Mushroom Poisoning Outbreaks - China, 2021.

What is already known about this topic?: Mushroom poisoning is one of the most serious food safety issues in China. Most poisoning incidents resulted from eating mushrooms causing gastroenteritis and psycho-neurological disorder from which patients usually could fully recover. Most deaths resulted from species causing acute liver failure and rhabdomyolysis, and the remaining deaths were attributed to acute renal failure and hemolysis. What is added by this report?: In 2021, the total number of investigations was 327 from 25 provincial-level administrative divisions, involving 923 patients and 20 deaths, and the overall mortality was 2.17%. Overall, 74 poisonous mushrooms causing 6 different clinical syndromes were successfully identified, 15 of which were newly recorded in China as poisonous mushrooms. What are the implications for public health practice?: Considering the potential huge risks for collecting and eating wild mushrooms, we strongly advise not collecting and eating unfamiliar wild mushrooms. Promoting knowledge about poisonous mushrooms is essential and urgent to reduce mushroom poisonings. Precise species identification timely after mushroom poisoning is important for appropriate diagnosis and treatment. Many deaths were ascribed to delayed hospitalization.

Mushroom Poisoning Outbreaks - China, 2020.

SUMMARY: What is already known about this topic? Acute liver failure, rhabdomyolysis, acute renal failure, and hemolysis caused by poisonous mushrooms are the most important mushroom poisoning threats to the Chinese population. The most notorious lethal mushrooms are the species from genera Amanita, Lepiota, and Galerina that cause acute liver failure, and Russula subnigricans that leads to rhabdomyolysis.What is added by this report? In 2020, the total number of investigations reached 676, involving an estimated 102 species of poisonous mushrooms, 24 of which were newly recorded in China. Gyromitra venenata was newly discovered in incidents in Yunnan and Guizhou provinces and were the first reported poisonings due to gyromitrins in China since 2000. The rare poisoning Shiitake mushroom dermatitis was recorded in China. Hemolysis poisoning caused by Paxillus involutus was recorded for the second time since the beginning of the new century, resulting in one death in Inner Mongolia Autonomous Region.What are the implications for public health practice? Promoting knowledge about safe consumption of mushrooms is essential to reduce mushroom poisonings. It is not wise to collect and eat wild mushrooms. For southwestern provinces such as Yunnan, especially, caution must be exercised with unfamiliar mushroom species.

Energy disorders caused by mitochondrial dysfunction contribute to α-amatoxin-induced liver function damage and liver failure.

Mushroom toxicity is the main branch of foodborne poisoning, and liver damage caused by amatoxin poisoning accounts for more than 90 % of deaths due to mushroom poisoning. Alpha-amatoxin (α-AMA) has been considered the primary toxin from amatoxin-containing mushrooms, which is responsible for hepatotoxicity and death. However, the mechanism underlying liver failure due to α-AMA remains unclear. This study constructed animal and cell models. In the animal experiments, we investigated liver injury in BALB/c mice at different time points after α-AMA treatment, and explored the process of inflammatory infiltration using immunohistochemistry and western blotting. Then, a metabonomics method based on gas chromatography mass spectrometry (GCMS) was established to study the effect of α-AMA on liver metabonomics. The results showed a significant difference in liver metabolism between the exposed and control mice groups that coincided with pathological and biochemical indicators. Moreover, 20 metabolites and 4 metabolic pathways related to its mechanism of action were identified, which suggested that energy disorders related to mitochondrial dysfunction may be one of the causes of death. The significant changes of trehalose and the fluctuation of LC3-II and sqstm1 p62 protein levels indicated that autophagy was also involved in the damage process, suggesting that autophagy may participate in the clearance process of damaged mitochondria after poisoning. Then, we constructed an α-AMA-induced human normal liver cells (L-02 cells) injury model. The above hypothesis was further verified by detecting cell necrosis, mitochondrial reactive oxygen species (mtROS), mitochondrial permeability transition pore (mPTP) opening, mitochondrial membrane potential (Δψ m), and cellular ATP level. Collectively, our results serve as direct evidence of elevated in vivo hepatic mitochondrial metabolism in α-AMA-exposed mice and suggest that mitochondrial dysfunction plays an important role in the early stage of α-AMA induced liver failure.

The cyclopeptide -amatoxin induced hepatic injury via the mitochondrial apoptotic pathway associated with oxidative stress.

In order to explore the role of apoptosis in alpha-amatoxin (α-AMA) induced liver injury and probable upstream activation signals, we established animal and cellular models, respectively, for this pathophysiological condition. To this end, we evaluated the survival rate and serum biochemical parameters in BALB/c mice exposed to α-AMA at different time periods, along with the levels of oxidative and antioxidant enzymes in the liver tissue of these mice and proteins involved in apoptosis-related pathways. Our results reveal that α-AMA-induced apoptosis occurs primarily through the mitochondrial apoptotic pathway and is associated with oxidative damage. Further, in order to verify the key nodes and important upstream activators in this apoptotic pathway, we estimated the levels of p53 protein and downstream mitochondrial apoptotic pathway-related proteins in L-02 cells, all of which were found to change significantly. We also found that the levels of total and mitochondrial reactive oxygen species (ROS) in L-02 cells increased with time. Collectively, our findings suggest that α-AMA affects many cellular processes, including the expression of p53 independent of transcription and the expression of Bax and Bcl-2, thereby activating the subsequent caspase cascade pathways. In addition, we identified ROS to be an upstream signaling molecule involved in the α-AMA-induced apoptosis of mouse liver cells and L-02 cells.

Mushroom Poisoning Outbreaks - China, 2019.

What is already known about this topic? Mushroom poisoning is becoming one of the most serious food safety issues in China, which is responsible for nearly a half of all oral poisoning deaths. What is added by this report? In China, many mushrooms were previously "recorded" as poisonous. In this study, about 70 species obtained from mushroom poisoning incidents including several new records were confirmed accurately by morphological and molecular evidence in 2019, and spatial and temporal distribution characters of 13 lethal mushrooms were summarized systematically. What are the implications for public health practice? Precise and timely species identification is of pivotal importance in mushroom incidents. More efforts and cooperation are continued to be needed urgently for the governments, CDC staff, doctors and mycologists in future.

Waterborne Arsenic Poisoning Caused by Discarded Slags - Yongzhou City, Hunan Province, China, 2018.

What is already known about this topic? Overexposure to arsenic is toxic and affects bodily systems. In severe cases, loss of motor function and death can occur. What is added by this report? At the end of 2018, a waterborne acute arsenic poisoning event occurred in Yongzhou City of Hunan Province because arsenic-containing slags contaminated the water supply, which resulted in 10 people being poisoned. Patients were poisoned through domestic use of contaminated well water excluding drinking. What are the implications for public health practice? Clinicians should be trained to correctly and promptly identify and diagnose acute arsenic poisoning. The arsenic slags and byproducts should be strictly managed by corresponding enterprises to avoid similar poisoning incidents. When dealing with such events, water intended for domestic use should be closely monitored and environmental pollution should be assessed and controlled.

Utility of brain CT for predicting delayed encephalopathy after acute carbon monoxide poisoning.

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a serious complication that occurs several days or weeks after carbon monoxide (CO) intoxication. This study identified computed tomography (CT) findings in the prediction of DEACMP development. Adults with CO poisoning admitted to Beijing Chaoyang Hospital, Shenyang Ninth People's Hospital, Shanxi Second People's Hospital and Shandong Provincial Hospital in China from January 2013 to January 2016 were retrospectively analyzed. Baseline demographic and clinical characteristics were extracted from the medical records. Brain CT imaging was carried out within 24 h of admission, and an integrated CT score was calculated to semi-quantify lesion severity. Patients were followed-up for 6 months. Baseline characteristics and CT findings were compared among patients who developed DEACMP (DEACMP group) and those who did not (non-DEACMP group). The receiver operating characteristic (ROC) curve analysis was used to examine the utility of integrated CT score for predicting DEACMP. Among the 123 patients included in the analysis, 27 (22.0%) developed DEACMP. The DEACMP and non-DEACMP groups did not differ with regard to age, sex and carboxyhemoglobin (COHb) level at admission. However, compared with the non-DEACMP group, the patients in the DEACMP group had longer onset time of symptoms and duration of exposure to CO, higher acute physiology and chronic health evaluation-II (APACHE-II) score, lower Glasgow Coma Scale (GCS) score, and there was a higher proportion of patients with severe symptoms and brain CT abnormalities (81.5 vs. 51.0%; P<0.05). Integrated CT score in the DEACMP group was significantly higher than that in the non-DEACMP group (73.63 vs. 51.39; P<0.01). ROC curve was used to analyze the utility of integrated CT score in the prediction of DEACMP. The area under the ROC curve was 0.700 (95% confidence interval, 0.584-0.817; P<0.01). In conclusion, brain integrated CT score has the potential to identify DEACMP in patients.

Effect of Biliary Drainage on the Toxicity and Toxicokinetics of Amanita exitialis in Beagles.

Amatoxin poisoning induces delayed-onset acute liver failure, which are responsible for more than 90% of deaths in mushroom poisoning. It has been postulated from animal and human studies that biliary drainage interrupting enterohepatic amatoxin circulation may affect amatoxin poisoning. Dogs were randomly divided into four groups of six animals each. In 20 mg/kg and 60 mg/kg with biliary drainage groups, after accepting bile drainage operation, beagles were fed Amanita exitialis powder (20 or 60 mg/kg) in starch capsules. In control and bile drainage groups, the beagle dogs were fed with empty capsules. They were assessed for toxicity signs, biochemical and pathological changes, and peptide toxins in plasma, urine and bile. The data were directly compared with those from our published studies on Amanita exitialis-exposed beagles without biliary drainage. Amatoxins were rapidly absorbed and eliminated from plasma after Amanita exitialis ingestion. Amatoxins in 0⁻1-day urine accounted for more than 90% of the total urine excretion, and amatoxins in bile accounted for less than 20% of the total urine and bile excretion. The dogs with biliary drainage showed less severe toxicity signs and biochemical and pathological changes and much lower internal exposure than dogs without biliary drainage. Biliary drainage caused a more than 70% reduction in intestinal amatoxin absorption and could reduce amatoxin absorption from the gastrointestinal tract.

Toxicity and toxicokinetics of Amanita exitialis in beagle dogs.

In this study, the toxicology of A. exitialis, a lethal mushroom found in China, and the toxicokinetics of peptide toxins contained in it were evaluated. Beagles were fed A. exitialis powder (20 or 60 mg/kg) in starch capsules, after which they were assessed for signs of toxicity, as well as biochemical and pathological changes. Ultra-performance liquid chromatography-electrospray ionization-tandem mass spectrometry was used to assay the peptide toxins. The total peptide toxins in A. exitialis was 3482.6 ±â€¯124.94 mg/kg. The beagles showed signs of toxicity, such as vomiting and diarrhea, at 12-48 h following ingestion of A. exitialis. Furthermore, alanine transaminase and aspartate transaminase levels in plasma, as well as prothrombin time and activated partial thromboplastin time peaked at 36 h post A. exitialis ingestion. Furthermore, total bilirubin and alkaline phosphatase levels peaked at 48 h after A. exitialis ingestion. Three dogs that were administered 60 mg/kg A. exitialis died at 24-72 h after ingesting the capsules. Additionally, liver histopathological examinations showed hemorrhagic necrosis of hepatocytes. α-Amanitin, ß-amanitin, and phallacidin were rapidly absorbed and eliminated from plasma after A. exitialis was ingested. A long latency period (12-24 h post A. exitialis ingestion) was observed in the dogs before the onset of gastrointestinal symptoms. There was acute liver damage thereafter. Gastric lavage and enhanced plasma clearance methods such as hemodialysis, hemoperfusion, or plasma exchange may be ineffective in removing amatoxins from blood at 12 h post A. exitialis ingestion. Enhanced excretion of amatoxins in urine could be effective within 2 days after ingestion of A. exitialis because amatoxins in 0-2 d urine accounted for more than 90% of the total urine excretion.

[Evaluation of therapeutic project on acute tetramethylene disulphotetramine poisoning and effect on intelligence in children].

OBJECTIVE: To evaluate four therapeutic measures on acute tetramethylene disulphotetramine (TETS) poisoning and the effects of it on intelligence of children. METHODS: All 86 patients of acute TETS poisoning were randomly divided into 4 groups (the control group, sodium valproate group, sodium dimercaptopropane sulfonate group and the hemoperfusion group). The therapeutic effects were observed after the arranged treatment was administrated. According to age, residence, sex, education and domestic economy, 30 children were matched by 1:1 with children of TETS poisoning. RESULTS: The termination time of seizure, doses of diazepam, mental symptoms and the continual time of mental symptoms were not significantly different among these three groups. After hemoperfusion, the seizure of patients was terminated or the frequency was obviously decreased, but the level of TETS in blood was not reduced. The average scores of full intelligence quotient (FIQ), the verbal intelligence quotient (VIQ) and the performance intelligence quotient (PIQ) of children in poisoning group were 9.1, 8.8 and 7.7 less than the controls. The average scores of FIQ of children with bad state were 15 less than the controls. CONCLUSION: Therapeutic effects of sodium valproate and sodium dimercaptopropane sulfonate on acute TETS poisoning should be not better than using diazepam and sodium phenobarbital. Therapeutic effects of hemoperfusion on TETS poisoning is good. TETS poisoning should have a great influence on intelligence of children.

[Study on the effect using hemoperfusion to treat tetramine poisoned patients].

OBJECTIVE: To evaluate the effect of hemoperfusion on tetramine poisoned patients. METHODS: Three tretramine poisoned cases treated with hemoperfusion were selected. The samples during and after hemoperfusion were collected and analyzed by gas chromatography. RESULTS: Tetramine concentration at the inlet of the artificial kidney kept the same level during hemoperfusion. After hemoperfusion, the tetramine concentration in patient plasma changed little in 72 hours. 1.03-1.55 mg of tetramine was adsorbed by the instrument of hemoperfusion after two hours' hemoperfusion. CONCLUSION: Although hemoperfusion was not so effective to reduce blood tetramine concentration in patients, it could clear about 1 mg tetramine for one time.