Alopecia is a frequent finding in ferrets. Within the differential diagnostic list three groups should be distinguished: infectious diseases, hormonal diseases and a miscellaneous group. The infectious disease group consists of dermatophytosis, mange and bacterial dermatitis. The most important diseases within the hormonal group are persistent oestrus, a functional remnant ovary and hyperadrenocorticism. Although the case has not been published, one ferret has been diagnosed with hypothyroidism. Seasonal alopecia is the most important diagnosis within the miscellaneous group. The animals in this group have hair loss only on the tail and the cause is not known. This condition is considered unimportant. It may, however, be the first signs of a ferret with hyperadrenocorticism. The latter disease is also the most common diagnosis of an alopecic ferret.

Approach to Alopecia in Ferrets is Described

This is very similar to the approach to alopecia in other companion animals.

Signalment

Within the signalment, age is an important factor. Symmetrical alopecia and swelling of the vulva in female ferrets under the age of 3 years is most likely due to a functional remnant ovary, while in ferrets over 3 years of age hyperadrenocorticism is more likely.

History

Important questions which should be asked are:

 Where and when was the animal purchased? Dermatophytosis and mange are most often seen directly after purchase.

 Does the animal have pruritus? With this question you can generally differentiate between an infectious cause and a metabolic cause (often hormonal). Infectious diseases are commonly associated with pruritus, while animals with a hormonal skin disease do not have pruritus. Hyperadrenocorticism in ferrets is an exception to this rule.

 Are there any other animals or persons in the household who have cutaneous symptoms? If lesions are seen in people (especially children) in the household, it is likely you are dealing with dermatophytosis, although ectoparasites in humans may result in self-limiting papules as well.

 What is the progression of the disease? Are the clinical signs static, are they constantly getting worse or are there periods of improvement? Dermatophytosis, for instance, may be self-limiting, with flare-ups during times of immunosuppression.

Physical Examination

Cutaneous signs may be a reflection of systemic disease. It is therefore mandatory that a physical examination is performed for every patient which is presented with skin disease.

Dermatological Examination

After an inspection of the animal from a distance, a closer inspection of the hairs and skin is performed. Attention is paid to the quality of the hairs; is there (symmetrical) alopecia, or are any broken hairs found? Are any lesions present? If so, how should they be characterised (papule, pustule, vesicle, wheal, nodule or tumour)? Are there any scales or crusts present? Are there signs of hypo-or hyperpigmentation?

Specific Tests

In the majority of cases no skin abnormalities are seen in alopecic ferrets. In these cases hyperadrenocorticism is very likely. In those cases in which skin lesions are found, skin scrapings, vacuuming of the fur, impression smears and brushing of the hairs with a new tooth brush (McKenzie tooth brush method) can be performed. Sabouraud's agar to which a colour indicator is added (Dermatophyte test medium (DTM)) is commercially available enabling in-house testing. In cases of dermatophytosis the agar will change colour during the growth of the fungus. This test method, however, does not enable you to differentiate between the different dermatophytes.

In hyperadrenocorticism, an abdominal ultrasound scan will provide you with the most valuable information.

Treatment

Treatment of infectious causes of alopecia in ferrets is similar to that reported for other companion animals.

Hyperadrenocorticism

In neutered pet ferrets hyperandrogenism is the most common form of hyperadrenocorticism. In recent years, evidence has been gathered which shows that increased concentrations of gonadotrophins, which occur after neutering (due to the loss of negative feedback), stimulate the adrenal cortex, eventually leading to an adrenocortical neoplasm. This may also explain why hyperadrenocorticism has, up to now, been considered a rare condition in ferrets in the United Kingdom.

Clinical signs of hyperadrenocorticism in ferrets include symmetrical alopecia, vulvar swelling in neutered female ferrets, recurrence of sexual behaviour after neutering, urinary blockage in males (due to periprostatic or periurethral cysts), occasional mammary gland enlargement in female ferrets, and pruritus. The skin is usually not affected, although some excoriations may be seen. Alopecia usually begins in spring, which coincides with the start of the breeding season, and may disappear without treatment. The next year the alopecia usually returns after which it usually does not resolve spontaneously at the end of the breeding season. Polyuria and polydipsia are reported in ferrets with hyperadrenocorticism. It is not clear, however, whether adrenal hormone production is responsible for these signs, or whether these (elderly) ferrets have concurrent kidney disease.

The most important differential diagnoses for a ferret with signs of hyperadrenocorticism are a non-ovariectomised female or a ferret with active remnant ovaries. Severe alopecia and pruritus in a ferret, however, has also been seen due to a food allergy. All signs in this ferret resolved after it had been converted to a different brand of ferret food.

Although many advanced techniques can be used in diagnosing hyperadrenocorticism in ferrets, the clinical signs remain the most important. Further confirmation can sometimes be obtained by palpating a (tiny) firm mass craniomedial to the cranial pole of the kidneys. The right adrenal gland is more difficult to palpate due to the overlying right caudate process of the caudate liver lobe.

Hormones that are commonly elevated are androstenedione, oestradiol and 17-hydroxyprogesterone. Elevation of one or more of these hormones has been considered to be diagnostic for hyperadrenocorticism. Plasma concentrations of the latter hormones are identical in intact female ferrets compared to those in hyperadrenocorticoid ferrets. It is therefore likely that this hormone panel does not aid in differentiating between a ferret with hyperadrenocorticism and one with an active ovarian remnant. The author therefore does not routinely measure these hormones in the diagnosis of this disease. Plasma cortisol concentrations have, just as in dogs, been found to be of no use for the diagnosis of hyperadrenocorticism in ferrets. Although an increased urinary corticoid-creatinine ratio (UCCR) has been found in ferrets with hyperadrenocorticism, this is not considered to be of diagnostic value because this ratio is also increased in intact ferrets during the breeding season and in ferrets with an active ovarian remnant.

The most useful tool in diagnosing hyperadrenocorticism in ferrets is abdominal ultrasonography. This is especially of great value prior to surgery, if you want to determine which adrenal gland is affected, or whether an ovarian remnant is present. In this way the owner can be informed about the potential surgical risks that may be encountered. Another advantage of this technique is that other abdominal organs can be evaluated during the same procedure. By using specific landmarks the adrenal glands can fairly easily be detected in nearly 100% of the cases.

When attempting to treat a ferret with hyperadrenocorticism, the most ideal treatment would probably be a combination of surgery and placement of an implant containing deslorelin (a depot gonadotropin-releasing hormone (GnRH) analogue). Surgical removal of the left adrenal gland is fairly easy. The location of the right adrenal gland makes it much more difficult to remove. The most effective drugs at present are the depot GnRH agonists, of which leuprolide acetate (Lupron Depot, TAP Pharmaceutical Products Inc.) is the most well known. Deslorelin is another pharmaceutical GnRH analogue. Advantages of these implants over leuprolide acetate are that the drug does not need to be reconstituted, lasts much longer than the depot injections, will be registered for use in animals and will probably be cheaper. These implants have already been used in ferrets with hyperadrenocorticism and seem to be very effective. Until the deslorelin implants are commercially available leuprolide acetate provides a suitable alternative. The Lupron 30 day Depot formulation is given in a dose of 100 µg i.m. for ferrets less than 1 kg and 200 µg i.m. for ferrets over 1 kg. This drug will suppress adrenocortical hormone release for at least 1 month in ferrets and may even last up to 3 months.

Melatonin has also been proposed as a therapeutic option for hyperadrenocorticoid ferrets. Melatonin supposedly suppresses the release of GnRH. Clinical improvement is seen in hyperadrenocorticoid ferrets receiving either 0.5 mg melatonin daily orally or an implant containing 5.4 mg melatonin. In the study in which melatonin was given orally, however, hormone concentrations, in general, rose and the tumours continued to grow. This treatment may therefore pose a risk to the ferrets as their condition deteriorates, because it will remain unnoticed by the owner.

References

1.  Nico Schoemaker's PhD thesis on Hyperadrenocorticism in Ferrets can be found online at: http://igitur-archive.library.uu.nl/dissertations/2003-1128-094343/inhoud.htm