Hyperplastic and Seborrheic Syndromes in Animals

Many anomalies affect keratinization; some are associated with hereditary hypotrichoses, whereas others are associated with systemic metabolic derangements. Those for which none of these associations has yet been made are a diverse group of syndromes that may affect localized parts of the epithelium or that may be generalized. Among the latter are the poorly characterized congenital or familial seborrheic syndromes, the best known of which is idiopathic seborrhea of Spaniels and idiopathic facial dermatitis of Persian cats. Hereditary congenital follicular parakeratosis is a syndrome of female Rottweilers and Siberian Huskies. It is a severe keratinization defect associated with various noncutaneous abnormalities.

Cutaneous ichthyoses are characterized by abnormal and hypertrophic epithelial proliferation, with accumulation of extensive scale and hyperkeratosis on the skin surface. Cases have been described mostly in cattle and dogs, but chicken and several mouse models are also known, and there is one report in a llama. In cattle, the severity varies; some forms are lethal shortly after birth. Affected breeds include Red Poll, Friesian, Holstein, Brown Swiss, Pinzgauer, and Chianina.

Canine ichthyosiform dermatoses are also heterogeneous and occur sporadically in a number of dog breeds, including Doberman Pinschers, Rottweilers, Irish Setters, Collies, English Springer Spaniels, Cavalier King Charles Spaniels, Golden Retrievers, Labrador Retrievers, American Bulldogs, and terriers (including Parson Russell Terriers). There is some evidence of a familial inheritance pattern in Parson Russell Terriers and Golden Retrievers. It is now known to be an autosomal recessive gene mutation in PNPLA1. In the American Bulldog the gene mutation has been identified as NIPAL4. In dogs, the body is covered with large adherent scales that may flake off in large sheets. The planum nasale and digital pads may be markedly thickened in some forms; the latter usually is associated with apparent discomfort. Clinical management is difficult, but signs may be ameliorated with keratinolytic shampoos or solutions (eg, selenium disulfides, lactic acid, benzoyl peroxide) and with humectants (eg, lactic acid, urea, propylene glycol, and essential fatty acid preparations). Experimental use of synthetic retinoids has been helpful. Control of secondary pyoderma is frequently required.

Nasal parakeratosis of Labrador Retrievers is a hereditary condition characterized by marked accumulations of thick keratinized material on the dorsal nasal planum. It is associated with a gene mutation in SUV39H2. Diagnosis is based upon clinical signs. This is a longterm condition that can be managed but not cured. Treatment should include emollients.

Psoriasiform-lichenoid dermatosis affects young English Springer Spaniels and is presumed to be genetic. The erythematous, symmetric lesions, which consist of papules and plaques on the pinnae and inguinal region, are covered with scales and become increasingly hyperkeratotic if left untreated. In some affected dogs, the lesions may eventually spread, and the skin is severely greasy. Spontaneous remissions and a waxing and waning course are recorded. Some dogs respond to antibiotic treatment or to synthetic retinoids, but most are refractory to therapy. Cyclosporine therapy has been used with mixed results in some dogs.

Pityriasis rosea of pigs is a familial disease in which the mode of inheritance is not known. Dermatosis vegetans of Landrace pigs is a hereditary, possibly congenital, disorder with an autosomal recessive mode of inheritance. It must be differentiated in the early stages from pityriasis rosea. This is a more serious disease and affects the hooves as well as the skin. Lesions begin as macules and papules and are scaly as in pityriasis rosea. They later become covered with brown-black crusts and are associated with coronitis and hoof deformity. Piglets fail to thrive and eventually develop pneumonia; the disease is not uniformly fatal, but affected survivors are stunted. There is no effective treatment.

Familial footpad hyperkeratosis is reported in Irish Terriers and Dogues de Bordeaux. All pads of all feet are involved from a young age, although the disease is not usually congenital. When hyperkeratosis is severe, horns, fissures, and secondary infection cause pain and lameness. No other skin lesions are present. Treatment is symptomatic, with soaking, keratolytic and emollient treatments, with treatment of bacterial pyoderma. No reports of the use of synthetic retinoids are available. Major differential diagnoses for footpad hyperkeratosis include hepatocutaneous syndrome, a disorder of keratinization, and pemphigus.

Granulomatous sebaceous adenitis is an idiopathic disease that destroys the sebaceous glands and, in some breeds of dogs, is associated with a severe seborrheic and alopecic dermatosis. It is hereditary in Standard Poodles and suspected to be familial in Akitas. It first manifests itself in young adults, but inapparent carriers are known in Poodles. Marked hyperkeratosis precedes development of hair coat abnormalities, which begin as loss of normal hair kinkiness and progress to patchy alopecia. Akitas tend to have more seborrhea oleosa and less alopecia than Poodles. Response to treatment is inconsistent and incomplete. Mildly affected dogs are treated with antiseborrheic shampoos and treatment of pyoderma as needed. Severely affected dogs have benefited from propylene glycol or hot oil treatments. Some dogs respond to oral supplementation with omega-3 fatty acids, and some respond to synthetic retinoids. Spontaneous remission has been recorded. Recently, modified cyclosporine A (5 mg/kg/day, PO) has been very effective in the treatment of many dogs.