Cardiovascular disease is a leading cause of death in both humans and dogs. Dilated cardiomyopathy (DCM) accounts for a large number of these cases, reported to be the third most common form of cardiac disease in humans and the second most common in dogs. In human studies of DCM there are more than 50 genetic loci associated with the disease. Despite canine DCM having similar disease progression to human DCM studies into the genetic basis of canine DCM lag far behind those of human DCM. In this review the aetiology, epidemiology, and clinical characteristics of canine DCM are examined, along with highlighting possible different subtypes of canine DCM and their potential relevance to human DCM. Finally the current position of genetic research into canine and human DCM, including the genetic loci, is identified and the reasons many studies may have failed to find a genetic association with canine DCM are reviewed.

Myasthenia, a syndrome of impaired neuromuscular transmission, occurs as either an acquired or congenital condition. Myasthenia gravis (MG) is an acquired autoimmune disorder with autoantibodies against the neuromuscular junction (NMJ) of skeletal muscle whereas congenital myasthenic syndromes (CMSs) are a clinically heterogeneous group of genetic disorders affecting the NMJ with a young age of onset. Both conditions are diseases for which recognition is important with regard to treatment and outcome. We review the published literature on MG and CMSs in dogs and cats, and by comparison with published classification used in humans, propose a classification system for MG and CMSs in dogs and cats. Myasthenia gravis is first classified based on focal, generalized, or acute fulminating presentation. It then is subclassified according to the autoimmune disease mechanism or seronegativity. Autoimmune disease mechanism relates to the presence or absence of a thymoma, or administration of thiourylene medication in cats. Congenital myasthenic syndromes are classified according to the affected NMJ component, the mechanism of the defect of neuromuscular transmission, the affected protein, and ultimately the mutated gene responsible. In proposing this categorization of MG and CMSs, we hope to aid recognition of the disease groups for both conditions, as well as guide treatment, refine prognosis, and provide a framework for additional studies of these conditions.

Background: Acquired myasthenia gravis (AMG) is increasingly recognized in cats, yet information regarding the natural history of the disease, treatment, and outcome including occurrence of immune and spontaneous remission remains limited.Objective: To determine the long-term outcome of cats with AMG without evidence of a cranial mediastinal mass (CMM).Animals: Eight cats diagnosed with AMG without evidence of a CMM. Methods: Retrospective case series. The medical records of cats diagnosed with AMG between 2005 and 2018 from 2 veterinary referral hospitals were reviewed for inclusion. Inclusion criteria consisted of a diagnosis of AMG, thoracic imaging, serum biochemistry including measurement of creatine kinase, and a CBC. Exclusion criteria were the presence of an identifiable CMM, or administration of methimazole or carbimazole.

Background Bacterial meningitis (BM) and meningoencephalitis (BMEM) are associated with high case fatality rates and neurologic sequelae in people, but limited data exists on outcome in dogs. Hypothesis/Objectives To report the clinicopathologic features, treatment and outcome of BM/BMEM in dogs, with a focus on clinical presentation, relapse and long‐term neurological deficits. Animals Twenty‐four client‐owned dogs diagnosed with BM/BMEM without empyema. Methods Retrospective case series of dogs diagnosed with BM/BMEM from 5 veterinary referral hospitals between January 2010 and August 2020. Results Twenty‐four dogs were included. Median duration of clinical signs was 2 days (range ≤24 hours to 30 days) and signs recorded included pyrexia (3) and cervical hyperesthesia (10). Neurological deficits were present in 18 dogs including altered mentation (12), ataxia (8), nonambulatory status (8), head tilt (8), and cranial nerve deficits (13). Intracellular bacteria were visualized on cerebrospinal fluid (CSF) analysis in 15/24 dogs, with positive CSF bacteriological culture in 8/21. Otitis media/interna (OMI) was diagnosed in 15/24 dogs, of which 6/15 dogs underwent total ear canal ablation and lateral bulla osteotomy. Twenty dogs survived to hospital discharge. Median duration of antibiotic administrations was 8 weeks (range, 2‐16 weeks). Glucocorticoids were administered to 15 dogs. Median follow‐up time was 92 days (range, 10‐2233 days). Residual neurological deficits were reported in 9 dogs, with a single case of suspected relapse. Conclusions and Clinical Importance Clinical signs were variable in dogs with BM/BMEM, the nidus of bacterial infection was often OMI and the majority of dogs made a full recovery with treatment.

Myasthenia gravis is an immune mediated disorder of neuromuscular transmission. Both an acquired and a congenital form have been reported in cats. Generalised weakness is considered a hallmark of myasthenia gravis, but in cats, due to their sedentary nature, this may not be as evident as in dogs. Feline acquired myasthenia gravis is associated with a significant incidence of cranial mediastinal masses, and a lower percentage of associated megaoesophagus than myasthenia gravis in dogs. The diagnosis of acquired myasthenia gravis remains challenging for the clinician, and there are currently no evidence-based treatment protocols. Reports describing outcomes in acquired feline myasthenia gravis are conflicting, with survival rates ranging from 42–85%. Data concerning the rate of spontaneous remission in feline acquired myasthenia gravis is limited, however the reported incidence appears low (9.2%). Recently, a mutation affecting the COLQ gene has been identified in the Sphynx and Devon Rex breeds, demonstrating a genetic basis to feline congenital myasthenia gravis.