Small animal disease surveillance: GI disease and salmonellosis.

Presentation for gastrointestinal (GI) disease comprised 2.2 per cent of cat, 3.2 per cent of dog and 2.2 per cent of rabbit consultations between April 1, 2016 and March 31, 2017Diarrhoea and vomiting without blood were the most frequently reported GI disease clinical signs (34.4 and 38.9 per cent in cats and 42.8 and 37.3 per cent in dogs, respectively)The mean percentage of samples testing positive for Salmonella in dogs was double that in cats (0.82 per cent and 0.41 per cent, respectively) from January 1, 2011 to December 31, 2016In dogs, autumn was associated with a greater proportion of Salmonella-positive sample submissions; no clear suggestion of seasonal variation in cats was observedIn both cats and dogs, isolates belonging to Salmonella enterica group B serotypes were the most common (68.9 per cent in cats and 55.0 per cent in dogs).

Small animal disease surveillance: pruritus, and coagulase-positive staphylococci.

Presentation for pruritus comprised 6.5 per cent, 3.6 per cent and 2.0 per cent of canine, feline and rabbit consultations, respectively, between January 2014 and June 2016Topical antimicrobials were the most commonly prescribed pruritus treatments for dogs (33.6 per cent of consultations); for cats, it was systemic glucocorticoids (53.5 per cent)In surveillance of coagulase-positive staphylococci, 16 per cent of 176 coagulase-positive staphylococci isolated from canine diagnostic samples were sensitive to all tested antibacterial classes; multidrug resistance (resistance to three or more antibacterial classes) was found in 6.8 per cent.

Small animal disease surveillance: respiratory disease.

Presentation for respiratory disease comprised 1.7 per cent, 2.3 per cent and 2.5 per cent of canine, feline and rabbit consultations, respectively, between January 2014 and December 2015. Coughing was the most frequent respiratory sign reported in dogs (71.1 per cent of consultations); in cats it was sneezing (42.6 per cent). Mean percentage of samples testing positive for feline calicivirus (FCV) was 30.1 per cent in 2014 and 27.9 per cent in 2015. January was the month with the highest percentage of FCV-positive samples in both 2014 and 2015.

Small animal disease surveillance.

This is the first UK small animal disease surveillance report from SAVSNET. Future reports will expand to other syndromes and diseases. As data are collected for longer, the estimates of changes in disease burden will become more refined, allowing more targeted local and perhaps national interventions. Anonymised data can be accessed for research purposes by contacting the authors. SAVSNET welcomes feedback on this report.

Barium toxicosis in a dog.

CASE DESCRIPTION: A 2-year-old 14.9-kg (32.8-lb) neutered female Shetland Sheepdog was admitted to the University of Liverpool Small Animal Teaching Hospital for evaluation of acute collapse. CLINICAL FINDINGS: At admission, the dog was tachypneic and had reduced limb reflexes and muscle tone in all limbs consistent with diffuse lower motor neuron dysfunction. The dog was severely hypokalemic (1.7 mEq/L; reference range, 3.5 to 5.8 mEq/L). Clinical status of the dog deteriorated; there was muscle twitching, flaccid paralysis, and respiratory failure, which was considered a result of respiratory muscle weakness. Ventricular arrhythmias and severe acidemia (pH, 7.18; reference range, 7.35 to 7.45) developed. Intoxication was suspected, and plasma and urine samples submitted for barium analysis had barium concentrations comparable with those reported in humans with barium toxicosis. Analysis of barium concentrations in 5 control dogs supported the diagnosis of barium toxicosis in the dog. TREATMENT AND OUTCOME: Fluids and potassium supplementation were administered IV. The dog recovered rapidly. Electrolyte concentrations measured after recovery were consistently unremarkable. Quantification of plasma barium concentration 56 days after the presumed episode of intoxication revealed a large decrease; however, the plasma barium concentration remained elevated, compared with that in control dogs. CLINICAL RELEVANCE: To our knowledge, this case represented the first description of barium toxicosis in the veterinary literature. Barium toxicosis can cause life-threatening hypokalemia; however, prompt supportive treatment can yield excellent outcomes. Barium toxicosis is a rare but important differential diagnosis in animals with hypokalemia and appropriate clinical signs.

Determination of serum fPLI concentrations in cats with diabetes mellitus.

Diabetes mellitus (DM) is one of the most common feline endocrinopathies. Pancreatitis is a reported cause for poor control of DM in cats; however, its prevalence in diabetic cats is unknown. Measurement of serum feline pancreatic lipase immunoreactivity (fPLI) has been proposed as a sensitive and specific test for the detection of pancreatitis in cats. The aim of this study was to assess fPLI concentrations in diabetic cats and compare these with non-diabetic cats of similar age. Samples from 29 cats with DM and 23 non-diabetic cats were analysed. Serum fPLI concentrations were significantly higher in samples from diabetic cats (P<0.01). A weak association was found between serum fructosamine and fPLI concentrations (R(2)=0.355, P=0.015), but there was no association between fPLI concentrations and the degree of diabetic control. There were no significant differences in reported clinical signs between cats with or without DM regardless of serum fPLI concentration. This is the first study to demonstrate elevated serum fPLI concentrations in cats with DM, suggesting that pancreatitis could be a significant comorbidity in these cats.

Stimulation of gastrin-CCKB receptor promotes migration of gastric AGS cells via multiple paracrine pathways.

Responses to G protein-coupled receptor stimulation may be mediated by paracrine factors. We have developed a coculture system to study paracrine regulation of migration of gastric epithelial (AGS) cells after stimulation of gastrin-CCK(B) receptors. In cells expressing this receptor, G-17 stimulated migration by activation of protein kinase C. However, G-17 also stimulated the migration of cells expressing green fluorescent protein, but not the receptor, when they were cocultured with receptor-expressing cells consistent with activation of paracrine signals. The use of various pharmacological inhibitors indicated that gastrin stimulated migration via activation of the EGF receptor (EGR-R), the erbB-2 receptor tyrosine kinase, and the MAP kinase pathway. However, gastrin also released fibroblast growth factor (FGF)-1, and migration was inhibited by the FGF receptor tyrosine kinase inhibitor SU-5402. Flow cytometry indicated that in both cell types, gastrin increased MAP kinase via activation of EGF-R but not FGF-R1 or erbB-2. We conclude that gastrin-CCK(B) receptors stimulate epithelial cell migration partly via paracrine mechanisms; transactivation of EGF-R is only one component of the paracrine pathway.