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 testsAdmission After 24 hAfter 4 days Discharge
White blood cells (RV: 4.50–10.80 9 10^3/lL)
pH (RV: 7.37–7.45)
14500 231008800 7160
7.297.50 7.54 7.4
pO2(RV: 83–108 mHg)
pCO2(RV: 32–45 mmHg)
Bicarbonate (RV: 22–29 mmol/L)
64 173(*)76 100
19.2 32.035 24.0
Lactate (RV: 0.6–2.3 mmol/L)
C–Reactive protein (RV: ‹5.00 mg/L)
3.220 5.86 3.22
Creatine kinase MB (RV: 0.1–4.0 ng/mL)64.6 228.20.6
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 Download full-text
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.