Preliminary evaluation of two bathing methods for the management of Malassezia overgrowth in dogs with atopic dermatitis.

BACKGROUND: Antifungal shampoos are widely used for canine Malassezia dermatitis. Few studies have evaluated effective bathing methods for atopic dogs with Malassezia overgrowth. OBJECTIVES: To evaluate the efficacy of an emollient bathing product (AFLOAT VET) and 2% miconazole/2% chlorhexidine shampoo (2% MIC/CHX) in atopic dogs, and to evaluate the influence on skin barrier function of both products in healthy dogs. ANIMALS: Sixteen atopic dogs with secondary Malassezia overgrowth and 11 healthy dogs. METHODS AND MATERIALS: This study was a randomized, single-blinded trial. The dogs were randomly treated with either emollient bathing or 2% MIC/CHX, twice weekly for four weeks. Clinical assessment used the Canine Atopic Dermatitis Extent and Severity Index, 4th iteration (CADESI-04), pruritus Visual Analog Scale (pVAS), and cytological evaluation of yeast numbers at Day (D)0, D14 and D28. Skin barrier function was determined by measuring transepidermal water loss (TEWL) after a single bathing procedure with each product in the healthy dogs. RESULTS: The pVAS scores and yeast counts were significantly reduced on D28 compared with D0 in both groups (P < 0.05). CADESI-04 was significantly decreased on D28 in the emollient bathing group (P = 0.003). There were no significant differences in each endpoint score between the groups. In healthy dogs, TEWL was significantly increased after bathing in both groups (P < 0.01). CONCLUSION: An emollient bathing product can be effective for Malassezia overgrowth in dogs with atopic dermatitis. Bathing with shampoo products might affect skin barrier function even when using an emollient product.

Efficacy and safety of 0.0584% hydrocortisone aceponate topical spray and systemic oclacitinib combination therapy in dogs with atopic dermatitis: a randomized, double-blinded, placebo-controlled trial.

BACKGROUND: Oclacitinib is an effective systemic therapy for dogs with atopic dermatitis (AD). Few studies have evaluated concurrent topical treatment with oclacitinib in dogs. OBJECTIVES: To evaluate the efficacy and safety of combination therapy of oclacitinib and 0.0584% hydrocortisone aceponate (HCA) spray in dogs with AD. ANIMALS: Eighteen dogs with AD. METHODS AND MATERIALS: This study was a randomized, double-blinded, placebo-controlled trial. All dogs were treated with oclacitinib (0.4-0.6 mg/kg twice daily for 14 days, then once daily for 14 days) and randomized to receive either HCA spray or placebo spray, applied once daily for seven days then every other day through to Day (D)28. Clinical assessments included the Canine Atopic Dermatitis Extent and Severity Index, 4th iteration (CADESI-4) and the pruritus Visual Analog Scale (PVAS) every seven days, and blood and urine tests every 14 days. RESULTS: The mean CADESI-4 and PVAS scores were significantly reduced on D7 and D14 compared to D0 in both groups (P < 0.05). From D14 to D21, CADESI-4 and PVAS scores were significantly increased in the placebo group (P < 0.005), and not in the HCA-treated group. The mean reduction from baseline of the HCA-treated group was significantly higher than that of the placebo group for the PVAS and CADESI-4 on D21 (59.9% versus 27.6%, P = 0.0216) and D28 (56.0% versus 30.5%, P = 0.0109), respectively. One dog in the HCA-treated group was withdrawn as a consequence of developing diarrhoea. CONCLUSION: Topical application of 0.0584% HCA spray may be useful for preventing exacerbation of pruritus and clinical lesions when tapering oclacitinib therapy in dogs with AD.

Characterization of canine filaggrin: gene structure and protein expression in dog skin.

BACKGROUND: Filaggrin (FLG) is a key protein for skin barrier formation and hydration of the stratum corneum. In humans, a strong association between FLG gene mutations and atopic dermatitis has been reported. Although similar pathogenesis and clinical manifestation have been argued in canine atopic dermatitis, our understanding of canine FLG is limited. HYPOTHESIS/OBJECTIVES: The aim of this study was to determine the structure of the canine FLG gene and to raise anti-dog FLG antibodies, which will be useful to detect FLG protein in dog skin. METHODS: The structure of the canine FLG gene was determined by analysing the publicly available canine genome DNA sequence. Polyclonal anti-dog FLG antibodies were raised based on the canine FLG sequence analysis and used for defining the FLG expression pattern in dog skin by western blotting and immunohistochemistry. RESULTS: Genomic DNA sequence analysis revealed that canine FLG contained four units of repeated sequences corresponding to FLG monomer protein. Western blots probed with anti-dog FLG monomer detected two bands at 59 and 54 kDa, which were estimated sizes. The results of immunohistochemistry showed that canine FLG was expressed in the stratum granulosum of the epidermis as a granular staining pattern in the cytoplasmic region. CONCLUSIONS AND CLINICAL IMPORTANCE: This study revealed the unique gene structure of canine FLG that results in production of FLG monomers larger than those of humans or mice. The anti-dog FLG antibodies raised in this study identified FLG in dog skin. These antibodies will enable us to screen FLG-deficient dogs with canine atopic dermatitis or ichthyosis.