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Background Factors known to be associated with outcome of acquired myasthenia gravis (MG) in dogs are limited. Hypothesis/Objectives Of dogs with MG, advancing age and comorbid neoplasia are associated with poor long‐term prognosis and low rates of remission. Animals Ninety‐four client‐owned dogs with MG diagnosed by acetylcholine receptor antibody (AChR Ab) assay between 2001 and 2019 from a university clinic and 3 private clinics in the United States. Methods Cases were retrospectively evaluated and data were collected to determine clinical signs, treatment, and response to therapy defined by means of a clinical scoring rubric. Immunological remission was defined as a return of the AChR Ab concentration to

Meningoencephalitis of unknown origin (MUO) is a relatively common and very serious canine neurologic condition, which is typically associated with a poor long term prognosis despite treatment. This case series chronicles two dogs diagnosed with MUO who were treated with long term corticosteroids and cytosine arabinoside and lived well-beyond the typical survival time for this condition. Both eventually succumbed to respiratory signs associated with mineralized thrombi in their pulmonary arteries. Adverse effects from the two drugs used for treatment are reviewed in order to propose a possible mechanism to explain how long term use of these medications could result in such a phenomenon.

Myasthenia gravis (MG) is a T cell-dependent, B cell-mediated autoimmune disease. Little is known about its cellular pathogenesis in dogs. This study provides the first preliminary assessment of the frequency of myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs) in the peripheral blood of dogs with seropositive generalized MG. No alteration in frequency of either MDSCs or Tregs in dogs with MG was observed when compared to those in either seronegative dogs with diagnoses other than MG, or healthy dogs. A longitudinal study in three dogs with MG revealed no correlation between the relative numbers of either population and the clinical course of disease. Neither the frequency of MDSCs nor of Tregs showed a correlation with anti-AChR antibody titer in dogs with MG. These findings suggest that aberrations in the frequency of either immunosuppressive population do not occur in MG, but they need to be validated in large-scale prospective studies.

Objective To determine the incidence of in-hospital adverse outcomes including acute kidney injury (AKI) and death in a population of dogs admitted to the intensive care unit (ICU) receiving 10% hydroxyethyl starch (HES) [250/0.5/5:1] compared with the general ICU population, while controlling for illness severity. Design Cohort study conducted between January 2007 and March 2010. Setting Veterinary teaching hospital. Animals Consecutive sample of dogs receiving HES (n = 180) were compared with a randomly selected sample of dogs (n = 242) admitted to the ICU over the same period. Interventions None Measurements and Main Results AKI was defined as an at least 2-fold increase in baseline creatinine concentration or new onset of oliguria/anuria persisting for ≥12 hours. The primary outcome was a composite of in-hospital death or AKI. Unadjusted and adjusted analysis controlling for illness severity using the acute patient physiologic and laboratory evaluation (APPLEfast) score and other confounders was performed. HES was administered either as incremental boluses (median dose 8.2 mL/kg/day, interquartile range [IQR] 5.0–11.3 mL/kg/day) or as a continuous rate infusion (CRI; median dose 26mL/kg/day, IQR 24.0–48 mL/kg/day). In unadjusted analysis, HES administration was associated with increased risk of mortality (odds ratio [OR] = 2.33, 95% confidence interval [CI] = 1.51–3.58, P < 0.001) or AKI (OR = 3.87, 95% CI = 1.21–12.37, P = 0.02). In an adjusted analysis after controlling for illness severity, admission type, and concurrent administration of blood products, HES administration remained an independent risk factor for the composite adverse outcome (OR = 1.98, 95% CI = 1.22–3.22, P = 0.005), with a number needed to harm (NNH) = 6 (95% CI = 4–23). Conclusions HES therapy is associated with increased risk of an adverse outcome including death or AKI in dogs. A randomized controlled trial investigating the safety of HES therapy in canine patients is warranted.

The objectives of this study were to investigate the relationship between cerebrospinal fluid lactate and serum concentrations in dogs with clinical signs of central nervous system disease and to establish if cerebrospinal fluid lactate (CSF) concentrations are higher in dogs with structural intracranial disease (Group Pos-MRI) compared to dogs that have clinical signs of intracranial disease but no structural brain disease (Group Neg-MRI) based on magnetic resonance imaging (MRI) findings. Using a prospective study canine blood and cerebrospinal fluid were collected in 24 dogs with neurological signs after undergoing brain MRI. Dogs were divided in 2 groups. No significant difference between serum lactate (1.57 ± 0.9 mmol/L) and CSF lactate concentration (1.34 ± 0.3 mmol/L) was detected. There was a direct correlation between CSF and serum lactate concentration (Les objectifs de la présente étude étaient d’examiner la relation entre les concentrations de lactate du liquide céphalo-rachidien (LCR) et du sérum chez des chiens présentant des signes cliniques de pathologie du système nerveux central et établir si les concentrations de lactate du LCR sont plus élevées chez les chiens avec une maladie intracrânienne structurale (Groupe Pos-IRM) comparativement à des chiens avec des signes cliniques de maladie intracrânienne mais sans maladie structurale du cerveau (Groupe Nég-IRM) sur la base des trouvailles en imagerie par résonnance magnétique (IRM). Utilisant une étude prospective, du sang canin et du LCR ont été prélevés chez 24 chiens avec des signes neurologiques après un examen par IRM du cerveau. Les chiens ont été séparés en deux groupes. Aucune différence significative ne fut détectée entre les concentrations de lactate sérique (1,57 ± 0,9 mmol/L) et de lactate du LCR (1,34 ± 0,3 mmol/L). Il y avait une corrélation directe entre les concentrations de lactate du LCR et du sérum (