title: Dermatoses affecting desmosomes in animals: a mechanistic review of acantholytic blistering skin diseases.
abstract: Failure of desmosomal adhesion with ensuing keratinocyte separation - a phenomenon called acantholysis - can result from genetic, autoimmune or infectious proteolytic causes. Rare hereditary disorders of desmosomal formation have been identified in animals. Familial acantholysis of Angus calves and hereditary suprabasal acantholytic mechanobullous dermatosis of buffaloes appear to be similar to acantholytic epidermolysis bullosa of human beings. A genetic acantholytic dermatosis resembling human Darier disease has been rarely recognized in dogs. In autoimmune blistering dermatoses, circulating autoantibodies bind to the extracellular segments of desmosomal proteins and induce acantholysis. Autoantibodies against desmoglein-3 are found in canine pemphigus vulgaris and paraneoplastic pemphigus. Autoantibodies against desmoglein-1 have been rarely detected in dogs with pemphigus foliaceus. When circulating autoantibodies target desmogleins-1 and -3, mucocutaneous pemphigus vulgaris develops in dogs. Finally, several infectious agents can release proteases that cleave desmosomal bonds. In superficial pustular dermatophytosis of dogs and horses, Trichophyton hyphae colonize the stratum corneum, and acantholysis presumably develops because of proteases secreted by the dermatophytes. In exudative epidermitis of piglets, Staphylococcus bacteria - usually Staphylococcus hyicus- release exfoliatin toxins that bind to and specifically cleave desmoglein-1. Any of the above mechanisms can result in impairment of desmosomal function with subsequent acantholysis. The end point of adhesion failure is identical among these diseases: there is cleft formation where desmosomes are affected. The similarity of mechanisms explains why clinical and microscopic skin lesions overlap between entities, thus leaving clinicians and dermatopathologists with the conundrum of determining whether the acantholysis is of genetic, autoimmune or infectious origin.
authors.affiliation: Department of Clinical Science, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606, USA. thierry_olivry@ncsu.edu
authors.forename: Thierry
authors.initials: T
authors.lastname: Olivry
authors.forename: Keith E
authors.initials: KE
authors.lastname: Linder
mesh_terms: D000818:Animals; D002448:Cell Adhesion; D003881:Dermatomycoses / Q000235:genetics / Q000473:pathology / Q000503:physiopathology / Q000662:veterinary*; D003896:Desmosomes / Q000473:pathology*; D004820:Epidermolysis Bullosa / Q000235:genetics / Q000473:pathology / Q000503:physiopathology / Q000662:veterinary*; D017192:Skin Diseases, Bacterial / Q000235:genetics / Q000473:pathology / Q000503:physiopathology / Q000662:veterinary*