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Emergency Medicine (2003) 15, 293–295 Case Report Something fishy: Six patients with an unusual cause of food poisoning! Michael Hall Emergency Department, The Canberra Hospital, Garran, Australian Capital Territory, Australia Abstract Scombroid fish poisoning is a clinical syndrome attributed to the ingestion of contam- inated fish. A toxin or toxins, known as scombrotoxin, result from decomposition by endogenous flora of the amino acid histidine liberating bioactive amines, predominantly histamine. The presentation has features of histamine toxicity, typically with urticaria, flushing, headache, abdominal cramps, diarrhoea and vomiting. The course is usually mild and self-limiting. The author describes six cases of scombroid poisoning after ingestion of fish from the same Canberra restaurant. One case resulted in significant hypotension necessitating a prolonged stay in the ED. Key words: histamine fish poisoning, hypotension, scombroid, scombrotoxin. Introduction Scombroid fish poisoning is a global phenomenon with public health, economic and industry implications. It has been described extensively in overseas literature but only three case reports exist from Australia. 1–3 Substantial underestimation of the incidence is likely, as many patients fail to present for medical attention. Of those that seek help, it is likely that many are not diagnosed. Symptoms are usually mild and transient 3 but severe reactions and deaths have been reported. 4 Case reports Four patients presented to the triage nurse at The Canberra Hospital around midnight. Their symptoms bore great similarity and on questioning, were all found to have eaten at the same restaurant. They had all consumed yellow fin tuna (Thunnus albacares) with wasabe and Japanese spices. The clinical features of these cases are shown in Table 1. Case 3 A 59-year-old man presented at 00.24 h. He had a past history of MI and hypertension and was taking metoprolol 50 mg bd, aspirin 150 mg daily, and trandolapril 1 mg daily. He reported eating a full serve of the tuna dish at approximately 23.45 h, despite noting a ‘strong peppery, bitter taste’. He immediately noticed tingling in the lips, before becoming flushed and lightheaded, associated with nausea and dia- rrhoea. He was dizzy on standing and generally ‘itchy’. Marked circumoral pallor was noted. Initial obser- vations were normal apart from a blood pressure of 77/37 mmHg. He was agitated and had a pruritic Correspondence: Dr Michael Gavin Hall, Emergency Department, The Canberra Hospital, Yamba Drive, Garran, ACT 2605, Australia. Email: [email protected] Michael Hall, MBBS, Emergency/Toxicology Registrar.

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Page 1: Something fishy: Six patients with an unusual cause of food poisoning!

Emergency Medicine (2003) 15, 293–295

Blackwell Publishing Ltd. Case ReportScombroid fish poisoning

Something fishy: Six patients with an unusual cause of food poisoning!Michael HallEmergency Department, The Canberra Hospital, Garran, Australian Capital Territory, Australia

Abstract

Scombroid fish poisoning is a clinical syndrome attributed to the ingestion of contam-inated fish. A toxin or toxins, known as scombrotoxin, result from decomposition byendogenous flora of the amino acid histidine liberating bioactive amines, predominantlyhistamine. The presentation has features of histamine toxicity, typically with urticaria,flushing, headache, abdominal cramps, diarrhoea and vomiting. The course is usuallymild and self-limiting. The author describes six cases of scombroid poisoning afteringestion of fish from the same Canberra restaurant. One case resulted in significanthypotension necessitating a prolonged stay in the ED.

Key words: histamine fish poisoning, hypotension, scombroid, scombrotoxin.

Introduction

Scombroid fish poisoning is a global phenomenon withpublic health, economic and industry implications. Ithas been described extensively in overseas literaturebut only three case reports exist from Australia.1–3

Substantial underestimation of the incidence is likely,as many patients fail to present for medical attention.Of those that seek help, it is likely that many are notdiagnosed.

Symptoms are usually mild and transient3 but severereactions and deaths have been reported.4

Case reports

Four patients presented to the triage nurse at TheCanberra Hospital around midnight. Their symptomsbore great similarity and on questioning, were all found

to have eaten at the same restaurant. They had allconsumed yellow fin tuna (Thunnus albacares) withwasabe and Japanese spices. The clinical features ofthese cases are shown in Table 1.

Case 3

A 59-year-old man presented at 00.24 h. He had apast history of MI and hypertension and was takingmetoprolol 50 mg bd, aspirin 150 mg daily, andtrandolapril 1 mg daily. He reported eating a fullserve of the tuna dish at approximately 23.45 h, despitenoting a ‘strong peppery, bitter taste’. He immediatelynoticed tingling in the lips, before becoming flushedand lightheaded, associated with nausea and dia-rrhoea. He was dizzy on standing and generally ‘itchy’.Marked circumoral pallor was noted. Initial obser-vations were normal apart from a blood pressureof 77/37 mmHg. He was agitated and had a pruritic

Correspondence: Dr Michael Gavin Hall, Emergency Department, The Canberra Hospital, Yamba Drive, Garran, ACT 2605, Australia. Email: [email protected]

Michael Hall, MBBS, Emergency/Toxicology Registrar.

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M Hall

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urticarial cutaneous eruption across his trunk andupper limbs. The remainder of his examination wasnormal, as was a 12 lead ECG. After application ofoxygen therapy, he was treated with metoclopramide10 mg IV, promethazine 25 mg IV (diluted to 250 mLsin N/Saline) and ranitidine 300 mg PO. 2 L of NormalSaline were administered over the first 90 min, 50 g ofactivated charcoal was given orally. Over 8 h his bloodpressure returned to normal. All other symptomsresolved completely. He was discharged on ranitidine150 mg bd for 2 days and promethazine 10 mg on an asrequired basis.

Cases 5 and 6

In response to information given to the above cases,two other persons phoned the Emergency Departmentin the morning. Both reported circumoral paraesthesiaand diarrhoea, which had resolved by midnight.

Public Health

The ACT Department of Public Health was notifiedand obtained specimens of the fish involved. Thiswas analysed at the Agency for Food and FibreSciences in Queensland and returned histaminelevels of 470 mg/kg and 490 mg/kg. Normal fishhas levels of less than 1 mg/kg. The Australian FoodStandards Code states that histamine must not exceed100 mg/kg.5

The restaurant stated that eight portions of thedish were served that night, giving a case attackrate of at least 75%. The fish had been bought fromthe Sydney fish markets and remaining portions wereremoved from further use. No MSG was used in thepreparation.

Discussion

Scombroid poisoning, also known as histamine fishpoisoning (HFP) is arguably the most common formof fish-related toxicity.6 The earliest report was in1830, when five of the crew of the Triton of Leith becameill after eating bonito, a known scombroid fish.7 Hista-mine fish poisoning has been reported world wide,although due to the mild nature of the syndrome andvariability in reporting practice, the true incidence isunknown. By nature episodic, the largest recordedoutbreak came from Japan in 1973, and involved 2656cases, from the consumption of dried horse mackerel(Trachurus japonicas).3 Instances have been reportedin Australia from tailor (Pomatorus saltatrix)3 juvenileWestern Australian salmon (Arripis truttaceus)2 andfrom an unknown tuna (Thunnus sp.).1

Traditionally, scombroid was thought to occur infish with dark flesh, particularly the family Scom-bridae (mackerel, tuna) and Scomberosocidae (bonito,saury) but has also been documented in numerous‘non-scombroid’ fish such as mahi-mahi, sardines,pilchards, anchovies and herring.3 These fish havehigh levels of histidine. It is postulated that followingdeath, endogenous enterobacteria convert the histidinein the flesh of the fish into histamine and otherbioactive amines. This process may occur at any timebetween harvest and consumption.

The mechanism of toxicity in scombroid poisoningremains unclear. Histamine levels within fish correlatewell with clinical toxicity, but an equivalent dose oforal histamine produces few symptoms.3 Other theoriesinclude an inhibition of histamine detoxification,synergy with other biologically active amines, releaseof endogenous amines by a scombroid toxin, anddisruption of gastrointestinal barriers.8 Interestingly,

Table 1. A cluster of six cases of scombroid fish poisoning presenting to The Canberra Hospital

Case Age Gender Latency (hours) Abnormal Taste Paraesthesiae or numbness

Diarrhoea Headache Rash Hypotension

1 41 F 2.3 Y Y Y Y N N2 52 M 2.3 N Y N Y Y N3 59 M 0.7 Y Y Y N Y Y4 27 M 3.3 N Y Y N Y N5 M ? Y Y Y N ? ?6 F ? N Y Y Y ? ?

In light of the symptom distribution a reasonable case definition would be essential: 1. Consumption of fish within 6 h of symptom onset;2. Circumoral paraesthesiae or numbness; 3 One of: diarrhoea, headache, rash.

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an association has been noted between severity ofscombroid toxicity and the use of isoniazid, a knowninhibitor of histamine metabolism.3

There may be marked variations in symptoma-tology between individuals and between differentportions of the same fish. Symptoms classically occurin the first hour after eating the fish, and the usualduration is 8–12 h, although they may persist up toseveral days. There are no known long-term sequelae.All of the patients described demonstrated some signsor symptoms of scombroid toxicity. Hypotension is arare complication, but may have been exacerbated bythe beta-blocker that patient three was taking. Anothermechanism may have involved the potentiation of his-tamine and bradykinin toxicity due to his angiotensinconverting enzyme inhibitor.

The diagnosis is clinical. A history of a strong pepperytaste, as in these cases, should alert the practitioner.It requires recognition of the time course, signs andsymptoms of the illness, and is made more obviousin the setting of multiple presenters. The commonclinical features are shown in Table 2. The differentialdiagnosis includes fish allergy, ciguatera toxicity andother forms of gastroenteritis.

The majority of patients will require no treatment.If symptoms are minor and already settling then patientsmay be discharged. There is no specific evidence forefficacy, but the author would recommend givingactivated charcoal to severe cases. Intravenous fluidsshould be used to treat hypotension or dehydration.Specific treatment involves a combination of H1 and H2blockers (e.g. promethazine 10–50 mg and ranitidine150–300 mg). Adrenaline may be indicated for airwaycompromise or refractory hypotension and should begiven in similar doses to that used for anaphylaxis.Steroids are thought to be unhelpful and may prolongthe illness.9

Most patients will respond quickly and can besafely discharged. For patients requiring adrenaline,

bronchodilators or intravenous fluids, a period ofobservation would be prudent.

Conclusions

Scombroid poisoning is an unusual cause of food poison-ing. It can occasionally cause significant hypotension.Decontamination and supportive care is supplementedwith combination H1 and H2 blockade. Education ofthe general public and those involved in food prepar-ation of the hazards of eating fish with a ‘peppery taste’may reduce the frequency of this problem.

Acknowledgements

The author would like to thank Dr Paul Dugdale,Chief Health Officer ACT Department of Health: MrJohn Woolard, General Manager ACT Health ProtectionService: and Mr Ralph Anthony, Public Health OfficerACT Health Protection Service, for assistance inpreparing this paper.

Accepted 21 November 2002

References

1. Brown C. Scombroid poisoning. Med. J. Aust. 1993; 158: 435–6.

2. Smart DR. Scombroid poisoning. A report of seven casesinvolving the Western Australian salmon, Arripis truttaceus.Med. J. Aust. 1992; 157: 748–51.

3. Taylor SL. Histamine food poisoning: toxicology and clinicalaspects. Crit. Rev. Toxicol. 1986; 17: 91–128.

4. Eitenmiller RR, Wallis JW, Orr JH, Phillips RD. Production ofhistidine decarboxylase and histamine by Proteus morganii.J. Food Protection 1981; 44: 815–20.

5. ANZFA. Australian Food Standard Code. (Issue 41) Canberra:Australia New Zealand Food Authority, 1998.

6. Lipp EK, Rose JB. The role of seafood in foodborne diseasesin the United States of America. Rev. Sci. Tech. 1997; 16:620–40.

7. Henderson PB. Case of poisoning from the bonito (ScomberPelamis). Edinburgh Med. J. 1830; 34: 317–18.

8. Lehane L, Olley J. Histamine fish poisoning revisited. Int. J.Food Microbiol. 2000; 58: 1–37.

9. Knight J. Scombroid poisoning. South Pacific Underwater Med.Soc. J. 1987; 17: 116–18.

Table 2. Signs and symptoms of scombroid poisoning

Cutaneous – rash (particularly exposed areas /neck/ face), urticaria, flushing

Gastrointestinal – cramps, diarrhoea, epigastric painNeurological – itching, pain, headacheCardiovascular – hypotension (rare)Respiratory – bronchospasm (rare)