Interpretation of the Reptile Blood Profile

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Exotic PetP R A C T I C E

VOLUME 3 ISSUE 5 MAY 1998

SCIENTIFIC ARTICLE

Hematologic and blood biochemical evaluations are frequently used toassess the health of the reptilian patient.1 The hemic response of reptiles isinfluenced by a wide array of variables that include the age, sex, season,

species, environment, sample handling, nutritional status, physiological sta-tus, method of testing, and blood sampling technique (blood samples arefrequently contaminated with lymphatic fluid). There are normal refer-ence values available in the literature for a few species of reptiles; however,information concerning environmental conditions, physiological parame-ters, and sample handling methods is often omitted.2, 3 Because of a generallack of experimental study involving the hematology, blood biochemistries,and meaningful reference values of reptiles, interpretation of the results canbe challenging. In general, interpretation of changes in the blood profile ofreptiles is similar to that of domestic mammals and birds. Ideally, a uniqueset of normal reference values should be obtained for the reptilian patientduring times of health and under a given set of environmental and nutri-

tional parameters for comparison when that animal becomes ill. The samplesize may limit the blood profile to a few tests, so the clinician must decidewhich tests may provide the most useful information. In general, informa-tion evaluating liver, kidneys, glucose, proteins, calcium, phosphorus, andthe hemogram are the most useful in the assessment of the reptilian patient.

Reptiles have larger but fewer numbers of circulating erythrocytes comparedwith birds and mammals. Among reptiles, there is an inverse relationship be-tween erythrocyte size and total red blood cell count (TRBC). For example, lizardshave smaller red blood cells but higher TRBC than snakes and chelonians. TheTRBC, hemoglobin concentration, and packed cell volume (PCV) vary according tosex, nutritional status, environmental conditions, and sample collection andhandling. In general, the PCV of most normal reptiles ranges between 20% and40%. A PCV less than 20% is suggestive of an anemia. Anemias are classified as

hemorrhagic, hemolytic, or depression, depending on their cause and response.Regenerative responses to anemia include moderate to marked polychromasia,anisocytosis, poikilocytosis, immature erythrocytes, and stippled basophilia.Marked regenerative responses demonstrate binucleate erythrocytes, abnormalnuclear shapes, and mitotic activity. Hemolytic and hemorrhagic (blood loss)anemias usually demonstrate a regenerative response depending on the durationof the anemia. Hemorrhagic anemia is often caused by traumatic injury, ulcer-ated lesions, and blood-feeding parasites. Hemolytic anemia is frequentlyassociated with toxemia, septicemia, and parasitemia. Depression anemia resultsfrom chronic inflammation, renal or hepatic diseases, or chemical toxicity andexhibits little or no regenerative response. Hypochromatic erythrocytes are associ-ated with dietary iron deficiency or chronic inflammation. A PCV greater than40% usually suggests dehydration; however, a true polycythemia is possible.

Meaningful normal referenceleukogram values are difficult toobtain in reptiles because of thevariables affecting the hemic cellsand the lack of standard methods forassessing the leukocytes. In general,total and differential leukocyte

counts must differ greatly from thenorm to be considered significant. Insome cases, the morphologic featuresof the leukocytes may be more valu-able than the actual cell counts inthe assessment of the reptilianpatient. The value of hematologicstudies is in the assessment of the rep-tilian patients response to treatmentor the examination of the course ofthe disease. Favorable responsesinclude the resolution of an anemia,leukocytosis, leukopenia, lym-

phopenia, heterophilia, monocytosis,and thrombocytopenia. The disap-pearance of toxic heterophils andreactive lymphocytes from bloodfilms is also a favorable response.

ISSUE HIGHLIGHTS:Clinical Chemistries

ROUNDTABLE

page 35

Abdominal Tumors inBudgerigars

FROM THE LITERATURE

page 37

Food Allergy in a Ferret

CASE REPORT

page 39

Interpretation of the Reptilian Blood ProfileTerry Campbell, D.V.M., Ph.D.

continues on page 34


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Editor in Chief

Shawn Messonnier, D.V.M.Paws and Claws Animal HospitalPlano, Texas

Editorial Board

Terry Campbell, D.V.M., Ph.D.Department of Clinical ScienceColorado State UniversityFort Collins, Colorado

James K. Morrisey, D.V.M.Special Species Medicine and SurgeryUniversity of WisconsinSchool of Veterinary MedicineMadison, Wisconsin

Wm. Kirk Suedmeyer, D.V.M.Senior Staff VeterinarianKansas City Zoological GardensAdjunct Assistant Professor ofZoological MedicineUMC College of Veterinary MedicineKansas City, Missouri

Valarie V. Tynes, D.V.M.Punta Gorda Animal HospitalPunta Gorda, Florida

Amy Beth Worell, B.S., D.V.M.,Diplomate A.B.V.P.-Avian SpecialistAll Pets Medical CentreWest Hills, California

Advisory Board

Michael A. Dutton, D.V.M.,Diplomate A.B.V.P.-CompanionAnimal PracticeWeare Animal HospitalWeare, New Hampshire

Cathy A. Johnson-Delaney, D.V.M.

Senior Veterinarian, Primate MedicineWashington Regional Primate ResearchCenter

University of WashingtonSeattle, Washington

EXOTICPETPRACTICE

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VOLUME 3 ISSUE5 MAY1998

34

Interpretation of theReptilian Blood Profilecontinues from page 33

The blood biochemical profiles of reptiles often resemble those of mam-mals and birds. The clinician must choose which may be more appropriatefor the reptilian patient.

The primary nitrogen excretory product of a reptile depends on its nat-

ural environment. For example, terrestrial reptiles excrete uric acid,whereas semi-aquatic turtles excrete urea. Because most pet reptiles areterrestrial, uric acid is often used to investigate the presence of renal dis-ease. Normal plasma uric acid concentrations of reptiles are less than 10mg/dL. Uric acid is not a sensitive nor a specific test for renal disease inreptiles. Hyperuricemia can result from gout, recent ingestion of a highprotein diet, or severe renal disease (loss of renal function greater than75%). In reptiles, normal plasma urea nitrogen values are typically lessthan 15 mg/dL; however, healthy desert chelonians, to increase the plasmaosmolarity for water conservation, often have values as high as 100 mg/dL.

Because few critical studies have been performed to evaluate reptilianliver diseases, plasma enzymes and biochemical tests used to evaluate liver dis-ease 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 liverdisease. Increases in plasma AST activity above 250 IU/L can be associated withhepatocellular or muscle disease and often occur with general diseases, such assepticemia and toxemia. Plasma creatine kinase activity is muscle-specific and isused along with AST to rule out coexistent muscle injury when searching forthe presence of liver disease in reptiles. Plasma AST activity increases above275 IU/L with trauma, systemic infections, intramuscular injections, and exer-tion, such as occurs with handling. Lactate dehydrogenase has a wide tissuedistribution and normal high plasma activity. Increases in plasma lactatedehydrogenase activity above 1,000 IU/L occur with hemolysis or with insultto the liver, skeletal muscle, or cardiac muscle. Alanine aminotransferase activityis 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 littlestudy of plasma alkaline phosphatase activity in reptiles; however, increasedactivity may reflect osteoblastic activity and not hepatic disease. Biliverdin is theprimary bile pigment of reptiles, and plasma elevations may indicate liver dis-ease. Most commercial veterinary laboratories do not test for biliverdin. A greenplasma is suggestive of hyperbiliverdinemia and severe liver disease.

The total plasma protein values (biuret method) of normal reptiles usu-ally ranges from 3 to 7 g/dL. Healthy female reptiles demonstrate a hyper-proteinemia (primarily a hyperglobulinemia) during active folliculogenesis,and the protein concentration returns to normal following ovulation.Pathologic increases in protein include dehydration and hyperglobulinemiaassociated with chronic inflammation. Hypoproteinemia usually occurswith chronic malnutrition but can also result from maldigestion, malab-

sorption, 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, hypo-glycemia is associated with starvation, malnutrition, severe liver disease,and, more commonly, septicemia. Hyperglycemia usually occurs with gluco-corticosteroid excess or iatrogenic delivery of excess glucose.

The normal plasma calcium concentration of most reptiles ranges from 8to 11 mg/dL. Hypercalcemia (2- to 4-fold increase in calcium) normallyoccurs in healthy females during active folliculogenesis, and calcium concen-trations return to normal after egg laying. Hypocalcemia occurs with alkalo-sis, hypoalbuminemia, excessive dietary phosphorus, secondary nutritional



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VOLUME 3 ISSUE5 MAY1998 EXOTICPETPRACTICE

ROUNDTABLE

WHATS YOUR DIAGNOSIS ???

A 2-year-old male ferret (Mustela putorius furo) was evaluated dur-ing his annual visit; the owner said the animal had been feeling sick.The results of the physical examination were unremarkable, the micro-

scopic fecal examination came up negative, and blood was drawn fora CBC and biochemical profile. The ferret was vaccinated and dis-charged. Results of the blood tests showed elevated-glutamyl trans-ferase (75 IU/L) and alinine aminotransferase (354 IU/L) and slightlyicteric serum; other test results were normal. Symptomatic treatmentwith oral amoxicillin (10 mg/kg PO q12hr for 1 week) resulted in animprovement in the ferrets attitude and appetite. After the positiveresponse to amoxicillin, the owner declined a recheck of the blood.

Eight months later, the ferret was again feeling sick and had lost0.3 pounds. A recheck of the blood profile showed elevated alinineaminotransferase (381 IU/L), -glutamyl transferase (116 IU/L), serumalkaline phosphatase (117 IU/L), and decreased glucose (57 mg/dL;normal, 90130 mg/dL). Radiographs appeared normal. An explor-atory laparotomy was recommended. Because of scheduling problems,the procedure was performed 2 months later. At that time, the ferretwas pawing at his mouth and exhibiting weakness in his hindlimbs.

Questions1. 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?continues on page 37

Clinical Chemistries in the Exotic Patient

Q. What clinical chemistries doyou recommend for the avianpatient?

Dr. Campbell: I recommend

testing glucose, calcium, phos-phorus, potassium, uric acid,aspartate aminotransferase(AST), creatine kinase (CK), and

protein (using the biuretmethod). An albumin test maybe requested, but results maybe unreliable when tested on

plasma vs. serum. Protein elec-trophoresis may be preferredfor testing albumin and globu-lin. Cholesterol and fasting bileacids may be needed if hepato-biliary disease is suspected; elec-trolytes can also evaluated.

Dr. Tynes:At minimum I recom-mend testing AST, CPK, glucose,uric acid, bile acids, and lactatedehydrogenase (LDH). Total

protein and calcium are usuallyincluded on most profiles.

Q. What clinical chemistries do

you recommend for the reptilepatient?

Dr. Campbell: I recommend thesame profile as for avian patients.Blood urea nitrogen (BUN) testsare preferred for aquatic turtles,whereas uric acid tests are pre-ferred for terrestrial turtles.

Dr. Tynes: I like to get the sameinformation as for my avian

patients, including a test forcalcium and phosphorus. If Ican get enough blood, I alsolike to check electrolytes.

Q. What clinical chemistries doyou recommend for the smallmammal patient?

Dr. Campbell: I recommend the

same profile as for canine andfeline patients. If only a small

sample size is obtained, themore valuable tests include glu-cose, calcium, phosphorus, total

protein, blood urea nitrogen,and AST or alinine aminotrans-

ferase (ALT).Dr. Tynes: Sometimes the sizeof the patient limits blood test-ing and the amount of bloodthat can be safely removed. If Ican get a CBC, that is fine. Ifmore blood is available, I willask for ALT, BUN, glucose, andtotal protein tests.

Q. What abnormalities do youexpect in the bird or reptile withrenal disease?

Dr. Campbell: Birds with severerenal disease may haveincreased uric acid, phosphorus,and potassium; less severe renaldisease may not be detected onthe biochemical profile. At leastthree fourths of the renal massmust be destroyed before uricacid concentration increases.Hyperuricemia may also occurwith gout, starvation, and

postprandially after ingestion ofa high-protein meal. Reptiles

with renal disease would also beexpected to have increased levelsof phosphorus and potassium.Hyperuricemia in terrestrial rep-tiles and increased BUN concen-tration in aquatic reptiles mayoccur. Acidemia, hyponatremia,hyperkalemia, hyperphos-

phatemia, and hypocalcemiamay also occur in birds and rep-tiles with severe renal disease.

Dr. Tynes: There is no sensitive

indicator of renal disease inbirds and reptiles, but once thekidney damage is advanced,uric acid levels will be high.Hyperphosphatemia also occurswith renal disease in reptiles.

Q. What abnormalities do youexpect in the bird or reptile withliver disease?



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VOLUME 3 ISSUE5 MAY1998EXOTICPETPRACTICE

36

Interpretation of theReptilian Blood Profilecontinues from page 34

hyperparathyroidism, and lack ofadequate exposure to ultraviolet Blight. Plasma calcium concentra-tions greater than 20 mg/dL occur

with excessive dietary or parenteralcalcium or vitamin D3.

Most reptiles have phosphorusconcentrations ranging from 1 to 5mg/dL. Hypophosphatemia occurswith starvation and nutritional lackof phosphorus. Hyperphosphatemia

occurs with excess dietary phospho-rus, hypervitaminosis D3, and renaldisease. A false increase in phospho-rus can occur with failure to quicklyseparate the plasma from the cells.

In conclusion, the cellular andbiochemical responses in reptilian

blood are less predictable than those ofendothermic mammals and birdswhose cellular microenvironments aremore stable than reptilian ones. Vari-ables such as age, sex, sample han-dling, blood collection, environmen-tal conditions, and analytical methods

must be considered when interpretingthe blood profile of the reptilianpatient.

References

1. Campbell TW: Clinical pathology, inMader DR (ed): Reptile Medicine andSurgery. Philadelphia, WB Saunders,

1996, pp 248257.2. Frye FL: Biomedical and Surgical As-pects of Captive Reptile Husbandry, ed 2.Malabar, Fla, Krieger Publishing, 1991.3. Stein G: Hematologic and bloodchemistry values in reptiles, in MaderDR (ed): Reptile Medicine andSurgery. Philadelphia, WB Saunders,1996, pp 473483.

Clinical Chemistriescontinues from page 35

Dr. Campbell: Increases in AST,cholesterol, and fasting bile

acids may be seen in birds withsevere hepatobiliary disease.Hyperbiliverdinuria (greenurates) might also be seen.Tests performed on reptilesreveal similar findings, al-though there are fewer studiesvalidating results in reptiles.Decreased glucose and proteinconcentrations may also occurwith chronic hepatic disease inbirds and reptiles.

Dr. Tynes: Elevated bile acidsoccur in birds with hepatic dis-ease. In birds and reptiles, ASTand LDH levels will usually ele-

vate, yet the CPK level will usu-ally be normal.

Q. What are expected abnormali-ties in the bird with chlamydiosis?

Dr. Campbell: Increased ASTand fasting bile acid levels canoccur when the liver is involved.Hyperproteinemia with hyper-globulinemia also is seen.Hyperbiliverdinuria or hyper-biliverdinemia may occur with

severe hepatic insult, whichmay indicate end-stage disease.

A marked leukocytosis, het-erophilia, and possible monocy-

tosis may occur. The heterophilsmay appear toxic and reactivelymphocytes may be seen.

Dr. Tynes:Abnormal lab resultsdepend on the organ affected.Usually, increases in AST, LDH,bile acids, or uric acid willresult. Diagnosis of chlamydio-

sis cannot be definitively madesolely on the basis of clinicalchemistries.

HOW I . . .

Force-feed FerretsShawn Messonnier, D.V.M.

Hospitalized ferrets are occa-sionally anorectic. Feeding is nec-essary to prevent further catabo-lism of body tissue, which isresponsible for an overall declinein the ferrets condition and aworsening prognosis.

Force-feeding can be done orallywith a syringe or, alternatively, withan esophagostomy tube for longerterm nutritional support. Severalproducts are available, dependingon the diagnosis. Hills a/d is a pop-ular brand of supplement for dogsand cats and can be used in ferrets.Meat-based baby foods are also

applicable. Human enteral productssuch as Ensure or Isocal brand sup-plements are also popular; differentflavors can be tried to see which ispreferred by the ferret. I prefer todilute the diets with Pedialyte orintravenous fluids (e.g., lactated

Ringers solution, Normosol-Rbrand) rather than plain tap waterto add extra electrolytes. Thehuman enteral products are densein quick calories; they should prob-ably be diluted at least 1:1 whenfirst fed to the ferret. On average,feeding at least 5 mL per feeding34 times per day is a good guide-

line. When using feline supple-ments, you can use the guidelinesestablished for cats and kittens. Asits appetite improves, the ferretmay take the supplement directlyfrom a bowl. After discharge fromthe 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 madeavailable.


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37

FROM THE LITERATURE

Abdominal Tumors in BudgerigarsBudgerigars (Melopsittacus undulatus) have a high incidence of abdominal

tumors, many of which are primary renal tumors. These may be adenomas,lymphomas, or adenocarcinomas. Common signs of these tumors include uni-lateral or bilateral lameness and abdominal distention. The lameness results

from sciatic nerve compression by the tumor as the nerve passes over the kid-ney. Early diagnosis is difficult because signs are usually not seen until thebird is brought in with lameness from organ enlargement. Hematuria, but notusually polyuria, is seen. The cranial pole of the kidney is the most commonlocation for the tumor. The ventriculus, which is displaced caudally by thetumor, may often be palpated during the physical examination. Radiology,laparoscopy, and ultrasonography can be used for definitive diagnosis. Thetumor is usually not able to be resected by the time the diagnosis is reached.Symptomatic therapy including analgesics may offer temporary benefit.

Newsletter of the AAVSept/Nov:22, 1997.

Editors Note: I frequently see budgeri-gars with lameness; the lameness is usu-ally unilateral. Most owners think thebird has fractured a leg. Although thismay be the cause of the lameness, in myexperience renal or gonadal enlargementcaused by a tumor is the most commoncause. The ventriculus is usually palpable,and many birds have pasting of the fecesor urates around the cloaca. Diarrheamay be present from compression of thecolon. I rarely perform diagnostic testingsuch as radiology because I am fairlyconfident of the diagnosis. Although Ioffer radiology to my clients, mostdecline because of the expense. I havehad short-term resolution of the lame-ness in some birds by using prednisolone(0.250.50 mg/kg PO q24hr); with thistreatment the tumor seems to shrink orneural inflammation is temporarilyresolved. The long-term prognosis isgrave for recovery.

Skin disorders commonly seen in chinchillas (Chinchilla lanigera) includebarbering, dermatophytosis, fur slip, poor haircoats, and bite wounds withabscesses. Dermatophytosis is usually caused by Trichophyton mentagrophytesbut may be caused occasionally byMicrosporum gypseum orMicrosporumcanis. Small scaly spots of alopecia are seen. Oral griseofulvin (25 mg/kg POq24hr for 34 weeks) is the treatment; captan mixed with the dust bath (1tsp/2 cups of dust) or lime sulfur dips can also be used concurrently.

Abscesses caused byStreptococcus spp. andStaphylococcus spp. result-ing from bite wounds are seen in chinchillas housed in groups. Surgicaldbridement and administration of antibiotics based on culture and sensi-tivity test results are indicated.

Barbering may result from cagemates or self-trauma; poor coats may becaused by improper environmental humidity, failure to provide a dust bath, orfatty acid or zinc deficiency. Fur slip can occur if the chinchilla is handled roughlyand may occur during the veterinary examination.

Editors Note: A thorough physicalexamination, medical history, and diag-nostic testing are important parts of theassessment of dermatologic disorders inall exotic pets. As in dogs and cats, skinscrapings, fungal cultures, and skin biop-sies (when indicated) can reveal a cause.Skin abscesses from bite wounds should

be treated early and aggressively usingsafe antibiotics. Providing the properdiet and environment will prevent manyskin disorders.

Chinchilla Dermatology

Whats Your Diagnosis ???continues from page 35

Answers1. The decreased glucose level is

suggestive of insulinoma. Hypo-glycemia can also be seen with sep-sis, starvation, and liver disease.

Increased hepatic enzymes areassociated with hepatic damageand cholestasis. In this case, theywere caused by hepatic lipidosis.

2. Common geriatric diseases includeinsulinoma, lymphosarcoma, renalfailure, and adrenal disease. Bloodvalues associated with insulinomainclude decreased blood glucose (lessthan 60 mg/dL) and normal or ele-vated insulin levels. The amendedinsulinglucose ratio, though contro-

versial, may assist in the laboratorydiagnosis of insulinoma.

3. Common signs of insulinoma includeseizures, collapse, weight loss, a nor-mal or decreased appetite, weakness(especially of the rear limbs), andnausea (hypersalivation, pawingat the mouth, jaw chomping).

4. Medical treatment can be usedin lieu of surgical therapy. Treat-ment begins with oral pred-nisolone or prednisone (0.52.0mg/kg q12hr). When symptomscan no longer be controlled withcorticosteroids, the dosage canbe increased or oral diazoxide(510 mg/kg q12hr) can be addedto the regimen.The prognosis for ferrets with

insulinoma is guarded; therapy is

not usually considered curative butrather prolongs the life of the pet.

Exploratory laparotomy revealeda single nodule in the right limbof the pancreas that was removedusing the shelled out technique.Numerous small round yellownodules were detected in the

liver. These were presumed to bemetastatic lesions from the pan-creatic lesion. However, hepaticbiopsy showed hepatic lipidosis.

Because of the advanced natureof the disease, the ferret wasdischarged with oral prednisolonesyrup (0.5 mg/kg q12hr). Afollow-up visit 2 weeks latershowed the ferret was doing well.Further follow-up was not pos-sible.

Hoefer H: Chinchillas, in TheVeterinary Clinics of North America:Small Animal Practice: Exotic PetMedicine II. Philadelphia, WBSaunders, 1994, p 107.


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Bird

C A R E S H E E TTerry Campbell , D.V.M., Ph.D.

Aspergillosis is a disease caused by fungiAspergillus. These fungi are ubiquitous innature; birds are exposed to them continuously. A healthy bird with a normalimmune system is resistant to aspergillosis. The disease may develop in any birdsthat have a poor immunity; however, certain birdswaterfowl, mynah birds, cap-tive penguins, African grey parrots, blue-fronted Amazon parrots, and several ofthe birds of preyare especially prone to developing aspergillosis.

Conditions that cause a birds immune system to fail and predispose them toaspergillosis include chronic stress, poor husbandry, respiratory irritants, andoveruse of certain medications. A bird can be chronically stressed when subjectedto an improper environment, such as overcrowded conditions, inadequate temper-ature, abnormal photoperiods, and constant exposure to potential predators oraggressive cagemates. Malnutrition and poor hygiene will also predispose a birdto aspergillosis. Poor ventilation and exposure to toxic chemicals (cigarette smoke,disinfectant fumes, aerosol sprays) will damage the respiratory system, making thebird more susceptible to aspergillosis. Young and geriatric birds and birds that aresick from other diseases are also susceptible to the disease.

Aspergillosis usually affects the respiratory tract of birds but can also occur inother parts of the body. Birds with aspergillosis typically exhibit chronic weightloss and difficulty breathing as indicated by open-mouthed breathing, tail bob-

bing when breathing, and labored breathing after mild exercise. Sometimesaffected birds make unusual noises when breathing. Infections in the nasal cavityresult in the development of a dry mass in the swollen nostril. Birds with systemicaspergillosis appear extremely ill and generally have a poor appetite. Other signsinclude regurgitation, abnormal droppings, neurological disorders, and a changein the voice.

Whenever a bird becomes ill or demonstrates a significant weight loss (greaterthan 10% of its body weight), it should be examined by a veterinarian. Diagnosisof aspergillosis can be challenging, and often the veterinarian relies on a numberof tests that include serology, cytology, endoscopy, radiographs, blood profile,fungal culture, and exploratory surgery.

Treatment of aspergillosis can be difficult, and the success depends upon the loca-tion and extent of the infection. Obviously, the earlier the diagnosis can be made

the better the chances of a positive response to treatment. Treatment may requiresurgery as well as antifungal medications.

In general, bird owners know their birds behavior better than anyone elsebecause they live with the pet and can detect subtle changes in its behavior. Anyabnormal change in the birds behavior should be brought to your veterinariansattention.

Aspergillosis in Birds

Copy and use in partnership with your clients.

Client Teaching Guide

38


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39


CASE REPORT

Food Allergy in a FerretMichael A. Dutton, D.V.M., Dipl. A.B.V.P.Companion Animal Practice

A 15-month-old, 0.5 kg maleneutered ferret (Mustela putorius

furo) was referred for intense facialpruritis and facial edema and exco-riations. Two weeks previously, thereferring veterinarian had placedhim on amoxicillin suspension for aswollen lip. The animal was housedwith numerous other ferrets, noneof which exhibited similar symp-toms. The ferrets diet was approxi-mately 75% meat-based kittenchow (Excel Kitten Chow) and25% ferret kibble (Totally Ferret,Performance Foods, Dayton, OH)

with water given as desired.Physical examination revealedpitting edema of the face, serousnasal discharge, bilateral conjunc-tivitis in both eyes, and excoriationson the facial skin, most notably onthe ears. Auscultation of the heartand lungs had normal results.

Diagnostic testing included tho-racic radiographs, skin scrapings(negative for mites), and a com-plete blood count (hemocrit =24.8%; white blood cell count =

15,800/L; platelets = 768,000).The radiographs revealed normallung and heart silhouette.

Rule-outs for the facial symp-toms included scabies, contactallergy, drug eruption, and otherallergic diseases.

The ferret was given an injectionof dexamethasone (2 mg/kg SC) anddiphenhydramine (20 mg/kg SC).

A recheck in 2 weeks revealedsignificant reduction in symptomswith the excoriations healing.

Minimal pruritis was present, andthe edema had resolved.

A routine examination 4 monthslater revealed total resolution ofsymptoms and no new recurrence.

Eleven months after the initialvisit, the patient was brought in fornumerous excoriations on the ven-

tral and dorsal neck. The left pinnawas edematous. A skin scrapingwas negative for scabies. Thepatient was given both a injectionof prednisolone (2 mg/kg) and iver-mectin (200 g/kg). A recheck visitwas scheduled for 2 weeks.

At the recheck visit, the historyrevealed improvement during thefirst week after the injections, butworsening since. The physical exam-ination revealed minimal improve-ment. At the owners request theprednisolone and ivermectin injec-tions were repeated and any diag-

nostic testing postponed. Anotherrecheck visit was scheduled.Two weeks later, the symptoms

had not changed. The patient wasadmitted for a dermal punch bi-opsy. A complete blood count hadnormal results. The ferret waspremedicated with acepromazine(20 mg/kg SC) and anesthetizedwith isoflurane by mask. A 6-mmbakers dermal punch was usedfor the biopsy and the samplefixed in formaldehyde solution

(Formalin). Numerous skin scrap-ings proved negative for scabies.

The biopsy revealed moderateepidermal hyperplasia with mildorthokeratotic and focal parakera-totic hyperkeratosis. Moderatemixed superficial dermal and peri-adnexal inflammatory cells infil-trated with a predominance ofmononuclear cells were also pres-ent. No evidence of infectious,parasitic, or endocrine disease wasnoticed. Allergic disease could not

be ruled out.A presumptive diagnosis of a food

allergy was made based on histo-pathology and poor response to previ-ous therapies. The patient was startedon a meat-based high-protein dietwith main ingredients of lamb and rice(Natures Life Kibble). The protein

level was 26%, the fat was 15%, andit was palatable to the ferret.

The patient was started on pred-nisone elixir (fed orally) to controlthe pruritis pending the outcome ofthe elimination diet trial.

The swelling regressed in 7weeks, and the ferret was weanedoff of the prednisone elixir.

The ferret was reintroduced tothe original meat-based kittenchow, and the facial edema recurredwithin 5 days. Prednisone wasstarted again and the diet switchedback to the lamb/rice product. Theedema resolved in 2 weeks.

One month later the ferret was feda commercially available chickenbaby food. The facial edema

recurred within 1 week. The edemaresolved when the ferret was againplaced on the lamb/rice product.Discussion

A definitive diagnosis of adversefood reaction is made if the ani-mals former diet and other ingestedsubstances subsequently offered asa challenge are associated with areturn of clinical signs within a fewminutes to a week.1 In this case,this criterion was satisfied anddemonstrates that food allergy

should be considered as a rule-outfor facial pruritis in a ferret.

The diagnostic approach to pru-ritis in a ferret is similar to thatused with dogs and cats. And as indogs and cats, the diagnosis of afood allergy needs to be substanti-ated by the use of an eliminationdiet. This can be particularly diffi-cult in the case of a ferret becausethe protein requirements are high-er than those commonly found inpet foods. Palatability is also a

consideration, given the limitedchoices available for ferret foods.

Reference

1. Roudebush P: Diagnosis and man-agement of adverse food reactions,in Bonagura JD (ed): Kirks CurrentVeterinary Therapy XII Small AnimalPractice. Philadelphia, WB Saunders,1995, p 62.


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Q&

A

Answer by Shawn Messonnier, D.V.M.

What are common dental problems in rabbits androdents?

The most commonly seen problem is malocclusion,leading to overgrown molars, incisors, and premo-

lars. Far less commonly, we will see apical abscessesand dental tartar. On occasion, we will see frac-tured or chipped teeth, often present with over-grown teeth.

Rodents, especially guinea pigs, are especially sus-ceptible to malocclusion problems. These animalsalso often experience more apical abscesses thando rabbits.1

Reference

1. Brown SA: Rabbit Dentistry. Proceedings of the SmallMammalReptile Medicine and Surgery for the Practitioner.Middleton, Wis, 1990.

UPCOMING

MEETINGSAssociation of Avian Veterin-

arians Annual Conference

and Expo, St. Paul, MN;August 2529. (303) 756-8380.

Central Veterinary Confer-ence, Bartle Hall ConventionCenter, Kansas City, MO;August 2931. (800) 255-6864.Dr. Shawn Messonnierwill be speaking.

Readers: We welcome your questions, practice tips, and casereports. Please submit any materials to Tania Banak,Mosby, Inc., 11830 Westline Industrial Drive, St. Louis,MO 63146; [email protected]; (800)325-4177;fax (314)453-4191.

Documents

Interpretation of the Reptile Blood Profile