Approach to Keratinization Disorders in Small Animal
World Small Animal Veterinary Association World Congress Proceedings, 2015
Alberto Martin Cordero1, DVM
1VETDERM: Dermatologia Veterinaria Especializada, Guadalajara, Mexico

Dr. Alberto Martin Cordero received the degree of Doctor in Veterinary Medicine by the University of Guadalajara. He studied Veterinary Dermatology in the European School for Advanced Veterinary Studies, University of Luxembourg. He is a member of the American Academy of Veterinary Dermatology and a founder member of the Latin American Society of Veterinary Dermatology. Is an assistant professor in University of Guadalajara, Department of Veterinary Medicine. He has been a speaker in numerous conferences in Mexico, Latin America and Eastern Europe; and presented articles and clinical cases in Latin America, USA, and Europe. He has been a coordinator in videotoscopy wetlabs and dermatology workshops. He is the coordinator of the dermatology program in Leon Conference (CVDL), currently the second largest veterinary meeting in the world. Dr. Alberto has published articles and clinical cases national and international. He works in private practice and it is the owner of VETDERM: the first veterinary dermatology referral practice the west of Mexico. He has realized visits in the Animal Dermatology Clinics in Southern California and in the Ludwig Maximilian University in Munich and Colorado State University.

Keratinization disorders are conditions that affect skin's surface appearance. Epidermis in mammals is constantly being replaced by new cells that transform from the bottom layer of the epidermis up to the stratum corneum.

Cells from deepest layers of the epidermis are nucleated and cubed shape; as cells start to emerge and transform themselves into upper layer cells, they lose their nuclei and the shape become more squamous until they are part of the stratum corneum and they are finally eliminated as dead cells. This process that occurs every 22 days in mammals is named epidermal turnover.

When the epidermal turnover time is decreased, eliminated cells become noticeable and sloughed cells are observed and become obvious. There are many causes of keratinization defects and they produce clinical signs by altering proliferation, differentiation, desquamation or combination between. Other changes are characterized by alteration in epidermal lipid formation and deposition.

Follicular casts are accumulations of keratin and follicular material that adheres to the hair shaft extending above the surface of the follicular ostia. Essentially this is scaling of the hair follicle that apparently is associated with failure to desquamate or exfoliate away from the hair shaft. It is a primary lesion in vitamin A-responsive dermatoses, primary seborrhea, and sebaceous adenitis. Follicular casts may be secondary lesions in demodectic mange, dermatophytosis and pyoderma.

Due to the high number of differential diagnosis associated with keratinization disorders a systematic clinical approach is needed.

History taking is very important to identify primary lesions, age of onset, evidence of pruritus, initial clinical signs. Physical examination will allow the clinician identify extension and type of lesions present. We must be aware that some of the lesions found in the patient may be the result of other primary lesions not observed in the moment of examination.

Pruritic seborrheic conditions include ectoparasites (Demodex, Notoedres, Cheyletiella, flea related conditions, Sarcoptes) allergies, infectious agents (staphylococcal pyoderma and Malassezia) and neoplastic conditions as epitheliotrophic lymphoma that may be present with erythroderma (combination of erythema, pruritus and scaling).

Skin scraping and cytology are two of the main tools we may use to rule out pruritic conditions. However, infectious agents like bacteria and yeast are secondary agents to other dermatosis, so in these cases we must identify the underlying cause in order to control secondary infection.

Non pruritic seborrhoea conditions include hormonal dermatosis (sex hormone, hypothyroidism and hyperadrenocorticism) ectoparasites (initial phase Demodex and Cheyletiella), immune mediated (pemphigus and lupus complex, drug eruption) infectious (distemper, FLV, FIV, Leishmania), metabolic (hepatocutaneous syndrome, liver and renal disease), paraneoplastic (thymoma), epitheliotrophic lymphoma may be present without pruritus.

Non pruritic seborrhoea may become pruritic where secondary infections become evident. Hypothyroid dogs may be pruritic if Malassezia proliferation occurs especially in keratoseborrheic patients. Even if the condition is evident secondary infections must be ruled out and controlled.

Hormonal dermatosis cause systemic signs and CBC or biochemistry alterations, these must be used as clues for the diagnostic approach.

Histopathology must be interpreted according to patients clinical findings to avoid misdiagnose. Biopsy samples must be submitted to the pathologist adding clinical information.

There are primary scaling conditions and some are breed related. Some of the scaling conditions are related to cornification disorders. Primary seborrhea in Cocker Spaniels, vitamin A responsive dermatosis, nasodigital hyperkeratosis in Labrador Retriever and Golden Retriever, Schnauzer comedo syndrome. Ichthyosis has been described in Labradors and other breeds.

Certain breeds have been described as developing primary idiopathic seborrhea and it is considered to be more common in the American Cocker Spaniel, English Springer Spaniel, West Highland White Terrier and Basset Hound. Other breeds described as having it also include the Irish Setter, Doberman Pinscher, Chinese Shar Pei, Dachshund, Labrador Retriever and German Shepherd dog.

Most of the conditions before mentioned have a genetic factor and are more characteristics in some breeds.

Other conditions related to nutritional and metabolic factors may be breed related. Zinc responsive dermatosis is more common in Nordic breeds, and lethal acrodermatitis in bull terrier.

Autoimmune and immune mediated conditions must be differentiated according to histopathology and clinical findings. One of the most common immune mediated keratinization disorder is sebaceous adenitis. In this conditions sebaceous glands are destroyed by an immune mediated process causing seborrhea in the dorsal region with subsequent alopecia that may progress to the trunk and distal extremities.


Dogs and cats may both develop a disease referred to as acne. There is little to no work suggesting canine or feline acne has similarities to human acne. In humans acne is a complex disease and there is a role played by hormones, diet, the bacteria Propionibacterium acnes, sebaceous glands, and possible keratinocyte activation.

Topical therapy for keratoseborrheic conditions is essential. Antiseborrheic shampoos are used to restore and normalize keratinocyte turnover. A cytostatic effect is exerted on basal cells, thereby reducing their rate of division (keratoplastic). Most antiseborrheic shampoos also eliminate excess corneal layers, by increasing desquamation. This is thought to be a result of ballooning of corneocytes that makes the stratum corneum softer and reduces the intercellular cohesion of the corneocytes and results in increased desquamation. Agents that function in this way are called keratolytic. There are many keratoplastic and keratolytic agents that are commercially available in shampoo formulations.

Moisturizing shampoos that are used for allergic skin disease management can also be used in mild dryer forms of keratinization defects. These function primarily by increasing the moisture content of the skin, with many products also having emollient effects. Salicylic acid, sulfur, selenium sulfide and zinc gluconate are the most common substances in shampoos used to regulate cornification.

Tar is a keratoplastic (cytostatic) agent. It reduces nuclear synthesis in the epidermal basal layers. It is also antiseptic and antipruritic. There are many different sources and varieties of this active agent. Tar shampoos are contraindicated in the cat. Benzoyl peroxide in addition to being antibacterial is antiseborrheic, by hydrolyzing sebum and reducing sebaceous gland activity.

Benzoyl peroxide exerts a follicular flushing action, which is very useful when treating comedone disorders and/or follicular hyperkeratosis. Irritant side effects have been reported especially in concentrations above 5%, the author prefers to avoid this shampoo in atopic patients unless seborrhea is severe.

A new group of products containing phytosphingosine (PS) have been used for a few years with success (DOUXO, Sogeval) for use in seborrheic conditions. PS is a key molecule in the natural defense mechanism of the skin and is a major component of ceramides.

Cyclosporine has recently been used in certain keratinization defects, is the treatment of choice for sebaceous adenitis at a long term management. I products have essential fatty acids, moisturizing and emollient agents to replace loss of essential fatty acids and to restore proper hydration to the epidermis.

Essential oils spot on are used as well to hydrate the skin and have demonstrate to have effect in keratoseborrheic patients in anecdotal reports Essential 6 spot on (Dermoscent, France).

Allerderm spot on (Virbac, France) are spot on ceramides that may help reducing scaling in some patients. These products are more focused in restoring epidermal barrier.

Approach to keratinization disorders require clinical examination and history taking as the prelude to diagnostic test. In order to unveil the correct diagnosis we must rule out and control secondary factors that may mimic pruritic conditions and may mislead us to and incorrect diagnosis.


1.  Carlotti DN, Bensignor E. Management of keratoseborrheic disorders. The European Journal of Companion Animal Practice. 2002;12:123–133.

2.  Kwochka KW. Symptomatic topical therapy of scaling disorders. In: Griffin CE, Kwochka KW, Mac Donald JM, eds. Current Veterinary Dermatology. St, Louis, MO: Mosby Year Book; 1993:191–202.

3.  Kwochka KW. Keratinization abnormalities: understanding the mechanism of scale formation. In: Ihrke PJ, Mason IS, White SD, eds. Advances in Veterinary Dermatology. Volume 2. New York, NY: Pergamon Press; 1993:91–111.

4.  Scott DW, Miller WH, Jr, Griffin CE. Muller and Kirk's Small Animal Dermatology. 6 edition. Philadelphia, PA: W.B. Saunders; 2001.


Speaker Information
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Alberto Martin Cordero, DVM
VETDERM: Dermatologia Veterinaria Especializada
Guadalajara, Mexico

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