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Dr. Michele Rosenbaum examines the causes of focal, non-pruritic, non-inflammatory alopecia.
Alopecia is a common and often frustrating problem in dogs. Alopecia may be strictly a cosmetic concern to the owner (especially if a show dog), or may indicate an underlying external or internal disease process.
Photo 1: Dachshund with pinnal alopecia. Note hyperpigmentation of skin. This breed is most commonly seen with alopecia of the pinna, but it is also seen in other breeds.
Parasites, allergy, bacterial or fungal infection, hormonal disease/imbalances and congenital or genetic disorders of hair growth may all contribute to alopecia. When evaluating a dog with alopecia, it is important to characterize the alopecia according to its age of onset (congenital or acquired), duration, location, pattern (focal, multifocal/patchy or diffuse/symmetrical), degree of pruritus and whether complete (no hair at all) or partial (stubble/broken hairs) alopecia exists.
It is also important to determine the relationship of the alopecia to the season of the year, vaccination date, medications, clipping, surgery, estrous cycle (whelping), and stress of illness or fever. Certain breeds are predisposed to specific causes of alopecia (Table 1, p. 13.)
This article will cover the less common causes of focal, non-pruritic, non-inflammatory alopecia other than alopecia caused by hypothyroidism, hyperadrenocorticism, seasonal (cyclic) flank alopecia and sex hormone imbalances.
Dachshunds are the breed most commonly seen with alopecia of the pinna (Photo 1), but this alopecia may also be seen in Italian Greyhounds, Chihuahuas, Boston Terriers, and Whippets. Age of onset is usually 6 months to 3 years. Progressive miniaturization of hairs causes a gradual thinning of pinnal hair, with only small vellus hairs remaining. Total pinnal alopecia may occur later in life as the disease progresses. The rest of the haircoat is normal. Differential diagnoses include iatrogenic alopecia due to application of corticosteroid ï¿½ï¿½ containing ear medications, hair follicle dysplasia, unusual causes of endocrine disease such as hyperadrenocorticism or hypothyroidism, sex hormone imbalances, dermatophytosis, demodicosis and alopecia areata. Diagnosis is made by physical examination findings, ruling out other differentials, and obtaining pinnal skin biopsies for histopathology, which shows a diminution in the size of anagen hair follicles. Therapy is for cosmetic appearance only. Melatonin at 3 mg orally every eight hours may be tried for eight to 12 weeks. Dogs that show a good response in that time period can have the melatonin gradually tapered to once daily, then every other day for long-term maintenance. In some cases, therapy can be discontinued, and then re-instituted if alopecia returns.
Photo 2: Post-clipping alopecia. Note lack of hair regrowth six months after surgery.
Pattern baldness is a non-inflammatory idiopathic alopecia most common in Dachshunds, but also seen in short-coated breeds such as Boxers, Boston Terriers, Chihuahuas, Whippets, Manchester Terriers, Greyhounds, and Italian Greyhounds. Females are predisposed. Beginning at about 6 months of age, hair begins to thin symmetrically on the skin on the pinna and behind the ears, ventral neck, ventrum and caudomedial thighs. Progressive, gradual, complete alopecia is seen in these areas over the next 12 months. Small fine hairs are present when the skin is closely examined. Remaining hairs do not epilate easily. The alopecic skin often becomes hyperpigmented. American Water Spaniels and Portuguese Water Dogs have a clinically distinct pattern baldness involving only the ventral neck, caudomedial thighs and tail. Diagnosis of pattern baldness is made by ruling out other differentials such as demodicosis, dermatophytosis, superficial pyoderma and causes of endocrine alopecia (hyperadrenocorticism, hypo-thyroidism, sex hormone imbalance), and by dermatohistopathology. Histopathology reveals miniaturization of hair follicles. Hair loss is often permanent, but some dogs respond to oral melatonin, 3-6 mg orally every eight to 12 hours. Treatment is not necessary. This is a cosmetic disease that does not affect the dog's quality of life.
This owner-caused localized alopecia has been described in dogs with barrettes, rubber bands or bows applied too tightly or for too long to tie up hair on the head. Initially the skin is erythematous, then if pressure is not relieved, this lesion progresses to an alopecic scarred patch where the hair was pulled back. Alopecia may be permanent if the lesion is allowed to progress for too long. If hair follicles are not destroyed, hair may regrow. Otherwise, surgical excision is required to remove the scarred patch if desired for cosmetic purposes. Hair ornaments should always be applied loosely to prevent this alopecia.
Post-clipping alopecia is the failure to regrow hair for months after clipping, usually after surgery (Photo 2, p. 13). or grooming. The author has also observed this alopecia in some dogs after clipping for intradermal skin tests or application of Fentanyl patches. It is most common in Nordic plush-coated dogs such as Siberian Huskies, Alaskan Malamutes, Keeshonds and Samoyeds, as well as in German Shepherds, Chow Chows and Labrador Retrievers.
The area over the back and rump is most commonly affected, and has a "just clipped" appearance, even months later. The reason the hair fails to regrow is unknown; it may be due to vasoconstriction of blood vessels in the skin that occurs with decreased skin surface temperature from loss of haircoat insulation after clipping. Histopathology shows a predominance of catagen hair follicles. Total hair regrowth may take six to 24 months, although most animals regrow hair within 12 months. Initially the regrown hair may be darker than normal.
Photo 3: Miniature poodle with hyperpigmented, inflamed alopecic patch due to rabies-vaccine-induced alopecia and vasculitis.
Differential diagnoses that should be ruled out with appropriate laboratory testing include causes of endocrine alopecia such as hyperadrenocorticism, hypothyroidism, and sex hormone imbalance. Vigorous brushing of the area, massage, hydrotherapy with warm water, and covering the alopecic area with a sweater to increase skin temperature and blood flow to the skin, may stimulate hair regrowth in some cases. Melatonin 3-6 mg orally every eight to 12 hours for eight to 12 weeks and short-term treatment with levothyroxine at 0.02mg/kg orally every 12 hours for four to six weeks may also increase hair regrowth in select cases.
This localized alopecia occurs at the injection site area after rabies vaccine or injection of long-acting corticosteroids or progestational compounds.
The post-rabies vaccine-induced alopecia most often is associated with an inflammatory panniculitis and/or vasculitis reaction, in addition to alopecia (Photos 3 and 4).
Breeds at risk for the rabies vaccine-associated alopecia include toy or small-breed dogs, especially Poodles, but also Bichon Frises, Shih Tzus, and Yorkshire and Silky Terriers. A hypersensitivity reaction to the subcutaneous injection of the vaccine is thought to be responsible for clinical signs. Signs develop two to four months after vaccination and consist of an alopecic patch at the injection site. Erythema, scaling, skin thickening and hyperpigmentation may develop, and alopecic patches or plaques may enlarge over time.
With the other injection reactions, two to four months after corticosteroid or progestational medication injection, the skin becomes atrophic, thin and hypopigmented, but no inflammation is present.
Photo 4: Close-up view of alopecic patch in Photo 3.
Differential diagnoses include localized demodicosis, dermatophytosis, superficial pyoderma, and alopecic areata. Diagnosis is made by history, clinical signs and histopathology. Histopathology reveals hair follicle, dermal, and adnexal atrophy with the corticosteroid/progestational injection form; and panniculitis, vasculitis, and follicular atrophy with rabies-vaccine-induced alopecia.
Treatment for the non-inflammatory injection reactions is not required.
Hair may take months to a year to regrow, and hair may be lighter or darker than normal when regrown. Surgical excision is curative for dogs with permanent alopecia. Future subcutaneous injections of corticosteroids or progesterone should be avoided in these animals. Treatments used for the rabies-vaccine-induced alopecia include surgical excision, corticosteroids and pentoxifylline (Trental ) which increases microvascular blood flow and decreases cutaneous inflammation.
Alopecia areata is a rare autoimmune disease characterized by non-inflammatory focal alopecia.
The production of autoantibiodies against bulbar hair follicle antigens results in loss of hair, most commonly on the head and neck, but lesions may occur anywhere on the body. Well-circumscribed focal to multi-focal alopecic patches develop that may expand over time.
The skin initially appears normal, but chronically alopecic areas may become hyperpigmented over time. Diagnosis is made by ruling out other causes of non-inflammatory alopecia, and by histopathology. Characteristic histopathologic findings include an accumulation of lymphocytes, histocytes and plasma cells around hair bulbs, described as resembling a "swarm of bees." More advanced lesions consist of follicular atrophy and distortion of hair follicles. No effective therapy is known for this cosmetic disease, and most dogs spontaneously regrow hair in six to 12 months, however, the hair may initially regrow as a lighter color. Corticosteroid therapy, either systemic or intralesional, as used in humans with alopecia areata, is usually ineffective in dogs.
Photo 5: Black hair follicle dysplasia in a mixed-breed dog. Note alopecia restricted to black-haired areas only.
Follicular dysplasia is an uncommon genetic cause of poor haircoat quality and alopecia recognized in certain breeds.
Doberman Pinschers (blue and fawn colors are most common but also seen in red and black dogs), Rottweilers, Siberian Huskies, Irish Water Spaniels, Portuguese Water Dogs, Curly-coated Retrievers, German Shorthaired Pointers, Chesapeake Bay Retrievers and German Wirehaired Pointers are predisposed to the development of this hair follicle disorder, but other breeds may be affected. The cause is unknown.
The condition begins gradually during the first three years of age with deterioration in haircoat quality. A "moth-eaten" or patchy pattern of hair loss that begins on the trunk occurs, often with dry scaling and changes in coat color in affected areas. The coat may take on a frizzy, woolly or puppy-like appearance due to loss of primary hairs. The head and legs are least affected. Pruritus is rare, unless secondary infection is present. The disease often waxes and wanes for months, but eventually the alopecia progresses and becomes widespread. Bilaterally symmetric alopecia of the trunk may occur in severe cases.
Diagnosis is by ruling out endrocrinopathies such as hypothyroidism, hyperadrenocorticism, and sex hormone imbalances, and by skin biopsy. Dermatohistopathology reveals one or more of the following abnormalities: distortion of hair follicles, hair shafts, and/or hair bulbs, a predominance of catagen or telogen follicles, follicular hyperkeratosis and macromelanosomes. Treatment involves antibiotics to treat secondary pyoderma, mild antiseborrheic or antibacterial shampoos and conditioners, moisturizing humectant rinses/sprays, melatonin, and retinoids (synthetic vitamin A derivatives) such as acitretin (Soriatane ). Treatment improves skin condition and may stimulate temporary fine hair regrowth, but in most cases alopecia is progressive and usually permanent. Affected dogs should not be bred.
Color dilution alopecia (CDA) is a form of hereditary adult-onset follicular dysplasia most commonly seen in blue and fawn Doberman Pinschers. CDA has also been reported in blue and fawn Miniature Pinschers, Irish Setters, Dachshunds, Chow Chows, Poodles, Great Danes, Whippets, Yorkshire Terriers, Chihuahuas, Italian Greyhounds, Salukis, Newfoundlands, Shetland Sheepdogs, Schipperkes and mixed-breed dogs. CDA is caused by abnormal melatonin distribution in hair shafts and a structural defect in hair growth. Dogs with CDA are born with normal skin and hair coats. The disease begins between 1-3 years of age with broken hairs (stubble alopecia) complicated by scaling, papules, and pustules that usually begin over the lower back and flanks in areas of dilute coat color. Tan points are normal. The trunk is most affected, with the head and legs much less involved. CDA is usually non-pruritic; however, recurrent pyoderma is common and may lead to pruritus if widespread. CDA may progress to complete permanent alopecia of all dilute-colored areas by middle age.
Photo 6: Follicular lipidosis in a Rottweiler. Note thinning of tan hairs on face, while black hairs are spared.
Diagnosis is made by microscopic evaluation of hair (trichogram) which shows large melanin granules (macro-melanosomes) and bulges within the hair shafts, and dermatohistopathology, which reveals dilated, cystic keratin-filled hair follicles and melanin clumps in epidermal and follicular basal cells and hair shafts. Treatment is lifelong and similar to that of follicular dysplasia. Dogs with color dilution alopecia should not be used for breeding.
Black hair follicular dysplasia is another related form of canine follicular dysplasia where dogs with bi-or tri-colored coats lose hairs in black areas only at a young age (Photo 5). Puppies appear normal at birth, but by 1 month of age begin losing black hairs only, progressing until all of these hairs are lost by 8-9 months of age. The skin is scaly in alopecic areas. A genetic defect in melanin transfer and hair shaft formation is thought to be involved.
Diagnosis is made by clinical signs and dermatohistopathology, which is similar to color dilution alopecia in black-haired areas, and normal in non-black-haired skin. Treatment is not necessary as this is a cosmetic problem only.
Follicular lipidosis of Rottweilers (Photo 6) is a rare localized follicular dysplasia that causes loss of hair over the tan points of the face and legs. Black hairs and tan points in other areas are normal. Clinical signs occur over the first 9 months of age. Histopathology reveals lipid swelling of the hair matrix cells and growing (anagen) hair follicles. Spontaneous hair regrowth is possible, or the alopecia may persist, but remains restricted to the above areas.
Focal alopecia can be a sign of parasitic, allergic, infectious, hormonal, metabolic, congenital/genetic, or neoplastic disease. All dogs with localized alopecia should be examined promptly to determine the underlying cause so that specific treatment can be prescribed if necessary. Often skin biopsy for histopathology is needed for definitive diagnosis. Clients should be discouraged from using home remedies and human hair-loss medications, as these are ineffective and can be toxic. For example, minoxidil or Rogaine can cause cardiac disease, weakness, lethargy, and collapse in dogs. Breeding of dogs with genetic causes of alopecia should be avoided.