Outbreak of fatal mushroom poisoning with Amanita franchetii and Ramaria rufescens

Abstract

Mushroom poisoning continues to occur worldwide. We report a cluster of sudden death in two villages of the Gan County, Jiangxi Province, People’s Republic of China in September 2005. Extensive investigations on the clinical presentation, epidemiological features, food and water sources have led to the identification of mushroom poisoning. Each of the 10 patients ate wild mushrooms, identified as Amanita franchetii and Ramaria rufescens, and suffered gastrointestinal symptoms prior to sudden deaths.

BACKGROUND

Reports of severe and fatal mushroom poisonings have increased worldwide.¹ Several new toxic species of mushrooms, including some previously edible ones, have also been described to cause unique toxidromes in recent years.^2–6 Ten people died suddenly in two villages of the Gan County, Jiangxi Province, People’s Republic of China within a few days in September of 2005. Some of their family members also suffered from mild to moderate symptoms. The authors report the investigations of the cluster death, and our findings suggest that the cause of the sudden deaths appeared to be poisoning from Amanita franchetii and Ramaria rufescens. It is very important to report mushroom poisonings, in particularly the previously edible ones.

CASE PRESENTATION

Ten sudden deaths occurred between 9 and 15 September 2005 in two villages (Hangfang and Dabu) of the Gan County, Jiangxi Province, PR China. We collected detailed medical histories of all the patients and their family members, and local epidemiological information. Tests of food specimen and environmental survey were also performed. The investigation and follow-up lasted for 14 months.

The demographics and clinical features of the 10 patients are summarised in the table. The patients ranged from 21 to 67 years old with a mean age of 48.6. There were nine women (90%) and one man (10%) from seven families. Their occupations were farmers or housewives. Two patients had a history of pulmonary tuberculosis and chronic colitis, respectively. Deaths occurred in seven families. There was no interaction between these families during the outbreak. Their daily food was rice and vegetables. They all suffered from gastrointestinal symptoms 3–6 days ante mortem.

Table 1.

Demographics and clinical features of the 10 patients

Pt	Age/sex	Kinship	PMH	Date of ingestion	Symptoms	Date of death
1	67/f	Mother	None	4 September	N/V, diarrhoea, general aching	9 September
2	30/f	Daughter-in-law	None	4 September	N/V	9 September
3	62/f	Mother	Chronic colitis	5 September	N/V, diarrhoea, general aching	10 September
4	43/f	Daughter-in-law	None	4 September	N/V	10 September
5	47/f		None	6 September	N/V, dizziness	11 September
6	60/f		None	7 September	N, abd distention and pain	12 September
7	67/m	Husband	Pulmonary TB	8 September	Dizziness, abd distention	15 September
8	60/f	Wife	None	8 September	N, dizziness	14 September
9	21/f		None	4 September	Dizziness	10 September
10	20/f		None	6 September	N, abd distention	11 September

abd, abdominal; N/V, nausea/vomiting.

The symptoms appeared to have decreased 2 days prior to deaths, and some of the patients went back to work. Eight of the 10 patients suddenly collapsed at work or after urinating. Transient spells of muscle spasms or tremors (80%) were witnessed. The other two patients (1 and 7) developed dyspnoea, chest distress and nausea, and were sent to the local hospitals for evaluation. Physical examination was significant for hypotension with a blood pressure of 40–60/20–30 mm Hg, tachycardia and diaphoresis. There was no bleeding. The lungs were clear, and the abdomen was soft. The liver and spleen were not palpated under the costal margin. Pathological reflexes were negative. Laboratory tests were unremarkable except moderately elevated AST. EKG showed sinus tachycardia, infrequent premature ventricular complexes and S-T depression. Despite fluid resuscitation and management with steroid and vasoactive agent, the patients deteriorated and passed away within 10 h.

INVESTIGATIONS

There were four surviving family members who were evaluated in hospitals. Their vital signs were stable. There was no jaundice, bleeding or ecchymosis. Laboratory test were significant for slightly elevated hepatic ALT. The coagulation study was normal. EKG and telemetry showed sinus tachycardia and T-wave inversion in some leads. They improved with supportive care. Their follow-up EKGs were normal.

The seven families lived in the same mountain area of 25 km². Based on an onsite investigation, there were no environmental pollution or unknown animal deaths in the area 2 months before and after the incident. We found no toxic substances, including pesticides, rodenticides and other toxic chemical agents in the water and food samples. The weather was moderate with a mean temperature of 26∼34°C without raining in the fall. There was no history of such cluster deaths in the area.

DIFFERENTIAL DIAGNOSIS

All of the patients ate wild mushrooms prior to the gastrointestinal symptoms. The time between mushroom ingestion and symptom onset was 2–15 h. After the inspection of 13 types of mushrooms collected in the area, the botanists identified A franchetii and R rufescens as being potentially poisonous and the cause of deaths (figs 1, 2).

Figure 1.

Amanita franchetii.

Figure 2.

Ramaria rufescens.

OUTCOME AND FOLLOW-UP

Following our recommendation, the local government has banned the picking, selling and ingestion of wild mushrooms. Since then, there have not been any unexplained deaths or mushroom poisonings in the last 14 months.

DISCUSSION

Mushroom poisoning is divided into four types as follows: (1) gastrointestinal; (2) neuropsychic; (3) haematolysis; and (4) toxic hepatitis. Gastrointestinal poisons are the most frequently encountered mushroom toxins. Amatoxins, which are responsible for more than 95% of mushroom-related fatalities, are cyclic octapeptides that are synthesised by a number of Amanita species and several of their relatives. At least five subtypes of amatoxins are known, the most significant being the alpha-amatoxin and beta-amatoxin. Both toxins are rapidly absorbed by the GI tract. Alpha-amanitin works by slowly attacking RNA polymerase, an enzyme in the liver. It ultimately affects the central nervous system and kidneys. Unlike many fungal toxins, it does not cause symptoms right away. Six to 24 h after ingestion, there may be an early feeling of unease, followed by violent cramps, severe abdominal pain, vomiting and diarrhoea. On the third day, there is a remission of symptoms, but this is a false remission. During this asymptomatic period, toxins severely affect the liver, resulting in gastrointestinal bleeding, coma, kidney failure and death usually within 7 days after eating the mushrooms if aggressive medical management or a liver transplant is not performed.

In this report, all the 10 patients developed GI symptoms 2–15 h after eating wild mushrooms, followed by a period of reduced symptoms and then died suddenly within 7 days after symptom onset. These clinical features and the identification of the ingested mushroom species suggested poisoning from A franchetii and R rufescens. In this outbreak, all patients were adults (21–67 years old). Nine of them were women. It was unclear whether men and children were less susceptible to the specific toxins from the A franchetii and R rufescens or they did not eat as many mushrooms as the women. After the ban on eating wild mushrooms, there were no further unexplained sudden deaths during the 14-month follow-up. However, there was no history of such outbreaks, despite the fact that farmers routinely picked and ate wild mushrooms in the past. To the best of our knowledge, there have been no reports of poisoning from ingestion of A franchetii and R rufescens. One possible explanation could be genetic mutation of the mushroom toxins. Several new mushroom poisoning syndromes have been described since the early 1990s.^2–7 Some previously edible species such as Tricholoma equestre (Yellow Trich) were reported as severely poisonous.^6,7 Therefore, our findings suggest that A franchetii and R rufescens should be considered toxic unless additional studies prove otherwise.

LEARNING POINTS

• Ingestion of Amanita Franchetii and Ramaria Rufescens may be fatal.

• Previously edible mushrooms may become poisonous.

• Picking and ingesting wild mushrooms are not safe and should be prohibited.