Mutations in the Gene Encoding Keratin 16 Cause Footpad Hyperkeratosis in Dogues de Bordeaux

Plassais J, Guaguère E, Lagoutte L, et al. A spontaneous KRT16 mutation in a dog breed: a model for human focal nonepidermolytic palmoplantar keratoderma (FNEPPK). J Invest Dermatol 2015; 135: 1187-1190. (Link to Pubmed). 

PubMed ID (PMID): 25521457

Reprints: Catherine André

Comments: The Dogue de Bordeaux breed has been long known for being predisposed to the development of a hereditary footpad hyperkeratosis. This paper reveals a lack of expression of keratin 16 in suprabasal footpad keratinocytes in affected dogs. Furthermore,  the authors detected a 1 base pair insertion in the KRT16 gene, which resulted in a truncation of keratin 16 due to the loss of the last 85 aminoacids. All affected dogs were found to be homozygotes for the mutated allele; carrier dogs that were heterozygous for the mutation did not exhibit any clinical signs, as is usually the case for the rare autosomal recessive keratinopathies.

Recommended by: Thierry Olivry, NC State University, Raleigh, North Carolina, USA

The Histopathology of Toxic Epidermal Necrolysis in Dogs is not What you Think!

Banovic F, Olivry T, Dazzle L, Tobias JR, Atlee B, Zabel S, Hensel N, Linder KE. Clinical and microscopic characteristics of canine toxic epidermal necrolysis. Vet Pathol 2015; 52: 321-330. Abstract. 

PubMed ID (PMID): 24907312

Reprints: Keith Linder

Comments: Traditionally, lesions associated with epidermal necrosis without dermal inflammation have been given the diagnosis of toxic epidermal necrolysis (TEN) while those exhibiting lymphocyte-mediated keratinocyte apoptosis at multiple epidermal levels are deemed representative of erythema multiforme (EM). This study shows that, using biopsy material of three dogs with TEN, "EM-like" keratinocyte apoptosis also occurs in canine TEN, as it does for the human disease. As a result, histopathology cannot (and should not) be used for accurately differentiating canine EM and TEN! As for many other diseases, the diagnosis should be made instead from collating information from the history, clinical signs and histopathology.

Recommended by: Thierry Olivry, NC State University, Raleigh, North Carolina, USA