Keeping your ferret healthy requires an understanding of the needs of these animals. Ferrets are strict carnivors with very rapid passage of food through their gastrointestinal system, that is why they require diets with highly digestible protein and available energy with minimal fiber. Ferrets are very susceptible to diseases associated with poorly balanced diets, such as yellow fat disease described in ferrets fed a high level of polyunsaturated fats and/or deficient in vitamin E. Young growing kits are found dead or cry when handled, and are reluctant to move. Affected kits have firm swellings under the skin and prominant lumps. Immediate removal of the offending diet is needed and daily injections of vitamin E.
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. The main way of transmission is by a penetrating wound that leads to an infection.
Signs of an abscess may include swelling, draining tracts, and fever. Prevention of penetrating wounds is accomplished by minimizing the animal's exposure to sharp objects in the cage and in the diet. Good husbandry practices can reduce the incidence of abscess formation. Abscesses are usually treated by drainage and flushing with dilute betadine solution. Systemic antibiotics are prescribed with local or topical therapy, especially when gram-negative bacteria are involved.
Generally, bacteria recovered from infections of the female reproductive tract include both gram-positive and gram-negative bacteria commonly found in the mouth and feces. E. coli, Streptococcus sp., and Corynebacterium sp. are frequently found. The frequency of infections of the reproductive tract is quite low in intact females, especially if they are on progesterone therapy.
It is generally believed that these pus-forming diseases are the result of infections that spread to 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. 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 result of repeated hormone therapy when hCG or GnRH is used to induce pseudopregnancy in jills.
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. Vulvar cellulitis is different from swelling associated with estrus. Physical examination, abdominal palpation, radiography and routine blood work can identify pyometra.
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.
Transmission of the bacteria causing proliferative colitis is probably by the fecal-oral route, is believed to be similar to intestinal proliferative diseases of hamsters. The infectious agent(s) may be present in inadequately cooked feed. What exactly causes the disease has not been established.
Clinical signs of proliferative colitis are seen in ferrets that are less than 10 months of age. The animals have green to bloody diarrhea that may persist intermittently for over 6 weeks. Affected ferrets have poor appetite, dehydrated, thin, and have a partial rectal prolapse. The history, presence of the rectal prolapse, and the palpation of a markedly thickened colon in a young ferret are major diagnostic features. Since the condition is unresponsive to therapy, the diagnosis should be confirmed by biopsy, and/or necropsy.
Supportive care with antimicrobial therapy are typical treatments of proliferative colitis in ferrets. However, antimicrobial therapy may not change the course of the disease if improvement is not observed after 48 hours of drug therapy. Metronidazole or chloramphenicol treatments for 2 weeks has been reported to be effective. Prevention is difficult without understanding the cause of the disease.
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 fever, lethargy, and extensive presence of the bacteria in the bloodstream. 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.
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 characteristic of ringworm are similar to those described for cats. There are round 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 relapses. Griseofulvin (25 mg/kg ) may also be used with topical therapy in advanced cases. Humans are susceptible to dermatophyte infections.
Ferrets do not appear to be highly susceptible to salmonellosis. Salmonella enterica serova Typhimurium has been found in ferrets with severe conjunctivitis, dysentery, rapid weight loss, and a fluctuating body temperature. The risks of medicating infected ferret needs to be weighed against the risk of exposing humans or other animals to Salmonella. The risk of human infections should always be considered when investigating ferrets with dysentery.
Avian, bovine, and human strains of mycobacteria can cause tuberculosis in ferrets, however clinical disease is uncommon. Clinically, infected ferrets may become emaciated and have paralysis of the hind limbs which may progress to affect all limbs. Disseminated disease caused by M. bovis is associated with weight loss, loss of appetite, lethargy, progressive muscle paralysis, enlarged liver and spleen, and death. Enlarged lymph nodes may be palpated. Euthanasia is recommended. Ferrets are susceptible to same forms of tuberculosis as humans and may be potential sources of human infection.
Ferrets are moderately susceptible to botulism types A and B, and highly susceptible to type C. The incidence of disease in pet ferrets fed commercial prepared dry or semi-moist diets is rare. Improper storage and handling of fresh meat diets leads to accumulation of botulism toxin, which causes flaccid paralysis in ferrets. Treatment consists of administration of type C antitoxin and supportive care. A bacterin for the C. botulinum type C is available for immunization of mink and ferrets fed fresh meat diets.
Urolithiasis is a common occurrence in ferrets. The signs are similar to those observed in cats, although urethral blockage in ferrets is rare. Uretheral obstruction is often accompanied by pyelonephritis. Medical treatment of urolithiasis is the same as that for feline urolithiasis and cystitis. Reducing dietary ash and providing adequate water may aid in decreasing the recurrence of uroliths.
Paralysis accompanied with urinary and/or fecal incontinence may occur. Paralysis may be due to hemivertebrae, veretbral fractures, intervertebral disc disease, hematomyelia, or myelitis. Ferrets with no radiographic lesions and those with intervertebral disc problems have responded variably to steroid and nonsteroidal anti-inflammatory therapy. This condition can recur.
Ulcers are induced by stress in the stomach, and can be frequently seen in ill ferrets. Hyperacidity has not been associated with formation of ulcers, and the presence of Helicobacter mustelae bacteria may play a role. Diagnosis is based on clinical test. Gastric ulceration may respond to cimetidine therapy (5 to 10 mg/kg orally t.i.d.) or triple medication therapy (bismuth, ampicillin and metronidazole) recommended for Helicobacter infections.
Mitral value insufficiency and cardiomyopathy, resembling the feline cardiomyopathy, have been observed in ferrets. Clinical signs include exercise intolerance, soft cough leading to difficulty breathing, and lethargy. Auscultation, palpation and radiographs can detect fluid accumulation in the chest and abdomen. Normal ferret EKG measurements are similar to those of the cat. Ferret heart disorders are treated similarly to feline heart disorders, with diuretics, antiarrhythmic drugs and calcium channel blockers.
Ferrets are prone to periodontal disease caused by accumulation of dental calculus. Regular preventive dental care is recommended as for the dog or cat. Teeth damaged by various causes, such as chewing on cages or bones, may require root canal repair or extraction.
Ferrets do not have well-developed sweat glands and are prone to heat exhaustion. Clinical signs include panting and inactivity. Hot and humid conditions should be minimized by adequate air circulation and/or cooling. Optimum temperatures are 40-65°F with a humidity range of 40-65%.
Ferrets are subject to some of the vitamin deficiencies, including thiamin (Chastek's paralysis), biotin (achromotrichia), vitamin E (anemia), and vitamin D coupled with a calcium-phosphorus imbalance (rickets). When ferrets are fed a balanced, formulated diet, no deficiencies have been reported. Exposure to excessive levels of zinc via galvanized feeding dishes or by licking cage bars may produce zinc toxicity. Zinc, in the form of zinc oxide, at levels in excess of 500 ppm is toxic to ferrets. Ferrets decrease their feed intake and lose weight on high-zinc diets. Greater than 3000 ppm of zinc is lethal to ferrets within 2 weeks. Affected animals become anemic and rapidly lose condition. Treatment by eliminating the source of zinc contamination (acid-washed galvanized cages or bowls), decreasing dietary zinc, and providing supportive therapy is indicated.