eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Scombroid

John D Patrick, MD, Assistant Professor of Medicine, Division of Emergency Medicine, Harvard Medical School; Staff, Walk-In Center, Mount Auburn Hospital

Updated: Feb 25, 2010

Introduction

Background

Scombroid fish poisoning (scombrotoxism, scombroid ichthyotoxicosis) is a food-related illness typically associated with the consumption of fish. Originally, the illness was associated with Scombroidea fish (eg, large dark meat marine tuna, albacore, mackerel); however, the Centers for Disease Control and Prevention (CDC) have identified the largest vector to be nonscombroid fish, such as mahi-mahi and amberjack. A case report documents a large outbreak related to escolar (rudderfish, oilfish) consumption, a species whose high waxy ester content can cause some gastrointestinal symptoms (keriorrhoea) that may overlap with those caused by scombroid poisoning.^{[1 ]}Epidemiologic data from the CDC suggest that scombroid poisoning is the principal chemical agent type of food-borne disease found in the United States; the second most common is ciguatera poisoning.^{[2 ]}

Pathophysiology

Most of the published literature suggests that symptoms are related to the ingestion of biogenic amines, especially histamine; others, like putrescine and cadaverine, may potentiate toxicity.^{[3 ]} Histamine is produced via bacterial decarboxylation of histidine and is normally present at levels less than 0.1 mg per 100 g of fish. In contrast, samples of fish that produce poisoning contain histamine levels of at least 20-50 mg per 100 g of fish. Serum histamine levels and urinary histamine excretion are elevated in humans with acute illness. Antihistamines (H1- and H2-blockers) have been used with good efficacy and safety to abate or abolish the symptoms.

Frequency

United States

Scombroid poisoning is relatively uncommon (although likely highly underreported), making up 5% of food-borne disease outbreaks reported to the CDC. The American Association of Poison Control Centers does not maintain specific data on scombroid poisoning, as noted in its 1998 annual toxic surveillance report.

International

Although scombroid poisoning is more common in nations with a warm water fishing industry, the illness is worldwide in scope. The most commonly implicated fish species are scombroid dark meat fish (eg, tuna, mackerel, skipjack, bonito, marlin) and nonscombroid species, such as mahi-mahi (dolphinfish), sardine, yellowtail, herring, and bluefish. Although rare, cases of whitefish scombrotoxism also have been reported.

Clinical

History

Scombroid toxicity is usually self-limited but may cause significant discomfort. The onset of symptoms is usually 10-30 minutes after ingestion of the implicated fish, which is said to have a characteristic peppery bitter taste. The symptoms are nonspecific and may include the following:

• Flushing
• Palpitations
• Headache
• Nausea
• Diarrhea
• Sense of anxiety of unease
• Prostration or loss of vision (rare)

Physical

• Diffuse, macular, blanching erythema (most common); this is shown in the images below
• 
  

  

  An example of a typical scombroid rash, in this case from tuna. Image courtesy of Amanda Oakley, MBChB, FRACP.

  
  {{mediacaption:818405_1}}  
• 
  

  

  An example of a typical scombroid rash, in this case from tuna. Posterior view of the same patient as in the image above. Image courtesy of Amanda Oakley, MBChB, FRACP.

  
  
• Tachycardia
• Wheezing (generally only in histamine-sensitive asthmatics)
• Hypotension or hypertension

Causes

• The bacterial decarboxylation of histidine usually present in fish tissue requires time and moderate temperatures. Thus, the most common causes of clinical illness are the consumption of spoiled fish, consumption of caught fish that has been cooled and refrigerated inadequately, or consumption of frozen fish that has been allowed to sit at room air temperature for a prolonged time after thawing. The most effective preventive measure is the maintenance of chilled temperatures (<40°F [<4.4°C]) from the time of catch until cooking or consumption.
• Generally, consumption of larger amounts of scombrotoxic fish produces more symptoms. Eating a portion of fish closer to the outside of a previously frozen mass of fish also causes more toxicity. Taste is a relatively insensitive measure of toxicity, since the lowest levels of histamine sufficient to cause symptoms cannot be tasted.
• Cooking does notinactivate the toxin.
• The degree of symptoms in individuals consuming the same meal may be quite variable. Magnitude of symptoms may be related to the following:
  • Individual differences in sensitivity to histamine (eg, symptoms may be markedly worse in persons taking isoniazid because of blockade of GI tract histaminase)
  • Size of the portion consumed
  • Whether the portion was from the same fish
  • How cold the fish was before cooking (ie, more thawing may have taken place at the surface, and a fish portion from this area may contain more histamine)

Differential Diagnoses

Other Problems to Be Considered

Acute allergic reaction
Carcinoid syndrome
Chinese restaurant syndrome (monosodium glutamate reaction)
Mastocytosis
Niacinlike reaction
Disulfiram, metronidazole, sulfonylurea reactions
Zollinger-Ellison syndrome
Pheochromocytoma
Migraine or cluster headache
Keriorrhoea, an oily diarrhea related to ingestion of marine wax esters

Workup

Laboratory Studies

• Generally, the diagnosis of scombroid toxicity is clinical; no laboratory tests are necessary.
• If the diagnosis requires confirmation, histamine levels can be measured in a piece of frozen suspect fish.

Other Tests

• In patients in whom palpitations are a predominant symptom, an ECG may be necessary.

Treatment

Prehospital Care

• Prehospital care is primarily supportive.
• Provide oxygen and monitor cardiac function as needed.
• Antihistamines and bronchodilators may be used as needed if advanced life support personnel are involved.

Emergency Department Care

If the patient only has minimal symptoms of scombroid toxicity, reassurance and observation may be the only treatment necessary.

• If clinically necessary, obtain an ECG and institute intravenous access, oxygen, and cardiac monitoring.
• Serum histamine levels and urinary histamine excretion are elevated in persons with acute illness. Treat with antihistamines as needed; H1- and H2-blockers may be useful.
• Consider use of activated charcoal only if presentation is very early and a large amount of fish was ingested.
• Although bronchospasm is rare, use standard treatment if it occurs.
• Extremely rare reported cases of myocardial dysfunction, ischemia, or infarction related to scombroid poisoning exist; standard treatment for these complications, including pressors, should be used. One reported case documents successful treatment of a 36-year-old woman with severe myocardial dysfunction refractory to pressor support by using a biventricular assist device for 8 days.^{[4 ]}

Consultations

Consult the regional poison control center or a local medical toxicologist (certified through the American Board of Medical Toxicology or the American Board of Emergency Medicine) for additional information and patient care recommendations.

Medication

If the patient is symptomatic enough to require treatment, antihistamines are used to counteract the excessive histamine-induced effects; H1- and H2-blockers may be useful. Epinephrine or other adrenergic agents are rarely necessary because the entire cascade of mediators released by a true allergic reaction is not found in scombroid poisoning. Blockade of histamine, the sole pharmacologic mediator of scombrotoxism symptoms, generally is the only treatment necessary. Adrenergic agents may be considered in the rare case of secondary bronchospasm or refractory hypotension associated with this type of poisoning.

Antihistamines

These agents directly counteract the symptom-causing histamine excess.

Diphenhydramine (Benadryl)

Oral or IV H1-receptor antagonists are DOC. Other antihistamines also may be used.

Dosing

Adult

25-50 mg PO/IV/IM q4-6h

Pediatric

1.25 mg/kg PO
<6 years: 12.5 mg PO q4-6h
6-12 years: 12.5-25 mg PO q4-6h; 1-1.5 mg/kg IV/IM
>12 years: Administer as in adults

Interactions

Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patients taking medications that can cause disulfiramlike reactions

Contraindications

Documented hypersensitivity; glaucoma; prostatic enlargement; MAOIs

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction

Cimetidine (Tagamet)

H2-receptor antagonist that may be used in conjunction with H1-blockers for severely symptomatic cases.

Dosing

Adult

300 mg PO/IV q6-8h

Pediatric

200 mg PO q8-12h or 10 mg/kg IV as a single dose

Interactions

Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Elderly persons may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur

Ranitidine (Zantac)

H2-receptor antagonist may be used in conjunction with H1-blockers for severely symptomatic cases. Has fewer drug interactions than cimetidine and may be better for patients who take other medications metabolized by the cytochrome p450 system.

Dosing

Adult

150 mg PO q12h or 50 mg IV q8-12h

Pediatric

75 mg PO 18-12h or 1 mg/kg IV as a single dose

Interactions

May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin; may reduce metabolism of ethanol

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment

Follow-up

Further Inpatient Care

• Admission is required only under exceptional circumstances.

Further Outpatient Care

• The vast majority of patients with scombroid toxicity may be discharged from the ED with oral histamine blockade treatment with H1- and H2-blockers for the next 3-5 days.

Deterrence/Prevention

• Avoid eating ocean fish that is partially spoiled or has been poorly refrigerated. Do not continue eating fish if an unusual peppery bitter taste is detected.

Prognosis

• The prognosis is generally excellent.

Miscellaneous

Medicolegal Pitfalls

• Failure to obtain appropriate history implicating the suspected toxic fish, thereby allowing others to become similarly afflicted

Special Concerns

• Remember public health issues. Notify the local board of health if the diagnosis is confirmed, especially if the source was public.

Multimedia

Media file 1: An example of a typical scombroid rash, in this case from tuna. Image courtesy of Amanda Oakley, MBChB, FRACP.

Media file 2: An example of a typical scombroid rash, in this case from tuna. Posterior view of the same patient as in the image above. Image courtesy of Amanda Oakley, MBChB, FRACP.

References

1. Feldman KA, Werner SB, Cronan S, Hernandez M, Horvath AR, Lea CS. A large outbreak of scombroid fish poisoning associated with eating escolar fish (Lepidocybium flavobrunneum). Epidemiol Infect. Feb 2005;133(1):29-33. [Medline].

2. Lynch M, Painter J, Woodruff R, Braden C. Surveillance for foodborne-disease outbreaks--United States, 1998-2002. MMWR Surveill Summ. Nov 10 2006;55(10):1-42. [Medline]. [Full Text].

3. Al Bulushi I, Poole S, Deeth HC, Dykes GA. Biogenic amines in fish: roles in intoxication, spoilage, and nitrosamine formation--a review. Crit Rev Food Sci Nutr. Apr 2009;49(4):369-77. [Medline].

4. Grinda JM, Bellenfant F, Brivet FG, et al. Biventricular assist device for scombroid poisoning with refractory myocardial dysfunction: a bridge to recovery. Crit Care Med. Sep 2004;32(9):1957-9. [Medline].

5. Bean NH, Goulding JS, Lao C, Angulo FJ. Surveillance for foodborne-disease outbreaks--United States, 1988-1992. MMWR CDC Surveill Summ. Oct 25 1996;45(5):1-66. [Medline].

6. Bedry R, Gabinski C, Paty MC. Diagnosis of scombroid poisoning by measurement of plasma histamine. N Engl J Med. Feb 17 2000;342(7):520-1. [Medline].

7. Bjeldanes LF, Schutz DE, Morris MM. On the aetiology of scombroid poisoning: cadaverine potentiation of histamine toxicity in the guinea-pig. Food Cosmet Toxicol. Apr 1978;16(2):157-9. [Medline].

8. Centers for Disease Control and Prevention. Scombroid fish poisoning associated with tuna steaks--Louisiana and Tennessee, 2006. MMWR Morb Mortal Wkly Rep. Aug 17 2007;56(32):817-9. [Medline]. [Full Text].

9. Chin KW, Garriga MM, Metcalfe DD. The histamine content of oriental foods. Food Chem Toxicol. May 1989;27(5):283-7. [Medline].

10. Eckstein M, Serna M, DelaCruz P, Mallon WK. Out-of-hospital and emergency department management of epidemic scombroid poisoning. Acad Emerg Med. Sep 1999;6(9):916-20. [Medline].

11. Ferran M, Yebenes M. Flushing associated with scombroid fish poisoning. Dermatol Online J. 2006;12(6):15. [Medline]. [Full Text].

12. Kipping R, Eastcott H, Sarangi J. Tropical fish poisoning in temperate climates: food poisoning from ciguatera toxin presenting in Avonmouth. J Public Health (Oxf). Dec 2006;28(4):343-6. [Medline].

13. Leask A, Yankos P, Ferson MJ. Fish, so foul! Foodborne illness caused by combined fish histamine and wax ester poisoning. Commun Dis Intell. 2004;28(1):83-5. [Medline].

14. Lipp EK, Rose JB. The role of seafood in foodborne diseases in the United States of America. Rev Sci Tech. Aug 1997;16(2):620-40. [Medline].

15. McInerney J, Sahgal P, Vogel M, et al. Scombroid poisoning. Ann Emerg Med. Aug 1996;28(2):235-8. [Medline].

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18. Morii H, Kasama K, Herrera-Espinoza R. Cloning and sequencing of the histidine decarboxylase gene from Photobacterium phosphoreum and its functional expression in Escherichia coli. J Food Prot. Aug 2006;69(8):1768-76. [Medline].

19. Morrow JD, Margolies GR, Rowland J, Roberts LJ 2nd. Evidence that histamine is the causative toxin of scombroid-fish poisoning. N Engl J Med. Mar 14 1991;324(11):716-20. [Medline].

20. Perkins RA, Morgan SS. Poisoning, envenomation, and trauma from marine creatures. Am Fam Physician. Feb 15 2004;69(4):885-90. [Medline].

21. Predy G, Honish L, Hohn W, Jones S. Was it something she ate? Case report and discussion of scombroid poisoning. CMAJ. Mar 4 2003;168(5):587-8. [Medline]. [Full Text].

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Keywords

scombroid toxicity, scombroid fish poisoning, seafood poisoning, scombrotoxism, scombroid ichthyotoxicosis, scombroid food poisoning, food poisoning, histamine reaction, scombroid poisoning, food-related illness, keriorrhoea, Scombroidea fish, marine tuna, albacore, mackerel, nonscombroid fish, mahi-mahi, amberjack, food-borne disease, seafood toxicity

Contributor Information and Disclosures

Author

John D Patrick, MD, Assistant Professor of Medicine, Division of Emergency Medicine, Harvard Medical School; Staff, Walk-In Center, Mount Auburn Hospital
John D Patrick, MD is a member of the following medical societies: American College of Emergency Physicians, Massachusetts Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert L Norris, MD, Associate Professor, Department of Surgery; Chief, Division of Emergency Medicine, Stanford University Medical Center
Robert L Norris, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, California Medical Association, International Society of Toxinology, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Fred Harchelroad, MD, FACMT, FAAEM, FACEP, Chair, Department of Emergency Medicine, Director of Medical Toxicology - Allegheny General Hospital, Associate Professor, Department of Emergency Medicine, Drexel University College of Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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