Alopecia is the partial or complete lack of hairs in areas where they are normally present. If a patient is presented for the problem of hair loss and the animal is pruritic, the problem of pruritus should be investigated first (see Integumentary System Introduction: Pruritus).
There are many causes of alopecia; any disease that can affect hair follicles can cause hair loss. There are two broad etiologic categories of alopecia—congenital or hereditary and acquired. Acquired alopecia is further divided into two categories: inflammatory and noninflammatory.
Congenital or hereditary alopecia (see Congenital and Inherited Anomalies of the Integumentary System: Hereditary Alopecia and Hypotrichosis) has been described in cows, horses, dogs, cats, and pigs. Hairless breeds of mice, rats, cats, and dogs have been bred and developed for personal and research interests. Congenital alopecia may or may not be hereditary; it is caused by a lack of development of hair follicles and is apparent at or shortly after birth. Animals with tardive alopecias are born with normal coats, and focal or generalized hair loss occurs when the animal sheds its juvenile coat or when it becomes a young adult. Examples of this include pattern baldness of Dachshunds, color dilution alopecia (most commonly seen in Doberman Pinschers), and certain types of follicular dysplasias.
Acquired alopecia encompasses all other causes of hair loss. In this type of alopecia, the animal is born with a normal hair coat, has or had normal hair follicles at one time, and is or was capable of producing structurally normal hairs. Acquired alopecia may be noninflammatory, as is seen in endocrine alopecia or some types of immune-mediated alopecia, or inflammatory. Inflammatory acquired alopecia is the most common cause of alopecia. Acquired alopecia develops because a disease destroys the hair follicle or shaft, interferes with the growth of hair or wool, or causes the animal discomfort (eg, pain, pruritus) leading to self-trauma and loss of hair.
Diseases that can directly cause destruction or damage to the hair shaft or follicle include bacterial skin diseases, dermatophytosis, demodicosis, severe inflammatory diseases of the dermis (eg, juvenile cellulitis, deep pyoderma), traumatic episodes (eg, burns, radiation), and rarely poisonings caused by mercury, thallium, and iodine. These diseases tend to be inflammatory.
Diseases that can directly inhibit or slow hair follicle growth include nutritional deficiencies (particularly protein deficiencies), hypothyroidism, hyperadrenocorticism, and excessive estrogen production or administration (hyperestrogenism, Sertoli cell tumors, estrogen injections for mismating). Temporary alopecia in horses, sheep, and dogs can occur during pregnancy, lactation, or several weeks after a severe illness or fever. Marked hair loss (effluvium) is common in cats following respiratory infection. These types of alopecia tend to be noninflammatory unless a secondary infection of the skin develops.
Pruritus or pain is a common cause of acquired inflammatory alopecia in animals. Diseases that commonly cause pruritus or pain include infectious skin diseases (eg, bacterial pyoderma and dermatophytosis), ectoparasites, allergic skin diseases (eg, atopic dermatitis, food allergy, contact, insect hypersensitivity), and less commonly, neoplastic skin diseases. Friction may cause local hair loss, eg, poorly fitted halters or collars. Rarely, excessive grooming may be the cause of hair loss in some animals, particularly cats.
Feline endocrine alopecia is no longer recognized as a bona fide syndrome; the new name is feline acquired symmetric alopecia. To date, there is no documented evidence of an endocrine disease in these cats, and the symmetric alopecia seen is a clinical sign of an underlying disease, most commonly a pruritic disease. The most common cause of feline symmetric alopecia is flea allergy dermatitis. In cats that do not have an obvious flea infestation, a CBC with differential is recommended; many cats that have flea allergy dermatitis have an eosinophilia. This finding may help convince clients to pursue flea control as a first diagnostic step.
Clinical Findings and Lesions
The clinical signs of hair loss may be obvious or subtle, depending on the disease. Congenital or hereditary hair loss is commonly symmetric and not accompanied by many inflammatory changes; in some cases, the areas of hair loss are localized to one region (eg, ear flaps) or to well-demarcated areas.
The clinical signs of acquired hair loss are varied and often influenced by the underlying cause(s); the pattern of hair loss may be focal, multifocal, symmetric, or generalized. Inflammatory changes such as hyperpigmentation, lichenification, erythema, scaling, excessive shedding, and pruritus are common. Some causes of acquired alopecia may predispose the animal to the development of secondary skin diseases, such as a bacterial pyoderma or seborrhea. Pruritus is variable, depending on the primary cause. In endocrine alopecias, the hair loss usually develops in a symmetric pattern, often in wear areas first; pruritus is uncommon unless there is a secondary infection. Contrary to previous thought, hair loss is not generally an early clinical sign of an endocrine alopecia.
Many owners seek veterinary assistance because of perceived excessive shedding. Shedding may be abnormal (excessive) if it results in obvious loss of the hair coat and areas of alopecia. A common cause of abnormal shedding is bacterial pyoderma. If, however, the shedding is not accompanied by development of patchy or symmetric hair loss, it is likely that it is just a stage in the natural replacement of the hair coat.
An accurate diagnosis of the cause of alopecia requires a careful history and physical examination. Key points in the history include recognition of breed predispositions for congenital or hereditary alopecias; the duration and progression of lesions; and the presence or absence of pruritus, evidence of contagion, or nondermatologic problems, eg, polyuria and polydipsia. On physical examination, the distribution of lesions should be noted (focal, multifocal, symmetric, generalized), and the hairs examined to determine if they are being shed from the hair follicle or broken off—the latter suggesting pruritus. Signs of secondary skin infections or ectoparasites should be noted, and a careful nondermatologic examination should be performed.
Initial diagnostic tests include skin scrapings for ectoparasites (particularly Demodex mites); combing of the hair coat for fleas, mites, and lice; impression smears of the skin for evidence of bacterial or yeast infections; fungal cultures for identification of dermatophytosis; and examination of plucked hairs, looking at both the shaft and the ends for evidence of dermatophytosis or that the hairs were chewed off. In many cases of bacterial pyoderma, impression smears of the skin do not show neutrophils and/or cocci, but they may show large numbers of shed keratinocytes. Neutrophils and cocci are seen if pustules or recently ruptured pustules are sampled.
If these tests do not identify or suggest an underlying cause, a skin biopsy may be indicated to evaluate hair follicle structures, numbers, and anagen/telogen ratios and to look for evidence of bacterial, fungal, or parasitic skin infections. In addition, skin biopsies are often needed to confirm congenital or tardive causes of hair loss and to identify inflammatory or neoplastic causes of hair loss. Skin biopsies from normal and abnormal sites should be submitted for evaluation. CBC, serum chemistry panels, and urinalyses are generally only helpful when an endocrinopathy is suspected. Specific endocrine function tests can be performed based on findings of routine laboratory work or clinical signs.
Successful therapy depends on the underlying cause and specific diagnosis.
Last full review/revision July 2011 by Karen A. Moriello, DVM, DACVD