Amanita phalloides poisoning is the most common form of mushroom poisoning. These mushrooms contain the poison amatoxin that affects primarily the liver and leads to disturbances in gastrointestinal and renal function, seizures, coma and death.
The clinical manifestations of poisoning by amatoxin may be grouped into four phases.
The first phase is a period of latency, with the onset of signs and symptoms delayed until 6 to 24 hours. In some instances, patients do not present until 2-3 days after mushroom consumption [1].
The second- or gastrointestinal- phase is marked by patients developing abdominal pain, vomiting and severe diarrhea that may contain blood. The fluid loss may progress to hypovolemia, electrolyte disturbances and circulatory shock [2] [3]. The levels of liver enzymes and bilirubin are usually normal at this stage.
In the third phase, patients experience a gradual resolution of dysentery over a 24-hour period, suggesting an apparent recovery. However, elevations in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) become evident at this stage, with jaundice clinically apparent in some individuals.
Two to four days after mushroom ingestion, severely poisoned patients may develop irreversible liver failure, often accompanied by acute renal failure. Multisystem organ failure, pancreatitis, disseminated intravascular coagulation, seizures, coma and death may occur within 1-3 weeks of poisoning [4] [5] [6]. Some patients may undergo full recovery with an improvement in both their symptoms and their liver profile.
The diagnosis of Amanita phalloides poisoning relies heavily on the accuracy of the various clinical findings and must be suspected in individuals presenting with a late onset of gastrointestinal symptoms coupled with hepatotoxic signs.
A complete liver profile may help document the hepatic injury caused by amatoxins. This includes aspartate transaminase (AST), alanine transaminase (ALT), serum bilirubin, alkaline phosphatase (ALP) and lactic acid dehydrogenase (LDH) levels. A coagulation profile measuring the prothrombin time (PT) and activated partial thromboplastin time (aPTT) is a reliable marker for mushroom intoxication and hence, should be measured routinely.
All patients with suspected ingestion of amatoxin-containing mushrooms must undergo certain baseline investigations including measurement of serum electrolyte and blood glucose levels, and a complete blood count [7]. Creatinine and blood urea nitrogen levels may be raised, especially in renal failure.
Microscopic hematuria may be present in the initial stages of poisoning, whilst acute renal failure may manifest as proteinuria and gross hematuria. Oliguria and anuria may be the other findings. Pancreatic amylase and lipase levels need to be measured as well.
Imaging studies in the form of abdominal X-rays, ultrasonography or a computed tomography (CT) scan may help to narrow the differential diagnosis. Histology of liver specimens shows centrilobular necrosis accompanied by areas of hemorrhage and necrosis.
The presence of amatoxin in the suspected mushroom samples may be detected via the Meixner test. The high number of false-positive cases with this test impairs its usage in a clinical setting. The spores of the implicated mushroom may be examined in gastric secretions, appearing smooth and turning blue on exposure to Melzer solution. Other tests used to measure the level of toxins include high-performance liquid chromatography, thin layer chromatography and radioimmunoassays [8].