II. Hyperadrenocorticism
III. Hyperestrogenism (Estrogen-Induced Anemia)
IV. Mastitis
V. Pyometra and Vaginitis/Vulvar Cellulitis
Pregnant and postparturient females are predisposed to eclamptogenic toxemia and "nursing sickness syndrome." Neither of these syndromes has been well documented, however, they are characterized by anorexia, muscular incoordination, weakness, weight loss, and death. Increasing the caloric intake from meat sources (infant meat diets), feeding kitten growth diet (Iams), and vitamin and mineral supplementation suitable for cats should be initiated during pregnancy and lactation. Ensuring that the dam's dietary needs are met during this critical period (including 0.5% NaCl in the diet) will help reduce pre-weaning deaths among kits due to lactational failure.
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.
III. 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).
Mastitis frequently occurs in nursing jills in early stages of lactation. Streptococcus sp., Staphylococcus sp., and Escherichia coli are the most frequent causes. Examination reveals enlarged, firm, slightly reddened mammary glands. Milk is expressed with difficulty. Hemolytic E. coli usually causes fulminating gangrenous mastitis, which is often accompanied by pyrexia, lethargy, and acute septicemia. Aggressive and immediate attention to coliform mastitis includes surgical resection of the involved gland combined with ampicillin (10 mg/kg b.i.d.) and gentamicin (5 mg/kg, divided t.i.d.) therapy.
V. Pyometra and Vaginitis/Vulvar Cellulitis
1. Etiology: Generally, bacteria recovered from infections of the female reproductive tract include both gram-positive and gram-negative bacteria commonly found in the oral cavity and feces. E. coli, Streptococcus sp., and Corynebacterium sp. are frequently isolated. The incidence of infections of the reproductive tract is moderate in intact females, especially if they are on progesterone therapy.
2. Transmission/Pathogenesis: It is generally believed that these pyogenic diseases are the result of localized infections that ascend the reproductive tract. Jills are predisposed to these infections during estrus, when conditions such as poor sanitation and aggressive hob behavior may cause vulvar cellulitis and vaginitis, especially if foreign material remains in the vagina. If bacteria gain access to the uterus via the open cervix, then pyometra may develop when the ferrets cycle out of estrus. Jills suffering from pancytopenia due to hyperestrogenism frequently have pyogenic infections of the reproductive tract to compound their debilitated state. Those ferrets on progesterone therapy, such as megesterol acetate, are at the same risk for developing pyometra as are dogs on similar hormone regimens. Vulvar inflammation can also occur in spayed jills that are in poor physiologic condition, and kept in dirty cages, or that are housed with intact hobs, which often attempt to breed neutered jills or hobs. Infections may develop as a sequela to repeated hormone therapy when hCG or GnRH is used to induce pseudopregnancy in jills.
3. Clinical signs: When the vulva is inflamed, it is swollen and often covered with a milky film. It may look much like it does during estrus. A vaginal discharge that is milky to purulent may be present. There may be no clinical signs associated with early vaginal or uterine infections, or obvious systemic signs (depression, diarrhea, anorexia, etc.) may be observed. A purulent vulvar discharge may be noted when the ferret is handled or palpated.
4. Diagnosis: Vulvar cellulitis is differentiated from swelling associated with estrus by history and cytology. Vaginitis is diagnosed by finding foreign material and exudate in the vaginal vault; uterine involvement needs to be considered if vaginitis is the tentative diagnosis. Physical examination, abdominal palpation, radiography and routine blood work can identify pyometra.
5. Treatment: Vulvar cellulitis may be treated topically with antibiotic/steroid
ointments. Removal of the foreign material from the vagina, administration
of localized and systemic antibiotics, and a change in the type of bedding
or nestbox material is indicated for treating vaginitis. Jills with
pyometra should be evaluated for hyperestrogenism. If hyperestrogenism
is diagnosed, the jill should be cycled out of estrus (see Hyperestrogenism
below), treated with antibiotics and, if needed, supportive therapy including
blood transfusions should be administered. Once the jill is stabilized,
ovariohysterectomy and antibiotic therapy are required.
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