BA is a potent toxin produced by Burkholderia cocovenenans subsp. Coconut milk-based products [2], corn flour products [5], Auricularia auricula [6], and Tremella fuciformis [7] can be contaminated with BA, resulting in human and animal poisoning and potentially causing death [8, 9]. BA is mainly absorbed through the digestive tract mucosa and distributed throughout the body in the blood [7]. Small amounts of BA can be fatal if taken orally [4, 10]. Therefore, food poisoning caused by BA has a high fatality rate and seriously threatens human health and food safety [11].

BA is a mitochondrial toxin with a unique mechanism of action. Unlike other mitochondrial toxins, such as cyanide, BA does not directly interfere with the electron transport chain [4]. It produces toxic effects by inhibiting the adenine nucleotide translocator (ANT) on the mitochondrial membrane. Thus, the exchange of adenosine diphosphate and adenosine triphosphate (ATP) in the mitochondrial inner membrane is blocked, which reduces ATP production and eventually blocks aerobic respiration, affecting various metabolic processes [4, 12]. The heart is an organ with high energy consumption, and BA can affect ATP production in cardiomyocytes [13], and interruption of the energy supply can cause cardiomyocyte injury, impaired contractility, and potential cardiac dysfunction [14]. As shown in Fig. 3, the patient in this study also exhibited acute myocardial injury.

The patient’s electrocardiogram (ECG) of the patient on the 4th day of admission, showing obvious ST-T segment abnormalities

BA has high activity in the liver and kidneys, and most of its metabolites are excreted in the feces and urine. In addition, a small proportion of metabolites are excreted into the intestine with bile and reabsorbed through the hepatoenteric circulation. This causes repeated liver damage during BA metabolism [12]. Liver functions such as detoxification, metabolism, and protein synthesis depend on ATP. Reduced ATP production can cause hepatocyte dysfunction and even hepatocyte necrosis, cholestasis, and destruction of liver function [4, 12]. BA also interferes with glucose metabolism in the liver, resulting in abnormal glucose metabolism and further liver injury [12]. Overall, the severe liver damage and dysfunction caused by BA may be due to a combination of ANT inhibition, disruption of ATP production, and the effects on hepatocyte energy expenditure and glucose metabolism [9]. Renal injury in BA poisoning often occurs in conjunction with severe liver damage and multiorgan failure [12].

The systemic effects of BA on the liver, kidneys, heart, and other organs determine the overall clinical manifestations and pathological features of BA poisoning. BA poisoning initially causes gastrointestinal symptoms and hyperglycemia, which rapidly progresses to hypoglycemia owing to the depletion of glycogen stores in various tissues, including the heart and liver [1, 3, 15]. In severe cases, multiple organ failure can ensue, and the mortality caused by BA poisoning is very high [4].

Currently, no specific antidote for BA poisoning exists, and supportive treatment is mainly adopted. In a study by Lv et al. [16], plasma exchange (PE) was significantly more effective than continuous blood purification in BA clearance. Liu et al. [17] also reported a case of BA poisoning that was successfully treated with PE. Although the patient in this case report were treated with PE, only ALT and AST indicators improved significantly, while bilirubin levels continued to increase without significant improvement in liver function. This may be because patients with irreversible organ damage missed the best opportunity for treatment when they arrived at our hospital.

The high mortality rate associated with BA poisoning may be attributed to several factors: (1) limited medical resources in the area where the poisoning occurs make it difficult to provide the required care and medical conditions; (2) no ability to detect BA or BA-producing bacteria; and (3) BA poisoning not being considered, leading to a misdiagnosis. Although BA poisoning is rare, medical staff familiar with its clinical manifestations must take corresponding measures to prevent and reduce the occurrence of BA poisoning. To prevent BA poisoning, safer fermentation processes and food handling should be emphasized. BA-contaminated food has the same appearance, smell, and taste as uncontaminated food; therefore, monitoring food sources to prevent food contamination with bacteria and toxins is crucial.