Background

Guinea pigs (Cavia porcellus) are popular companion animals with reported skin diseases, but most reports are accessed from textbooks or review articles.

Hypothesis/objectives

To document skin diseases and their prevalence in companion guinea pigs in northern California, USA, and to investigate predilections for the most common conditions over a 25 year period.

Animals

Two hundred and ninety three guinea pigs from the hospital population met inclusion criteria.

Methods

A retrospective study was performed by searching computerized medical records seen at the Veterinary Medical Teaching Hospital (VMTH), School of Veterinary Medicine, University of California from 1 January 1990 to 31 July 2015 using key words relevant to dermatology.

Results

Of the 580 guinea pigs seen at the VMTH, 50% (293) had skin disease. Of the 293 cases, 154 (52%) presented for nondermatological reasons. Guinea pigs with skin disease were significantly older than those without skin disease (P = 0.0002); females with skin disease were more likely to have cystic ovaries (P = 0.0203), although these were not always associated with alopecia. Pododermatitis and infestation with Trixacarus caviae or lice were the most common skin diseases. Ivermectin or selamectin was used for ectoparasite treatment. Abscesses unassociated with pododermatitis were the most common nodules. Benign follicular tumours were the most common neoplasm. Despite the frequent mention of dermatophytosis in the veterinary literature, only two cases of Trichophyton mentagrophytes were diagnosed.

Conclusions and clinical importance

Cutaneous conditions in companion guinea pigs in the USA are common. Clinicians should include a dermatological examination when examining these rodents regardless of the reason for presentation.

Background

Eosinophilic airway disease in cats is sometimes described as allergic in origin, but controversy exists in the documentation of allergy in cats and the utility of allergy testing for respiratory tract diseases.

Objective

To examine serum immunoglobulin E (IgE) response to aeroallergens in cats with airway eosinophilia.

Animals

Fifteen cats with idiopathic eosinophilic airway inflammation and 9 control cats.

Methods

Prospective, case-control study. Surplus serum from cats with airway eosinophilia documented by bronchoscopic bronchoalveolar lavage was submitted for IgE measurement using ELISA polyclonal antibody methodology. Responses for regional allergens (fungal organisms, weeds, grasses, trees, mites, insects) were assessed. Results were reported as ELISA absorbance units with scores 0 to 79 considered negative, scores between 80 and 300 considered intermediate, and scores >300 considered positive.

Results

Cats with airway eosinophilia had significantly more positive serum IgE responses (25/720) than did healthy controls (5/432, P = .02); however, the number of cats with positive IgE responses (5/15) did not differ from controls (1/9, P = .35). The allergen that most commonly resulted in positive serum IgE response in cats with airway eosinophilia was dust mite (n = 4) followed by 2 types of storage mites (n = 3 each). No control cat tested positive for these allergens.

Conclusions and clinical importance

Serum IgE production against aeroallergens was found in some cats with eosinophilic airway inflammation, but the number of affected cats with positive results did not differ from controls. Further investigation in cats with eosinophilic, mixed, and neutrophilic airway disease in comparison to control cats is warranted.

Bruton tyrosine kinase (BTK) is expressed in B cells and innate immune cells, acting as an essential signaling element in multiple immune cell pathways. Selective BTK inhibition has the potential to target multiple immune-mediated disease pathways. Rilzabrutinib is an oral, reversible, covalent BTK inhibitor designed for immune-mediated diseases. We examined the pharmacodynamic profile of rilzabrutinib and its preclinical mechanisms of action. In addition to potent and selective BTK enzyme and cellular activity, rilzabrutinib inhibited activation and inflammatory activities of B cells and innate cells such as macrophages, basophils, mast cells, and neutrophils, without cell death (in human and rodent assay systems). Rilzabrutinib demonstrated dose-dependent improvement of clinical scores and joint pathology in a rat model of collagen-induced arthritis and demonstrated reductions in autoantibody-mediated FcγR signaling in vitro and in vivo, with blockade of rat Arthus reaction, kidney protection in mouse Ab-induced nephritis, and reduction in platelet loss in mouse immune thrombocytopenia. Additionally, rilzabrutinib inhibited IgE-mediated, FcεR-dependent immune mechanisms in human basophils and mast cell-dependent mouse models. In canines with naturally occurring pemphigus, rilzabrutinib treatment resulted in rapid clinical improvement demonstrated by anti-inflammatory effects visible within 2 wk and all animals proceeding to complete or substantial disease control. Rilzabrutinib is characterized by reversible covalent BTK binding, long BTK residence time with low systemic exposure, and multiple mechanistic and biological effects on immune cells. Rilzabrutinib's unique characteristics and promising efficacy and safety profile support clinical development of rilzabrutinib for a broad array of immune-mediated diseases.

Cutaneous lupus erythematosus (CLE) in humans encompasses multiple subtypes that exhibit a wide array of skin lesions and, in some cases, are associated with the development of systemic lupus erythematosus (SLE). We investigated dogs with exfoliative cutaneous lupus erythematosus (ECLE), a dog-specific form of chronic CLE that is inherited as a monogenic autosomal recessive trait. A genome-wide association study (GWAS) with 14 cases and 29 controls confirmed a previously published result that the causative variant maps to chromosome 18. Autozygosity mapping refined the ECLE locus to a 493 kb critical interval. Filtering of whole genome sequence data from two cases against 654 controls revealed a single private protein-changing variant in this critical interval, UNC93B1:c.1438C>A or p.Pro480Thr. The homozygous mutant genotype was exclusively observed in 23 ECLE affected German Shorthaired Pointers and an ECLE affected Vizsla, but absent from 845 controls. UNC93B1 is a transmembrane protein located in the endoplasmic reticulum and endolysosomes, which is required for correct trafficking of several Toll-like receptors (TLRs). The p.Pro480Thr variant is predicted to affect the C-terminal tail of the UNC93B1 that has recently been shown to restrict TLR7 mediated autoimmunity via an interaction with syndecan binding protein (SDCBP). The functional knowledge on UNC93B1 strongly suggests that p.Pro480Thr is causing ECLE in dogs. These dogs therefore represent an interesting spontaneous model for human lupus erythematosus. Our results warrant further investigations of whether genetic variants affecting the C-terminus of UNC93B1 might be involved in specific subsets of CLE or SLE cases in humans and other species.

Fluconazole-induced alopecia is a significant problem for patients receiving long-term therapy. We evaluated the hair cycle changes of fluconazole in a rat model and investigated potential molecular mechanisms. Plasma and tissue levels of retinoic acid were not found to be causal. Human patients with alopecia attributed to fluconazole also underwent detailed assessment and in both our murine model and human cohort fluconazole induced telogen effluvium. Future work further examining the mechanism of fluconazole-induced alopecia should be undertaken.