Equine herpesvirus 1-associated ulcerative dermatitis in a horse.

This case report describes the clinical and histopathological findings of an infection caused by equine herpesvirus-1 (EHV-1) in a horse showing respiratory signs and a papular, crusted and ulcerative dermatitis involving mucosae. This diagnosis was supported by real-time PCR positive for EHV-1 on nasal swabs and tissues.

Cet article décrit les données cliniques et histopathologiques d'une infection due à EHV-1 (equine herpesvirus - 1) chez un cheval présentant des signes respiratoires et une dermatite papuleuse, croûteuse et ulcérative s'étendant aux muqueuses. Le diagnostic a été supporté par une PCR en temps réel positive pour EHV-1 sur tissus et écouvillon nasal. Dieser Fallbericht beschreibt die klinischen und histopathologischen Befunde einer Infektion durch das equine Herpesvirus-1 (EHV-1) bei einem Pferd, welches respiratorische Zeichen zeigte und eine papulöse, krustige und ulzerative Dermatitis, von der auch die Schleimhäute betroffen waren. Die Diagnose wurde durch eine Real-time PCR Untersuchung, die an Tupfern aus der Nase und aus Gewebe positiv auf EHV-1 verlief, unterstützt.

Este informe de caso describe los hallazgos clínicos e histopatológicos de una infección causada por herpesvirus equino tipo-1 (EHV-1) en un caballo que mostraba signos respiratorios y una dermatitis papular, con costras y ulceras afectando las mucosas. Este diagnóstico fue corroborado por una PCR en tiempo real positiva para EHV-1 en hisopos nasales y tejidos.

Este relato de caso descreve os achados clínicos e histopatológicos de uma infecção causada por herpesvírus equino tipo-1 (EHV-1) em um cavalo que apresentou sinais respiratórios e dermatite papular, crostosa e ulcerativa envolvendo mucosas. Este diagnóstico foi confirmado por PCR em tempo real positivo para EHV-1 em swabs nasais e tecidos.

Bacterial microbiota and proinflammatory cytokines in the anal sacs of treated and untreated atopic dogs: Comparison with a healthy control group.

The pathogenesis of anal sacculitis has not been extensively investigated, although atopic dogs seem to be predisposed to the disease. The aim of this study was therefore to characterize and compare the bacterial microbiota and pro-inflammatory cytokines in the anal sacs of dogs from three groups (healthy dogs, untreated atopic dogs and atopic dogs receiving antipruritic treatment or allergen-specific immunotherapy) in order to determine whether changes could be at the origin of anal sacculitis in atopic dogs. Bacterial populations of anal sac secretions from fifteen healthy dogs, fourteen untreated and six treated atopic dogs were characterized by sequencing the V4 region of the 16S rRNA gene using Illumina technology. Proinflammatory cytokines were analyzed with the Luminex multiplex test. Community membership and structure were significantly different between the anal sacs of healthy and untreated atopic dogs (P = 0.002 and P = 0.003, respectively) and between those of untreated and treated atopic dogs (P = 0.012 and P = 0.017, respectively). However, the community structure was similar in healthy and treated atopic dogs (P = 0.332). Among the proinflammatory cytokines assessed, there was no significant difference between groups, except for interleukin 8 which was higher in the anal sacs of untreated atopic dogs compared to treated atopic dogs (P = 0.02), and tumor necrosis factor-alpha which was lower in the anal sacs of healthy dogs compared to treated atopic dogs (P = 0.04). These results reveal a dysbiosis in the anal sacs of atopic dogs, which may partially explain the predisposition of atopic dogs to develop bacterial anal sacculitis. Treatments received by atopic dogs (oclacitinib, desloratadine and allergen-specific immunotherapy) shift the microbiota of the anal sacs towards that of healthy dogs. Further studies are required to identify significant cytokines contributing to anal sacculitis in atopic dogs.