ABSTRACT

Due to their small size and amenable behavior, ferrets have become common companion animals. They are susceptible to a variety of infectious and non-infectious diseases, including a variety of neoplastic syndromes. The clinical approach, diagnosis and treatment of selected diseases of the ferret are summarized here. A list of suggested readings follow this text.

Dirofilariasis (Heartworm Disease). Ferrets are susceptible to heartworm infection, but due to the fact that most ferrets are kept indoors, cases are still uncommon. Due to the small size of the ferret heart, as few as two heartworms may result in fatal cardiac insufficiency. The small numbers of heartworms in these animals also necessitates the use of occult heartworm tests due to the low levels of circulating microfilaremia. Lesions of heartworm disease in the ferret are essentially the same as cardiomyopathy, as infection commonly results in heart failure in this species. Aberrant cerebral heartworm migration has been noted in this species. The presence of heartworms within the right ventricles and pulmonary artery can be construed as the cause of death in any ferret in which it is observed. Prevention: Ferrets in heartworm endemic areas are usually maintained on monthly oral ivermectin at approximately 0.2 mg/kg, small Heartgard^© for cats or Revolution^©. Treatment: Heart Disease Immiticide^© Protocol: Immiticide once, then again in 1 mo, with prednisone; Very Slow Ivermectin Protocol:Ivermectin 50 mcg once/month.

Aleutian Disease. Aleutian disease is caused by the same parvovirus that causes Aleutian disease in mink, however, the disease is quite different between these two species. In mink, AD results in rapidly life-threatening immune-mediated glomerulonephritis, vasculitis, and hypergammaglobulinemia. In ferrets, there are notable similarities, including a hypergammaglobulinemia, and in late stages of the disease, an immune complex glomerulonephritis; however, the disease is much more insidious, with a progression of as long as 2 years. Ferrets in the late stages of disease will be hyperproteinemic (8-9 mg/dl, with >20% of this total being comprised of gammaglobulins). Diagnosis: Serologic testing, PCR or counterimmunoelectrophoresis. Gross lesions are seen only late in the course of disease. Splenomegaly and lymphadenopathy are the most common gross lesions with this disease; splenic infarction as a result of marked splenomegaly may complicate the clinical and pathologic picture. Enlarged, brown-tan kidneys may be present. In terminal cases, clotting abnormalities resulting from vasculitis and the marked hypergammaglobulinemia may result in petechial hemorrhage and hematuria. Treatment: Supportive care, anecdotally anti-inflammatories might help and antimicrobials to prevent secondary infections. Historically Most Ferrets Exposed to ADV Have Never Developed Clinical Disease.

Epizootic catarrhal enteritis. ECE is a diarrheal disease of ferrets which causes epizootics of high morbidity (up to 100%), but low mortality. The diarrhea is rapidly dehydrating and most mortalities occur in older animals with concurrent illness. Symptoms include vomiting and passage of a dark green stool with abundant mucus. During the recovery phase, stools assume a "birdseed" like appearance. The causative agent is a coronavirus. Diagnosis: history of recent exposure to a young ferret, or the owners handled a young ferret. Treatment: Aggressive supportive care, IV/IO or SQ fluids 70ml/kg/24 hr, Pepto-bismol©, antimicrobials, nutritional support (200-300 kcal/kg/day). Anecdotally, this disease appears to lead to chronic malabsorption syndrome. Older ferrets may not recover or take longer to recover. Isolate all infected animals. Affected animals will shed the virus for 4-6 months following infection.

Eosinophilic enteritis. Eosinophilic enteritis is not an uncommon disease. Although the etiology of this disease is unknown, parasitic cause or hypersensitivity to food have been suggested. The wasting disease is most commonly seen in young male ferrets under 14 months of age. Peripheral eosinophilia may be seen in affected animals. Treatment: hypoallergenic diet (feline Hill's Z/D) food trial, prednisone 1.25-2.5 mg/kg BID 7 days, then SID-7 dys, then EOD indefinitely.

Gastric ulcers. Ferrets are extremely susceptible to stress-related gastric ulcers. This is a common finding in animals with other systemic diseases and often contributes to debility in older animals. Gastric ulcers are often seen in association with gastric Helicobacter mustelae infection, however, a definitive cause-and-effect relationship has not been proven in this species. Two distinct forms of gastric ulceration may be seen in the ferret. The most common form is the presence of digested blood within the stomach lumen. Ulcers are pinpoint, extremely difficult to see, and are present in the highest numbers in the pyloric region of the stomach. The second, less common form, is the presence of a single, focally extensive, ulcer in the pyloric stomach. These large ulcers may result in sudden death due to erosion into the submucosal blood vessels. Treatment: Treatment: Amoxicillin 10 mgkg BID, Metronidazole 20 mg/kg BID, Bismuth 15-20 mg/kg BID, supportive care, highly digestible diet, transfusions if needed.

Proliferative colitis. Proliferative colitis is an uncommon disease which is usually seen in male ferrets under one year of age. The disease is sporadic. Clinical signs include tenesmus and production of small, frequent bowel movements which often contain frank blood and mucus. The disease is caused by a campylobacter-like organism which results in asymmetrical proliferation of immature epithelium, causing marked thickening of the wall. This condition is subject to periodic periods of recrudescence, often during times of stress. If untreated, it may be fatal. Treatment: chloramphenicol.

Adrenal-associated endocrinopathy. AAE is a common endocrine disorder of middle aged to older ferrets. The syndrome is the result of proliferative lesions in the adrenal cortex which secrete excess amounts of estrogenic hormones. As a result of this excess estrogen, affected ferrets exhibit a range of cutaneous, behavioral, and reproductive signs. While technically a form of hyperadrenocorticism, AAE should not be confused with Cushing's disease, or hypercortisolism. Only rarely are cortisol levels elevated in these patients. Interestingly, unlike dogs and cats, metastasis occurs extremely late in the course of disease with adrenocortical carcinoma, and early removal of affected adrenals carries a fair prognosis. Bilaterally symmetrical alopecia beginning over the tailhead and progressing forwards over the flanks and abdomen is strongly suggestive of AAE. Additionally, the presence of an enlarged vulva in a spayed female also strongly suggests AAE. These clinical signs may be the result of any of the three types of proliferative adrenocortical lesions--hyperplasia, adenoma, or carcinoma. The normal length of the ferrets adrenal gland ranges from 3-5 mm; glands exceeding 5 mm often contain proliferative lesions. Diameters exceeding 1 cm are highly suggestive of adrenocortical carcinoma in the ferret. Treatment: Surgical resection, Luprelide (100 mcg/kg q 3-4 wks), other drugs: Amiridex (anastrozole), Casodex (bicalutamide), Nolvadex (tamoxifen).

Islet cell tumors. Islet cell neoplasms are the most common neoplasm of this species. These neoplasms generally result in hypoglycemia as a result of inappropriate secretion of insulin. Clinical signs include lethargy, stupor, ptyalism, and ataxia, and may progress to coma and death. Non-functional islet cell tumors are commonly seen in older animals at necropsy.

While all islet cell tumors are potentially malignant, metastasis is rare, as opposed to islet cell neoplasms in the dog and cat. Islet cell tumors are reddish-brown, well-defined nodules which range in size from 2mm-1cm. They are firmer than the surrounding pancreatic tissue and may be multiple. These neoplasms must be differentiated grossly from foci of pancreatic exocrine hyperplasia, a common benign age-related finding. Small reddish brown nodules may also be present in the mesentery adjacent to the pancreas. Diagnosis: Diagnosis: Clinical signs, history, serum FASTING glucose (<60 mg/dl), serum insulin, Insulin:glucose ratio, abdominal ultrasound. Treatment: supportive care, surgical resection of nodules, partial pancreatectomy, liver biopsy, Diazoxide 10-30 mg/kg PO, Prednisolone 0.25-2 mg/kg PO SID-BID, frequent, high-protein meals.

Lymphosarcoma. Lymphosarcoma is the most common malignancy in the domestic ferret. These neoplasms most commonly arise spontaneously; however, a recent article documents horizontal transmission of malignant lymphoma in ferrets using cell or cell-free inoculum. This finding, coupled with the occasional clustering of lymphomas in a single facility, has prompted speculation that lymphosarcoma in the ferret may be the result of a retroviral infection, but a viral agent has not, as of yet, been isolated from cases of lymphosarcoma in the ferret. Several variants of lymphoma exist in the ferret. The most commonly seen form, in which the neoplastic cell is a mature, well-differentiated lymphocyte occurs in older ferrets, primarily resulting in peripheral lymphadenopathy, with visceral spread and subsequent organ failure late in the course of disease. A second form occurs primarily in young ferrets less than two years of age. This form, in which the neoplastic cell is a large blastic lymphocyte, is characterized by early visceral neoplasms, often with the production of a large thymic mass. An enlarging thymic neoplasm often results in compression of the lung lobes, dyspnea, and pleural effusion, and may often be misdiagnosed as pneumonia or heart disease by veterinarians with little experience in this species. A third, uncommon form, in which combinations of peripheral lymphadenopathy and visceral neoplasms may be seen and in which the neoplastic cells is often a large, atypical lymphoblast is known as the immunoblastic polymorphous variant. Adult (lymphocytic) form--diffuse lymphadenopathy. Splenic white pulp may be greatly expanded and grossly visible on cut section. In later stages, firm white nodules may be seen in a number of visceral organs, including the liver and kidney, and the spleen may be diffuse and enlarged. Juvenile (lymphoblastic) form--The presence of a thymic mass is strongly suggestive of this condition. Diffuse hepatosplenomegaly is often seen due to massive infiltration of these organs also. Neoplastic cells may be seen in any organ, including the bone marrow.

Tufts University: Harrington Oncology Program

Key:

Dose Reductions: If CBC * indicates myelosuppression, reduce dosage of drug by 25%.

References

Note, the above text was created with information from notes from Pathology of the Ferret by Bruce H. Williams, DVM, DACVP. Additional sources of information utilized and recommended are:

1.  Fernandez-Moran J, Mustelidae. In: M. Fowler and E. Miller. Zoo and Wild Animal Medicine, 5th ed. WB Saunders. St. Louis, Missouri. 2003.

2.  Fox J, Biology and Diseases of the Ferret, 2nd ed. Lippincott Williams and Wilkins. 1998.

3.  Orcutt C, Emergency and Critical Care of Ferrets. In: A. Rupley. The Veterinary Clinics of North America: Exotic Animal Practice, Critical Care. WB Saunders, Philadelphia. 1998.

4.  Quesenberry KE, and Carpenter JW. Ferrets, Rabbits and Rodents. 2^nd Edition. Saunders. St. Louis, MI. 2004.