Keracunan akibat memakan tempe bongkrek sudah seringkali kita dengar, khususnya yang terjadi di wilayah Karesidenan Banyumas. Tempe. Satu keluarga yang terdiri dari empat orang keracunan setelah memakan tempe goreng. Satu di antaranya tewas. Tempe gembus dan bongkrek sering dikonsumsi oleh beberapa orang, tempe bongkrek seringkali menyebabkan keracunan karena adanya.
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Bongkrekic acid BA has a unique mechanism of toxicity among the mitochondrial toxins: Bongkrekic acid is produced by the bacterium Burkholderia gladioli pathovar cocovenenans B. Our objective was to summarize what is known about the epidemiology, exposure sources, toxicokinetics, pathophysiology, clinical presentation, and diagnosis and treatment of human BA poisoning.
We identified a total of references which were reviewed. Outbreaks have been reported from Indonesia, China, and more recently in Mozambique. Very little is known about the toxicokinetics of BA. Bongkrekic acid produces its toxic effects by inhibiting mitochondrial ANT.
ANT can also alter cellular apoptosis. Signs and symptoms in humans are similar to the clinical findings from other mitochondrial poisons, but they vary in severity and time course. Management of patients is symptomatic and supportive. Bongkrekic acid is a mitochondrial ANT toxin and is reported primarily in outbreaks of food-borne poisoning involving coconut and corn. It should be considered in outbreaks of food-borne illness when signs and symptoms manifest involving the liver, brain, and kidneys and when coconut- or corn-based foods are implicated.
Bongkrekic acid BAa little-known mitochondrial toxin produced by the bacterium Burkholderia gladioli pathovar strain or set of strains with the same or similar characteristics that have been shown to be pathogenic to certain plants cocovenenans B.
Human illness from BA exposure is reported from consumption of bongkgek food, particularly fermented coconut tempe a traditional food made of fermented coconut pulp and corn products [ 13 ]. These outbreaks have occurred mainly in Indonesia and China [ 4 ]; however, one was recently reported in Mozambique [ 12 ].
Bongkrekic acid is odorless and tasteless; affected food products can have a normal appearance, smell, and taste [ 5 ].
Published epidemiological and toxicological reports about outbreaks and human illness from BA are scarce. Our search terms were: We manually searched reference lists of identified articles and performed Google searches for other online sources of information using the terms Burkholderia gladiolicocovenenansbongkrekic acid, asam bongkrekflavotoxin, tempe bongkrek, fermented corn flour, Tremellaand diaojiangba hanging keracuhan cake.
Sources were reviewed and selected for inclusion if they contained biochemical, epidemiologic, toxicological, or clinical information. On manual review of the references from articles and book chapters, the most original articles were identified and included. Websites were used if they were referred to in Pro-MED alerts or were from established and reliable news sources.
Once kerzcunan reviewed a source and extracted the pertinent information to answer questions in each section, we did not include other sources if it contained the same information. We identified articles, five book chapters, four Keradunan alerts, one PowerPoint presentation, and 12 websites using the search criteria listed in the Methods section. We included 18 articles, five book chapters, kerscunan Pro-MED alerts, bongkrke PowerPoint presentation, and three websites in this review.
It is thought to be a polyketide. Polyketides are biologically active secondary metabolites produced by bacteria, fungi, and plants to impart a survival advantage such as inhibiting the growth of other bacteria, fungi, viruses, parasites, or tumor cells. Doxycycline, erythromycin, and many other antibiotics are examples of polyketides [ 15 ].
Bongkrekic Acid—a Review of a Lesser-Known Mitochondrial Toxin
The gram-negative, aerobic, rod shaped bacteria B. The Burkholderia genus includes more than 60 species, but B. Its toxicity is relatively mild and secondary to that of BA [ 13 ]. Early studies reported that B. Later studies confirmed it has the same molecular formula as BA and may be the same molecule as BA or be a BA metabolite [ 416 ].
The authors of the original paper later state that they are the same molecule [ 17 ]. Outbreaks to date have been reported in only two settings: Summary of outbreaks, year, number affected and fatalities related to bongkrekic acid poisoning [ 1 — 12 ].
Tempe bongkrek is a locally produced, inexpensive protein source in Java, Indonesia. It is made by pressing the coconut meat by-product from coconut milk or oil production into a cake that is then inoculated with R.
The final product is sliced or cubed for frying or cooking in soup. If fermentation is incomplete, B. Deaths from BA poisoning related to tempe bongkrek consumption were first reported in [ 18 ]. Sinceconsumption of contaminated tempe bongkrek has resulted in almost cases of BA toxicity, including at least deaths [ 13 ].
After an outbreak inproduction of tempe bongkrek was banned, but production and occasional outbreaks continue to occur [ 113 ]. In northeastern China, fermented corn products used to make breads, noodles, and dumplings appear to be the primary source of BA poisoning [ 2 ].
In southern China, diaojiangba hanging syrup cake has been linked to BA poisoning events [ 3 ]. In addition, half of the Tremella fuciformis mushrooms consumed in China and other Asian countries might be contaminated with B. Outbreaks due to BA usually occur during warm summer months in both Indonesia and China. Inthe first outbreak of BA toxicity outside of Asia was reported. Bongkrekic acid production depends on two distinct and sequential environmental conditions: Production is also dependent on the presence of fatty acids, particularly those found in coconut and corn [ 1 ].
Bacterial growth media containing oleic acid produced the highest concentrations of BA [ 1 ]. Lauric, myristic, and palmitic acids make up Optimal conditions for proliferation of B. There is scarce information on the toxicokinetics and lethal dose of BA in humans. One source suggests that 1—1. Studies on mice suggest an oral LD 50 of 0. The absorption profile and volume of distribution for BA is unknown, although BA likely has a large volume of distribution because it is a highly unsaturated fat and is highly lipid soluble [ 22 ].
We do not know how BA is metabolized. Early studies reported Flavotoxin A a toxin also thought to be found in B. The route of elimination of BA is unknown. Bongkrekic acid produces its toxic effects by inhibiting mitochondrial adenine nucleotide translocase ANT.
There are three isoforms of ANT found in humans and they occur to differing extents in the heart, skeletal muscle, fibroblasts, and liver [ 24 ]. It plays a role in coordinated apoptosis and uncoordinated necrotic cell death by becoming a part of a lethal pore in the mitochondrial membrane called the mitochondrial permeability transition pore MPTP.
The MPTP is a protein-based channel that regulates the permeability of the mitochondrial membrane. Proteins, lipids, ions, pro-oxidants, and chemotherapeutic agents can all directly modulate the pore-forming activity of ANT [ 2324 ]. BA and its laboratory synthesized derivatives with varying functional groups have become tools in the study of apoptosis mechanisms, appearing in more than publications [ 25 ]. Illustration of bongkrekic acid site of action showing inhibition of adenine nucleotide translocase in the mitochondrial matrix membrane.
In the earliest studies investigating the cellular pathophysiology of BA, Welling et al. These findings led them to hypothesize that BA inhibits mitochondrial enzymes. Other natural toxins that also inhibit ANT include atractyloside, apoatractyloside, apocarboxyatractyloside, epiatractyloside, carboxyatractyloside, aryl azido atractyloside, n -ethyl maleimide, agaric acid, and isobongkrekic acid [ 27 ].
The primary target organs are the liver, brain, and kidneys [ 20 ]. Reported symptoms include malaise, dizziness, somnolence, excessive sweating, palpitations, abdominal pain, vomiting, diarrhea, hematochezia oliguria, hematuria, and urinary retention. Findings during patient examination include hypotension, arrhythmias, hyperthermia, icterus, jaundice, and rigidity of extremities, Cheyne-Stokes respirations, pulmonary rales, lethargy, delirium, shock, coma, and death [ 2414 ].
Laboratory abnormalities include an initial hyperglycemia followed by hypoglycemia, abnormal liver function tests, normal red blood cell count and hemoglobin, and an increase in white blood cell count [ 2 ]. Data from animal studies show a variable timeline in the development of signs, symptoms and death. In another study, dogs and rhesus monkeys fed B. Test animals did not die when fed organs of animals poisoned with contaminated food [ 4 ].
Apa Benar Tempe Gembus dan Tempe Bongkrek Nutrisinya Rendah?
Reported autopsy findings from outbreaks of BA poisoning in China [ 2 ]. It can be identified using commercial test kits such as the Biologic GN2 System [ 13 ]. The most commonly used method bonngkrek B. The most reliable method might be the multiplex PCR protocol [ 13 ]. We found no other reports of B. We could not locate any published reports of testing biological media for BA, but the presence and quantification of BA in environmental bongkdek can be tested using liquid thin layer chromatography, chromatography-mass spectroscopy, and high-pressure liquid chromatography [ 162021 ].
Standardized guidelines for treatment of BA-poisoned persons do not exist.
Treatment strategies may be extrapolated from recommendations for treatment of other mitochondrial toxins, such as carbon monoxide, cyanide, and hydrogen sulfide. However, antidotes used for other mitochondrial toxins e. Dextrose might be helpful for patients keeacunan develop hypoglycemia, although it has not been reported to reduce mortality [ 13 ].
We expect that the volume of distribution of BA is likely too large to be amenable to extracorporeal removal, such as hemodialysis; however, hemodialysis should still be considered in the setting of renal failure to support organ function. Bongkrekic acid has a unique mechanism of toxicity among the mitochondrial toxins: The limited data regarding kerracunan LD 50 in animals cannot be extrapolated to humans or other species.
Bongkrekic acid produces overt clinical toxicity keracknan to those of other mitochondrial toxins, although on a different timeline delayed compared to agents like cyanide, which can cause illness within seconds to minutes.
Diduga Keracunan Tempe, 1 Orang Tewas & 3 Dirawat
A high reported mortality rate may be due to difficulty accessing medical care in rural areas where outbreaks occurred and possibly due to limited resources in delivering the quality of supportive critical care necessary for treatment.
Medical toxicologists should be aware of its existence for possible inclusion in the differential diagnosis of food-borne illnesses.
Although illness from BA has not been reported outside of Asia until recently, this does not exclude the presence of BA-associated illness in other parts of the world. It is unclear why it has not been detected in other parts of the world previously as Burkholderia and possibly B. A lack of confirmatory testing capacity for detection of the bacteria or BA or a failure to consider the diagnosis could be contributing to misdiagnosis.
Bongkrekic acid poisoning appears to be somewhat rare, but it can significantly affect public health in those areas where fermented coconut or corn products serve as inexpensive sources of protein among largely food-insecure populations.
Interventions aimed at exposure prevention and safer fermentation processes should be emphasized. Foods contaminated with BA can look, smell, and taste the same as non-contaminated foods [ 7 ], and no reliable, commercially available method of screening food products for B.