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.
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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. 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. 
Photo 2: Post-clipping alopecia. Note lack of hair regrowth six months after surgery.
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Pinnal alopecia 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 �� 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. Pattern baldness 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.
Traction alopecia 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 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.
Photo 3: Miniature poodle with hyperpigmented, inflamed alopecic patch due to rabies-vaccine-induced alopecia and vasculitis.
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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. 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.
Post-injection alopecia 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.
Photo 4: Close-up view of alopecic patch in Photo 3.
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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. 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 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.
Photo 5: Black hair follicle dysplasia in a mixed-breed dog. Note alopecia restricted to black-haired areas only.
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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. Follicular dysplasia 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.
Photo 6: Follicular lipidosis in a Rottweiler. Note thinning of tan hairs on face, while black hairs are spared.
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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. 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.
Conclusion 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.
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