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.

Metaflumizone–amitraz (Promeris)‐associated pustular acantholytic dermatitis in 22 dogs: evidence suggests contact drug‐triggered pemphigus foliaceus

“…Distinct and consistent differences in the histopathology of PAPLR and AIPF were not identified, and the shared morphological features in these two conditions support shared mechanisms of pathogenesis. Importantly, histology alone is not considered sufficient to render a specific diagnosis of PAPLR, and clinical lesion location and history of PD application are required to differentiate PAPLR from other acantholytic pustular dermatitis reactions in the dog, including AIPF, exfoliative superficial pyoderma and pustular dermatophytosis 25 . Only one case exhibited noticeable apoptosis of keratinocytes at multiple levels of the epidermis with lymphocytic and histiocytic satellitosis; while this pattern is classically attributed to ADRs in humans and animals, this change was not a consistent feature in this case series.…”

“…Paraffin‐embedded blocks or 10 unstained paraffin sections of previously collected skin biopsies of all selected PAPLR were obtained from diagnostic pathology laboratories. Sections were stained routinely with haematoxylin and eosin, while periodic acid–Schiff (PAS) and Gram stains were also done to rule out postinfectious acantholytic pustular dermatoses due to fungal and bacterial pathogens, respectively 25 . Microscopic skin lesions were evaluated for any epidermal, adnexal and dermal changes.…”

Deficient Plakophilin-1 Expression Due to a Mutation in PKP1 Causes Ectodermal Dysplasia-Skin Fragility Syndrome in Chesapeake Bay Retriever Dogs

“…A disease similar to human acantholytic EB has so far been described only in cattle: the so-called “familial acantholysis” was first reported in Angus calves nearly 30 years ago [13], while “hereditary suprabasal acantholytic mechanobullous dermatosis” was seen more recently in Brazilian Murrah buffaloes [14]. A third occurrence of a similar phenotype was described briefly in Texas Brangus calves (cited in [15]). In none of these examples, however, has the genetic cause of acantholytic EB been determined.…”

Descripción clínica, histológica e histoquímica del pénfigo foliáceo equino: un reporte de caso

“…Monteiro et al (2008), manifestaron que el pénfigo foliáceo pertenece a un grupo de enfermedades llamadas "roído de polilla", que se caracterizan por placas o máculas con diferentes grados de alopecias, así como por áreas descamativas, eritematosas e hipercrómicas, distribuidas en cara, tronco, miembros y región cervical, pudiendo estar asociada a diferentes afecciones (acariasis, dermatofilosis, dermatofitosis, foliculitis bacterianas, hipersensibilidad a picada de insectos y desequilibrio nutricional), resaltando la importancia del diagnóstico definitivo en el presente estudio, por ser fundamental para la escogencia del tratamiento adecuado. Las manifestaciones clínicas concordaron con las reportadas por Vandenabeele et al (2004), Zabel et al (2005), Olivry (2006), Monteiro et al (2007), Oliveira et al (2007), Monteiro et al (2008), Olivry & Linder (2009 Oliveira et al (2007). De igual forma, los hallazgos histopatológicos en la tinción de HE coinciden con los reportados por Monteiro et al (2007) y Oliveira et al (2007, siendo la acantolisis la expresión diagnóstica más importante, es así como Olivry y Linder (2009), manifiestan que los equinos con PF presentan anticuerpos contra las moléculas de adhesión en la superficie de los queratinocitos, llevando a la perdida de la conexión intracelular y acantolisis, así mismo Vandenabeele et al (2004) y Zabel et al (2005, indican que los queratinocitos acantoliticos pueden ser observados en los exámenes citológicos e histológicos de las lesiones pustulares o costrosas.…”