II. Influenza
III. Epizootic Catarrhal Enteritis (ECE)
IV. Aleutian Disease of Ferrets
V. Rabies
VI. Other Viral Diseases
I. Distemper
A. Etiology: Canine distemper virus (CDV) causes ferret distemper. Incidence of infection is moderate to high in nonvaccinated ferrets.
B. Transmission: An outbreak of distemper can rapidly spread throughout a susceptible ferret colony, due to aerosolization of virus particles, with case-fatality rate approaching 100% in a susceptible populations. Canine distemper virus is a pantropic virus infection, infecting and replicating in all epithelial and lymphoid organs. In ferrets, however, the course of distemper virus infection is predictable unlike infection in the dog, and it always induces a catarrhal respiratory phase followed by central nervous system involvement.
C. Clinical Signs: Clinical signs of distemper appear 7 to 10 days after
exposure and include anorexia and mucopurulent ocular and nasal discharge.
A rash appears under the chin (see photo), around the anus, and in the
inguinal area 10 to 12 days after exposure. The footpads may become
hyperkeratotic. Death generally occurs 12 to 16 days after exposure
to ferret-adapted CDV strains and 21 to 35 days after exposure to canine
wild virus strains. Ferrets that survive the catarrhal phase may
die during a central nervous system phase of distemper, signs of which
include hyperexcitability, excess salivation, muscular tremor, convulsions
and coma. Vaccine strains of canine distemper virus that have been
propagated in cell lines of canine origin can also induce disease in ferrets.
Signs of vaccine-induced distemper may include mild purulent upper respiratory
tract infection with pyrexia that resolves in a week, or progresses to
fulminating distemper during that same time frame.
D. Pathology: Macroscopic postmortem findings include bilateral mucopurulent nasal and ocular discharge with accompanying eye lesions. Often the ferrets die acutely within 3 to 4 days, and few macroscopic lesions are evident other than skin rash, hard pad, pneumonia, gastric ulcers and tarry feces. Histologic lesions include intranuclear or intracytoplasmic inclusion bodies in a variety of cell types. A productive area to examine for inclusion bodies is the epithelium lining the stomach, trachea, urinary bladder and conjunctiva. Inclusions are less frequently found in epidermal and neuronal or glial cells.
E. Diagnosis: Because the progressive signs of distemper are so typical, the disease is rarely confused with other conditions. Early in the disease, the fever and serous discharges resemble influenza. Clinical diagnosis of CDV infection can be confirmed with fluorescent antibody (FA) techniques on conjunctival scrapings at onset and throughout clinical disease. Less commonly, FA tests on peripheral blood smears may reveal CDV inclusions in neutrophils. A post-mortem diagnosis can be confirmed by virus isolation or by histopathology.
F. Prevention and Control: With the high case-fatality rate, treatment of ferret distemper is not warranted, and euthanasia is a practical alternative to treatment. Prophylaxis by vaccination using a modified-live CDV vaccine of chick embryo (not canine cell) origin is effective. In the face of an outbreak in a susceptible colony, sick animals should be removed from apparently healthy ferrets, and the healthy ferrets should be vaccinated immediately.
A. Etiology: Ferrets are susceptible to infection with several strains of human influenza virus (orthomyxovirus).
B. Transmission: Influenza virus is transmitted from humans to ferrets by droplet infection. Reciprocal transmission (from ferrets to human) has not been recognized.
C. Clinical Signs: Within 48 hours of exposure, the ferret become listless, febrile, anorexic, and exhibits a serous oculonasal discharge. Paroxysmal sneezing, occasionally accompanied by a purulent nasal discharge may develop. The fever is usually biphasic throughout the 7 to 14 days of the disease. Neonates may die from interstitial pneumonia. Otherwise, the disease is not fatal.
D. Pathology: Usually catarrhal rhinitis is observed clinically. In neonatal infections, interstitial pneumonia is observed.
E. Diagnosis: Clinical signs are similar to those of distemper. Influenza causes biphasic fever, catarrhal oculonasal discharge that does not change in character over the course of the disease and recovery usually occurs within 4 to 5 days of the onset of clinical signs. Other nonviral causes of pneumonia, such as bacterial and mycotic infections, can be ruled out on the basis of culture, duration, and response to treatment.
F. Treatment and Control: Respiratory tract congestion may be relieved with antihistamines. Treatment is usually not necessary, although antibiotics may be needed to control secondary bacterial infections. Recovery from infection confers immunity for at least 5 weeks against the homologous strains of influenza.
VIII. Epizootic Catarrhal Enteritis (ECE)
Epizootic catarrhal enteritis is a diarrheal disease caused by a coronavirus that can produce epizootics of high morbidity, but low mortality. Ferrets rapidly dehydrate and mortalities occur in older animals with concurrent illness. Clinical signs include vomiting and watery dark green feces with abundant mucus. The small intestine contains a moderate amount of watery ingesta. Histopathologic lesions include vacuolar degeneration and necrosis of apical enterocytes with resultant villous fusion and blunting. Treatment with parenteral and oral fluids promote recovery.
IV. Aleutian Disease of Ferrets
A. Etiology: Aleutian disease is caused by a parvovirus that is antigenically distinct from that that causes feline distemper. There appears to be a biologic difference between Aleutian disease virus (ADV) isolates of mink and ferret origin. Serologic surveys of a large ferret colony revealed low to moderate exposure (up to 41%) to ADV. Incidence of clinical disease was unknown.
B. Transmission and Pathogenesis: Both horizontal (fecal-oral and aerosol) and vertical transmission are suspected to occur in ferrets as in mink. The virus infection is persistent and induces a systemic proliferation of lymphocytes and plasma cells. A significant, chronic, increase in serum gamma globulins (greater than 20% of the total protein value) is associated with the plasma cell proliferation in most infected ferrets.
C. Clinical Signs: ADV infection is usually subclinical in ferrets but clinical signs may occur. A syndrome of posterior ataxia, progressive paresis, quadriplegia, cachexia, and melena may be seen. Stressed animals may die acutely. Hypergammaglobulinemia can be detected in affected animals.
D. Pathology: Gross necropsy lesions include mild splenomegaly and hepatomegaly. Lymphocytic and plasmacytic infiltration of liver, spleen, lungs, and kidneys, and follicular hyperplasia of lymph nodes are prominent histologic alterations.
E. Diagnosis: Aleutian disease may need to be differentiated from acute episodes of nonspecific enteritis, proliferative enteritis, and gastric ulcers. Confirmation of hypergammaglobulinemia and of plasmacytic visceral infiltration provides a strong tentative diagnosis of ADV infection. For definitive diagnosis, serum should be tested for ADV antibody by counterimmunoelectrophoresis: an assay available at the Rocky Mountain Reference Laboratory (Bozeman, Montana), United Vaccine (Madison, WI) or certain research institutions.
F. Prevention and Control: There is no treatment. Affected ferrets should be isolated or euthanatized to decrease the spread of the virus. Aleutian disease virus probably persists in infected ferrets for years. There is no cross antigenicity between ADV and other parvovirus vaccines, and there is no specific vaccine due to the immune-mediated nature of the disease.
Ferrets are susceptible to rabies virus, but the latency or duration of spontaneous infection is unknown. Rabies has been diagnosed in 6 ferrets since 1980, and in one case the ferret might have been vaccinated with a modified live rabies vaccine. Another case of ferret rabies was diagnosed in a ferret with no history of vaccination or exposure to a wild carnivore. There are now several USDA-approved killed vaccine products for use in ferrets: Imrab3, Rhone Merieux, Inc. and Prorab 1, Intervet. The dose and schedule for ferret vaccination is the same as that for cats, and the vaccine is effective in protecting ferrets from live virus challenge. However, the Public Health Service, through the CDC, currently recommends that vaccinated ferrets that bite a human should be euthanatized for rabies examination. The 10-day postbite quarantine is not known to be adequate for ferrets, and cannot be used as a standard until enough clinical data is collected from vaccinated ferrets. When faced with such a bite case, it may be best to contact the state public health official for the latest recommendations. Decreasing the risk of exposure to wild carnivores markedly decreases the chance of ferrets contracting the disease. There are other conditions that can cause central nervous system diseases in ferrets, particularly canine distemper virus infection. If there is any doubt as to the progression of a CNS disorder in a ferret, the affected ferret should be isolated and or euthanatized so the brain can be submitted for laboratory examination of rabies virus infection.
Public Health Significance: The concern of humans contracting rabies from unvaccinated pet ferrets is one of the major issues that precipitated the passage of laws and ordinances preventing private ownership of ferrets in many cities and states.
Feline leukemia virus (FeLV) does not appear to produce clinical disease
in ferrets, however some practitioners have reported positive results to
FeLV tests. Ferrets are not susceptible to mink virus enteritis.
Ferrets display no clinical disease from feline panleukopenia virus (parvovirus)
infection although virus may be briefly shed after exposure. Vaccination
with multivalent products is not recommended (to prevent overstimulation
of the immune system).
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