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Case Reports
. 2025 Jun 18:12:1542020.
doi: 10.3389/fvets.2025.1542020. eCollection 2025.

Case Report: α-amanitin toxicosis leading to acute death in a puppy

Affiliations
Case Reports

Case Report: α-amanitin toxicosis leading to acute death in a puppy

Zachary Lake et al. Front Vet Sci. .

Abstract

A 12-week-old, male intact, Shetland Sheepdog presented with acute onset vomiting and diarrhea, rapidly progressing to stupor and hypoglycemic shock following ingestion of α-amanitin-containing mushrooms. Despite aggressive therapeutic interventions, the patient exhibited rapid systemic deterioration characterized by recurrent hypoglycemia, hypotension, and multi-organ failure, leading to cardiopulmonary arrest within 22 h of presentation. Definitive diagnosis was unable to be elucidated prior to death, leading to an untailored treatment plan. Post-mortem analysis confirmed extensive necrosis of the liver, kidneys, and brain. Presence of α-amanitin was confirmed in the hepatic tissue via post-mortem liquid chromatography-tandem mass spectrometry analysis. Serum collected at presentation was submitted post-mortem for an insulin level which was found to be discordantly elevated, which may demonstrate an alternative mechanism of hypoglycemia in this case. This case highlights the rapidly lethal potential of α-amanitin in pediatric patients and the non-classical case presentation. This report contributes to the limited veterinary literature on this toxin in pediatric patients and underscores the need for heightened awareness and rapid diagnosis and treatment in suspected cases.

Keywords: amanita; canine; hepatic necrosis; hypoglycemia; toxicity.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Hepatocellular necrosis. There is diffuse disruption of the hepatocyte cords. Individualized hepatocytes exhibit variable cell size, rounding of cytoplasmic margins, and cytoplasmic hypereosinophilia. Most of the hepatocytes lack a nucleus and others have karyorrhectic or pyknotic nuclear remnants.
Figure 2
Figure 2
Renal cortical tubule epithelial necrosis. The cortical tubules are commonly affected by necrosis of the epithelial cells characterized by cytoplasmic vacuolation and/or hypereosinophilia, nuclear pyknosis, karyorrhexis, or karyolysis, and sloughing into the tubule lumina. Sloughed epithelial cells are admixed with amorphous, eosinophilic debris within the tubular lumina.
Figure 3
Figure 3
Neuronal necrosis. Neurons within the deep cerebrocortical laminae exhibit neuronal degeneration and necrosis characterized by shrunken, angular cell bodies with hypereosinophilic cytoplasm and karyolytic or pyknotic nuclei. The neurons and blood vessels are commonly surrounded by a clear space indicative of edema.

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