Abnormal sebaceous gland differentiation in 10 kittens (‘sebaceous gland dysplasia’) associated with generalized hypotrichosis and scaling

Abstract

A rare congenital dermatosis, characterized by progressive hypotrichosis with variable scaling and crusting, occurred in 10 short-haired kittens in North America and Europe. Lesions appeared at between 4 and 12 weeks of age, commencing on the head and becoming generalized. The tail was spared in two kittens. Generalized scaling was mild to moderate, often with prominent follicular casts. Periocular, perioral, pinnal and ear canal crusting was occasionally severe. The skin was thick and wrinkled in two kittens. Histologically, the main lesion was abnormal sebaceous gland morphology. Instead of regular differentiation from basal cells to mature sebocytes, the glands were composed of a haphazard collection of undifferentiated basaloid cells, some partly vacuolated and a few containing eosinophilic globules. Mitotic figures and apoptotic cells were present in an irregularly thickened follicular isthmus. Lymphocytic mural folliculitis and mild sebaceous adenitis were rare. Orthokeratotic hyperkeratosis and follicular casts were present. Hair follicles were of normal density and were mostly in anagen, but some contained malacic hair shafts. Perforating folliculitis, leading to dermal trichogranuloma formation, occurred occasionally. Further biopsy samples taken at 2 years and at 3 and 4 years, respectively, from two kittens revealed similar but often more severe sebaceous gland lesions. Hair follicles were smaller, with many in telogen. The young age of onset suggests a genetic defect interfering with sebaceous and, possibly, follicular development. These lesions are discussed with reference to studies of mouse mutants in which genetic defects in sebaceous differentiation cause a similar phenotype of hyperkeratosis and progressive alopecia.

Alopecia in four kittens caused by abnormal maternal licking behaviour

“…2 Abnormal sebaceous gland differentiation is a rare cause of progressive hypotrichosis with variable scaling and crusting, usually beginning on the head and becoming generalised. 3 In this case, there was evidence of hair regrowth on trichograms and the remaining hair coat of the kittens was normal. The presence of broken hairs and longitudinal splitting on microscopic hair examination suggested intense trauma on the hairs as the main cause of alopecia.…”

“…1 Congenital and hereditary defects, such as congenital hypotrichosis, ectodermal dysplasia and abnormal sebaceous gland differentiation, are rare. 2,3 Grooming plays an important role in feline maternal behaviour, 4 but excessive licking or grooming can lead to alopecia or skin lesions, although typically this behaviour is selfdirected. 5 The aim of this report is to describe a case of alopecia in a litter of kittens caused by abnormal maternal licking behaviour.…”

Scaling dermatosis in three dogs associated with abnormal sebaceous gland differentiation

“…Abnormal sebaceous gland differentiation (‘sebaceous gland dysplasia’) is a rare, poorly understood condition of cats . A few reports indicate that sebaceous gland dysplasia also occurs in dogs, although these cases are not fully described .…”

“…Kittens presented at 4–12 weeks with progressive hair loss, often beginning on the face, and variable degrees of scaling, harsh dry hair coat and hair cast formation. The juvenile onset of this condition suggests a genetic basis, and it is postulated that a genetic defect causes abnormal sebaceous gland development . Histopathologically, sebaceous glands are markedly reduced in size with irregular profiles and are composed of aggregates of haphazardly arranged basaloid epithelial cells and sebocytes .…”

“…The juvenile onset of this condition suggests a genetic basis, and it is postulated that a genetic defect causes abnormal sebaceous gland development . Histopathologically, sebaceous glands are markedly reduced in size with irregular profiles and are composed of aggregates of haphazardly arranged basaloid epithelial cells and sebocytes . The orderly progression from reserve cells to mature sebocytes is lost.…”