Cortinarius orellanosus and Cortinarius rubellus
These mushrooms have a colorful but mostly brownish cap, stalk, and thick gills; the matured gills are orange-rust in color. The spores are bright rust, orange-brown, or gray-brown, but not purple-brown. They have a cobweb-like partial veil called a cortina that often remains as a faint band of fibers around the stalk. In North America, C rubellus (also known as C rainierensis) is found in northern areas of the east and west coasts, while C orellanosus has been reported in Michigan.
The toxic Cortinarius mushroom species contain orellanine, a bipyridyl compound similar to the herbicides paraquat and diquat. Toxin concentrations vary greatly with the portion of the mushroom and the species. Orellanine is highly nephrotoxic; however, the mechanism of toxicity is not yet fully understood. Orellanine is thought to inhibit protein synthesis in renal tubular epithelium and decrease cellular NADPH, resulting in free radical damage, lipid peroxidation, and membrane destruction. In humans, a dose of 0.04 mg of orellanine/kg (contained in 2–3 mushrooms) can lead to disease requiring lifelong dialysis. There are no confirmed cases of animal poisoning in North America; however, lack of awareness among veterinarians about the toxicity of these mushrooms, coupled with a lack of confirmatory diagnostic tests for orellanine, may limit diagnosis of poisoning by these mushrooms. Orellanine is not degraded by cooking, freezing, or drying.
Clinical Findings of Orellanine Toxicosis in Animals
There is a latent phase between ingestion and onset of clinical signs. Gastrointestinal signs may occur within 72 hours. Within 3–20 days, clinical signs of renal failure may develop. The onset of clinical signs is delayed (3–14 days after ingestion). Gastrointestinal signs include anorexia, vomiting, diarrhea or constipation, and abdominal pain. Clinical signs of renal failure include polyuria and polydipsia. Oliguria, followed by diuresis and recovery or chronic renal failure, may occur. The kidney seems to be the target organ; lesions include interstitial nephritis, tubular damage, and fibrosis. Hepatic damage is infrequently reported. In most cases, marked improvement over an extended period (6 months) occurs; however, chronic renal failure occurs in some cases.
Diagnosis of Orellanine Toxicosis in Animals
Monitoring of renal function parameters, acid-base status, electrolytes, and CBC are important diagnostic components. Urinalysis may reveal isosthenuria, glucosuria, pyuria, proteinuria, cylindruria, and hematuria. Activities of liver enzymes typically remain within normal limits. Orellanine can be detected in mushrooms, stomach contents, and urine within 24 hours after exposure. Unfortunately, due to the lag time between ingestion and onset of clinical signs, this may not be clinically useful. Orellanine can be detected in the renal cortex up to 6 months after exposure, suggesting that the toxin is sequestered in the kidney. Renal pathological changes include acute tubular injury, interstitial edema, and interstitial nephritis, with no hepatic involvement. Mushroom identification can differentiate Cortinarius spp from Paxillus involutus, a mushroom reported to cause hypersensitivity leading to renal failure.
Treatment of Orellanine Toxicosis in Animals
Treatment should be focused on decontamination, mushroom identification (often difficult), and intensive supportive care. Due to the long latent period and onset of clinical signs days after exposure, decontamination is not useful. Treatment consists of supportive care for renal failure and gastrointestinal signs. Intravenous fluid therapy, gastrointestinal protectants (sucralfate, famotidine, ranitidine, or omeprazole), and antiemetics (maropitant or metoclopramide) may be used. In humans, forced diuresis is not recommended due to increased renal damage, and chronic hemodialysis is often necessary and, in some cases, renal transplantation is performed. Complete recovery of renal function occurs in only 30% of patients with orellanine poisoning. Furosemide increases toxicity in rats when injected before C orellanoides ingestion. In animals, peritoneal or hemodialysis may be considered; however, data on efficacy do not exist. Experimental treatments, in humans, include use of corticosteroids, N-acetylcysteine, and selenium but results have been inconclusive.