukopenia, lymphopenia, heterophilia, monocytosis, and thrombocytopenia. The disappearance of toxic heterophils and reactive lymphocytes from blood films is also a favorable response.
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ISSUE HIGHLIGHTS:
Clinical Chemistries
ROUNDTABLE
page 39
Editor in Chief
Shawn Messonnier, D.V.M.
Paws and Claws Animal Hospital Plano, Texas
Editorial Board
Terry Campbell, D.V.M., Ph.D.
Department of Clinical Science Colorado State University Fort Collins, Colorado
Advisory Board
Michael A. Dutton, D.V.M., Diplomate A.B.V.P.-Companion Animal Practice
Weare Animal Hospital Weare, New Hampshire
ISSN 1086-4288 May 1998 by Mosby, Inc. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without prior written permission from the publisher. Vol. 3, No. 5, May 1998. Exotic Pet Practice (ISSN 1086-4288) is published monthly by Mosby, Inc., 11830 Westline Industrial Drive, St. Louis, MO 63146-3318. POSTMASTER send address changes to Exotic Pet Practice, 11830 Westline Industrial Drive, St. Louis, MO 63146-3318. Annual subscription rates for 1998: individual $49.00, resident $31.00, institutional $77.00. For multiple-copy pricing, contact Journal Subscription Services, Mosby, Inc., 11830 Westline Industrial Drive, St. Louis, MO 63146; (800) 453-4351. periodical.service@mosby.com Editorial address: Tania Banak, Mosby, Inc., 11830 Westline Industrial Dr., St. Louis, MO 63146; (800) 325-4177.
The blood biochemical profiles of reptiles often resemble those of mammals and birds. The clinician must choose which may be more appropriate for the reptilian patient. The primary nitrogen excretory product of a reptile depends on its natural environment. For example, terrestrial reptiles excrete uric acid, whereas semi-aquatic turtles excrete urea. Because most pet reptiles are terrestrial, uric acid is often used to investigate the presence of renal disease. Normal plasma uric acid concentrations of reptiles are less than 10 mg/dL. Uric acid is not a sensitive nor a specific test for renal disease in reptiles. Hyperuricemia can result from gout, recent ingestion of a high protein diet, or severe renal disease (loss of renal function greater than 75%). In reptiles, normal plasma urea nitrogen values are typically less than 15 mg/dL; however, healthy desert chelonians, to increase the plasma osmolarity for water conservation, often have values as high as 100 mg/dL. Because few critical studies have been performed to evaluate reptilian liver diseases, plasma enzymes and biochemical tests used to evaluate liver disease in birds and mammals are applied to reptiles. Aspartate aminotransferase (AST) has high activity in the reptilian liver, but is not a specific test for liver disease. Increases in plasma AST activity above 250 IU/L can be associated with hepatocellular or muscle disease and often occur with general diseases, such as septicemia and toxemia. Plasma creatine kinase activity is muscle-specific and is used along with AST to rule out coexistent muscle injury when searching for the presence of liver disease in reptiles. Plasma AST activity increases above 275 IU/L with trauma, systemic infections, intramuscular injections, and exertion, such as occurs with handling. Lactate dehydrogenase has a wide tissue distribution and normal high plasma activity. Increases in plasma lactate dehydrogenase activity above 1,000 IU/L occur with hemolysis or with insult to the liver, skeletal muscle, or cardiac muscle. Alanine aminotransferase activity is usually less than 20 IU/L in the plasma of normal reptiles, and increases are not reliable in the detection of hepatocellular disease. There has been little study of plasma alkaline phosphatase activity in reptiles; however, increased activity may reflect osteoblastic activity and not hepatic disease. Biliverdin is the primary bile pigment of reptiles, and plasma elevations may indicate liver disease. Most commercial veterinary laboratories do not test for biliverdin. A green plasma is suggestive of hyperbiliverdinemia and severe liver disease. The total plasma protein values (biuret method) of normal reptiles usually ranges from 3 to 7 g/dL. Healthy female reptiles demonstrate a hyperproteinemia (primarily a hyperglobulinemia) during active folliculogenesis, and the protein concentration returns to normal following ovulation. Pathologic increases in protein include dehydration and hyperglobulinemia associated with chronic inflammation. Hypoproteinemia usually occurs with chronic malnutrition but can also result from maldigestion, malabsorption, protein-losing enteropathies, and chronic liver or kidney disease. The normal glucose concentration of reptiles ranges between 60 and 100 mg/dL but is subjected to marked physiologic variation. In general, hypoglycemia is associated with starvation, malnutrition, severe liver disease, and, more commonly, septicemia. Hyperglycemia usually occurs with glucocorticosteroid excess or iatrogenic delivery of excess glucose. The normal plasma calcium concentration of most reptiles ranges from 8 to 11 mg/dL. Hypercalcemia (2- to 4-fold increase in calcium) normally occurs in healthy females during active folliculogenesis, and calcium concentrations return to normal after egg laying. Hypocalcemia occurs with alkalosis, hypoalbuminemia, excessive dietary phosphorus, secondary nutritional
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R O U N D TA B L E
same profile as for canine and feline patients. If only a small sample size is obtained, the more valuable tests include glucose, calcium, phosphorus, total protein, blood urea nitrogen, and AST or alinine aminotransferase (ALT). Dr. Tynes: Sometimes the size of the patient limits blood testing and the amount of blood that can be safely removed. If I can get a CBC, that is fine. If more blood is available, I will ask for ALT, BUN, glucose, and total protein tests. Q. What abnormalities do you expect in the bird or reptile with renal disease? Dr. Campbell: Birds with severe renal disease may have increased uric acid, phosphorus, and potassium; less severe renal disease may not be detected on the biochemical profile. At least three fourths of the renal mass must be destroyed before uric acid concentration increases. Hyperuricemia may also occur with gout, starvation, and postprandially after ingestion of a high-protein meal. Reptiles with renal disease would also be expected to have increased levels of phosphorus and potassium. Hyperuricemia in terrestrial reptiles and increased BUN concentration in aquatic reptiles may occur. Acidemia, hyponatremia, hyperkalemia, hyperphosphatemia, and hypocalcemia may also occur in birds and reptiles with severe renal disease. Dr. Tynes: There is no sensitive indicator of renal disease in birds and reptiles, but once the kidney damage is advanced, uric acid levels will be high. Hyperphosphatemia also occurs with renal disease in reptiles. Q. What abnormalities do you expect in the bird or reptile with liver disease?
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W H AT S Y O U R D I A G N O S I S ? ? ?
A 2-year-old male ferret (Mustela putorius furo) was evaluated during his annual visit; the owner said the animal had been feeling sick. The results of the physical examination were unremarkable, the microscopic fecal examination came up negative, and blood was drawn for a CBC and biochemical profile. The ferret was vaccinated and discharged. Results of the blood tests showed elevated -glutamyl transferase (75 IU/L) and alinine aminotransferase (354 IU/L) and slightly icteric serum; other test results were normal. Symptomatic treatment with oral amoxicillin (10 mg/kg PO q12hr for 1 week) resulted in an improvement in the ferrets attitude and appetite. After the positive response to amoxicillin, the owner declined a recheck of the blood. Eight months later, the ferret was again feeling sick and had lost 0.3 pounds. A recheck of the blood profile showed elevated alinine aminotransferase (381 IU/L), -glutamyl transferase (116 IU/L), serum alkaline phosphatase (117 IU/L), and decreased glucose (57 mg/dL; normal, 90130 mg/dL). Radiographs appeared normal. An exploratory laparotomy was recommended. Because of scheduling problems, the procedure was performed 2 months later. At that time, the ferret was pawing at his mouth and exhibiting weakness in his hindlimbs. Questions 1. What are possible explanations for the abnormal laboratory results? 2. What are common geriatric diseases in ferrets? 3. What are common signs and laboratory findings in ferrets with insulinoma? 4. If the owner declines exploratory and surgical treatment of insulinoma, what is the recommended medical treatment?
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hyperparathyroidism, and lack of adequate exposure to ultraviolet B light. Plasma calcium concentrations greater than 20 mg/dL occur with excessive dietary or parenteral calcium or vitamin D3. Most reptiles have phosphorus concentrations ranging from 1 to 5 mg/dL. Hypophosphatemia occurs with starvation and nutritional lack of phosphorus. Hyperphosphatemia
occurs with excess dietary phosphorus, hypervitaminosis D3, and renal disease. A false increase in phosphorus can occur with failure to quickly separate the plasma from the cells. In conclusion, the cellular and biochemical responses in reptilian blood are less predictable than those of endothermic mammals and birds whose cellular microenvironments are more stable than reptilian ones. Variables such as age, sex, sample handling, blood collection, environmental conditions, and analytical methods
must be considered when interpreting the blood profile of the reptilian patient.
References
1. Campbell TW: Clinical pathology, in Mader DR (ed): Reptile Medicine and Surgery. Philadelphia, WB Saunders, 1996, pp 248257. 2. Frye FL: Biomedical and Surgical Aspects of Captive Reptile Husbandry, ed 2. Malabar, Fla, Krieger Publishing, 1991. 3. Stein G: Hematologic and blood chemistry values in reptiles, in Mader DR (ed): Reptile Medicine and Surgery. Philadelphia, WB Saunders, 1996, pp 473483.
Clinical Chemistries
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Dr. Campbell: Increases in AST, cholesterol, and fasting bile acids may be seen in birds with severe hepatobiliary disease. Hyperbiliverdinuria (green urates) might also be seen. Tests performed on reptiles reveal similar findings, although there are fewer studies validating results in reptiles. Decreased glucose and protein concentrations may also occur with chronic hepatic disease in birds and reptiles.
Dr. Tynes: Elevated bile acids occur in birds with hepatic disease. In birds and reptiles, AST and LDH levels will usually elevate, yet the CPK level will usually be normal. Q. What are expected abnormalities in the bird with chlamydiosis? Dr. Campbell: Increased AST and fasting bile acid levels can occur when the liver is involved. Hyperproteinemia with hyperglobulinemia also is seen. Hyperbiliverdinuria or hyperbiliverdinemia may occur with
severe hepatic insult, which may indicate end-stage disease. A marked leukocytosis, heterophilia, and possible monocytosis may occur. The heterophils may appear toxic and reactive lymphocytes may be seen. Dr. Tynes: Abnormal lab results depend on the organ affected. Usually, increases in AST, LDH, bile acids, or uric acid will result. Diagnosis of chlamydiosis cannot be definitively made solely on the basis of clinical chemistries.
HOW I ...
Force-feed Ferrets
Shawn Messonnier, D.V.M. Hospitalized ferrets are occasionally anorectic. Feeding is necessary to prevent further catabolism of body tissue, which is responsible for an overall decline in the ferrets condition and a worsening prognosis. Force-feeding can be done orally with a syringe or, alternatively, with an esophagostomy tube for longer term nutritional support. Several products are available, depending on the diagnosis. Hills a/d is a popular brand of supplement for dogs and cats and can be used in ferrets. Meat-based baby foods are also applicable. Human enteral products such as Ensure or Isocal brand supplements are also popular; different flavors can be tried to see which is preferred by the ferret. I prefer to dilute the diets with Pedialyte or intravenous fluids (e.g., lactated Ringers solution, Normosol-R brand) rather than plain tap water to add extra electrolytes. The human enteral products are dense in quick calories; they should probably be diluted at least 1:1 when first fed to the ferret. On average, feeding at least 5 mL per feeding 34 times per day is a good guideline. When using feline supplements, you can use the guidelines established for cats and kittens. As its appetite improves, the ferret may take the supplement directly from a bowl. After discharge from the hospital, a pets owner can be taught to force-feed the ferret. Or, for those who prefer not to do so, outpatient therapy can be made available.
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F R O M T H E L I T E R AT U R E
Editors Note: I frequently see budgerigars with lameness; the lameness is usually unilateral. Most owners think the bird has fractured a leg. Although this may be the cause of the lameness, in my experience renal or gonadal enlargement caused by a tumor is the most common cause. The ventriculus is usually palpable, and many birds have pasting of the feces or urates around the cloaca. Diarrhea may be present from compression of the colon. I rarely perform diagnostic testing such as radiology because I am fairly confident of the diagnosis. Although I offer radiology to my clients, most decline because of the expense. I have had short-term resolution of the lameness in some birds by using prednisolone (0.250.50 mg/kg PO q24hr); with this treatment the tumor seems to shrink or neural inflammation is temporarily resolved. The long-term prognosis is grave for recovery.
Chinchilla Dermatology
Skin disorders commonly seen in chinchillas (Chinchilla lanigera) include barbering, dermatophytosis, fur slip, poor haircoats, and bite wounds with abscesses. Dermatophytosis is usually caused by Trichophyton mentagrophytes but may be caused occasionally by Microsporum gypseum or Microsporum canis. Small scaly spots of alopecia are seen. Oral griseofulvin (25 mg/kg PO q24hr for 34 weeks) is the treatment; captan mixed with the dust bath (1 tsp/2 cups of dust) or lime sulfur dips can also be used concurrently. Abscesses caused by Streptococcus spp. and Staphylococcus spp. resulting from bite wounds are seen in chinchillas housed in groups. Surgical dbridement and administration of antibiotics based on culture and sensitivity test results are indicated. Barbering may result from cagemates or self-trauma; poor coats may be caused by improper environmental humidity, failure to provide a dust bath, or fatty acid or zinc deficiency. Fur slip can occur if the chinchilla is handled roughly and may occur during the veterinary examination.
Hoefer H: Chinchillas, in The Veterinary Clinics of North America: Small Animal Practice: Exotic Pet Medicine II. Philadelphia, WB Saunders, 1994, p 107.
Editors Note: A thorough physical examination, medical history, and diagnostic testing are important parts of the assessment of dermatologic disorders in all exotic pets. As in dogs and cats, skin scrapings, fungal cultures, and skin biopsies (when indicated) can reveal a cause. Skin abscesses from bite wounds should be treated early and aggressively using safe antibiotics. Providing the proper diet and environment will prevent many skin disorders.
Answers 1. The decreased glucose level is suggestive of insulinoma. Hypoglycemia can also be seen with sepsis, starvation, and liver disease. Increased hepatic enzymes are associated with hepatic damage and cholestasis. In this case, they were caused by hepatic lipidosis. 2. Common geriatric diseases include insulinoma, lymphosarcoma, renal failure, and adrenal disease. Blood values associated with insulinoma include decreased blood glucose (less than 60 mg/dL) and normal or elevated insulin levels. The amended insulinglucose ratio, though contro-
versial, may assist in the laboratory diagnosis of insulinoma. 3. Common signs of insulinoma include seizures, collapse, weight loss, a normal or decreased appetite, weakness (especially of the rear limbs), and nausea (hypersalivation, pawing at the mouth, jaw chomping). 4. Medical treatment can be used in lieu of surgical therapy. Treatment begins with oral prednisolone or prednisone (0.52.0 mg/kg q12hr). When symptoms can no longer be controlled with corticosteroids, the dosage can be increased or oral diazoxide (510 mg/kg q12hr) can be added to the regimen. The prognosis for ferrets with insulinoma is guarded; therapy is
not usually considered curative but rather prolongs the life of the pet. Exploratory laparotomy revealed a single nodule in the right limb of the pancreas that was removed using the shelled out technique. Numerous small round yellow nodules were detected in the liver. These were presumed to be metastatic lesions from the pancreatic lesion. However, hepatic biopsy showed hepatic lipidosis. Because of the advanced nature of the disease, the ferret was discharged with oral prednisolone syrup (0.5 mg/kg q12hr). A follow-up visit 2 weeks later showed the ferret was doing well. Further follow-up was not possible. 37
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CASE REPORT
level was 26%, the fat was 15%, and it was palatable to the ferret. The patient was started on prednisone elixir (fed orally) to control the pruritis pending the outcome of the elimination diet trial. The swelling regressed in 7 weeks, and the ferret was weaned off of the prednisone elixir. The ferret was reintroduced to the original meat-based kitten chow, and the facial edema recurred within 5 days. Prednisone was started again and the diet switched back to the lamb/rice product. The edema resolved in 2 weeks. One month later the ferret was fed a commercially available chicken baby food. The facial edema recurred within 1 week. The edema resolved when the ferret was again placed on the lamb/rice product. Discussion A definitive diagnosis of adverse food reaction is made if the animals former diet and other ingested substances subsequently offered as a challenge are associated with a return of clinical signs within a few minutes to a week.1 In this case, this criterion was satisfied and demonstrates that food allergy should be considered as a rule-out for facial pruritis in a ferret. The diagnostic approach to pruritis in a ferret is similar to that used with dogs and cats. And as in dogs and cats, the diagnosis of a food allergy needs to be substantiated by the use of an elimination diet. This can be particularly difficult in the case of a ferret because the protein requirements are higher than those commonly found in pet foods. Palatability is also a consideration, given the limited choices available for ferret foods.
Reference
1. Roudebush P: Diagnosis and management of adverse food reactions, in Bonagura JD (ed): Kirks Current Veterinary Therapy XII Small Animal Practice. Philadelphia, WB Saunders, 1995, p 62.
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Q & A
What are common dental problems in rabbits and rodents? The most commonly seen problem is malocclusion, leading to overgrown molars, incisors, and premolars. Far less commonly, we will see apical abscesses and dental tartar. On occasion, we will see fractured or chipped teeth, often present with overgrown teeth. Rodents, especially guinea pigs, are especially susceptible to malocclusion problems. These animals also often experience more apical abscesses than do rabbits.1
Reference
1. Brown SA: Rabbit Dentistry. Proceedings of the Small MammalReptile Medicine and Surgery for the Practitioner. Middleton, Wis, 1990.
MEETINGS
Association of Avian Veterinarians Annual Conference and Expo, St. Paul, MN; August 2529. (303) 7568380. Central Veterinary Conference, Bartle Hall Convention Center, Kansas City, MO; August 2931. (800) 2556864. Dr. Shawn Messonnier will be speaking.
UPCOMING
Readers: We welcome your questions, practice tips, and case reports. Please submit any materials to Tania Banak, Mosby, Inc., 11830 Westline Industrial Drive, St. Louis, MO 63146; tania.banak@mosby.com; (800)325-4177; fax (314)453-4191.