A scombroid poisoning causing a life-threatening acute pulmonary edema and coronary syndrome in a young healthy patient.
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Article: Histamine fish poisoning revisited.[show abstract] [hide abstract]
ABSTRACT: Histamine (or scombroid) fish poisoning (HFP) is reviewed in a risk-assessment framework in an attempt to arrive at an informed characterisation of risk. Histamine is the main toxin involved in HFP, but the disease is not uncomplicated histamine poisoning. Although it is generally associated with high levels of histamine (> or =50 mg/100 g) in bacterially contaminated fish of particular species, the pathogenesis of HFP has not been clearly elucidated. Various hypotheses have been put forward to explain why histamine consumed in spoiled fish is more toxic than pure histamine taken orally, but none has proved totally satisfactory. Urocanic acid, like histamine, an imidazole compound derived from histidine in spoiling fish, may be the "missing factor" in HFP. cis-Urocanic acid has recently been recognised as a mast cell degranulator, and endogenous histamine from mast cell degranulation may augment the exogenous histamine consumed in spoiled fish. HFP is a mild disease, but is important in relation to food safety and international trade. Consumers are becoming more demanding, and litigation following food poisoning incidents is becoming more common. Producers, distributors and restaurants are increasingly held liable for the quality of the products they handle and sell. Many countries have set guidelines for maximum permitted levels of histamine in fish. However, histamine concentrations within a spoiled fish are extremely variable, as is the threshold toxic dose. Until the identity, levels and potency of possible potentiators and/or mast-cell-degranulating factors are elucidated, it is difficult to establish regulatory limits for histamine in foods on the basis of potential health hazard. Histidine decarboxylating bacteria produce histamine from free histidine in spoiling fish. Although some are present in the normal microbial flora of live fish, most seem to be derived from post-catching contamination on board fishing vessels, at the processing plant or in the distribution system, or in restaurants or homes. The key to keeping bacterial numbers and histamine levels low is the rapid cooling of fish after catching and the maintenance of adequate refrigeration during handling and storage. Despite the huge expansion in trade in recent years, great progress has been made in ensuring the quality and safety of fish products. This is largely the result of the introduction of international standards of food hygiene and the application of risk analysis and hazard analysis and critical control point (HACCP) principles.International Journal of Food Microbiology 06/2000; 58(1-2):1-37. · 3.43 Impact Factor
Article: Scombroid fish poisoning syndrome.[show abstract] [hide abstract]
ABSTRACT: Two patients presented to the emergency department with features of a histamine-like reaction and were subsequently determined to have scombroid fish poisoning. It is important to recognize the syndrome as an intoxication rather than an allergic reaction in order that the source of the toxin can be identified and further cases prevented. A review of the features and pathogenesis of the syndrome is presented.Annals of Emergency Medicine 10/1982; 11(9):487-9. · 4.29 Impact Factor
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ABSTRACT: Histamine poisoning results from the consumption of foods, typically certain types of fish and cheeses, that contain unusually high levels of histamine. Spoiled fish of the families, Scombridae and Scomberesocidae (e.g. tuna, mackerel, bonito), are commonly implicated in incidents of histamine poisoning, which leads to the common usage of the term, "scombroid fish poisoning", to describe this illness. However, certain non-scombroid fish, most notably mahi-mahi, bluefish, and sardines, when spoiled are also commonly implicated in histamine poisoning. Also, on rare occasions, cheeses especially Swiss cheese, can be implicated in histamine poisoning. The symptoms of histamine poisoning generally resemble the symptoms encountered with IgE-mediated food allergies. The symptoms include nausea, vomiting, diarrhea, an oral burning sensation or peppery taste, hives, itching, red rash, and hypotension. The onset of the symptoms usually occurs within a few minutes after ingestion of the implicated food, and the duration of symptoms ranges from a few hours to 24 h. Antihistamines can be used effectively to treat this intoxication. Histamine is formed in foods by certain bacteria that are able to decarboxylate the amino acid, histidine. However, foods containing unusually high levels of histamine may not appear to be outwardly spoiled. Foods with histamine concentrations exceeding 50 mg per 100 g of food are generally considered to be hazardous. Histamine formation in fish can be prevented by proper handling and refrigerated storage while the control of histamine formation in cheese seems dependent on insuring that histamine-producing bacteria are not present in significant numbers in the raw milk.Journal of toxicology. Clinical toxicology 02/1989; 27(4-5):225-40.
A Scombroid Poisoning Causing a Life-Threatening Acute
Pulmonary Edema and Coronary Syndrome in a Young Healthy
Antonio D’Aloia•Enrico Vizzardi•Paolo Della Pina•
Silvia Bugatti•Francesca Del Magro•Riccardo Raddino•
Antonio Curnis•Livio Dei Cas
? Springer Science+Business Media, LLC 2011
Scombroid poisoning, also called histamine fish poisoning,
is an allergy-like form of food poisoning that represents
one of the major problems in seafood safety. It consists in a
clinical syndrome associated with consumption of fish and,
less frequently, cheese containing high levels of histamine
[1, 2]. Usually certain families of dark meat fish are
involved, mainly Scombroidae and Scomberesocidae (e.g.,
tuna, mackerel, skipjack, Bonito, and Cero). Other non-
scombroid fish (e.g., mahi—mahi, herring, anchovies,
sardines, Australian salmon, swordfish) was also reported
to be associated with scombroid fish poisoning [1–5]. High
fish histamine concentrations have been found responsible
for this kind of poisoning. Histamine and histamine-like
substances are generated from histidine by a decarboxylase
activity of bacteria such as Proteus, Klebsiella, Aerobacter,
Serratia, Enterobacter, and Escherichia coli [6, 7]. The
presence of this bacteria and the massive histamine pro-
duction detected in the fish is usually secondary to con-
tamination of handlers and improper refrigeration . The
clinical presentation is generally characterized by flushing,
rash, swelling of face or tongue, sweating, headache, diz-
ziness, abdominal cramps, diarrhea, nausea, vomiting,
palpitations, respiratory distress, and hypotension. The
onset of symptoms generally occurs few minutes after
ingestion of contaminated food. Usually the course is self-
limiting and antihistamines can be used to relieve symp-
toms. We report a rare case of a life-threatening scombroid
poisoning with myocardial ischemia and acute pulmonary
edema after tuna ingestion.
A 16-year-old girl without previous history of cardiac or
pulmonary abnormalities, allergies, or others relevant dis-
eases, presented to the emergency department after the
onset of flushing and palpitations within a short time of
eating a grilled tuna. On examination, she had arterial
systemic hypotension (90/60 mmHg), tachycardia, and a
diffuse skin erythematous rash. She reported nausea and
abdominal pain. The first ECG revealed a sinus tachycardia
without ventricular repolarization abnormalities (Fig. 1).
The patient was initially treated with steroid and chlor-
pheniramine (Histamine H1 receptor antagonist) intrave-
nous infusion resulting only in cutaneous rash resolution.
After few minutes, a supraventricular tachycardia occurred
at rate of 160 bpm with diffuse severe ST segment
depression (Fig. 2) reversed to sinus rhythm after diltiazem
intravenous infusion. Gradually the cardiovascular status
worsened with severe hypotension, cardiogenic shock
signs, and onset of flush acute pulmonary edema. The
patient received norepinephrine, epinephrine, and diuretics
in order to stabilize the hemodynamic parameters. Myo-
cardial necrosis markers increased (max Troponin I of
45 ng/ml) and the echocardiogram documented left ven-
tricle (LV) diffuse hypokinesis with severe decrease in
ejection fraction (EF) of 30% and severe mitral valve
regurgitation. Blood gas analysis showed hypoxemia and
lactic acidosis; the urine culture and drug tests were neg-
ative. During the next 30 h period, the patient underwent to
mechanical ventilator support. In the next days, gradually
the hemodynamic, metabolic, and respiratory parameters
A. D’Aloia ? E. Vizzardi (&) ? P. Della Pina ? S. Bugatti ?
F. Del Magro ? R. Raddino ? A. Curnis ? L. Dei Cas
Department of Experimental and Applied Medicine, University
of Brescia, Piazzale Spedali civili, 125100 Brescia, Italy
Fig. 1 First ECG recorded at emergency department showing sinus tachycardia
Fig. 2 Second ECG recorded showing supraventricular tachycardia and diffuse severe ST segment depression
improved (see Table 1), and ventilatory support and the
inotropic therapy were removed. The echocardiogram
performed 4 days after the acute event, documented an EF
improving from 30 to 52% and mild mitral regurgitation.
The blood tests after ten days showed a myocardial enzyme
curve normalization (see Table). Subsequent analysis of the
tuna ingested by the young girl documented an extremely
high histamine level in the flesh fish ([1,000 mg/gr),
secondary to a prolonged poor conservation.
Scombroid poisoning is a form of ichthyosarcotoxism
causing a clinical syndrome resulting from the ingestion of
mishandled fish, mainly of the scombroid family. Histamine
and other decomposition products (such as Putrescine and
Cadaverine) are generated by the conversion of free histi-
dine, found at high levels in the muscle of several fishes.
Inappropriate storage of these fishes can lead to the decar-
boxylation of histidine in the flesh to histamine by entero-
bacteria. Although high flesh histamine concentrations are
typically demonstrated in the fish implicated in scombroid
poisoning (generally levels greater than 50 mg/100 g), the
pathogenesis ofthis syndrome isnot totally explainedby the
only action of histamine. In fact, there is not a clear dose–
response relationship between oral administration of hista-
mine and histamine levels in the decomposed fish, with
scombrotoxic fish showing higher toxicity than an equiva-
lent oral dose of pure histamine. These observations have
leaded to the research of further mechanisms of toxicity.
potentiation of histamine control enzymes; (2) a mast cell
degranulators (Scombrotoxin) present in spoiled fish but not
individuated yet; (3) the presence of other histamine ago-
nists; (4) histamine intolerance, that could explain the wide
variations between individuals in their susceptibility to
histamine in decomposed fish.
Diagnosis is generally clinical, based on the history of
the patient and the symptoms. Often, the fish poisoning as
the cause of illness is detected after the resolution of
clinical syndrome. The symptoms of histamine poisoning
mimic those of an IgE-mediated food allergy, as well as
flushing, headache, diarrhea, and palpitations. However, in
some cases, the scombroid poisoning can be characterized
by very serious symptoms, as well as cardiovascular
compromission. Indeed Scombroid syndrome is often
misdiagnosed and therefore under reported. Nevertheless,
this condition represents the 38% of all seafood associated
outbreaks in United States, and the 32% in England and
Wales, with an incidence (in the highest reported outbreak
rates) of 2–5 outbreaks/year/million people (Denmark,
New Zealand, France, Finland), and the singularly high rate
of 31 outbreaks/year/million in Hawaii . About the
therapy, there are not data from clinical trials. H1 and H2
antihistamines generally are effective to relieve clinical
symptoms. Support therapy with rehydratation and antie-
metic could ameliorate the behavior of patient. In some
cases is necessary an aggressive therapy like in anaphy-
lactic shock. Our report serves to highlight a really rare
case of cardiac presentation of Scombroid syndrome that
has triggered a severe acute coronary acute syndrome
complicated by cardiogenic shock requiring mechanical
respiratory assistance and continuous intravenous inotrop-
ics with resolution of symptoms only several days later.
Since Scombroid fish poisoning can easily be confused
with food allergy or bacterial food poisoning, the physi-
cians should stay alert assessing the previous consumption
of fish that must alert to the possibility of this syndrome.
1. Taylor, S. L., Stratton, J. E., & Nordlee, J. A. (1989). Histamine
poisoning (Scombroid fish poisoning): An allergy-like intoxica-
tion. Journal of Toxicology Clinical Toxicology, 27, 225–240.
Table 1 Time course of main laboratory parameters
Laboratory testsAdmissionAfter 24 h After 4 days Discharge
White blood cells (RV: 4.50–10.80 9 10^3/lL)
pH (RV: 7.37–7.45)
pO2(RV: 83–108 mHg)
pCO2(RV: 32–45 mmHg)
Bicarbonate (RV: 22–29 mmol/L)
Lactate (RV: 0.6–2.3 mmol/L)
C–Reactive protein (RV: ‹5.00 mg/L)
Creatine kinase MB (RV: 0.1–4.0 ng/mL)64.6228.20.6
Troponine I (RV: C 0.04 ng/mL)9.60456.64
(*)Patient subjected to mechanic ventilator support. RV Reference Values
2. Dickinson, G. (1982). Scombroid fish poisoning syndrome. Annals
of Emergency Medicine, 11, 487–489.
3. Muller, G. J., Lamprecht, J. H., Barns, J. M., et al. (1992).
Scombroid poisoning. South African Medicine Journal, 81,
4. Morrow, J. D., Margolies, G. R., Rowland, B. S., et al. (1991).
Evidence that histamine is the causative toxin of scombroid fish
poisoning. New England Journal of Medicine, 324, 716–720.
5. Scoging, A. C. (1991). Illness associated with seafood. CDR
(London England: Review), 1(11), 117–122.
6. Lehane, L., & Olley, J. (2000). Histamine fish poisoning revisited.
International Journal of Food Microbiology, 58, 1–37.
7. Staruszkiewicz, W. F., Barnett, J. D., Rogers, P. L., et al. (2004).
Effects of on-board and dockside handling on the formation of
biogenic amines in mahimahi (Coryphaena hippurus), skipjack
tuna (Katsuwonus pelamis), and yellowfin tuna (Thunnus albac-
ares). Journal of Food Protection, 67, 134–141.