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Poisonous animals
 
Cnidarians (Jellyfish, Corals and Anemones)
 
Venomous fish
 
Scorpions
 
Spiders
 
Hymenopterans (Bees, Wasps and Ants)
 
Sea snakes
 
Terrestrial snakes
 
Miscellaneous animals
 
 
 
 
 
 
 
 

Clinic

 

Scombrotoxic fish

Studies

Bartholomew et al. 1987: retrospective study. 638 cases in 258 outbreaks. The 94 outbreaks in which the consumed fish contained >5 mg% are histamine are described. The results for signs and symptoms are based on the number of outbreaks, with the argument that the symptoms within a single outbreak are always very uniform. Determination of histamine from fish samples in 240/258 outbreaks.

Gilbert et al. 1980: retrospective study. 196 cases in 50 outbreaks. The 30 outbreaks (= 150 cases) for which there were sufficient clinical data are described. The results for signs and symptoms are based on the number of outbreaks, with the argument that the symptoms within a single outbreak are always very uniform. Determination of histamine from fish samples in 37/50 outbreaks.

Kow-Tong and Malison 1987: retrospective study, N = 115. Determination of histamine from fish samples.
Maire et al. 1992: retrospective study, N = 31.
Murray et al. 1982: retrospective study. 71 cases in 26 outbreaks. The results for signs and symptoms are based on the number of outbreaks, with the argument that the symptoms within a single outbreak are always very uniform. Determination of histamine from fish samples.

 

Results of these studies are shown in Table 4.5 below.

Further studies and reviews

Arnold and Brown 1978, Taylor and Bush 1988, Taylor et al. 1989.

Case reports

Borysiewicz and Kirkler 1981, Kasha and Norins 1988, Morrow et al. 1991.

Signs & symptoms

Effects due to exogenous substances with a direct pharmacological effect and autopharmacological effects

Skin rash (erythema), flushing, sweating, pruritus, angio-oedema, nausea, vomiting, diarrhoea, abdominal pain, burning sensation (mouth), peppery taste, palpitations (tachycardia), arterial hypotension, headache, fever (Table 4.5).
Time between ingestion and onset of symptoms: 10 min–2 h (Bartholomew et al. 1987).

Table 4.5 Signs and symptoms of scombroid poisoning: comparison of various studies (see also below, Comments)

 

Country Study n 1 2 3 4 5 6 7 8 9 10 11 12 13 14
Great Britain
Gilbert et al. 1980
n = 150 in 50 outbreaks+




 


 



Great Britain

Murray et al. 1982
n = 71 in 26 outbreaks+



Great Britain Bartholomew et al. 1987
94 outbreaks+



Switzerland
Maire et al. 1992
n = 31








Taiwan
Kow-Tong and Malison 1987
n = 115 in 1 outbreak






 

1
Nausea 12 Skin rash (erythema)
2 Vomiting 13 Flushing and sweating
3 Diarrhoea 14 Pruritus   
4

Abdominal pain

15 Angio-oedema
5 Palpitations/tachycardia
16 Burning (mouth), peppery taste
6 Arterial hypotension
17 Headache
7 Vertigo
19 Fever

 


<10%

n = number of sick people who were included in documentation of the symptoms of poisoning

+ = percentage values for signs and symptoms are based on the number of outbreaks

10–25%
26–50%
51–75%
76–90%
>90%

not mentioned

Differential diagnosis

Skin rash (erythema), flushing and burning in the mouth, combined with a short incubation period of 10 min–2 h, distinguish scombroid poisoning clinically from other types of food poisoning. Several criteria support the differential diagnostic distinction between scombroid poisoning and "true" seafood allergies. Scombroid poisoning generally occurs in "small epidemics", i.e. there are usually other ill persons besides the index patient. High concentrations of histamine are found in the consumed fish. The patient has no history of allergies.

Patients on isoniazid therapy

Isoniazid is a histamine inhibitor. Tuberculosis patients on isoniazid develop the typical signs of scombroid fish poisoning at much lower concentrations of histamine in fish than persons not taking this medication. If the interval between taking isoniazid and consumption of the poisonous fish is sufficiently long, the levels of isoniazid may already be so low that this reaction does not occur (Uragoda 1980, Uragoda and Kottegoda 1977).

Morbidity

Without treatment the symptoms disappear after 12–24 h with no lasting effects.

Case fatality rate

From 1973 to 1986, 178 outbreaks of scombroid poisoning with a total of 1,096 persons involved were reported to the Foodborne Disease Outbreak Surveillance System of the CDC (USA). There were no fatalities among these cases (MMWR 1989).

Laboratory and physical investigations

1. Detection of toxin
Detection of histamine in fish tissue (indirect evidence of poisoning due to scombrotoxic fish)
Thin-layer and gas chromatography (Taylor and Bush 1988,  Henion et al. 1981).
Detection of increased clearance of histamine and its metabolite N-methylhistamine in urine

Detection of increased clearance of histamine and its metabolite N-methylhistamine in urine with normal PGD-M levels (PGD-M is the main metabolite of prostaglandin D2, a secretory product of mast cells, which can be used to evaluate mast cell activation as the cause of raised histamine levels) (Morrow et al. 1991).

Contention: it is not exogenous histamine that causes the symptoms of poisoning, but rather an unidentified toxin, scombrotoxin, which degranulates basophilic cells or mast cells without causing the release of prostaglandin D2 (Clifford et al. 1991).


2. ECG
Tachycardia, supraventricular arrhythmias (atrial flutter) (Borysiewicz and Krikler 1981).

First aid

Gastric evacuation, if this has not occurred spontaneously. However, there has been no study to prove the value of this method.

Treatment (specific)

H1 and H2 receptor antagonists

H1 antagonists (diphenhydramine, chlorpheniramine) and H2 antagonists (cimetidine) (Blakesley 1983, Morrow et al. 1991). As the illness is generally mild and self-limiting, the role of H1 and H2 receptor antagonists in treatment for this form of poisoning needs to be clarified (Hughes and Potter 1991).


Comments

The clinical picture of scombroid poisoning appears to be very uniform, according to all of the existing clinical data, which are, however, almost invariably retrospective. Differences between individuals can almost always be explained by the dose-effect relationship.

The diagnosis of scombroid poisoning is primarily based on patient history and clinical criteria. The detection of increased clearance of histamine and its metabolite in urine with normal PGD-M levels (Morrow et al. 1991) and the detection of histamine in remaining tissue from the consumed fish support the diagnosis.

Correlation of signs and symptoms with the histamine concentration in the consumed fish gives the following picture (Bartholomew et al. 1987): if the samples investigated contained >20 mg% histamine, there was close agreement (94%) with clinically manifest scombroid poisoning (skin rash, flushing, burning in the mouth, short incubation period). If the samples contained 5–20 mg% histamine, this agreement was only 38%. However, also in cases where the consumed fish caused symptoms and in which the samples contained <5 mg% histamine, 39% of the observed symptom complexes were characteristic for scombroid poisoning in terms of the symptoms listed above.