Abstract: This paper reviews the aetiology, pathogenesis and clinical aspects of alopecic dermatosis with a non-hormonal cause.

In the dog, chronic non-pruritic bilateral symmetrical alopecia is typical of hormonal diseases. Other clinical presentations of alopecia may be less extensive, not symmetrical and may show various associated lesions, with a variable pruritus. In the cat, true hormonal alopecia is extremely rare and most cases of alopecia are secondary to other disorders, particularly excessive grooming due to pruritus. The following classification is essentially based on the aetiology of the hair loss.

Suspected or confirmed hereditary alopecias (inherited hair production defects)

1. Feline alopecia universalis (sphinx cat) and feline congenital hypotrichosis (Siamese, Devon rex)

Sphinx cats are appreciated by "amateurs" but hypotrichosis is considered as a defect.

2. Canine alopecic breeds (Chinese crested dog, Xoloitzcuintl)

Again, the peculiar aspect of these dogs is the reason for their selection.

3. Rare inherited congenital canine alopecia

More or less extensive alopecia has been reported in Cocker spaniels, Belgian shepherds, poodles, whippets, beagles, bichons frisés, basset hounds, Labrador retrievers and Irish water spaniels.

4. Pinnal alopecia

This localized non-congenital alopecia has been reported in Yorkshire terriers, Dachshunds, Chihuahuas, whippets and Italian greyhounds. In the Yorkshire terrier, alopecia of the dorsum of the muzzle is often associated. Ear margin seborrhoea reported in Dachshunds and Cocker spaniels may be somehow alopecic. Pinnal alopecia is seen in the Siamese cat.

5. Pattern baldness

This non-congenital alopecia has been reported mainly in Dachshunds, but exists also in Chihuahuas and miniature pinschers. This syndrome affects the ears, ventral neck, chest, abdomen and caudal thighs.

6. Preauricular alopecia

This non congenital feline alopecia is a physiologic condition.

7. Dermatomyositis

This is a hereditary skin and muscle disease, seen in Collies, Shetlands, and Beaucerons (and possibly other breeds as well). The mode of inheritance is believed to be autosomal dominant.

Transient papules and vesicles may be seen. Erosions, ulcers and crusting are much more common. Alopecia is an early sign of the disease which can begin at 6 months of age. Face, bony prominences, ear pinnae, limbs, fingers, tail and footpads are involved. Muscle lesions (lymphocytic myositis) are discrete with mainly temporal and masseter muscles atrophy. Skin biopsy reveals follicular atrophy, perifolliculitis and perifollicular fibrosis, hydropic degeneration of epidermal basal cells with some Civatte bodies and dermo-epidermal clefting. Systemic prednisolone is indicated during acute phases of the disease. Sunlight avoidance and oral vitamin E (100 to 400 mg per day) may be helpful. Pentoxifylline (10 mg/kg TID) might also be effective.

8. Follicular dysplasia

Colour mutant alopecia (CMA) is a hereditary tardive alopecia seen in the blue and fawn mutants of Doberman pinschers, miniature pinschers, Irish setters, Dachshunds, chow-chows, poodles, great Danes, whippets, Yorkshire terriers, Chihuahuas and Italian greyhounds. Black hair follicular dysplasia has been reported in bearded collies, Dachshunds, Schipperke, basset hounds, papillon spaniels, Cocker spaniels, pointers, Gordon setters and mongrels. Both diseases appear a few months after birth. Colour mutant alopecia only appears in the diluted colour areas. In breeds with tan points, these points remain normal and in the one-colour breeds, all the skin is affected. The alopecia is partial and the hair looks dry and dull. Secondary seborrhoea sicca and bacterial folliculitis are common. Black hair follicular dysplasia affects only the black hair coat areas of partially black dogs. The alopecia is partial to subtotal and associated with scaliness. Diagnosis of both conditions is made by assessment of history, physical examination and histopathology which shows mild to moderate epidermal melanosis, orthokeratotic hyperkeratosis, cystic hair follicles and follicular keratosis, variable follicular atrophy and hair dystrophy, prominent clumping of melanin both within and around hair follicles with many melanophages surrounding the base of the follicles and aggregates of melanin in the hair cortex and medulla. Alopecia can be explained, thus, by hypoactive follicles, blockage of follicular orifices and breakage of hair shafts at the site of melanin aggregates. The genetic factors of both diseases are not known but might be identical, since CMA does not seem to be linked to the d allele. The dd genotype could increase the incidence of the disease. Topical antiseborrhoeic therapy is partially effective. Retinoids (acitretin, lmg/kg/day) could be useful.

Other alopecia of this group include follicular dysplasia of Portuguese water dog and other curly coated dogs, follicular dysplasia of Siberian Husky, follicular dysplasia of Weimaraners and above all cyclic (flank) alopecia. The latter, more common in Boxers and Airedale terriers, is linked to photoperiod and reversible. Lesions are well demarcated and hyperpigmented. Diagnosis is based on clinical signs and histopathology which shows primary and secondary follicular hyperkeratosis with a "medusoid" or "octopus" shape. Therapy and prevention with melatonine has been (successfully ?) tried.

Suspected or confirmed hereditary keratinisation defects

Hair follicle is unproductive because of hyperkeratosis.

1. Deficiencies

 EFA deficiency could be a cause of abnormal keratinisation resulting in alopecia. However, true EFA deficiency is rare since most pets are correctly fed nowadays.

 Vitamine A deficiency (vitamin A responsive dermatosis) is mainly seen in Cocker spaniels. Follicular orthokeratotic hyperkeratosis explains alopecia seen in this very seborrhoeic skin disease.

 Zinc deficiency is seen mainly in Nordic breeds. Parakeratotic hyperkeratosis is seen on the surface of the epidermis and inside the hair follicle as well. The latter may explain the hair loss.

2. Ichthyosis

Although a genetic condition, this disease generates alopecia because of hyperkeratosis which affects also the hair follicle rather than by a follicular atrophy.

3. Idiopathic acanthosis nigricans

This condition is seen in the Dachshund and must be differentiated from acanthosis nigricans secondary to allergic skin disease, endocrinopathies, obesity or visceral neoplasia. There is a bilateral alopecia associated to lichenification and hyperpigmentation of the ventral aspect of the body (particularly the axillae) and the face, ear pinnae and limbs. Seborrhoea is usually severe. Hyperplastic superficial dermatitis, epidermal melanosis and pigmentary incontinence are associated to follicular keratosis. The disease may be controlled by topical antiseborrhoeic therapy and long-term low-dose steroid therapy.

4. Idiopathic hyperplastic dermatitis

This rare and controversial condition is probably a hereditary disorder. It is mainly seen in West Highland White Terriers but could also exist in other breeds (Scottish terrier, Wire-haired fox terriers, Newfoundlands). Parakeratotic hyperkeratosis is associated to other histopathological features, such as irregular acanthosis and prominent hyperplasia of basal cell layer. Secondary Malassezia pachydermatis infection is very frequent in West Highland white Terriers, but antifungal therapy is only partially beneficial. Retinoids could be useful in some cases.

Follicular diseases and cicatricial alopecia (follicular destruction)

1. Follicular dermatoses

Follicular dermatoses are caused by demodex, bacteria (mainly Staphylococcus sp.), and dermatophytes. There is a mechanical destruction of the hair by the infectious agent which lives and develops around (demodex, bacteria) or inside and around the hairshaft (dermatophytes). In addition, an inflammatory reaction contributes to the destruction and elimination of hair, particularly in the advanced stages of the disease (cf infra). Alopecia is often nummular and peripherally expanding.

2. Cicatricial alopecia

Cicatricial alopecia (follicular destruction) is seen in:

 Severe inflammation of the skin which leads to destruction of the adnexae (deep pyoderma, intermediate and systemic mycoses).

 Necrotizing diseases of the skin (severe trauma, chemical necrosis, burns, superficial necrolytic dermatitis due to hepatopathy or glucagon secreting pancreatic islet neoplasm, immune-mediated necrotizing skin diseases e.g., erythema multiforme and Lyell's disease).

 Neoplastic processes.

Immunological alopecia

1. Inflammatory alopecia (telogen arrest)

Any inflammatory skin disease may generate a telogen arrest, of unknown mechanism. This process may be extensive (allergies) or more localized such as in folliculitis with peripheral alopecic spots. Inflammation could then decrease the number of hair and thus the development of a pathogen, mainly a dermatophyte.

Perifolliculitis is seen mainly in leishmaniasis and sebaceous adenitis and could also lead to a telogen arrest. Granulomatous perifollicular reaction is very often seen in leishmaniasis. Leishmaniads are not always visible. Alopecia is more or less prominent. The face and ears are frequently involved. Seborrhoea may be severe and hyperkeratosis could contribute to the loss of hair. Sebaceous adenitis is characterized by the destruction of sebaceous glands by a granulomatous reaction, without hair follicle involvement. Lesions are more or less nummular, particularly in short-haired dogs, and seborrhoea may be severe, particularly in long haired dogs (Samoyeds) in which alopecia is less prominent. Alopecia due to chemotherapy and post-clipping alopecia are also due to telogen arrest.

2. Immune-mediated alopecia

 Alopecia areata ("pelade"): This disease, of unknown cause, leads to focal or multifocal areas of non-inflammatory alopecia. Lesions are circumscribed and more frequent on the face. Histopathology shows a lymphoplasmacytic and histiocytic perifolliculitis ("swarm of bees"). No therapy is known but spontaneous healing occurs in a few months.

 Morphea is a localized scleroderma of unknown aetiology characterized clinically by circumscribed lesions of alopecia on the trunk and limbs. Histopathologically, there is a fibrosing dermatitis with a mild lymphohistiocytic reaction. No therapy is known but spontaneous healing occurs in a few weeks.

Self-traumatic alopecia: hair fracture

This form of alopecia is very common in pruritic diseases, such as hypersensitivities and ectoparasitosis. Other lesions are variable (erythema, excoriation, crusts) and alopecia is visible in localized to extensive areas. Self-traumatic alopecia should be differentiated from inflammatory telogen arrest. Good examples are pyotraumatic dermatitis and feline symmetric alopecia. Aetiological and symptomatic antipruritic therapy will control such conditions.

Telogen effluvium = telogen defluxion

In particular circumstances, such as severe disease, postpartum, surgery, a sudden synchronisation of hair follicles in telogen phase may occur. This results in an excessive shedding and alopecia. Shedding is also seen a few weeks later when normal hair growth reoccur (anagen). History is very useful to establish a diagnosis. Trichogram will show mainly "club" (telogen) hair. This condition resolves spontaneously in a few weeks.

Non-hormonal metabolic alopecia in the cat

Feline pancreatic paraneoplastic alopecia is probably non hormonal, and is characterized by a progressive hairloss and a shiny skin due to follicular atrophy and absence of stratum corneum respectively. Prognosis is very poor.

References

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