Helicobacter mustelae is found in the stomach and duodenum of all ferrets after weaning. It is an opportunistic pathogen and can induce chronic, persistent gastritis and ulcer formation similar to the disease in people. Gastric lymphoma may occur in chronic cases. Clinical signs include inappetence, vomiting, bruxism, diarrhea, melena, and hypersalivation. Lethargy, weight loss, and dehydration can also occur. These animals may be painful on cranial abdominal palpation because of the ulcers induced or enhanced by the presence of this bacterium. Definitive diagnosis requires examination of tissue from surgical or endoscopic biopsy but is not commonly performed because of the ubiquitous nature of this organism in the ferret GI tract. Silver stains and urease tests should be performed on the biopsy specimens when attempting to determine a definitive diagosis. A molecular assay is available for fecal samples. Treatment is with multidrug regimens, including amoxicillin (20 mg/kg, PO, bid), metronidazole (20 mg/kg, PO, bid), and bismuth subsalicylate (1 mL /kg, PO, bid). Clarithromycin (25 mg/kg/day, PO) and omeprazole (1 mg/kg/day, PO) can be used for refractory cases. Treatment is usually for 21 days. Because of the opportunistic nature of this pathogen, it is important to look for underlying problems such as gastroenteritis, foreign bodies, or stress. Treatment for Helicobacter is commonly initiated when gastroenteritis or foreign bodies are diagnosed or when a gastrotomy is peformed.
Lawsonia intracellularis can cause a proliferative bowel disease, especially in younger ferrets. Signs include diarrhea, weight loss, and rectal prolapse. Treatment is with chloramphenicol (25 mg/kg, PO, bid) for 14–21 days.
Salmonellosis in ferrets is rare but associated with feeding raw or undercooked meat or unpasteurized milk. Signs include bloody diarrhea, conjunctivitis, and anemia. Salmonella tymphimurium, S newport, and S choleraesuis may be involved. Treatment is with aggressive supportive care and antibiotics. Ferrets are susceptible to Mycobacterium avium, M bovis, and Mycobacterium tuberculosis. Intradermal testing is not reliable. Bacterial cystitis is rare in ferrets and is usually associated with urolithiasis and prostatomegaly. Escherichia coli, Staphylococcus aureus, and Proteus spp are most commonly identified. Bacterial pneumonias in ferrets are caused by Streptococcus zooepidemicus, Mycobacterium spp, and gram negative-bacteria such as E coli and Klebsiella pneumoniae. Other bacterial infections are similar to those seen in other carnivores.
Ferrets are susceptible to canine distemper virus. Transmission is by aerosol or exposure to infected secretions. Clinical signs begin 7–10 days after infection and start as fever and dermatitis on the chin and inguinal area, progressing to anorexia, erythema of mucus membranes, and mucopurulent ocular and nasal discharge. Brown crusts on the face and eyelids and hyperkeratosis of the footpads also occur. Respiratory signs develop and progress rapidly. Diagnosis is by history, clinical signs, and positive immunofluorescent antibody testing or histopathology. Mortality is close to 100% and typically occurs 12–14 days after infection.
The human influenza virus causes fever, lethargy, anorexia, nasal discharge, sneezing, and depression in ferrets. Treatment is supportive and includes antibiotics for secondary infections, antihistamines, and amantadine (6 mg/kg, nasally, bid). Recovery is usually within 7–14 days.
Two coronaviruses cause disease in ferrets. The ferret enteric coronavirus causes epizootic catarrhal enteritis. This disease is highly transmissible and is often brought into a group of ferrets by an asymptomatic juvenile animal. Clinical signs begin 2–14 days after introduction of the new ferret or exposure through fomites and include anorexia, vomiting, green or mucoid diarrhea, melena, dehydration, lethargy, and weight loss. The disease is most severe in older ferrets, which may take months to fully recover. The virus causes blunting of the intestinal villi and consequent maldigestion and malabsorption. Definitive diagnosis is difficult, although scanning electron microscopy of the feces may identify coronavirus. Increased ALT and alkaline phosphatase may occur secondary to hepatic lipidosis. Treatment is supportive and includes fluids, nutritional support, broad-spectrum antibiotics, and GI protectants. Prevention is by quarantine of new ferrets, thorough cleaning of new bedding and toys, and washing hands and changing clothes after handling other ferrets.
A second related coronavirus called ferret systemic coronavirus causes a systemic pyogranulomatous inflammatory disease resembling the dry form of feline infectious peritonitis. This disease is seen in young ferrets (average age 11 mo) and is progressive throughout several weeks to months. Clinical signs include anorexia, weigh loss, diarrhea, and enlarged intra-abdominal and, less commonly, peripheral lymph nodes. Hypergammaglobulinemia, anemia, and CNS signs can be seen as the disease progresses. This disease was initially called disseminated idiopathic myofasciitis because of the white nodules found in many tissues on necropsy. These nodules are pyogranulomatous inflammation and involve many organs, including peritoneum, adipose tissue, viscera, and blood vessels. A pyogranulomatous pneumonia has also recently been reported. Treatment is supportive with immunosuppressants such as prednisolone and anecdotal reports of use of polyprenyl immunostimulants, which have resultedin some increase in survival time. Average survival time is ~2 mo.
Aleutian disease is a parvovirus originally seen in mink, but at least two distinct ferret strains of the virus have been identified (see Viral Diseases of Mink). The virus causes immune complex deposition on organs, which results in a variety of nonspecific clinical signs such as progressive weight loss, weakness, ataxia, hepatomegaly, and splenomegaly. A severe hypergammaglobulinemia is the most consistent finding on blood work. A presumptive diagnosis is based on clinical signs and hyperglobulinemia. The two most common tests for the virus antibody are counterimmunoelectrophoresis and immunofluorescent antibody tests. Definitive diagnosis is difficult, because many apparently normal ferrets have positive titers. The organism has been found in the urine, feces, and blood of symptomatic and asymptomatic animals. Treatment with anti-inflammatories and immunosuppresants such as prednisolone and cyclophosphamide can be considered and may have clinical benefit. Treatment of infected mink kits with gamma globulin-–containing Aleutian disease virus antibody has decreased mortality rates, but this treatment has not been attempted on ferrets. There is currently no vaccine available for this disease in ferrets.
Ferrets are susceptible to Microsporum canis and Trichophyton mentagrophytes. Transmission is by direct contact or fomites and is often associated with overcrowding and exposure to cats. Infection is more common in kits and young ferrets and is often seasonal and self-limiting. A pyogranulomatous dermatitis and fungal pododermatitis has been associated with Microsporum nanum. Other fungal diseases in ferrets include cryptococcal meningitis and blastomycosis causing granulomatous meningoencephalitis. Fungal pneumonia is uncommon in ferrets but can be caused by Blastomyces dermatitidis and Coccidioides immitis in endemic areas. Cryptococcosis from Cryptococcus bacillisporus and C neoformans var grubii has been diagnosed in ferrets. Signs include pneumonia, pleuritis, rhinitis, and regional lymph node enlargement.
Ear mites are the most common ectoparasite in ferrets and are caused by Otodectes cynotis. The same ear mite is found in dogs and cats, and it can be passed between species. Diagnosis and treatment are as for dogs and cats (see Otitis Externa). Fleas are also common in ferrets and can be transmitted between ferrets and other household pets. Diagnosis is by visualization, and treatment is the same as for dogs and cats (see Fleas and Flea Allergy Dermatitis). Many of the long-acting topical treatments, such as fipronil, last longer in ferrets because of the increased sebum in the coat. Mange in ferrets is caused by Sarcoptes scabiei and can be seen as a generalized dermatitis or can be limited to the feet, toes, and pads in a pedal form unique to ferrets.
Heartworm disease, caused by Dirofilaria immitis, can be found in ferrets, especially if given outdoor access in endemic areas. Disease can be caused by even a single worm. Clinical signs include lethargy, coughing, dyspnea, and ascites. Ferrets are typically infected with a very small number of worms (1–20), making diagnosis difficult. Echocardiography is warranted, because the parasites often obstruct blood flow and cause right-sided heart failure. Echocardiography may also be helpful in identification of the worms in the right ventricle, pulmonary arteries, and vena cavae . Peripheral microfilaremia is uncommon in ferrets; therefore, antigen testing is more beneficial. Treatment using longterm antithrombotic drugs and adulticides can be done but may cause problems. Low-dose ivermectin (0.05 mg/kg, SC, monthly until clinical signs and microfilaremia resolve) is the current recommended treatment (see Heartworm Disease).
Coccidiosis can cause disease in young ferrets including diarrhea, lethargy, and rectal prolapse. Diagnosis and treatment are similar to those in dogs. Rectal prolapse can also occur with coccidiosis and usually resolves after treating the underlying disease. Topical hemorrhoidal creams may be helpful.
Last full review/revision July 2013 by James K. Morrisey, DVM, DABVP (Avian)