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Hyperadrenocorticism in a ferret
J. G. Fox, DVM, MS; M. E. P. Goad, DVM, PhD; B. A. Garibaldi, DVM; L. M. Wiest, Jr., VMD
A7 7-year-old adult male ferret was referred to our laboratory because of progressive weight loss and alopecia. The referring clinician had seen radio- graphic signs of fluid in the thorax and had removed 50 ml of serosanguineous thoracic fluid one week before referral. The ferret also had had progressive hair loss during. the preceding 10 months. More recently, the owner had noticed increased water consumption, decreased stamina, and labored breathing. Clinical examination revealed severe dehydration (>8% on the basis of skin turgor), muffled heart sounds, weak femoral pulses, hepatomegaly, lethargy, alopecia, weakness, tem- poral muscle atrophy, dyspnea, and emaciation. The animal weighed approximately 1 kg. The striking hair loss was bilaterally symmetric over 80% of the body and extended from the neck to the tip of the tail, but did not involve the head or limbs (Fig 1). The skin was thin and had numerous linear abrasions; abdominal vessels were prominent. Pleural effusion and ascites were seen on radiographs. The tentative diagnoses were hyperadrenocorticism and con- gestive heart failure. The ferret was euthanatized because of a rapidly deteriorating condition and poor prognosis. Blood samples for serologic and hormone assays, CBC, and serum biochemical analyses were obtained via cardiac puncture after anesthesia and before euthanasia.
The profound leukopenia (1.4 x 103 wBc/ul) was characterized by lymphopenia (8%; 112 lym- phocytes/jul) and eosinopenia (0%). Phosphorus (14.4 mg/dl; normal, 5.6 to 8.7 mg/dl), BUN (127 mg/dl; normal, 12 to 43 mg/dl), creatinine (0.9 mg/dl; normal, 0.2 to 0.6 mg/dl), and potassium (7.9 mEq/L; normal, 4.3 to 5.3 mEq/dl) concentra- tions were high,1,2 as was aspartate transaminase activity (134 U/L; normal, 20 to 120 U/L). Albumin concentration (2.4 g/dl; normal, 3.3 to 4.1 g/dl) was low.1,2 Results of a serum counterelectrophoresisª to
From the Division of Comparative Medicine, Massachusetts Institute of Technology, 37 Vassar St, Cambridge, MA 02139 (Fox, Goad, Garibaldi), and the Patuxent Valley Animal Hospital, 7363 Old Columbia Rd, Columbia, MD 21046 (Wiest).
Supported in part by grant No. RR1046 from the Division of Research Resources, National Institutes of Health, Bethesda, Md. *Counterelectrophoresis, United Veterinary Laboratories, Middleton, Wis.
detect antibody to the parvovirus causing Aleutian disease and of a test for FeLVb were negative. Examination of blood for circulating microfilariae, using Knott’s technique, did not detect organisms. The serum cortisol concentration was 8.1 µg/dl.
The thoracic cavity contained approximately 160 ml of transparent pale red fluid (sp gr, 1.014), with erythrocytes and nondegenerate lymphocytes. Listeria monocytogenes was isolated from the pleural fluid. The heart was large and globoid and had a double apex. Both ventricles were dilated and had thin ventricular free walls. The aortic, pulmonary, and atrioventricular valves were normal. The ab- dominal cavity contained 20 ml of transparent pale
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red fluid (sp gr, 1.022), with many erythrocytes and lymphocytes. The left adrenal gland measured 0.5 cm × 0.75 cm ×1 cm, was irregular in shape, and had numerous nodules protruding from the sur- face (Fig 2). The right adrenal gland was small (1 mm × 2 mm × 1 mm). The liver was large, moder- ately friable, and pale brown and had a marked reticular pattern; it weighed 380 g (38% of the body weight). The renal surfaces were pitted.
The normal architecture of the left adrenal gland was effaced by anaplastic cells that varied from round or cuboidal to spindle-shaped. Cytoplasmic staining characteristics ranged from pale eosino- philic to dark basophilic. Nuclei also differed in size, shape, and staining characteristics. Nucleoli were prominent. Tumor cells were arranged in irregular rows or in sheets of cells; they invaded the adrenal gland capsule. Tumor cells were seen also in vessels of the adrenal gland adventitia. The right adrenal gland was atrophied; the cortex had only 3 to 5 cell layers. Lymphocytes and macrophages were scat- tered throughout the cortex of the right adrenal gland.
The myocardium had moderate fibrous connec- tive tissue between myocytes. Fibrocytes and fibro- blasts were prominent throughout the myocardium, but especially along blood vessels. The appearance of cardiac vessels was within normal limits.
The liver had mild centrilobular and periportal fibrosis and lymphoplasmacytic infiltrates. The skin was atrophic; the epithelium consisted of only 1 to 2 cell layers. Hyperkeratosis was mild. Hair follicles were sparse; those seen were in catagen or telogen phases. The dermal collagen was arranged irreg- ularly.
The renal cortex was decreased in thickness.
Glomeruli were reduced in size and number; many were sclerotic, with thick basement membranes. Scattered foci of mineralization were seen through- out the cortex. Fibrosis was evident, and diffuse plasma cell and lymphocyte infiltrates were scattered throughout the interstitium.
The diagnosis was functional adrenocortical carcinoma, complicated by dilatative cardiomyopa- thy, chronic active hepatitis, and renal disease. The significant lymphopenia and eosinopenia, bilateral symmetric alopecia with dermal atrophy, and tem- poral muscle atrophy are findings characteristic of hyperadrenocorticism in human beings and dogs.3-5
The pathologic findings in this ferret were similar to those described in other ferrets with cardiomyopathy.6 The hypoproteinemia and hepati- tis also may have contributed to the fluid accumula- tion in the thorax and abdomen. Listeria mono- cytogenes (isolated from the pleural effusion) has been isolated from lung homogenates of ferrets used in canine distemper studies.7 Listeria monocytogenes may cause septicemia and pneumonia, as well as meningoencephalitis in human beings treated for prolonged periods with corticosteroids or other immunosuppressive agents.8 Patients with hyper- adrenocorticism have increased susceptibility to infectious diseases. The high BUN concentration, hyperkalemia, and hyperphosphatemia probably were attributable to end-stage renal disease and undoubtedly complicated the hyperadrenocorticism and cardiomyopathy.
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6. Lipman NS, Murphy JC, FoxJG. Clinical, functional, and pathologic changes associated with a case of dilatative cardiomy- opathy in a ferret. Lab Anim Sci 1987;37:210-212.
7. Morris JA, Norman MC. The isolation of Listeria mono- cytogenes from ferrets. J Bacteriol 1950;59:313-314.
8. Armstrong D. Listeria monocytogenes In: Mandell GL, Douglas RG, Bennett JE, Eds. Principles and practice of infectious diseases. 2nd ed. New York: Wiley Publications, 1985;1177-1182.