Allergic reactions usually impact individuals with a known history of allergies to the specific food item. But, scombroid poisoning can affect multiple people, even those without any prior history of allergies. Scombroid poisoning occurs when certain dark meat fish, which have undergone bacterial decomposition, are consumed. This type of poisoning is caused by ingesting a heat-stable toxin produced during the decomposition process (Hungerford, 2010). It is needed to differentiate scombroid poisoning from both fish poisoning and fish allergies.
Fish poisoning, also known as ichthyosarcotoxism, can occur from consuming certain species, primarily from tropical regions, whose flesh contains potent toxins (Stratta & Badino, 2012). However, there is no consistent evidence that these so-called poisonous species are always toxic or toxic in every location. The freshness of the fish does not influence its potential to cause illness.
The term scombroid comes from the Scombridae family, which comprises mackerels, tunas, and bonitos. Over the years, this group has been responsible for most cases of scombroid poisoning. However, they are not the sole culprits. The dolphinfish (Coryphaena hippurus) has also been linked to several outbreaks, despite having no relation to the mackerel group. When fish that has been improperly stored, typically at temperatures above 4°C is consumed, scombroid poisoning can occur.
These conditions promote the growth of bacteria, which convert histidine (found in the meat of oily fish) into histamine through the action of bacterial enzymes, specifically histidine decarboxylase. This conversion can happen rapidly, with fish stored at 20°C accumulating toxic levels of histamine within just two hours. Histamine levels exceeding 50 mg per 100 g of fish are required to trigger the clinical symptoms of scombroid poisoning (Guergué-Díaz de Cerio et al., 2016).
Histamine physiological role and metabolism
Histamine is a messenger molecule in the human body and not inherently a toxin. It is widely distributed and released from mast cells, enterochromaffin-like cells, and neurons. Histamine interacts with various "histaminergic" receptors, specifically H1, H2, H3, and H4 receptors, mediating its diverse actions (Russell & Maretić, 1986). In healthy individuals, histamine plays many crucial roles, including regulating gastric acid secretion and acting as a neurotransmitter in the central nervous system. The various roles of histamine as a naturally occurring messenger in the human body have significant implications for understanding the true nature of scombroid poisoning, particularly its mechanisms and treatment.
Histamine and its receptors mediate responses such as vasodilation, smooth muscle contraction, change in blood pressure, stimulation of nociceptive nerve fibers, tachycardia, and arrhythmias, which align with the symptoms of scombroid poisoning. The H1 and H2 receptors are specifically involved in mediating symptoms like hives, itching, and flushing, which are characteristic of scombroid poisoning (Russell & Maretić, 1986).
Histidine, an amino acid naturally found in fish, is broken down into histamine by bacteria when the fish is not refrigerated. Histamine is produced from free histidine through the action of bacterial histidine decarboxylase (HDC) when fish is subjected to time-temperature abuse. Histamine, produced by the decarboxylation of histidine in the fish's muscle, is primarily responsible for the condition. This decarboxylation process is triggered by enzymes produced by enteric gram-negative bacteria, such as Morganella morganii, Escherichia coli, Klebsiella species, and Pseudomonas aeruginosa, which are found in the fish's skin and intestines.
While scombroid poisoning is typically associated with spoiled fish and fish products, histamine and other biogenic amines are also present in various foods and beverages. Histidine, a common amino acid, undergoes bacterial decarboxylation to form histamine in many other foods and beverages, such as wine, cheese, and fermented meat. In fermented products like wine, cheese, and fish sauce, histamine is produced by gram-positive lactic acid bacteria, whereas in raw fish products, it is primarily produced by gram-negative enteric bacteria. While preventing time-temperature abuse is the most effective way to control histamine formation, it is now known that certain bacteria can produce high levels of histamine even at temperatures as low as 0–5°C (Hungerford, 2010).
The mechanism of scombroid food poisoning can be influenced by a combination of three external factors: the species of fish, the saprophytic microorganisms that convert histidine to histamine, and environmental conditions. As well as, internal individual factors such as the amount of exogenous histamine consumed, the speed of histamine inactivation, and individual sensitivity also play a role (Lerke et al., 1978).
Symptoms of Scombroid Poisoning
Symptoms of scombroid poisoning include flushing, rash, urticaria (generally widespread erythema, usually without wheals), palpitations, headache, dizziness, sweating, and a burning sensation in the mouth and throat. Gastrointestinal symptoms can include abdominal cramps, nausea, vomiting, and diarrhea. Bronchospasm, respiratory distress, and vasodilatory shock have also been reported. Symptoms typically begin within 10 to 90 minutes after consuming the affected fish. The rash usually lasts 2–5 hours, while other symptoms generally resolve within 3–36 hours. Diagnosis is often clinical and can be confirmed by measuring histamine levels in the spoiled food. Additionally, determining the patient's histamine level in plasma or the level of histamine metabolites (e.g., N-methylhistamine) in urine can support the diagnosis (Russell & Maretić, 1986).
Treatment of Scombroid Poisoning
Given the mild nature of scombroid poisoning and its tendency to resolve on its own, many patients do not require treatment. For mild symptoms such as flushing, burning, rash, or swelling around the mouth, the most effective treatment is the prompt administration of oral antihistamines for 1 to 2 days. H1 antihistamines, like cetirizine, are preferred because they are non-sedating. These can be combined with an H2 antihistamine, such as cimetidine, famotidine, or ranitidine. With this treatment, symptoms should resolve within 6 to 8 hours. It is unnecessary to extend treatment beyond 2 days, as this is the time it takes for the toxin to be fully absorbed or eliminated, leading to the disappearance of clinical symptoms (McInerney et al., 1996).
Prevention of Scombroid Poisoning
The key to preventing scombroid poisoning is to quickly refrigerate fish intended for consumption. Ideally, fish should be stored at a temperature of 0°C or lower to inhibit bacterial growth and the activation of histidine decarboxylase. It's important to remember that while cooking or freezing contaminated fish can eliminate the bacteria, it does not destroy the toxin, which remains stable in both heat and cold. Additionally, any outbreaks of scombroid poisoning should be reported to the health department to prevent further cases (Guergué-Díaz de Cerio et al., 2016).
Conclusion
Scombroid poisoning is a common yet likely underdiagnosed cause of fish poisoning. It typically manifests with cutaneous lesions and is treated with oral antihistamines for 1 to 2 days, with complications being rare. Prevention is undoubtedly the best approach, as once histamine has formed; reactions cannot be prevented by cooking, freezing, or canning. Dermatologists' familiarity with this condition can help avoid confusion with allergic reactions to fish. Given that scombroid poisoning presents with skin lesions, it well be encouraged to be called upon by the emergency department to evaluate us of scombroid poisoning.
Did you find this article useful?
YES
NO
References
Guergué-Díaz de Cerio, O., Barrutia-Borque, A., & Gardeazabal-García, J. (2016). Scombroid Poisoning: A Practical Approach. Actas Dermo-Sifiliograficas, 107(7), 567–571. https://doi.org/10.1016/j.adengl.2016.06.003
Hungerford, J. M. (2010). Scombroid poisoning: A review. Toxicon, 56(2), 231–243. https://doi.org/10.1016/j.toxicon.2010.02.006
Lerke, P. A., Werner, S. B., Taylor, S. L., & Guthertz, L. S. (1978). Scombroid poisoning. Report of an outbreak. Western Journal of Medicine, 129(5), 381–386.
McInerney, J., Sahgal, P., Vogel, M., Rahn, E., & Jonas, E. (1996). Scombroid poisoning. Annals of Emergency Medicine, 28(2), 235–238. https://doi.org/10.1016/S0196-0644(96)70067-7
Russell, F. E., & Maretić, Z. (1986). Scombroid poisoning: Mini-review with case histories. Toxicon, 24(10), 967–973. https://doi.org/10.1016/0041-0101(86)90002-4
Stratta, P., & Badino, G. (2012). Five things to know about...: Scombroid poisoning. CMAJ. Canadian Medical Association Journal, 184(6), 674. https://doi.org/10.1503/cmaj.111031
Comentarios