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Background Pancreatitis in cats, although commonly diagnosed, still presents many diagnostic and management challenges. Objective To summarize the current literature as it relates to etiology, pathogenesis, diagnosis, and management of pancreatitis in cats and to arrive at clinically relevant suggestions for veterinary clinicians that are based on evidence, and where such evidence is lacking, based on consensus of experts in the field. Animals None. Methods A panel of 8 experts in the field (5 internists, 1 radiologist, 1 clinical pathologist, and 1 anatomic pathologist), with support from a librarian, was formed to assess and summarize evidence in the peer reviewed literature and complement it with consensus clinical recommendations. Results There was little literature on the etiology and pathogenesis of spontaneous pancreatitis in cats, but there was much in the literature about the disease in humans, along with some experimental evidence in cats and nonfeline species. Most evidence was in the area of diagnosis of pancreatitis in cats, which was summarized carefully. In contrast, there was little evidence on the management of pancreatitis in cats. Conclusions and clinical importance Pancreatitis is amenable to antemortem diagnosis by integrating all clinical and diagnostic information available, and recognizing that acute pancreatitis is far easier to diagnose than chronic pancreatitis. Although both forms of pancreatitis can be managed successfully in many cats, management measures are far less clearly defined for chronic pancreatitis.

Chronic enteropathy (CE) in dogs is common worldwide, but little data is available from Australia. The aim of this study was to describe treatment response and long-term outcome in a cohort of dogs with CE. Dogs were prospectively enrolled at Murdoch University and the University of Melbourne. After diagnostic investigation to rule out diseases other than CE, dogs underwent sequential therapeutic trials until achieving a clinical response (diet then antibiotics, and finally immunosuppressants). Success was defined as 75% reduction of clinical severity for a minimum of five weeks. A total of 21 dogs were enrolled, and 19 completed the study. One dog was euthanised for lack of response to treatment and one excluded for lack of owner compliance. Most dogs responded to diet (n = 10), followed by antibiotics (n = 7) and immunosuppressants (n = 2). Long-term remission (median 21.1 months, [3.0-44.7]) was achieved in eight out of ten dietary responders without additional treatment. In contrast, only two dogs with antibiotic response remained in long-term remission, of which one needed on-going antibiotic treatment. Longer term remission was achieved in the two dogs treated with immunosuppressants with on-going low dose therapy. This study concludes that most dogs referred for CE in Australia respond to dietary treatment (even after previous dietary interventions), and remission is long-term compared to dogs treated with an antibiotic. Furthermore, the need for long-term antibiotics in some dogs to maintain response may lead to antibiotic resistance. This study supports adequate dietary trials for CE in dogs, and a need for alternative second-line treatments.

Key Clinical Message Disseminated toxoplasmosis is a potentially fatal complication in dogs receiving immunosuppressive therapy, particularly if multiple immunosuppressive drugs are used. Toxoplasmosis should be considered if signs of acute respiratory or hepatic disease develop, and diagnosis would rely on demonstration of organisms via cytology or PCR rather than a single time‐point serological assay.

A pharmacodynamic assay has been previously developed to monitor ciclosporin treatment in dogs by assessing inhibition of cytokine transcription after whole blood stimulation with 12‐myristate 13‐1 acetate and ionomycin (PMA/I). In this study, whole blood stimulation with either PMA/I or lipopolysaccharide (LPS) was used to assess the effect of multiple drugs (azathioprine, ciclosporin, mycophenolate, leflunomide and prednisone) after a 7‐day treatment course on production of cytokines measured with a multiplex assay in healthy dogs (n = 4 for each treatment). Interleukin‐10 (IL‐10), interferon gamma (IFN γ) and tumour necrosis factor alpha (TNF α) were significantly activated by PMA/I stimulation and IL‐6, IL‐10 and TNF α by LPS stimulation, in the absence of immunosuppressive drugs. After ciclosporin treatment, IL‐10, IFN γ and TNF α production was significantly reduced after stimulation with PMA/I compared to pre‐treatment. After prednisone treatment, TNF α production was significantly reduced after stimulation with PMA/I or LPS compared to pre‐treatment. No significant change was observed after treatment with azathioprine, leflunomide or mycophenolate. This methodology may be useful to monitor dogs not only treated with ciclosporin, but also with prednisone or a combination of both. Further studies are needed to assess the use of this assay in a clinical setting.

Background The objectives of this study were to establish the prevalence, risk factors and comorbidities/sequelae for diabetes mellitus (DM) in Australian dogs presented to first-opinion veterinary practices. Methods Electronic patient records of dogs (n=134,329) attending 152 veterinary clinics during 2017 were sourced through VetCompass Australia. They included 418 dogs with DM; a prevalence of 0.36 per cent (95 per cent CI 0.33 per cent to 0.39 per cent) in Australian dogs attending these veterinary clinics. By comparing with the reference group of rarer breeds and unidentified crossbreeds, multivariable modelling was used to reveal breeds (and their crosses) with significantly higher odds of having DM. Results The results revealed that breeds (and their crosses) with significantly higher odds of having DM were Australian terriers (ORs=7.93 (95 per cent CI 2.83 to 22.27)), Siberian huskies (OR=6.24 (95 per cent CI 2.51 to 15.54)), English springer spaniels (OR=5.37 (95 per cent CI 1.48 to 19.53)), West Highland white terriers (OR=4.85 (95 per cent CI 2.55 to 9.25)), miniature schnauzers (OR=3.47 (95 per cent CI 1.16 to 10.35)), all types of poodles (OR=3.41 (95 per cent CI 2.07 to 5.61)), bichon frises (OR=3.41 (95 per cent CI 1.65 to 7.01)), schnauzers (OR=3.18 (95 per cent CI 1.42 to 7.11)) and cavalier King Charles spaniels (CKCS; OR=1.84 (95 per cent CI 1.08 to 3.13)). Breeds with lower risk were German shepherd dogs (OR=0.11 (95 per cent CI 0.01 to 0.84)), golden retrievers (OR=0.09 (95 per cent CI 0.01 to 0.68)) and boxers (no cases identified). Fisher’s exact tests showed that labradoodles were diagnosed significantly more often than purebred Labradors (P=0.04) and did not differ significantly from poodles (P=0.81). Cavoodles did not differ significantly from either CKCS (p~1.00) or poodles (P=0.12). Spoodles were significantly less diagnosed than poodles (P=0.003) but did not differ from cocker spaniels (P=0.66). Desexed male dogs had a higher odds of DM than entire male (OR=0.62 (95 per cent CI 0.39 to 0.98)) and desexed female dogs (OR=0.76 (95 per cent CI 0.61 to 0.96)). Comorbidities/sequelae associated with canine DM included suspected pancreatitis (OR 10.58 (95 per cent CI 5.17 to 22.78)), cataracts (OR 9.80 (95 per cent CI 5.65 to 17.35)), hyperadrenocorticism (OR 6.21 (95 per cent CI 3.29 to 11.88)), urinary tract infection (OR 5.09 (95 per cent CI 1.97 to 13.41)) and hypothyroidism (OR 4.10 (95 per cent CI 1.08 to 15.58)). Conclusions Breeds at most risk included Australian terriers and Siberian huskies as previously reported, as well as, for the first time, English springer spaniels. In contrast to other populations where there is female predisposition for DM, desexed male dogs in Australia were at increased risk for DM compared with both entire males and desexed females. This predisposition for desexed males to develop DM warrants further investigation.

Objective To describe 5 cases of conservative management of substantial esophageal perforation in dogs. Series Summary Five dogs presented with an esophageal foreign body (EFB) and resultant esophageal perforation. Clinical signs at presentation included tachycardia, tachypnea, and increased respiratory effort. Thoracic radiography was performed in all cases, and in each case, pleural and mediastinal effusion was present, suggesting esophageal perforation prior to endoscope‐guided removal. A full thickness esophageal defect was visualized after foreign body removal in 4/5 cases. Treatment included IV crystalloid fluid therapy, IV antimicrobials, analgesia, and proton pump inhibitors in all cases. Two dogs had a percutaneous endoscopically placed gastrostomy feeding tube placed and 1 dog received prednisolone sodium succinate IV because of marked pharyngeal inflammation. Complications after EFB removal included pneumothorax (n = 2) and pneumomediastinum (n = 4). Four of the 5 dogs survived to discharge and did not have complications 2–4 weeks following discharge. One dog was euthanized as result of aspiration pneumonia following EFB removal. New or Unique Information Provided Traditionally, surgical management of esophageal perforations has been recommended. This can be a costly and invasive procedure and requires a high degree of surgical skill. In this report, conservative management of substantial esophageal perforation in 5 dogs is described; medical management may be a viable treatment option in dogs with perforation of the esophagus due to EFB.

AIM: A prospective, observational study to determine the prevalence of post-exercise conditions at Australian Greyhound race meetings and to assess association with race performance and other environmental, race- and dog-related factors was undertaken. METHODS: A total of 4020 starters were observed (2813 Greyhounds, 1009 trainers, 536 races, 52 race meets, 48 race dates and 11 race tracks) following a race. The presence of diaphragmatic flutter (DF), ataxia, seizure, collapse or sudden death was recorded. Risk factors were screened by univariable logistic regression prior to multivariable backward stepwise model building. RESULTS: In this study, 962 starters (n = 768 dogs) had DF (23.9%), 16 starters were ataxic (0.4%) and there were no observed cases of collapse, seizure or sudden death. Race track location, increasing race distance, race grade based on increasing 1st place prize value, lower (earlier) race number at the meeting, age, a previous observation of DF at the last start, females, colour (white) and better finishing position were all associated with an increased risk of a Greyhound being observed with DF. However, when logistic regression assessing the random effect of dog was performed, the presence of previous DF was not significant. In this cohort, DF was common following strenuous exercise in Greyhounds and on its own does not appear to result in reduced performance or distress to the animal. CONCLUSION: The incidence of ataxia was low and collapse, seizure and sudden death were not observed. However, even though uncommon, ataxia has welfare concerns for racing Greyhounds that warrants further investigation.

Background Aerosolized medications are increasingly being used to treat respiratory diseases in dogs. No previous studies assessing respiratory tract deposition of radiolabeled aerosols have been performed in conscious dogs. Hypothesis/Objectives Assess respiratory tract deposition of radiolabeled, inhalant corticosteroid (fluticasone propionate labeled with 99mTc) delivered from a nebulizer and metered dose inhaler (MDI) to healthy dogs. Animals Ten healthy Foxhounds. Methods Prospective, randomized, cross-over pilot study. Initial inhalation method (nebulizer or MDI) was randomly assigned. Treatments were crossed over after a 7-day washout period. Treatments initially were performed using sedation. Dogs were imaged using 2-dimensional planar scintigraphy, with respiratory tract deposition quantified by manual region-of-interest analysis. Deposition calculated as percentage of delivered dose. Six of 10 dogs were randomly selected and reassessed without sedation. Results Inhalation method had significant effect on respiratory tract deposition (P = 0.027). Higher deposition was achieved by nebulization with mean deposition of 4.2% (standard deviation [SD], 1.4%; range, 1.9–6.1%); whereas MDI treatment achieved a mean of 2.3% (SD, 1.4%; range, 0.2–4.2%). Nebulization achieved higher respiratory tract deposition than MDI in 7 of 10 dogs. No statistical difference (P = 0.68) was found between mean respiratory tract deposition achieved in dogs when unsedated (3.8%; SD, 1.5%) or sedated (3.6%; SD, 1.7%). Conclusions and Clinical Importance Study confirms respiratory tract deposition of inhalant medications delivered from a nebulizer and MDI in healthy dogs, breathing tidally with and without sedation. Respiratory tract deposition in these dogs was low compared to reported deposition in adult humans, but similar to reported deposition in children.

Case report An 11-year-old male neutered Miniature Poodle was investigated for ptyalism, weight loss and anorexia. Cricopharyngeal dysphagia was diagnosed using fluoroscopy, and non-inflammatory salivary disease was diagnosed using a combination of cytology and computed tomography. The dog was successfully managed with phenobarbitone. Conclusion To the authors’ knowledge this is the first time acquired cricopharyngeal dysphagia and phenobarbitone-responsive sialoadenosis have been described together.

Knowledge about acute pancreatitis has increased recently in both the medical and veterinary fields. Despite this expansion of knowledge, there are very few studies on treatment interventions in naturally occurring disease in dogs. As a result, treatment recommendations are largely extrapolated from experimental rodent models or general critical care principles. General treatment principles involve replacing fluid losses, maintaining hydrostatic pressure, controlling nausea and providing pain relief. Specific interventions recently advocated in human medicine include the use of neurokinin-1 antagonists for analgesia and early interventional feeding. The premise for early feeding is to improve the health of the intestinal tract, as unhealthy enterocytes are thought to perpetuate systemic inflammation. The evidence for early interventional feeding is not supported by robust clinical trials to date, but in humans there is evidence that it reduces hospitalisation time and in dogs it is well tolerated. This article summarises the major areas of management of acute pancreatitis in dogs and examines the level of evidence for each recommendation.

Objectives To (i) assess the clinical diagnostic accuracy of SNAP canine pancreatic lipase (cPL) and specific canine pancreatic lipase (Spec cPL) and (ii) assess the agreement of an abnormal test result between SNAP cPL and Spec cPL in dogs presenting with acute abdominal disease. Design Prospective observational cohort study. Setting University teaching hospital emergency center. Animals Thirty-eight client-owned dogs that presented with acute abdominal disease, with a known final diagnosis between March 2009 and April 2010. Dogs were retrospectively assigned into 2 groups, dogs with acute pancreatitis (AP) (Group 1) and dogs without AP (Group 2). Interventions Paired serum samples obtained within 24 hours of presentation were analyzed using the SNAP cPL test and Spec cPL assay. Measurements and Results SNAP cPL clinical sensitivity and specificity was 82% (9/11 dogs of group 1) and 59% (16/27 dogs of group 2), respectively. Spec cPL clinical sensitivity and specificity was 70% (7/10 dogs of group 1) and 77% (20/26 dogs of group 2), respectively. Accuracy of the SNAP and Spec cPL for a clinical diagnosis of pancreatitis was found to be 66% and 75%, respectively. Agreement between a positive SNAP (cPL ≥ 200 μg/L) and a clinical diagnosis pancreatitis resulted in κ = 0.33. Agreement between an increased Spec (cPL ≥ 400 μg/L) and a clinical diagnosis of pancreatitis resulted in a κ = 0.43. The agreement between SNAP and Spec cPL (cPL ≥ 200 μg/L) for the entire cohort resulted in κ = 0.78. Conclusion SNAP cPL and Spec cPL results may provide a "false positive" diagnosis of pancreatitis in up to 40% of dogs presenting with acute abdominal disease. There is good overall agreement between SNAP cPL and Spec cPL; however, there were 4/38 dogs with positive SNAP cPL and "normal" Spec cPL.

Background: Confocal endomicroscopy (CEM) is an endoscopic technology that permits in vivo cellular and subcellular imaging of the gastrointestinal mucosa. Objective: To determine the feasibility of CEM to evaluate small intestinal mucosal topologic morphology in dogs and to characterize the appearance in healthy dogs. Animals: Fourteen clinically healthy research colony dogs. Methods: Experimental study. Dogs were anesthetized for standard endoscopic evaluation of the small intestine followed by CEM. Two fluorophores were used to provide contrast: fluorescein (10% solution, 15 mg/kg IV) before administration of topical acriflavine (0.05% solution) via an endoscopy spray catheter. A minimum of 5 sites within the small intestine were assessed and at each location, sequential adjustment of imaging depth allowed collection of a three-dimensional volume equivalent to an 'optical biopsy'. CEM-guided pinch biopsies were obtained for histologic examination. Results: CEM provided high-quality in vivo cellular and subcellular images. Intravenous administration of fluorescein provided sufficient contrast to allow assessment of the vasculature, cellular cytoplasmic features and goblet cell numbers, and distribution. Topical application of acriflavine preferentially stained cellular nucleic acids, allowing evaluation of nuclear morphology. Quality of captured images was occasionally affected by motion artifact, but improved with operator experience. Conclusion and Clinical Importance: CEM provides in vivo images that allow for cellular and subcellular assessment of intestinal mucosal morphology during endoscopy. This has implications for aiding in vivo diagnosis of gastrointestinal disease. © 2013 by the American College of Veterinary Internal Medicine.

Sinonasal aspergillosis is an uncommon, yet debilitating and often frustrating condition to treat in dogs despite years of research evaluating pathogenesis, diagnosis and treatment. The disease is most commonly caused by non-invasive fungal infection, thought to be secondary to altered innate and/or adaptive immune responses. Attempts to confirm this have however failed. A variety of conflicting opinions regarding the diagnosis and treatment of sinonasal aspergillosis exist. Often the use of a particular treatment protocol is based upon personal or regional preference. Evaluation of the veterinary literature demonstrates that the evidence base in support of individual treatment recommendations is weak. A number of recent publications have helped to expand the current knowledge base and therefore our understanding of important practicalities for both diagnostic options and treatment protocols. The following review examines the current evidence for the pathogenesis of sinonasal aspergillosis in dogs, as well as the various diagnostic options. The available evidence for frequently utilised -therapeutic options and their likely outcomes is also explored.

The cellular events leading to pancreatitis have been studied extensively in experimental models. Understanding the cellular events and inciting causes of the multisystem inflammatory cascades that are activated with this disease is of vital importance to advance diagnosis and treatment of this condition. Unfortunately, the pathophysiology of pancreatitis in dogs is not well understood, and extrapolation from experimental and human medicine is necessary. The interplay of the inflammatory cascades (kinin, complement, cytokine) is extremely complex in both initiating leukocyte migration and perpetuating disease. Recently, nitric oxide (NO) and altered microcirculation of the pancreas have been proposed as major initiators of inflammation. In addition, the role of the gut is becoming increasingly explored as a cause of oxidative stress and potentiation of systemic inflammation in pancreatitis.

Background: The putative role of the gut in amplification of systemic inflammation in acute pancreatitis is gaining credence, and intraluminal nutrition has been shown to decrease inflammation in experimental models of pancreatitis. Prepyloric feeding often is used in people with acute pancreatitis, but has not been evaluated in dogs. Hypothesis: Early intervention with enteral nutrition (EN) delivered proximal to the pylorus will be well tolerated in dogs with acute pancreatitis and provide justification for further larger trials. Animals: Ten dogs with severe acute pancreatitis in an open-label, prospective pilot study. Methods: Dogs were treated with plasma transfusion and standard care, and then consecutively assigned to receive either EN via esophagostomy tube feeding or parenteral nutrition (PN). Outcome was used to determine optimal study size for future studies, and complications were compared between the 2 groups. Results: A significantly greater number of vomiting or regurgitating episodes occurred in dogs receiving PN. The dogs receiving EN did not demonstrate any noticeable postprandial pain. There were more catheter-related complications in the PN group. There was no difference in outcome between the 2 treatments, and 43 dogs for each treatment would be required in future studies to determine a difference in outcome. Conclusions and Clinical Relevance: Early EN delivered proximal to the pylorus is well tolerated in dogs with severe pancreatitis and resulted in fewer complications than PN. Prospective trials in a larger cohort are justified to fully establish the potential benefit of early EN, preferably compared with minimal enteral nutrition.

Background: Four dogs presented with clinical signs of severe hepatic disease after consuming a commercial camel meat diet. Methods: Laboratory investigation revealed evidence of severe liver disease, including markedly increased serum alanine aminotransferase (ALT) activity and total bilirubin concentration, and prolonged clotting times. Results: Two dogs deteriorated despite supportive therapy and were euthanased. Histologically, both livers appeared similar, with the main lesion being extensive periacinar necrosis and haemorrhage. Indospicine, a toxic amino acid of plant origin, was detected in the serum and/or plasma from all four dogs, as well as in tissues of a dog that was necropsied and in a sample of the camel meat fed to this animal. Serum biochemistry tests using blood samples collected from 15 additional dogs identified as having eaten the diet detected indospicine was in the serum of 14 and 3 had increased ALT activity. One of the latter dogs subsequently developed clinical signs of severe liver disease and was euthanased. Conclusion: To the authors' knowledge, this is the first published report of the detection of indospicine residues in camel meat and the occurrence of severe, sometimes fatal, liver disease in dogs that consumed this contaminated meat.

BACKGROUND: Historically, histiocytic ulcerative (HUC) (or granulomatous) colitis of Boxer dogs was considered an idiopathic immune-mediated disease with a poor prognosis. Recent reports of dramatic responses to enrofloxacin and the discovery of invasive Escherichia coli within the colonic mucosa of affected Boxer dogs support an infectious etiology. HYPOTHESIS: Invasive E. coli is associated with colonic inflammation in Boxer dogs with HUC, and eradication of intramucosal E. coli correlates with clinical and histologic remission. ANIMALS: Seven Boxer dogs with HUC. METHODS: Prospective case series. Colonic biopsies were obtained at initial evaluation in 7 dogs, and in 5 dogs after treatment with enrofloxacin. Biopsies were evaluated by standardized histopathology, and fluorescence in situ hybridization (FISH) with probes to eubacteria and E. coli. RESULTS: Intramucosal E. coli was present in colonic biopsies of 7/7 Boxers with HUC. Clinical response was noted in all dogs within 2 weeks of enrofloxacin (7 + or - 3.06 mg/kg q24 h, for 9.5 + or - 3.98 weeks) and was sustained in 6 dogs (median disease-free interval to date of 47 months, range 17-62). FISH was negative for E. coli in 4/5 dogs after enrofloxacin. E. coli resistant to enrofloxacin were present in the FISH-positive dog that relapsed. CONCLUSIONS AND CLINICAL RELEVANCE: The correlation between clinical remission and the eradication of mucosally invasive E. coli during treatment with enrofloxacin supports the causal involvement of E. coli in the development of HUC in susceptible Boxer dogs. A poor response to enrofloxacin treatment might be due to colonization with enrofloxacin-resistant E. coli.

Idiopathic hypereosinophilic syndrome (HES) is a rare syndrome for which Rottweilers appear to over-represent the canine cases. A 6-month-old female entire Rottweiler presented with seizures following a traumatic incident. The dog was identified as having a marked, sustained eosinophilia and investigations did not identify an underlying cause. Concurrently, the dog had chronic eosinophilic hepatitis with impaired liver function and mesenteric eosinophilic lymphadenitis. The dog went on to have spontaneous resolution of HES and normal liver function was subsequently documented. To date, the dog is still alive, more than 4 years after initial presentation. The diagnosis of idiopathic HES in Rottweilers may not carry a poor prognosis and the condition may spontaneously resolve, even in cases with documented organ damage.

Accumulation of a pure transudate abdominal effusion in the absence of significant hypoalbuminaemia is uncommon in dogs and is due to pre-sinusoidal portal hypertension. Reported causes of pre-sinusoidal portal hypertension vary, but suggest a reasonable prognosis. A retrospective analysis of 17 dogs that presented to our institution with ascites due to pre-sinusoidal portal hypertension identified idiopathic hepatic fibrosis or canine chronic hepatitis as the underlying cause in the majority of cases. Twelve (70.5%) dogs were 4 years of age or younger at time of presentation. Total serum protein was higher in dogs with chronic hepatitis than it was in dogs without inflammatory disease. The prognosis was generally poor and no histological, imaging or biochemical parameters were useful as prognostic indicators. Dogs died or were euthanased due to severe clinical signs associated with the portal hypertension and/or perceived poor prognosis.

An 18-month-old boxer was presented for investigation of profound lethargy, and primary hypothyroidism was diagnosed. A strong antithyroglobulin antibody titre was also present, indicating lymphocytic (immune-mediated) thyroiditis as the cause of hypothyroidism. A concurrent protein-losing glomerulonephropathy was also detected, although the aetiology could not be determined at initial presentation. Thyroid replacement and dietary therapy were prescribed. The dog improved clinically for approximately 12 months when it was re-presented with poorly controlled hypothyroidism and renal failure. Postmortem examination confirmed the presence of lymphocytic-plasmacytic thyroiditis, in conjunction with membranoproliferative glomerulonephritis and renal failure.

An eight-year-old, female springer spaniel was treated for metastatic insulinoma with a single intravenous dose of 500 mg/m2 streptozotocin (SZN), and pre- and post-treatment diuresis. A tapering dose of corticosteroids was also administered over a 28 day period. SZN and corticosteroid administration resulted in resolution of hypoglycaemia and subsequent development of diabetes mellitus. Further metastases caused cervical spinal pain and the dog was euthanased 118 days after SZN administration. SZN can be safely used for the treatment of canine insulinoma, but, when compared with other published cases, a marked variation in clinical response to this drug exists and further study is warranted.

A 12-year-old female neutered ragdoll crossbred cat was presented for investigation of generalised weakness and regurgitation. The cat was being treated with transdermal methimazole for hyper-thyroidism, which had been diagnosed 10 weeks previously. An acetylcholine receptor antibody titre was consistent with acquired myasthenia gravis. Withdrawal of methimazole and treatment with pyridostigmine was followed by resolution of clinical signs and reduction of the acetylcholine -receptor antibody titre. Medical control of hyperthyroidism was subsequently achieved with carbimazole, administered in conjunction with pyridostigmine, and no recurrence of clinical signs was observed. Myasthenia gravis is an uncommon but clinically significant adverse effect of methimazole therapy in cats, and may be caused by immunomodulatory properties of this drug. An adverse drug reaction should be considered in cats receiving methimazole that develop myasthenia gravis, and potentially also other immune-mediated disorders.

Objective: To determine the specificity of a snake venom detection kit in urine samples from dogs and cats presenting to a referral centre for diseases unrelated to snake envenomation. Design: Urine was collected from 50 dog and 25 cats presented for investigation and treatment of diseases unrelated to snake envenomation. Urine was collected as a voided sample, by cystocentesis or by catheterisation, and routine urinanalysis was performed. Snake venom testing was performed within 2 h of collection using a commercially available snake venom detection kit, which was observed continuously during the 10-min colour reaction phase for evidence of a visible colour indicating a positive test. Results: No false-positive reactions occurred in any sample analysed. Conclusion: The snake venom detection kit appears to have 100% specificity for using urine as a test sample.

A six-year-old Staffordshire bull terrier had a four-week history of progressive lethargy, ascites and exercise intolerance. A mass 3 cm in diameter obliterating the right atrial lumen was detected by echocardiographic examination. There were lactescent pericardial and serosanguineous pleural effusions. Histological and immunochemical examinations showed that the mass was a primary rhabdomyoma.

A 7-year-old neutered male Somali cat, bred in Western Australia, was presented for investigation of jaundice and severe anaemia. Splenomegaly and hepatomegaly were evident on physical examination. Severe anaemia, along with leukopenia and increased liver enzymes, were present on laboratory evaluation. Clinical investigation identified cholangitis and treatment for this resolved the jaundice but failed to resolve the anaemia. Treatment for Mycoplamsa haemofelis was administered concurrently. Genetic testing was then performed and pyruvate kinase deficiency was identified, the first time this has been reported in an Australian cat. Treatment with immunosuppressive medication was not successful.