I. Arthropods
II. Dermatophytosis
III. Distemper
IV. Hyperadrenocorticism
V. Hyperestrogenism (Estrogen-Induced
Anemia)
VI. Pyogenic Infections
I. Arthropods
Infestation with Sarcoptes scabei may take two forms: 1) a focal
to generalized alopecia and intense pruritus associated with the mite,
which can be found in skin scraping of affected areas, or 2) sarcoptic
lesions which are confined to the toes and feet where feet are swollen,
scabby, and if not treated, clawless. Diagnosis is made by scraping
affected areas and observing the typical sarcoptid mite (see photo).
Treatment consists of application of sulfur ointment or lime and sulfur dips and washes, and trimming the claws and removing the scabs after softening them in warm water. Other topical treatments used for dogs have been used successfully on ferrets. Ivermectin is probably the most successful treatment available and has been successfully used to treat Sacroptes in ferrets (0.2mg/kg repeated in 2 weeks). Pruritus may be reduced by administration of corticosteroids.
Ferrets may also be infected with fleas (Ctenocephalides sp.) and may be treated with mild flea products, similar to those used on cats. Ear mites (Otodectes cynotis) may be treated with ivermectin (0.2mg/kg) repeated in 2-3 weeks.
Public Health Significance: Humans may be bitten by fleas and become infected with Sarcoptes
scabei, which manifests as pruritis beginning in the areas of the skin
having contact with the animal. The skin frequently becomes encrusted and
excoriated as the disease progresses.
Ringworm (Microsporum canis and Trichophyton mentagrophytes)
has been reported in young ferrets. Stored litter or shavings for
nest boxes are often the source of infection. The lesions are similar
to those described for cats. There are circumscribed areas of alopecia
and scaley crusts spread all over the body. Topical fungicides and
time will clear up the crusty, hairless lesions while fresh nest box material
will help prevent recrudescence. Griseofulvin (25 mg/kg ) may also
be used with topical therapy in advanced cases. 
Public Health Significance: Humans are susceptible to dermatophyte
infections.
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.
Hyperadrenocorticism is a disease affecting both male and female ferrets,
average age 5 years (range 1-8 yrs.) Typically, bilateral, non-pruritic
alopecia is reported which begins at the base of the tail and may become
generalized.
Ovariohysterectomized female ferrets typically have vulvar enlargement
similar to the intact estrus female. A mucopurulent to hemorrhagic
vaginal
discharge may be noted, and polydipsia and polyuria are infrequently
reported. Diagnosis is based on clinical signs, abdominal ultrasonography,
and finding enlarged adrenal gland(s) during laparotomy.
Removal of the affected gland(s) is generally curative, and clinical signs
generally resolve quickly
after adrenalectomy. Results of ACTH stimulation tests are variable,
however clinical signs and elevated estradiol concentrations may support
a
diagnosis of hyperadrenocorticism. Histologically, the mass may
appear as nodular hyperplasia, adrenocortical adenoma, or carcinoma.
Adrenal
carcinomas are often diagnosed (about 50% of the time in one review
of 117 cases), however they have a very low metastatic rate (one in the
aforementioned study). There has been a suggestion in the literature
that early neutering (5-6 weeks of age) may predispose the ferret to development
of adrenocortical tumors. However, there is no evidence to date
to support this theory.
V. Hyperestrogenism (Estrogen-Induced Anemia)
A. Etiology: High endogenous estrogen levels during prolonged estrus leads to bone marrow depression. The incidence of estrogen toxicity is high in intact jills that have not been bred.
B. Clinical Signs: Clinical signs of bone marrow depression are
common and variable. Affected ferrets are generally pancytopenic
and therefore are predisposed to bleeding disorders and secondary bacterial
infections. Common clinical findings include an enlarged vulva, pale
mucous membranes often flecked with petechia, bilaterally symmetrical alopecia,
skin petechia, pneumonia, tarry feces, posterior paresis or paralysis,
and affected ferrets are often obtunded. Affected ferrets commonly
have mild anemia and leukopenia, and they can be profoundly thrombocytopenic.
Severe anemia is commonly associated with hemorrhagic diathisis.
Pneumonia and vaginal discharge from pyometra are common.
C. Necropsy: Gross pathologic changes include pale tissues, thin watery blood, pale fatty bone marrow, petechial or ecchymotic hemorrhages throughout the subcutis and gastrointestinal tract, hydrometra or pyometra, and occasionally pyogenic infections in other organs. The major histopathologic changes are hemorrhages, hypocellular bone marrow and decreased splenic extramedullary hematopoiesis.
D. Pathogenesis: Prolonged high levels of endogenous estrogens depress the bone marrow, resulting in pancytopenia. Thrombocytopenia predisposes the ferret to bleeding disorders (subcutaneous ecchymoses, gastrointestinal hemorrhages, and hematomyelia), while neutropenia predisposes ferrets to secondary bacterial infections (pyometra, pneumonia, etc.).
E. Differential Diagnosis: Diagnosis of bone marrow depression is based on clinical presentation of a female in estrus with a mild anemia and profound thrombocytopenia. In ferrets with a PCV less than 30%, hemorrhage should be suspected. Since the clinical presentation of these animals can vary from lethargy to paralysis to pneumonia, the clinician should pay strict attention to the history and clinical signs of estrus, which are a swollen vulva and, occasionally, mild bilateral symmetrical alopecia.
F. Treatment: If estrus has not extended beyond 2 to 3 weeks ovariohysterectomy can be performed if the CBC is normal. Unlike the technique used in cats, manual stimulation of the cervix will not reliably bring the ferret out of estrus. Also, the use of the antiestrogenic drug, tamoxifen citrate, is estrogenic and therefore is contraindicated in ferrets. If a jill has been in estrus for at least 2 weeks and has not developed severe thrombocytopenia, she can be treated with an IM injection of 50 to 100 IU of human chorionic gonadotropin (hCG) or with 20 ug GnRH IM. If the size of the vulva has not decreased 10 to 14 days after treatment, a second dose of either hormone may be given. The jill can also be bred to a vasectomized hob to induce ovulation. Exogenous hormone therapy or breeding to a vasectomized hob will induce a 42 day pseudopregnancy. When the CBC returns to normal, the jill should be ovariectomized to prevent recrudescence. In cases of marked thrombocytopenia, the jill will need supportive care in addition to ovulatory manipulations. Use of whole blood transfusions (5 to 10 mls per transfusion), anabolic steroids, vitamins and antibiotics may also be necessary to save the jill's life. Ferrets appear to lack detectable blood groups thus transfusions pose little clinical risk, even without crossmatching. If the jill returns to estrus and still has an abnormal hemogram, additional hormone therapy or sterile breeding should be performed to remove estrogenic influences. The jill can be spayed when thrombocyte numbers approach normal. In general, treatment of severe bone marrow depression is difficult and almost uniformly unsuccessful, so a poor prognosis should be offered to any ferret that has been in estrus for more than 8 weeks.
G. Prevention: Female ferrets not intended for breeding should undergo ovariohysterectomy prior to their first estrus (at about 6 to 8 months of age).
Subcutaneous Abscesses
1. Etiology: Staphylococcus sp., Streptococcus sp., Pasteurella sp., Corynebacterium sp., Actinomyces israeli, and Escherichia coli cause abscesses of the skin (infected bite wounds during mating), and oral abscesses secondary to injuries by ingested bones. Incidence of pyogenic infections is common.
2. Transmission and Pathogenesis: The primary mode of transmission is by a penetrating wound that leads to a localized infection. In most cases, the infection will be walled off and few systemic signs will be seen.
3. Clinical Signs: A fluctuant swelling, local draining tract, fever, and neutrophilia may be noted depending on the location of the lesion.
4. Differential Diagnosis: Biopsy, aspiration, or draining the affected area differentiates inflammation from neoplasia.
5. Prevention and Control: Prevention of penetrating wounds is accomplished by minimizing the animal's exposure to sharp objects in the cage and in the diet. Limiting the time the female is with the male after successful mating may decrease the number and severity of bite wounds associated with breeding. Good husbandry practices can reduce the incidence of abscess formation.
6. Treatment: Treat localized abscesses by drainage and flushing
with dilute betadine solution. Systemic antibiotics should be prescribed
with local or topical therapy, especially when gram-negative bacteria are
involved.
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