Early diagnosis of amanitin exposure (amatoxicosis) in a dog with a point-of-care diagnostic test.

OBJECTIVE: To describe the rapid diagnosis, treatment, and clinical course of a dog that ingested an amanitin-containing mushroom. CASE SUMMARY: A 2-month-old female intact Australian Shepherd presented with diarrhea and vomiting, along with a possible mushroom exposure. Upon presentation, the dog's urine was collected and tested positive by a point-of-care rapid diagnostic test specific for detecting amanitins, the causative agents of amatoxicosis. NEW OR UNIQUE INFORMATION PROVIDED: This is the first reported case of amatoxicosis that was diagnosed using a point-of-care test prior to starting treatment. An early diagnosis helps to guide early treatment decisions in this frequently fatal toxicosis.

[Acute liver failure in a dog after mushroom intake, presumably of the genus Amanita]. / Akutes Leberversagen bei einem Hund nach Aufnahme eines Pilzes, vermutlich der Gattung Amanita.

A 4-year-old, neutered male Husky-mix dog weighing 29.4 kg that reportedly ingested a mushroom most likely of the genus Amanita one day prior to presentation exhibited signs of diarrhea, vomitus, inappetence and progressively worsening lethargy. Clinical chemistry revealed hypoglycemia, hyperbilirubinemia, decreased prothrombin and thromboplastin time, as well as increased liver enzyme activities. Despite hospitalization and supportive therapy over a period of 3 days the dog's general condition worsened leading to euthanasia. The pathomorphological findings were characterized by hemorrhage in several organs, hemorrhagic ingesta, icterus, and marked hepatic cellular necrosis.

Clinical recovery of 5 dogs from amatoxin mushroom poisoning using an adapted Santa Cruz protocol for people.

OBJECTIVE: To describe the clinical course, treatment, and outcome of 5 dogs following ingestion of toxic Amanita spp. mushrooms containing amatoxins using an adapted version of the Santa Cruz protocol developed for people. CASE SERIES SUMMARY: Five dogs were presented with clinical signs compatible with amanitin toxicity with witnessed ingestion noted in 3 of 5 dogs. Clinical findings included acute onset vomiting and diarrhea, lethargy, and hepatopathy including signs of fulminant hepatic failure (increased liver enzyme activities, hyperbilirubinemia, prolonged clotting times, and hypoglycemia were noted among these cases). Urine toxicological screening confirmed the presence of Amanita toxins in 4 cases with expert mycologist speciation in the fifth. Core interventions included percutaneous biliary drainage, use of octreotide, and early nil per os orders. All dogs survived to discharge with this treatment strategy. NEW OR UNIQUE INFORMATION PROVIDED: This case series describes the use of a modified version of the Santa Cruz protocol to address amatoxin-induced fulminant hepatic failure in dogs. The protocol was safe, well tolerated, and all patients made a full clinical recovery.

Rapid, Sensitive, and Accurate Point-of-Care Detection of Lethal Amatoxins in Urine.

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 ß-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.

Fatal Amanita muscaria poisoning in a dog confirmed by PCR identification of mushrooms.

Diagnosing mushroom poisoning in dogs can be difficult and often includes identification of suspect mushrooms. Visual identification may be hindered by mastication, oral medications, or poor quality of environmental mushroom samples. Other analytical techniques may thus be necessary to aid in mushroom identification. A 5-y-old neutered male Labrador Retriever dog developed acute onset of vomiting, diarrhea, tremors, seizures, and somnolence. The dog was treated at a veterinary clinic and was briefly stabilized, but died during transport to an emergency clinic. On postmortem examination at the University of Kentucky Veterinary Diagnostic Laboratory, the dog's stomach was full of mushrooms covered with activated charcoal. Mushrooms were damaged, fragmented, and discolored, precluding accurate visual identification. Mushroom pieces were sent to the Department of Plant Pathology at the University of California-Davis for PCR identification; the neurotoxic mushroom Amanita muscaria was identified. A qualitative liquid chromatography-mass spectrometry (LC-MS) method was developed to detect ibotenic acid and muscimol, the toxic compounds present in A. muscaria. Mushrooms, stomach contents, and urine were analyzed by LC-MS; ibotenic acid and muscimol were detected in all samples. Because identification of ingested mushrooms is sometimes necessary to confirm mushroom poisoning, PCR can identify ingested mushrooms when visual identification is unreliable.

Mushroom Poisoning Cases in Dogs and Cats: Diagnosis and Treatment of Hepatotoxic, Neurotoxic, Gastroenterotoxic, Nephrotoxic, and Muscarinic Mushrooms.

Ingestion of poisonous mushrooms by small animals can lead to liver failure, neurotoxicity, or gastrointestinal irritation. Although amanita poisoning can be lethal, ingestion of other toxic mushrooms is generally self-limiting and not life threatening. Most cases are undiagnosed, as routine diagnostic tests only exist for amanitins and psilocin. Early detection of amanitin exposure can greatly aid in the therapeutic intervention by allowing veterinarians to make timely decisions regarding patient management. Treatment is generally supportive, but specific therapeutic measures exist for amanitin and psilocin exposures.

Acute Inocybe mushroom toxicosis in dogs: 5 cases (2010-2014).

OBJECTIVE: To describe the clinical course, treatment, and outcome of 5 dogs following ingestion of mushrooms belonging to the Inocybe genus. CASE SERIES SUMMARY: Five dogs with witnessed Inocybe ingestions were presented with clinical signs compatible with poisoning. Vomiting, ptyalism, diarrhea, depression, and tachycardia were common clinical findings in the dogs in this case series. The prognosis with Inocybe toxicosis appears to be excellent as all dogs fully recovered following supportive care. NEW OR UNIQUE INFORMATION PROVIDED: This is the first reported case series of Inocybe mushroom ingestions in dogs where identification of the mushrooms were confirmed by an expert mycologist.

A novel orellanine containing mushroom Cortinarius armillatus.

Orellanine (3,3',4,4'-tetrahydroxy-2,2'-bipyridine-1,1'-dioxide) is a tetrahydroxylated di-N-oxidized bipyridine compound. The toxin, present in certain species of Cortinarius mushrooms, is structurally similar to herbicides Paraquat and Diquat. Cortinarius orellanus and Cortinarius rubellus are the major orellanine-containing mushrooms. Cortinarius mushrooms are widely reported in Europe where they have caused human poisoning and deaths through accidental ingestion of the poisonous species mistaken for the edible ones. In North America, Cortinarius orellanosus mushroom poisoning was recently reported to cause renal failure in a Michigan patient. Cortinarius mushroom poisoning is characterized by delayed acute renal failure, with some cases progressing to end-stage kidney disease. There is debate whether other Cortinarius mushroom contain orellanine or not, especially in North America. Currently, there are no veterinary diagnostic laboratories in North America with established test methods for detection and quantitation of orellanine. We have developed two diagnostic test methods based on HPLC and LC-MSMS for identification and quantitation of orellanine in mushrooms. Using these methods, we have identified Cortinarius armillatus as a novel orellanine-containing mushroom in North America. The mean toxin concentration of 145 ug/g was <1% of that of the more toxic C. rubellus. The HPLC method can detect orellanine at 17 µg g(-1) while the LC-MSMS method is almost 2000 times more sensitive and can detect orellanine at 30 ng g(-1). Both tests are quantitative, selective and are now available for veterinary diagnostic applications.

Modulation of the spleen transcriptome in domestic turkey (Meleagris gallopavo) in response to aflatoxin B1 and probiotics.

Poultry are highly susceptible to the immunotoxic effects of the food-borne mycotoxin aflatoxin B1 (AFB1). Exposure impairs cell-mediated and humoral immunity, limits vaccine efficacy, and increases the incidence of costly secondary infections. We investigated the molecular mechanisms of AFB1 immunotoxicity and the ability of a Lactobacillus-based probiotic to protect against aflatoxicosis in the domestic turkey (Meleagris gallopavo). The spleen transcriptome was examined by RNA sequencing (RNA-seq) of 12 individuals representing four treatment groups. Sequences (6.9 Gb) were de novo assembled to produce over 270,000 predicted transcripts and transcript fragments. Differential expression analysis identified 982 transcripts with statistical significance in at least one comparison between treatment groups. Transcripts with known immune functions comprised 27.6 % of significant expression changes in the AFB1-exposed group. Short exposure to AFB1 suppressed innate immune transcripts, especially from antimicrobial genes, but increased the expression of transcripts from E3 ubiquitin-protein ligase CBL-B and multiple interleukin-2 response genes. Up-regulation of transcripts from lymphotactin, granzyme A, and perforin 1 could indicate either increased cytotoxic potential or activation-induced cell death in the spleen during aflatoxicosis. Supplementation with probiotics was found to ameliorate AFB1-induced expression changes for multiple transcripts from antimicrobial and IL-2-response genes. However, probiotics had an overall suppressive effect on immune-related transcripts.

Dog intoxication by lizard's claw mushroom, Lysurus cruciatus (higher Basidiomycetes) in southern Brazil.

A case of mushroom poisoning of a dog caused by a phalloid fungus is reported for the first time. The phalloid caused gastrointestinal syndrome in a 1-year-old dog, and was identified as Lysurus cruciatus, a common phalloid fungus in southern Brazil.

Respiratory arrest following ingestion of wild mushrooms in 3 dogs (2006-2011).

OBJECTIVE: To describe the clinical course, treatment, and outcome of 3 dogs with respiratory arrest following mushroom ingestion. CASE SERIES SUMMARY: Three dogs were presented for mushroom toxicosis that developed respiratory arrest. Two of the dogs were treated with diazepam just prior to the development of respiratory arrest; 1 dog received no medications prior to respiratory arrest. Of the 3 dogs, 1 was euthanized and the remaining 2 recovered fully with assisted and mechanical ventilation. NEW OR UNIQUE INFORMATION PROVIDED: This is the first documentation of respiratory arrest associated with mushroom toxicosis in dogs.

Mushroom toxicosis in dogs in general practice causing gastroenteritis, ptyalism and elevated serum lipase activity.

Mushroom toxicosis is rarely diagnosed in dogs and is poorly reported in the veterinary literature. This report suggests that mushroom toxicosis is a potentially under-diagnosed condition in first opinion practice in the UK. Nine dogs with clinical signs consistent with mushroom toxicosis were identified from the records of an out-of-hours emergency service between August 2010 and January 2011. Four dogs were later excluded because of clinical inconsistencies. Clinical signs included acute profuse ptyalism (5/5), diarrhoea (5/5), vomiting (4/5), hypovolaemia (4/5), stuporous (3/5) or obtunded mentation (1/5), miosis (2/5) and hypothermia (2/5). Serum lipase activity was elevated in 4/4 dogs; canine-specific pancreatic lipase was elevated in the remaining dog. Four dogs recovered with aggressive intravenous fluid therapy, analgesia and supportive care; the remaining dog was euthanased due to severe clinical signs and financial constraints. Mushroom toxicosis is an important differential diagnosis for acute gastroenteritis and one possible cause of some cases of "Seasonal Canine Illness". Affected dogs may demonstrate elevated pancreatic enzymes and mushroom toxicosis should be considered in cases of elevated lipase or abnormal semi-quantitative canine-specific pancreatic lipase activities.

Suspected muscarinic mushroom intoxication in a cat.

A 3-year-old domestic shorthair cat was witnessed ingesting mushrooms and developed signs of muscarine intoxication. After stabilisation and treatment with atropine the cat recovered well and was discharged from hospital in 2 days. This report describes the features and successful management of this unusual toxicosis in cats.

Mushroom poisoning cases in dogs and cats: diagnosis and treatment of hepatotoxic, neurotoxic, gastroenterotoxic, nephrotoxic, and muscarinic mushrooms.

Of the several thousand species of mushrooms found in North America, less than 100 are toxic. Species in the genus Amanita are responsible for the vast majority of reported mushroom poisonings. In general, the number of reported mushroom poisonings in animals is low, most likely because toxicology testing is available for a limited number of mushroom toxins and thus many cases are not confirmed or reported. Also, only a limited number of mushrooms are submitted for identification purposes. Mushroom intoxications require tremendous efforts from clinicians and toxicologists in terms of making a diagnosis and treatment, and management is challenging.

Amanitin intoxication in two beef calves in California.

Two 2- and 3-month-old beef calves from 2 separate herds, locations, and times were found dead and were submitted to the veterinary diagnostic laboratory for diagnostic work-up. In both cases, no premonitory signs were seen by the owners. Histopathology revealed acute panlobular hepatic necrosis in both calves. In addition, calf A had copper and selenium deficiency, and calf B had oxalate nephrosis, and selenium and zinc deficiencies. Alpha-amanitin was detected in the urine from calf A, and in the liver and rumen contents from calf B using liquid chromatography-mass spectrometry. The cause of panlobular hepatic necrosis and death of both calves was determined to be amanitin toxicosis from ingestion of amanitin-containing mushrooms based on microscopic changes and toxicological analysis of tissues. In cases of sudden death in cows with histopathological findings of panlobular hepatic necrosis, toxicological analysis for amanitin is needed for a definitive diagnosis of poisoning by amanitin-containing mushrooms.

Amanitin toxicosis in two cats with acute hepatic and renal failure.

Amanitin is a toxic cyclopeptide present in several species of poisonous mushrooms. Amanitin toxicosis was diagnosed in 2 cats from separate premises. Both cats initially had lethargy and vomiting, and they rapidly developed depression and neurological signs over 24-48 hours. Marked elevation of alanine aminotransferase was the primary finding, with subsequent serum chemistry values compatible with hepatic and renal failure. Histopathological findings consisted of submassive to massive acute hepatic necrosis, renal proximal tubular epithelial necrosis, and foci of necrosis and inflammation in the gastrointestinal tract. Amanitin exposure was confirmed postmortem by detection of α-amanitin in the kidney by liquid chromatography-mass spectrometry. A similar clinical course and pathological changes are reported in human and canine amanitin intoxication; however, gastrointestinal lesions are not typically described.