Background: Treatment of canine otitis externa with owner‐administered products can be difficult.Objectives: To evaluate otic treatment administered by a veterinarian on quality of life (QoL) of dogs with otitis externa and their owners, and on clinical and cytology parameters of otitis; compared to an owner‐administered treatment.Animals: Fifty client‐owned dogs randomly randomized into two groups and treated for 2 weeks.Methods: Veterinarians treated Group A dogs with a veterinary licensed otic gel on two occasions at a 1 week interval; owners treated Group B dogs once daily with a veterinary licensed otic drop based product along with twice weekly cleaning. Veterinarians evaluated otitis with theOTI‐3 scale and semi‐quantitative cytological examination on days 0, 7, 14 and 28. At each visit, owners assessed QoL with a validated questionnaire and pruritus with a Visual Analog Scale. Scores before and after treatment of each group, and differences between groups were analysed statistically.Results: In both groups, all parameters improved significantly. There was a significantly higher improvement of QoL scores, for dogs and owners, in Group A, compared to Group B at all time points (P< 0.05), except for owner QoL on Day 28. There was no difference in improvement ofOTI‐3 between groups at any time point, whereas Group A cytology scores and pruritus improved significantly more by Day 7 (P= 0.0026 andP= 0.0294, respectively).Conclusion: A veterinarian‐administered otic gel provided equivalent efficacy and higher QoL to dogs with otitis externa and their owners, compared to an owner‐administered topical otic therapy.

Sebaceous adenitis and concurrent meibomian gland dysfunction (MGD) were diagnosed in a two-year-old mongrel dog presenting with hypotrichosis, exfoliative dermatitis and blepharitis. Diagnosis of sebaceous adenitis was based on history, clinical signs, the histological demonstration of multifocal lymphohistiocytic and neutrophilic inflammation targeting the sebaceous glands and sebaceous glands loss. MGD was diagnosed by non-contact infrared meibography followed by tear film lipid layer interferometric evaluation. Ciclosporin and sebolytic shampoos controlled the dermatological condition, while doxycycline, warm compresses, palpebral massages and tobramycin/dexamethasone ointment controlled the blepharitis. This case report should stimulate clinicians to investigate MGD in dogs suffering from sebaceous adenitis, because the meibomian and sebaceous glands share similar anatomy and physiology.

Case summary: A 5-year-old, spayed female, indoor-only domestic shorthair cat was referred with an acute history of multifocal cutaneous and mucocutaneous erosive-ulcerative lesions and skin detachment. The lesions occurred on the seventh day of therapy with cefadroxil. Erosive-ulcerative and occasionally crusted lesions were apparent on the medial and lateral canthus of both eyes, ventral neck, abdomen, perivulvar region, periungual skin and medial aspect of the front and hindlimbs. Diffuse and severe exfoliation was present on the dorsum and tail base and in both external ear canals. The cat was also dehydrated, tachycardic and febrile. Histopathological examination revealed extensive epidermal ulceration, interface dermatitis with vacuolar degeneration, apoptosis at multiple epidermal levels and basal, suprabasal and spinous dermoepidermal detachment. The histopathological diagnosis was consistent with Stevens–Johnson syndrome/toxic epidermal necrolysis (SJS/TEN). The recently reported Algorithm of Drug Causality in Epidermal Necrolysis (ALDEN), currently used in human medicine, was applied and a score of +6 was calculated; this supported the view that SJS/TEN in this cat was very likely to be associated with cefadroxil administration. Relevance and novel information: This clinical communication reports cefadroxil as a very probable cause of SJS/TEN in a cat; the ALDEN was applied in this case and supported diagnosis.

A two-year-old, intact female Scottish Terrier presented with one-and-a-half-year history of erosive and ulcerative lesions affecting the nasal planum. Clinical appearance, history, histopathology, and response to therapy were suggestive of a rare vasculopathy of the nasal planum that has been previously described in Scottish Terrier dogs. In previously published reports, medical treatments of the disease had failed, leading to euthanasia of five dogs, while a short-term follow-up was available for one case that was controlled with prednisolone and ciclosporin. The dog reported herein was successfully treated with medical therapy consisting initially of a combination of ciclosporin and prednisolone and endonasal stents applied over the first six months. Stents were inserted in order to prevent abnormal scarring and nostril stenosis. More than one and a half years after diagnosis, the dog is still being administered ciclosporin once daily, breathes normally, and has an optimal quality of life.

Janus kinase (JAK) pathways have emerged as targets of treatment, yet localization and expression of JAK1 and JAK3 in canine atopic skin have not been studied. This study aimed to compare the localization and expression of JAK1 and JAK3 in the skin of atopic dogs before and after allergen exposure. Skin biopsies taken from atopic beagles sensitized to house dust mites (HDM) before (D0) and after four weeks (D28) of allergen exposure were stained. Staining was subjectively scored by examiners unaware of the source of the slides. Image J was used for the semiquantitative assessment of staining intensity. JAK1 and JAK3 staining was epidermal and dermal. JAK1 staining was cytoplasmic, primarily found in basal keratinocytes and dermal cells, while JAK 3 was nuclear (all epidermal levels and on dermal inflammatory cells). Epidermal thickness was significantly higher on D28 than on D0 (p < 0.0001). For JAK1, epidermal staining divided by epithelial thickness was significantly lower on D28 (p = 0.0002) compared to D0. For JAK3 staining, intensity in the dermis was significantly higher on D28 (p = 0.0405) compared to D0. We conclude that decreased expression of JAK1 in the epidermis and increased expression of JAK3 in the dermis of atopic dogs occur after allergen exposure.