Hyperkeratotic erythema multiforme variant in 17 dogs.

BACKGROUND: A new canine subgroup defined as 'old-dog' or 'hyperkeratotic' erythema multiforme (HKEM) with marked hyperkeratosis and parakeratosis has been proposed without any detailed description of larger case series. OBJECTIVES: We report herein the signalment, clinical signs, treatment outcome, and histopathological and immunological findings in 17 dogs with HKEM. ANIMALS: Inclusion criteria were the presence of (i) scaly skin lesions with or without crusting; and (ii) microscopic lesions typical of EM (i.e. a panepidermal cytotoxic lymphocytic dermatitis with or without basal keratinocyte apoptosis); and (iii) microscopic ortho- and/or parakeratotic hyperkeratosis affecting the interfollicular epidermis. MATERIALS AND METHODS: Clinical questionnaires and skin biopsies were reviewed. Polymerase chain reactions for epidermotropic viruses and direct immunofluorescence were performed. RESULTS: Various breeds were affected with an over-representation of males in their mid-to-late adulthood (median age 9 years). Generalised skin lesions included multifocal-to-coalescing, linear and annular macules and plaques with erythema and adherent firm crusting. Microscopic lesions were specific for EM and featured prominent superficial epidermal apoptosis with lymphocytic satellitosis and parakeratosis. No drug triggers were identified. Polymerase chain reactions for canine herpesvirus polymerase gene, canine parvovirus and canine distemper virus were negative in all HKEM and canine erosive EM (15 dogs) biopsies. Lesions failed to respond to oral and/or topical antimicrobials. Complete remission of signs was achieved in 9 of 17 dogs (53%) using immunosuppressive regimens. CONCLUSIONS AND CLINICAL RELEVANCE: Hyperkeratotic erythema multiforme (HKEM) is a chronic, persistent and clinically distinctive erythema multiforme (EM) variant that differs from 'classic' vesiculobullous erosive-to-ulcerative EM in dogs.

A randomised controlled trial testing the rebound-preventing benefit of four days of prednisolone during the induction of oclacitinib therapy in dogs with atopic dermatitis.

BACKGROUND: A rebound of pruritus occasionally occurs after oclacitinib dose reduction in dogs with atopic dermatitis (AD). OBJECTIVES: To determine whether an initial 4-day course of prednisolone decreases the probability of a pruritus rebound after reducing the frequency of oclacitinib administration. ANIMALS: Forty dogs with mild-to-moderate AD lesions and moderate-to-severe pruritus. MATERIALS AND METHODS: Dogs were randomised to receive oclacitinib at 0.4-0.6 mg/kg twice daily for 14 days then once daily, alone or with prednisolone at 0.5 mg/kg, orally, twice daily for the first 4 days. Clinicians graded the Canine Atopic Dermatitis Extent and Severity Index (CADESI)4 and 2D-investigator global assessment (IGA) before and after 28 days; owners assessed the pruritis Visual Analog Scale (PVAS)10 and Owner Global Assessment of Treatment Efficacy (OGATE) on Day (D)0, D4, D14, D21 and D28. We considered a rebound any increase greater than one PVAS10 grade at D21 compared to D14. RESULTS: On D21, there were significantly fewer rebounds in the dogs receiving prednisolone (three of 20, 15%) compared to those given oclacitinib alone (nine of 20, 45%; Fisher's test, p = 0.041). Compared to oclacitinib monotherapy, the concurrent administration of prednisolone for the first 4 days led to significantly lower PVAS10 on D4 and D28, CADESI4 and 2D-IGA on D28, and OGATE on D21 and D28 (Wilcoxon-Mann-Whitney U-tests). Adverse effects of therapy were minor, intermittent and self-resolving. CONCLUSIONS AND CLINICAL RELEVANCE: The initial addition of 4 days of prednisolone significantly decreased the probability of a rebound of pruritus 1 week after oclacitinib dose reduction. This short concomitant glucocorticoid administration led to a higher skin lesion improvement and improved perception of treatment efficacy with minimal adverse effects.

Western blot analysis of sera from dogs with suspected food allergy.

BACKGROUND: Food allergy is often suspected in dogs with clinical signs of atopic dermatitis. This diagnosis is confirmed with an elimination diet and a subsequent challenge with regular food. Laboratory tests for the diagnosis of food allergy in dogs are unreliable and/or technically difficult. Cyno-DIAL® is a Western blot method that might assist with the selection of an appropriate elimination diet. HYPOTHESIS/OBJECTIVES: To evaluate the performance of Cyno-DIAL® for the selection of an elimination diet and diagnosis of food allergy. ANIMALS/METHODS: Thirty eight dogs with atopic dermatitis completed an elimination diet. Combining the results of the diet trials and the challenges, 14 dogs were classified as food allergic (FA), 22 as nonfood-allergic and two as ambiguous cases. RESULTS: Amongst all dogs and amongst dogs with a clinical diagnosis of FA, 3% and 7% (respectively) were positive to Royal Canin Anallergenic® , Vet-Concept Kanguru® or Vet-Concept Dog Sana® ; 8% and 7% to Hill's d/d Duck and Rice® ; 8% and 21% to Hill's z/d Ultra Allergen Free® ; 53% and 64% to Eukanuba Dermatosis FP® ; and 32% and 43% to a home-cooked diet of horse meat, potatoes and zucchini. The specificity and sensitivity of Cyno-DIAL® for diagnosing food allergy were 73% and 71%, respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: Although Cyno-DIAL® was considered potentially useful for identifying appropriate foods for elimination diet trials, it cannot be recommended for the diagnosis of food allergy. The Cyno-DIAL® test performed better than some previously evaluated ELISA-based tests.

Establishment of diagnostic criteria for feline nonflea-induced hypersensitivity dermatitis.

Hypersensitivity dermatitides (HD) are commonly seen in cats, and they are usually caused by environmental, food and/or flea allergens. Affected cats normally present with one of the following clinical reaction patterns: head and neck excoriations, usually symmetrical self-induced alopecia, eosinophilic skin lesions or miliary dermatitis. Importantly, none of these clinical presentations is considered to be pathognomonic for HD skin diseases, and the diagnosis of HD is usually based on the exclusion of other pruritic diseases and on a positive response to therapy. The objectives of this study were to propose sets of criteria for the diagnosis of nonflea-induced HD (NFHD). We recruited 501 cats with pruritus and skin lesions and compared clinical parameters between cats with NFHD (encompassing those with nonflea, nonfood HD and those with food HD), flea HD and other pruritic conditions. Using simulated annealing techniques, we established two sets of proposed criteria for the following two different clinical situations: (i) the diagnosis of NFHD in a population of pruritic cats; and (ii) the diagnosis of NFHD after exclusion of cats with flea HD. These criteria sets were associated with good sensitivity and specificity and may be useful for homogeneity of enrolment in clinical trials and to evaluate the probability of diagnosis of NFHD in clinical practice. Finally, these criteria were not useful to differentiate cats with NFHD from those with food HD.

Masitinib decreases signs of canine atopic dermatitis: a multicentre, randomized, double-blind, placebo-controlled phase 3 trial.

This study investigated the efficacy and safety of masitinib, a selective tyrosine kinase inhibitor capable of downregulating mast cell functions, for treatment of canine atopic dermatitis (CAD). Dogs with confirmed CAD received masitinib at 12.5 mg/kg/day (n = 202) or control (n = 104) for 12 weeks. A reduction in CAD Extent and Severity Index (CADESI-02) score of ≥ 50% at week 12 was observed in 61% of masitinib-treated dogs versus 35% of control dogs (P < 0.001), according to the modified intent-to-treat population. For dogs resistant to ciclosporin and/or corticosteroids (60% of the study population), CADESI-02 response rates were 60 versus 31%, respectively (P = 0.004). The mean reduction in pruritus score of severely pruritic dogs was 46 versus 29%, respectively (P = 0.045). Furthermore, 65% of owners with severely pruritic dogs assessed masitinib efficacy as good/excellent versus 35% control (P = 0.05). Overall, 63% of investigators assessed masitinib efficacy as good/excellent versus 35% control (P < 0.001). Premature discontinuations from the modified intent-to-treat population (28.2% masitinib versus 26.0% control) were mainly due to adverse events (13.4 versus 4.8%, respectively) or lack of efficacy (12.4 versus 18.3%, respectively). In total, 13.2% dogs presented with severe adverse events (16.0% masitinib versus 7.7% control). Masitinib showed a risk of reversible protein loss, although regular surveillance of blood albumin and proteinuria allowed for discontinuation of treatment while the dog was still clinically asymptomatic. Masitinib proved to be an effective and mostly well-tolerated treatment of CAD, including severe and refractory cases, with medically manageable adverse effects.

Clinical characteristics and causes of pruritus in cats: a multicentre study on feline hypersensitivity-associated dermatoses.

Hypersensitivity dermatitides (HD) are often suspected in cats. Cats with HD are reported to present with one or more of the following patterns: miliary dermatitis, eosinophilic dermatitis, self-induced symmetrical alopecia or head and/or neck excoriations. Previous reports on feline HD included small numbers of animals, took place in geographically restricted areas or did not compare these conditions with other causes of pruritus. The goal of the present study was to analyse 72 parameters covering signalment, clinical, laboratory and treatment characteristics from a large group of pruritic cats from different geographical areas. Of the 502 cats, the following diagnoses were made: flea HD (29% of cases), food HD (12%) nonflea/nonfood HD (20%) and other diseases in which pruritus was a feature (24%). Cats with signs consistent with a HD but which did not complete a food trial were not analysed further (15% of cases). Most cats with nonflea HD exhibited signs compatible with one or more of the four typical lesional patterns, but none of these patterns was found to be pathognomonic for any specific diagnosis. Food HD and nonflea/nonfood HD were found to be clinically undistinguishable. Young adult, purebred and female cats appeared predisposed to nonflea/nonfood HD. As many diagnoses presented with similar lesional patterns, a thorough clinical work-up is required for establishment of a specific diagnosis.

Follicular dysplasia in five Weimaraners.

This study evaluated the clinical and histopathological features and results of light and electron scanning microscopy assessments of follicular dysplasia in five Weimar Pointers. The data were compared with those obtained in three normal Weimaraners. In our study, this dermatosis affected young adults that showed progressive alopecia of the trunk (head and limbs were spared) associated with recurrent folliculitis/furunculosis. Exclusion of other dermatoses and the presence of histopathological lesions and hair shafts abnormalities seen in light and/or scanning electron microscopy similar to colour dilution alopecia led to the diagnosis of follicular dysplasia. The lesions we observed are the same as those described previously in colour dilution alopecia, but they were less pronounced in all our samples.

Colour dilution alopecia in seven Dachshunds. A clinical study and the hereditary, microscopical and ultrastructural aspect of the disease.

Abstract Seven Dachshunds from five different families were studied for late-onset alopecia. All were born blue and tan in litters containing unaffected wild boar coated animals. Six of the seven dogs changed their colour during the first months of their life from blue and tan to 'deadleaf' or grey and tan. Histopathology, light microscopy of hairs and scanning electron microscopy of the hairs showed similarities with those previously described in blue Doberman Pinschers and confirmed the diagnosis of colour dilution alopecia (CDA). Transmission electron microscopy of cross-sectioned hairs showed vacuoles containing melanin granules of different size in medullary, subcortical and intracortical areas. Some opened at the hair surface and released melanin granules. Study of the pedigree proved autosomal recessive inheritance. Résumé- 7 teckels de 5 families ont fait l'objet de cette étude. Tous sont nés bleu et feu et proviennent de portées comprenant des chiots sains couleur sanglier. Six de ces chiens ont changé leur couleur durant les premiers mois de leur vie, passant ainsi du bleu et feu à'feuilles mortes' ou gris et feu. Histologiquement, l'examen microscopique des poils et l'examen ultrastructural à balayage montrent des lésions similaires à celles décrites chez les Dobermanns Pinschers bleus, et confirment le diagnostic d'Alopécie des Robes Diluées (ARD). La microscopie électronique à transmission des poils sectionnés montre des vacuoles contenant des grains de mélanine dans les régions médullaires, subcorticales, et intracorticales des poils. Quelques poils montrent la sortie des granules de mélanine à la surface du poil. L'étude des pédigrés prouve un mode de transmission autosomal récessif de cette maladie. [Beco, L., Fontaine, J., Gross, T.L., Charlier, G. Colour dilution alopecia in seven Dachshunds. A clinical study and the hereditary, microscopical and ultrastructural aspects of the disease (Alopécie des Robes Diluées chez 7 teckels: étude clinique et aspects héréditaires, microscopiques et ultrastructuraux). Veterinary Dermatology 1996; 7: 91-97.] Resumen Se estudió la alopecia de aparición tardía en siete perros Dashshund de cinco familias diferentes. Todos los cachorros nacieron de color azul y canela en camadas que contenían animates con pelaje jabalí, sin afectación. Seis de los siete perros cambiaron su color durante los primeros meses de vida de azul y canela a 'hoja seca' o gris y canela. La histopatologia, la microscopía óptica de los pelos y la microscopía electrónica de barrido de los pelos mostraron similitudes con los previamente descritos en los Doberman Pinscher azules y confirmaron el diagnóstico de alopecia de color diluido (ACD). La microscopia electrónica de transmisión de cortes transversales del pelo mostraron vacuolas que contenían gránulos de melanina de tamaño variable en las zonas medular, subcortical e intracortical. Algunos se abrían a la superficie del pelo y liberaban gránulos de melanina. El estudio del pedigree reveló una forma de herenicia autosómica recesiva. [Beco, L., Fontaine, J., Gross, T.L., Charlier, G. Colour dilution alopecia in seven Dachshunds. A clinical study and the hereditary, microscopical and ultrastructural aspects of the disease (Alopecia de color diluido en siete Dachshunds. Estudio clinico y aspectos hereditarios, microscopicos y ultraestructurales de la enfermedad). Veterinary Dermatology 1996; 7: 91-97.] Zusammenfassung- Sieben Dackel aus fünf verschiedenen Familien wurden wegen Alopezie mit spätem Beginn untersucht. Alle wurden als 'blau und tan' in Würfen geboren, die gesunde saufarbene aufwiesen. Sechs der sieben Hunde änderten ihre Farbe während der ersten Lebensmonate von 'blau und tan' nach 'dürrlaub' oder 'grau und tan'. Histopathologisch zeigten Lichtmikroskopie der Haare und Elektronen-mikroskopabtastung der Haare Ähnlichkeiten mit denen früher beschriebener Veränderungen beim blauen Dobermann, und bestätigten die Diagnose Farbverdünnungsalopezie (CDA). Die Transmissionselek-tronenmikroscopie von quergeschnittenen Haaren zeigte Vakuolen, die Melaningranula verschiedener Größe in medullären, subkortikalen und intrakortikalen Zonen enthielten. Einige öffneten sich hin zur Haarober fläche und entließen die Melaningranula. Die Untersuchung der Abstammung zeigte eine autosomal rezessive Erblichkeit. [Beco, L., Fontaine, J., Gross, T. L., Charlier, G. Colour dilution alopecia in seven dachschunds. A clinical study and the hereditary microscopical and ultrastructural aspects of the disease (Farbverdünnungsalopezie bei sieben Dackeln. Eine klinische Studie über erbliche, mikroskopische und ultrastrukturelle Aspekte dieser Erkrankung). Veterinary Dermatology 1996; 7: 91-97.].