A. ocreata resembles several edible species commonly consumed by humans, increasing the risk of accidental poisoning.

The species occurs in the Pacific Northwest and California Floristic Provinces of North America, associating with oak trees.

Similar in toxicity to the death cap (A. phalloides) and destroying angels of Europe (A. virosa) and eastern North America (A. bisporigera), it is a potentially deadly fungus responsible for several poisonings in California.

[3] Its principal toxic constituent, α-Amanitin, damages the liver and kidneys, often fatally, and has no known antidote, though silybin and N-acetylcysteine show promise.

[12] It forms ectomycorrhizal relationships and is found in association with coast live oak (Quercus agrifolia),[13] as well as hazel (Corylus spp.).

[3][14] There is some evidence it may be the most toxic of all the North American phalloideae, as a higher proportion of people consuming it had organ damage and 40% perished.

[16] Amatoxins consist of at least eight compounds with a similar structure, that of eight amino-acid rings;[17] of those found in A. ocreata, α-Amanitin is the most prevalent and along with β-Amanitin is likely to be responsible for the toxic effects.

[17] Signs and symptoms of poisoning by A. ocreata are initially gastrointestinal in nature and include colicky abdominal pain, with watery diarrhea and vomiting which may lead to dehydration and, in severe cases, hypotension, tachycardia, hypoglycemia, and acid-base disturbances.

[25] Kidney failure (either secondary to severe hepatitis[26][27] or caused by direct toxic renal damage)[20] and coagulopathy may appear during this stage.

There are four main categories of therapy for poisoning: preliminary medical care, supportive measures, specific treatments, and liver transplantation.

[4][29] Supportive measures are directed towards treating the dehydration which results from fluid loss during the gastrointestinal phase of intoxication and correction of metabolic acidosis, hypoglycemia, electrolyte imbalances, and impaired coagulation.

[30] There is some evidence that intravenous silibinin, an extract from the blessed milk thistle (Silybum marianum), may be beneficial in reducing the effects of amatoxins, preventing their uptake by hepatocytes, thereby protecting undamaged hepatic tissue.

[4] Evidence suggests that, although survival rates have improved with modern medical treatment, in patients with moderate to severe poisoning up to half of those who did recover suffered permanent liver damage.