Globally, mushroom poisonings cause about 100 human deaths each year, with thousands of people requiring medical assistance. Dogs are also susceptible to mushroom poisonings and require medical assistance. Cyclopeptides, and more specifically amanitins (or amatoxins, here), are the mushroom poison that causes the majority of these deaths. Current methods (predominantly chromatographic, as well as antibody-based) of detecting amatoxins are time-consuming and require expensive equipment. In this work, we demonstrate the utility of the lateral flow immunoassay (LFIA) for the rapid detection of amatoxins in urine samples. The LFIA detects as little as 10 ng/mL of α-amanitin (α-AMA) or γ-AMA, and 100 ng/mL of β-AMA in urine matrices. To demonstrate application of this LFIA for urine analysis, this study examined fortified human urine samples and urine collected from exposed dogs. Urine is sampled directly without the need for any pretreatment, detection from urine is completed in 10 min, and the results are read by eye, without the need for specialized equipment. Analysis of both fortified human urine samples and urine samples collected from intoxicated dogs using the LFIA correlated well with liquid chromatography–mass spectrometry (LC-MS) methods.

Background: Benign esophageal strictures can recur despite multiple dilatation procedures and palliative management can be challenging.Objective: To describe the technique and determine the outcome of esophageal stenting for treatment of refractory benign esophageal strictures (RBES) in dogs.Animals: Nine dogs with RBES. Methods: Retrospective review of records for dogs with RBES. Indwelling intraluminal esophageal stents were placed transorally with endoscopy, fluoroscopic guidance, or both. Follow-up information was obtained via medical record or telephone interview.Results: Nine dogs had 10 stents placed including biodegradable stents (BDS) (6/10), self-expanding metallic stents (SEMS) (3/10), and a self-expanding plastic stent (SEPS) (1/10). All dogs had short-term improved dysphagia. Complications included ptyalism, apparent nausea, gagging, vomiting, or regurgitation (8/9), confirmed recurrence of stricture (6/9), stent migration (3/9), stent shortening (1/9), megaesophagus (1/9), incisional infection (1/9), and tracheal-esophageal fistula (1/9). Eight of 9 dogs required intervention because of the complications of which 4 of 8 dogs were eventually euthanized because of stent-related issues. One dog was lost to follow-up examination.Conclusions and Clinical Importance: Findings suggest that esophageal stent placement was safe and technically effective, but unpredictably tolerated in dogs with RBES. If a stent is placed, dogs should be monitored carefully for stent migration, dissolution of absorbable stents, and recurrence of strictures.

Background: Hereditary factor VII (FVII) deficiency is characterized as a mild bleeding disorder in Beagles, caused by a missense mutation in exon 5 of the FVII gene. An Alaskan Klee Kai dog with severe bleeding after trauma was diagnosed with FVII deficiency based on coagulation testing. Molecular analyses were undertaken to identify the genetic basis of the defect in this breed. Hypothesis: FVII deficiency in Alaskan Klee Kai dogs is caused by a mutation in the FVII gene. Animals: Eighteen client‐owned Alaskan Klee Kai. Methods: Coagulation screening tests and factor assays were performed to characterize the coagulopathy. All coding regions of the propositus' FVII gene were sequenced. Amplification of exon 5, sequencing, and Mnl I restriction digest experiments were performed to screen for a point mutation in the remaining 17 dogs. Results: FVII deficiency was diagnosed in 6 dogs with a median FVII activity (FVII:C) of 5% (reference range, 50–150%). All FVII‐deficient Alaskan Klee Kai were homozygous for the same mutation as FVII‐deficient Beagles (ie, a G to A transition), resulting in substitution of glycine 96 by glutamic acid. An overlap in the FVII: C values obtained from heterozygote and wild‐type dogs precluded accurate detection of carriers without genetic screening. Conclusions and Clinical Importance: FVII deficiency may be associated with a bleeding tendency and should be considered in Alaskan Klee Kai dogs with prolonged prothrombin times. Plasma FVII:C accurately identifies affected dogs, but deoxyribonucleic acid testing is required for identification of carriers.

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OBJECTIVE To report history, physical examination findings, clinicopathologic abnormalities, treatments, and outcomes of dogs with confirmed α-amanitin toxicosis resulting from ingestion of α-amanitin–containing mushrooms, and to report whether any differences were significant between survivors and nonsurvivors. ANIMALS 59 dogs. PROCEDURES Medical records of all dogs with confirmed α-amanitin toxicosis presented to a northern California emergency and specialty veterinary hospital between January 2006 and July 2019 were reviewed for signalment; body weight; history; physical examination findings including rectal temperature at presentation; results of serum biochemical analyses, coagulation tests, and a test for the detection of α-amanitin in urine; treatments; and outcomes. Differences for each were compared between survivors and nonsurvivors. RESULTS Among the 59 dogs, 36 were < 1 year of age; 56 had variable clinical signs that included vomiting, diarrhea, anorexia, and weakness or lethargy; and 22 had rectal temperatures > 39.2°C (102.5°F) at presentation. Cases were seen throughout the calendar year. At presentation, alanine aminotransferase activity was mildly to markedly increased in 97% of dogs, hypoglycemia was noted in 78%, and coagulation times were prolonged in 91%. Most dogs that rapidly decompensated died; however, 13 dogs survived to hospital discharge and completely recovered. CONCLUSIONS AND CLINICAL RELEVANCE Ability to recognize dogs with α-amanitin toxicosis on the basis of clinical signs, physical examination findings, and clinicopathologic test results is essential because mushroom ingestion is rarely observed and immediate treatment is necessary. Dogs that have marked hypoglycemia or coagulopathy may have a poor prognosis.