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SCOMBROID FISH POISONING

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Scombroid poisoning is a form of ichthyosarcotoxicosis (the toxin is contained within the flesh of the fish). Implicated fishes have free histidine present in their musculature which is metabolized during spoilage to histamine and saurine, a salt of histamine. The toxin involved in the reaction may not be histamine itself, but histamine is usually associated with scombrotoxicosis.

Specific Substances

    A) SCOMBRIDAE
    1) Auxis thazard (Lacepede) (frigate mackerel)
    2) Euthynnus alletteratur (Rafinesque) (black skipjack)
    3) E. pelamis (Linnaeus) (skipjack)
    4) Escolar
    5) Lepidocybium flavobrunneum
    6) Sarda sarda (Bloch) (bonito)
    7) Scomber japonicus (Houttuyn) (Pacific mackerel)
    8) S. scombrus Linneaus (Atlantic mackerel)
    9) Scomberomorus cavalla (Cuvier) (king mackerel)
    10) S. maculatus (Mitchill) (Spanish mackerel)
    11) S. regalis (Bloch) (Cero)
    12) Thunnus alalunga (Bonnaterre) (albacore)
    13) T. abbacares (Bonnaterre) (yellowfin tuna)
    14) T. obesus (Lowe) (bigeye tuna)
    15) T. thynnus (Linnaeus) (bluefin tuna)
    OTHER TYPES OF FISH IMPLICATED
    1) Mahi Mahi or Dolphinfish
    2) Bluefish (Pomatomus saletria) (SYNONYM)
    3) Bombay Duck (a dried fish)
    4) Kahawai
    5) Kingfish
    6) Pilchards
    7) Pacific Amberjack
    8) Japanese Saury (Cololabis saira)
    9) Salmon
    10) Trumpeter Fish
    11) ArripidaeArripis trutta (sea perch)
    12) CoryphaenidaeCoryphaena hippurus (Linnaeus) (dolphin)
    13) CupeidaeAmblygaster sirn (Walbaum) (sprat)
    14) ScomberesocidaeCololabis saira (Brevoort) (saury)
    15) XiphiidaeMakair audax (Poey) (striped marlin)Xiphias gladius (Linneaus) (swordfish)
    16) Prepared FishHerring, sardines, and anchovies
    17) Iwashi maruboshi (dried sardine)
    GENERAL TERMS
    1) SWORDFISH
    2) TUNA
    3) ALBACORE
    4) BONITO
    5) SCROMBROID FISH POISONING
    6) SKIPJACK
    7) DOLPHIN
    8) MACKERAL
    9) MARLIN
    10) PACIFIC DOLPHIN
    11) SWORDFISH (SCOMBROID FISH POISONING)
    12) TUNA (SCOMBROID FISH POISONING)
    13) ALBACORE (SCOMBROID FISH POISONING)
    14) BONITO (SCOMBROID FISH POISONING
    15) SCROMBROID FISH POISONING (MISSPELLING FOR SCOMBROID)
    16) SKIPJACK (SCOMBROID FISH POISONING)
    17) DOLPHIN (SCOMBROID FISH POISONING)
    18) MACKERAL (SCOMBROID FISH POISONING)
    19) MARLIN (SCOMBROID FISH POISONING)
    20) PACIFIC DOLPHIN (SCOMBROID FISH POISONING)

Available Forms Sources

    A) SOURCES
    1) SUMMARY: Fish of the families Scombridae, most commonly tuna and mackerel, and bonito and saury have large amounts of free histidine in their muscle. However, many non-scombroid species, like mahi-mahi or dolphin, and Australian salmon and sardines contain free histidine. Thus, the term "histamine fish poisoning" (HFP) may also be found in the literature to describe this condition and may more appropriately describe this food-related illness (Lehane, 2000; Becker et al, 2001).
    2) The Center for Disease Control (CDC), reported that 42% of all histamine outbreaks were related to non-scombroid fish poisoning in a study conducted in the late 1970's and early 1980's (Becker et al, 2001).
    a) Recently, the CDC reports that scombroid fish poisoning has been most often associated with the consumption of tuna, mahi-mahi, and bluefish (Anon, 2000).
    3) IMPLICATED FISHES (Feldman et al, 2005; Kanki et al, 2004; Russell & Maretic, 1986; Etkind et al, 1987; Mitchell, 1984; Becker et al, 2001):
    1) Scombridae
    a) Auxis thazard (Lacepede) (frigate mackerel)
    b) Euthynnus alletteratur (Rafinesque) (black skipjack)
    c) E. pelamis (Linnaeus) (skipjack)
    d) Lepidocybium flavobrunneum (escolar)
    e) Sarda sarda (Bloch) (bonito)
    f) Scomber japonicus (Houttuyn) (Pacific mackerel)
    g) S. scombrus Linneaus (Atlantic mackerel)
    h) Scomberomorus cavalla (Cuvier) (king mackerel)
    i) S. maculatus (Mitchill) (Spanish mackerel)
    j) S. regalis (Bloch) (Cero)
    k) Thunnus alalunga (Bonnaterre) (albacore)
    l) T. abbacares (Bonnaterre) (yellowfin tuna)
    m) T. obesus (Lowe) (bigeye tuna)
    n) T. thynnus (Linnaeus) (bluefin tuna)
    o) Auxis thazard (Lacepede) (frigate mackerel)
    p) Euthynnus alletteratur (Rafinesque) (black skipjack)
    q) E. pelamis (Linnaeus) (skipjack)
    r) Lepidocybium flavobrunneum (escolar)
    s) Sarda sarda (Bloch) (bonito)
    t) Scomber japonicus (Houttuyn) (Pacific mackerel)
    u) S. scombrus Linneaus (Atlantic mackerel)
    v) Scomberomorus cavalla (Cuvier) (king mackerel)
    w) S. maculatus (Mitchill) (Spanish mackerel)
    x) S. regalis (Bloch) (Cero)
    y) Thunnus alalunga (Bonnaterre) (albacore)
    z) T. abbacares (Bonnaterre) (yellowfin tuna)
    aa) T. obesus (Lowe) (bigeye tuna)
    ab) T. thynnus (Linnaeus) (bluefin tuna)
    2) Mahi Mahi or Dolphinfish
    3) Bluefish (Pomatomus saletria)
    4) Bombay Duck (a dried fish)
    5) Kahawai
    6) Kingfish
    7) Pilchards
    8) Pacific Amberjack
    9) Japanese Saury (Cololabis saira)
    10) Salmon
    11) Trumpeter Fish
    12) Arripidae
    a) Arripis trutta (sea perch)
    13) Coryphaenidae
    a) Coryphaena hippurus (Linnaeus) (dolphin)
    14) Cupeidae
    a) Amblygaster sirn (Walbaum) (sprat)
    15) Scomberesocidae
    a) Cololabis saira (Brevoort) (saury)
    16) Xiphiidae
    a) Makair audax (Poey) (striped marlin)
    b) Xiphias gladius (Linneaus) (swordfish)
    17) Prepared Fish
    a) Herring, sardines, and anchovies
    18) Iwashi maruboshi (dried sardine)
    4) Canned, dried, or smoked fish may also cause scombroid poisoning (Mitchell, 1984; Russell & Maretic, 1986; Lehane, 2000).
    5) OTHER: Ingestion rarely of aged cheeses such as swiss, cheddar, and gouda have been associated with toxicity (Burnett, 1990).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) DESCRIPTION: Scombroid is a condition that develops following ingestion of certain fish species that have been improperly stored. It can produce flushing, itching and allergic-type symptoms.
    B) TOXICOLOGY: In larger fish species, the amino acid histidine is converted to histamine and histamine-like substances by bacteria when freshly caught fish is allowed to warm. The implicated fish may have a pungent smell or peppery taste though absence of these findings does not exclude toxicity. No method of preparation or cooking will make the fish nontoxic when histamine is present. Cooking only destroys the histamine-producing bacteria. Individuals ingesting the spoiled fish can experience a histamine reaction.
    C) SOURCES: IMPLICATED FISH SPECIES: Fish of the families Scombridae, most commonly tuna and mackerel, and bonito and saury have large amounts of free histidine in their muscle. However, many non-scombroid species, like mahi-mahi or dolphin, and Australian salmon and sardines contain free histidine.
    D) EPIDEMIOLOGY: Toxicity is relatively uncommon, but may be under recognized; severe toxicity is rare.
    E) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Within minutes to hours of ingestion of the improperly stored fish, patients may experience headaches, nausea, flushing, and itching.
    2) SEVERE TOXICITY: Severe histamine reactions may occur, leading to fever, tachycardia, hypotension, bronchospasm, vomiting, diarrhea, urticaria, or angioedema. Symptoms may last up to 36 hours after ingestion.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) FEVER
    a) CASE REPORT: After ingesting sail fish fillets, a child experienced fever, chills, pale face, tachycardia (heart rate 182 bpm) and hypotension (BP 68/48 mmHg) (Wu & Chen, 2003).
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Facial flushing, conjunctival irritation, angioneurotic facial edema, and burning of gingivae or throat may develop.
    2) Implicated fish may have a normal or a "sharp" or "peppery" taste. A metallic taste has also been reported.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Palpitations are a common symptom; however, tachycardia, hypotension, and shock are rare. Sinus bradycardia with hypotension has been reported.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Chest tightness and mild respiratory distress have occurred; however, severe respiratory distress and respiratory collapse are rare.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Headache is common; dizziness, weakness, apprehension, tingling, and anxiety have occurred.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, diarrhea, and abdominal cramps are common.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) An erythematous rash, pruritus, or burning sensation are common; diaphoresis and urticaria are less common.
    0.2.19) IMMUNOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Angioedema has been reported following scombroid fish poisoning.

Laboratory Monitoring

    A) No laboratory tests are indicated in the evaluation of patients with scombroid toxicity.
    B) If laboratory confirmation is desired, quantitation of histamine in the implicated fish flesh may be performed by a health department or reference laboratory. Normal fish has less than 1 mg of histamine/100 g of flesh. Illness is usually associated with 100 mg of histamine/100 g of flesh, but 20 mg of histamine/100 g of flesh may cause illness in susceptible individuals.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Patients should be given antihistamines, both H1 (eg, Diphenhydramine every 6 hours as needed, 25 to 100 mg in adults; 0.5 to 1.5 mg/kg in children) and H2 blockers (eg cimetidine, ranitidine, famotidine).
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Patients should be given antihistamines, both H1 (eg, Diphenhydramine every 6 hours as needed, 25 to 100 mg in adults; 0.5 to 1.5 mg/kg in children) and H2 blockers (eg cimetidine, ranitidine, famotidine). The IV route is preferred for patients with severe toxicity. Administer isotonic fluids, if the patient is hypotensive. Treat airway edema, hypotension, or bronchospasm with epinephrine (ADULT: 0.3 mg IM; PEDIATRIC: 0.01 mg/kg IM) and corticosteroids (adults prednisone 60 mg orally or solumedrol 125 mg IV). Administer inhaled beta agonists (eg albuterol) for bronchospasm.
    C) DECONTAMINATION
    1) PREHOSPITAL: Decontamination is not indicated in the prehospital setting.
    2) HOSPITAL: Patients generally do not present until they are symptomatic, so there is little role for GI decontamination.
    D) AIRWAY MANAGEMENT
    1) Airway management should be considered for patients with angioedema or bronchospasm unresponsive to IV antihistamines and bronchodilators.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION
    1) There is no role for enhanced elimination techniques in scombroid toxicity.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with mild symptoms consisting of flushing, nausea, and itching can be observed at home with over-the-counter antihistamine treatment. Patients with respiratory symptoms, angioedema or recurrent vomiting should be referred to a healthcare facility.
    2) OBSERVATION CRITERIA: Mild cases should be observed for 2 to 4 hours after symptom control. Patients with severe symptoms should be observed for recurrence of symptoms for 8 hours after symptom control.
    3) ADMISSION CRITERIA: Admission is generally not required for patients with scombroid toxicity. Indications for admission to the hospital are inability to control vomiting, hypotension unresponsive to fluids and antihistamines, or angioedema unresponsive to antihistamines.
    4) CONSULT CRITERIA: A toxicologist should be consulted in cases of severe toxicity of if patients are unresponsive to antihistamine therapy. Notify the local health department to investigate the source and prevent further exposure.
    H) PITFALLS
    1) Failure to recognize the associated fish intake. Failure to notify the business that provided the fish may lead to numerous cases of toxicity.
    I) TOXICOKINETICS
    1) Symptoms are usually present within minutes to several hours and may last up to 36 hours.
    J) DIFFERENTIAL DIAGNOSIS
    1) Anything that cause an allergic histamine reaction may be confused with scombroid toxicity. However, a temporal history of an implicated fish species is strongly suggestive of scombroid toxicity.

Range Of Toxicity

    A) TOXICITY: A bite of spoiled fish may result in symptoms; individual variation to scombroid fish poisoning exists. The recognized toxic concentration of histamine in fish is greater than 100 mg/100 g of meat.

Clinical Effects

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) An erythematous rash, pruritus, or burning sensation are common; diaphoresis and urticaria are less common.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) WITH POISONING/EXPOSURE
    a) An erythematous rash is a frequent finding (Grinda et al, 2004; Wu & Chen, 2003; Hall, 2003; Kerr & Parke, 1998; Sanchez-Guerrero et al, 1997; Gilbert et al, 1980; Kim, 1979; Merson et al, 1974; Guss, 1998). Itching or pain do not always accompany rash (Borade et al, 2007).
    b) INCIDENCE: In a retrospective review, rash (41%; n=19) was the most common adverse evert reported in patients with scombroid fish poisoning with at least one dermatologic effect reported in 82% (n=38) of all patients exposed. Other common dermatologic symptoms included: flushing 37% (n=17), erythema 23.9% (n=11), and pruritus 15.2% (n=7) (Lavon et al, 2008).
    B) ITCHING OF SKIN
    1) WITH POISONING/EXPOSURE
    a) Pruritus or a burning sensation is often described (Lavon et al, 2008; Kim, 1979; Russell & Maretic, 1986; Etkind et al, 1987; Sanchez-Guerrero et al, 1997; Guss, 1998).
    C) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) Diaphoresis may be observed after scombroid poisoning (Gilbert et al, 1980; Anon, 2000). In a case series, sweating was reported in 14 of 42 patients (33%) with scombroid poisoning (Feldman et al, 2005).
    D) URTICARIA
    1) WITH POISONING/EXPOSURE
    a) Although urticaria occurs less frequently (Merson et al, 1974; Russell & Maretic, 1986), there have been several cases of urticaria following the ingestion of tuna fish (Sanchez-Guerrero et al, 1997).
    E) FLUSHING
    1) WITH POISONING/EXPOSURE
    a) Facial flushing or "feverish feeling" may develop (Lavon et al, 2008; Wu & Chen, 2003; Smart, 1992; Sanchez-Guerrero et al, 1997; Kerr & Parke, 1998; Sabroe & Kobza Black, 1998; Anon, 2000).
    b) INCIDENCE: In a series of 42 patients with scombroid poisoning after eating escolar fish, 26 (62%) developed facial flushing, and 13 (31%) developed whole body flushing (Feldman et al, 2005). In another outbreak, all 8 patients developed flushing within 20 to 120 minutes of exposure (Miki et al, 2005).

Immunologic

    3.19.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Angioedema has been reported following scombroid fish poisoning.
    3.19.2) CLINICAL EFFECTS
    A) ANGIOEDEMA
    1) WITH POISONING/EXPOSURE
    a) Two cases of angioedema (palpebral and glottis, respectively) occurred following scombroid poisoning. Onset of symptoms occurred within 30 minutes of ingestion and resolved following treatment (ie, epinephrine, antihistamines, and steroids) (Sanchez-Guerrero et al, 1997).

Summary Of Exposure

    A) DESCRIPTION: Scombroid is a condition that develops following ingestion of certain fish species that have been improperly stored. It can produce flushing, itching and allergic-type symptoms.
    B) TOXICOLOGY: In larger fish species, the amino acid histidine is converted to histamine and histamine-like substances by bacteria when freshly caught fish is allowed to warm. The implicated fish may have a pungent smell or peppery taste though absence of these findings does not exclude toxicity. No method of preparation or cooking will make the fish nontoxic when histamine is present. Cooking only destroys the histamine-producing bacteria. Individuals ingesting the spoiled fish can experience a histamine reaction.
    C) SOURCES: IMPLICATED FISH SPECIES: Fish of the families Scombridae, most commonly tuna and mackerel, and bonito and saury have large amounts of free histidine in their muscle. However, many non-scombroid species, like mahi-mahi or dolphin, and Australian salmon and sardines contain free histidine.
    D) EPIDEMIOLOGY: Toxicity is relatively uncommon, but may be under recognized; severe toxicity is rare.
    E) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Within minutes to hours of ingestion of the improperly stored fish, patients may experience headaches, nausea, flushing, and itching.
    2) SEVERE TOXICITY: Severe histamine reactions may occur, leading to fever, tachycardia, hypotension, bronchospasm, vomiting, diarrhea, urticaria, or angioedema. Symptoms may last up to 36 hours after ingestion.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) FEVER
    a) CASE REPORT: After ingesting sail fish fillets, a child experienced fever, chills, pale face, tachycardia (heart rate 182 bpm) and hypotension (BP 68/48 mmHg) (Wu & Chen, 2003).

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Facial flushing, conjunctival irritation, angioneurotic facial edema, and burning of gingivae or throat may develop.
    2) Implicated fish may have a normal or a "sharp" or "peppery" taste. A metallic taste has also been reported.
    3.4.2) HEAD
    A) WITH POISONING/EXPOSURE
    1) Facial flushing is common (Kim, 1979; Smart, 1992; Sanchez-Guerrero et al, 1997; Feldman et al, 2005).
    2) Swelling of face, lips, and tongue may occur secondary to angioedema (Grinda et al, 2004; Kim, 1979; Mitchell, 1984; Russell & Maretic, 1986; Sanchez-Guerrero et al, 1997).
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Conjunctival injection has been described (Nosanchuk et al, 1982; Russell & Maretic, 1986).
    2) Transient vision loss was reported in an adult with a history of diabetes and hypertension following scombroid poisoning (McInerney et al, 1996). Symptoms resolved within an hour of diphenhydramine administration; neurological exam was negative.
    a) It was suggested that vision loss was secondary to cerebral blindness caused by either vasospasm or by a compromise in circulation caused by hypertension exacerbation due to the effects of histamine.
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) An abnormal taste, a burning, hot, "sharp", or "peppery" sensation of the gingivae or throat may occur when eating the implicated fish (Feldman et al, 2005; Grinda et al, 2004; Hall, 2003; Gilbert et al, 1980; Russell & Maretic, 1986; Kim, 1979; Anon, 2000). A tight feeling in the throat has been reported after exposure (Becker et al, 2001).
    2) Oral blisters may also develop.

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Palpitations are a common symptom; however, tachycardia, hypotension, and shock are rare. Sinus bradycardia with hypotension has been reported.
    3.5.2) CLINICAL EFFECTS
    A) PALPITATIONS
    1) WITH POISONING/EXPOSURE
    a) Palpitations are frequently described (Predy et al, 2004; Merson et al, 1974; Gilbert et al, 1980; Sabroe & Kobza Black, 1998).
    b) Palpitations or tachycardia were reported in 24 of 42 patients (57%), who developed scombroid poisoning after eating escolar fish (Feldman et al, 2005).
    B) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Tachycardia may be observed following scombroid poisoning (Feldman et al, 2005; Grinda et al, 2004; Russell & Maretic, 1986; Sanchez-Guerrero et al, 1997).
    b) CASE SERIES: Three individuals experienced pulse rates between 119 to 150 with a normal blood pressure approximately 30 minutes after exposure (Kerr & Parke, 1998).
    c) CASE REPORT: After ingesting sail fish fillets, a child experienced fever, chills, pallor, tachycardia (heart rate 182 beats per minute) and hypotension (BP 68/48 mmHg) (Wu & Chen, 2003).
    C) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Two cases of bradycardia, one associated with hypotension, was reported in a case series of 30 patients (Eckstein et al, 1999).
    D) ATRIOVENTRICULAR BLOCK
    1) WITH POISONING/EXPOSURE
    a) Atrioventricular block (2:1) has been described in an adult following exposure; the patient converted to sinus rhythm after diphenhydramine (McInerney et al, 1996).
    E) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension has been reported, but is rare (MMWR, 1986)(Halstead, 1980).
    b) CASE REPORTS
    1) An 80-year-old woman with a history of stable hypertension and no other known cardiac risk factors, collapsed with a blood pressure of 60/40 mmHg shortly after eating mackerel. Physical, laboratory and diagnostic (ECG, chest x-ray) findings were within normal limits. Vital signs began to significantly improve with the addition of cyclizine for nausea. Chorpheniramine was also added for suspected scombroid poisoning, and the patient continued to improve and remained hemodynamically stable. The patient was discharged to home the following day (Borade et al, 2007).
    2) One patient experienced significant hypotension (BP 77/37 mmHg), requiring a prolonged stay at the hospital (Hall, 2003).
    3) CASE REPORT: After ingesting sail fish fillets, a child experienced fever, chills, pallor, tachycardia (heart rate 182 beats per minute) and hypotension (BP 68/48 mmHg) (Wu & Chen, 2003).
    F) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) A 51-year-old woman developed facial flushing, severe throbbing headache, nausea, palpitations, tachycardia (100 beats per minute) and hypertension (BP 200/120 mm Hg) 30 minutes after eating a tuna fish salad. The salad contained elevated histamine levels (35 mg histamine/100 g). Following supportive therapy, all symptoms resolved within 8 to 10 hours after onset. However, she experienced fatigue and intermittent palpitations for another 5 days (Predy et al, 2004).
    G) CARDIOGENIC SHOCK
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 36-year-old woman presented to the ED with dyspnea, lip edema, burning in the mouth, an erythematous rash, nausea, headache, tachycardia (120 beat per minute (bpm)), and tachypnea (40 breaths/min) approximately 20 minutes after consuming cooked fresh tuna (histamine levels in fish not reported). Over the next several hours, despite administration of antihistamines and corticosteroids, the patient's presenting symptoms persisted and she developed hypotension (BP 80/50 mmHg), requiring administration of fluids and epinephrine. Within the next 1 to 3 days, the patient's hemodynamic status worsened with the development of cardiogenic shock with pulmonary edema and respiratory distress, necessitating mechanical ventilation and continued administration of epinephrine with the addition of dobutamine. An ECG showed supraventricular tachycardia (150 bpm). The patient's troponin I level was elevated and a transesophageal echocardiography showed severe biventricular myocardial dysfunction that appeared to be refractory to the continued inotropic support.
    1) On hospital day 3, a biventricular assist device was implanted that consisted of 2 paracorporeal pneumatic pumps, providing mechanical circulatory support, and set at a rate of 70 bpm corresponding to an output of 5.6 L/min. Dobutamine and epinephrine were discontinued on postoperative days 0 and 3, respectively. On postoperative day 7, despite anticoagulation with heparin, a stroke, with left hemiplegia, occurred; however, a repeat transesophageal echocardiography showed almost complete recovery of myocardial function, resulting in the explantation of the device on postoperative day 8 (11 days postingestion). Follow-up of the patient over the next 3 years showed complete resolution of myocardial dysfunction without cardiac or neurologic sequelae (Grinda et al, 2004).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Chest tightness and mild respiratory distress have occurred; however, severe respiratory distress and respiratory collapse are rare.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) A sensation of "chest tightness" or respiratory distress has occurred (Feldman et al, 2005; Gilbert et al, 1980; Mitchell, 1984; Sabroe & Kobza Black, 1998). Of 7 cases reported, 2 developed dyspnea which resolved following medical intervention (Sanchez-Guerrero et al, 1997).
    b) INCIDENCE: In one retrospective review of 46 patients with scombroid fish poisoning, dyspnea was reported in 17.4% (n=8) of patients (Lavon et al, 2008).
    B) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) Although bronchospasm and severe respiratory distress occur rarely (Halstead, 1980; Russell & Maretic, 1986), several patients have developed severe symptoms including bronchospasm (Sanchez-Guerrero et al, 1997).
    C) APNEA
    1) WITH POISONING/EXPOSURE
    a) One case of respiratory collapse has been reported (Russell & Maretic, 1986).
    D) TACHYPNEA
    1) WITH POISONING/EXPOSURE
    a) Tachypnea (40 breaths/minute) occurred in a 36-year-old woman following scombroid fish poisoning resulting from ingestion of cooked fresh tuna (Grinda et al, 2004).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Headache is common; dizziness, weakness, apprehension, tingling, and anxiety have occurred.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) A throbbing temporal headache is common (Guly & Grant, 2006; Grinda et al, 2004; Wu & Chen, 2003; Hall, 2003; Gilbert et al, 1980; Sanchez-Guerrero et al, 1997; Sabroe & Kobza Black, 1998; Anon, 2000).
    b) INCIDENCE: Headaches were reported in 28 of 42 patients (67%) who developed scombroid poisoning following ingestion of escolar fish (Lepidocybium flavobrunneum) (Feldman et al, 2005). In another series of 46 patients with scombroid fish poisoning, headache (30.4%; n=14) was the most common neurologic symptom reported (Lavon et al, 2008).
    B) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) A feeling of giddiness or dizziness sometimes occurs (Guly & Grant, 2006; Feldman et al, 2005; Wu & Chen, 2003; Dickinson, 1982; Gilbert et al, 1980; Sanchez-Guerrero et al, 1997; Sabroe & Kobza Black, 1998). Weakness, apprehension and anxiety may develop (Russell & Maretic, 1986).
    b) INCIDENCE: In one retrospective review of 46 patients with scombroid fish poisoning, dizziness was reported in 10.9% (n=5) of patients (Lavon et al, 2008).
    C) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Tingling has been reported (Hall, 2003; Taylor et al, 1989).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, diarrhea, and abdominal cramps are common.
    3.8.2) CLINICAL EFFECTS
    A) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea is a common finding after scombroid poisoning (Wu & Chen, 2003; Hall, 2003; Gilbert et al, 1980; Kerr & Parke, 1998; Anon, 2000). Flatus may also be noted (Russell & Maretic, 1986).
    b) Diarrhea occurred in 17 of 42 patients (41%) who developed scombroid poisoning following ingestion of escolar fish (Lepidocybium flavobrunneum) (Feldman et al, 2005).
    B) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, and abdominal cramps are frequently reported, and is usually one of the presenting symptoms (Lavon et al, 2008; Feldman et al, 2005; Grinda et al, 2004; Wu & Chen, 2003; Sanchez-Guerrero et al, 1997; Lerke et al, 1978; Merson et al, 1974).
    1) ONSET: Symptoms may begin within a few minutes of consuming the implicated food. Although the effects are self-limited in most cases, symptoms may last for up to 24 hours (Borade et al, 2007).
    b) INCIDENCE: In a series of 42 patients who developed scombroid poisoning after eating escolar fish, 20 (48%) developed nausea and 8 (19%) developed vomiting (Feldman et al, 2005). In another series of 46 patients with scombroid fish poisoning, 9 (19.6%) developed diarrhea, 4 (8.7%) had nausea, and 2 (4.3%) developed vomiting (Lavon et al, 2008).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No laboratory tests are indicated in the evaluation of patients with scombroid toxicity.
    B) If laboratory confirmation is desired, quantitation of histamine in the implicated fish flesh may be performed by a health department or reference laboratory. Normal fish has less than 1 mg of histamine/100 g of flesh. Illness is usually associated with 100 mg of histamine/100 g of flesh, but 20 mg of histamine/100 g of flesh may cause illness in susceptible individuals.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) BLOOD HISTAMINE LEVELS: Histamine concentrations have been measured following exposure and have been elevated (Kim, 1979), but are not clinically useful.
    2) Tryptase is released at the same time as histamine and acts as an indicator of mast-cell activation. Elevated levels may be anticipated in an anaphylactic reaction; lower levels may indicate poisoning by an exogenous source of histamine (Sanchez-Guerrero et al, 1997).
    4.1.4) OTHER
    A) OTHER
    1) OTHER
    a) FISH HISTAMINE LEVELS: Fresh fish flesh contains normally less than 1 mg/100 g of histamine (Gilbert et al, 1980).
    1) Fish containing greater than or equal to 100 mg histamine/100 g flesh have been implicated in causing scombroid fish poisoning (Gilbert et al, 1980).
    2) Occasionally poisoning cases have been associated with findings of less than or equal to 20 mg histamine/100 g flesh (Gilbert et al, 1980).
    2) CULTURES
    a) Cultures are not considered useful (Gilbert et al, 1980); however common bacterial organisms capable of metabolizing histidine to histamine have been done from implicated fish (Lerke et al, 1978; Merson et al, 1974; Taylor et al, 1979; Gilbert et al, 1980).

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) LABORATORY DIAGNOSIS: The diagnosis is most often based on analysis of implicated fish flesh for histamine content (Foo, 1975).
    2) HISTAMINE CONCENTRATION: The concentration may vary considerably in specimens taken from the same fish; multiple sites should be sampled to improve accuracy (Lerke et al, 1978).
    3) QUANTITATION METHODS:
    1) Fluorometric method (Lerke et al, 1978)
    2) Paper chromatographic method (Foo, 1975)
    3) Capillary gas chromatographic-mass spectrometric method (Henion et al, 1981)

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Admission is generally not required for patients with scombroid toxicity. Indications for admission to the hospital are inability to control vomiting, hypotension unresponsive to fluids and antihistamines, or angioedema unresponsive to antihistamines.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with mild symptoms consisting of flushing, nausea, and itching can be observed at home with over-the-counter antihistamine treatment. Patients with respiratory symptoms, angioedema or recurrent vomiting should be referred to a healthcare facility.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) A toxicologist should be consulted in cases of severe toxicity of if patients are unresponsive to antihistamine therapy. Notify the local health department to investigate the source and prevent further exposure.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Mild cases should be observed for 2 to 4 hours after symptom control. Patients with severe symptoms should be observed for recurrence of symptoms for 8 hours after symptom control.

Monitoring

    A) No laboratory tests are indicated in the evaluation of patients with scombroid toxicity.
    B) If laboratory confirmation is desired, quantitation of histamine in the implicated fish flesh may be performed by a health department or reference laboratory. Normal fish has less than 1 mg of histamine/100 g of flesh. Illness is usually associated with 100 mg of histamine/100 g of flesh, but 20 mg of histamine/100 g of flesh may cause illness in susceptible individuals.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Decontamination is not indicated in the prehospital setting.
    B) DIPHENHYDRAMINE
    1) Prehospital administration of diphenhydramine and intravenous fluids has been successfully used in 2 multiple casualty incidents (57 patients total) involving scombroid poisoning in which the diagnosis was established by on scene medical personnel in one case and an index case presenting to the emergency department in the second case (Eckstein et al, 1999).
    2) DIPHENHYDRAMINE/ADULT
    a) DOSE: 10 to 50 mg intravenously at a rate not exceeding 25 mg/minute or deep intramuscularly; maximum dose: 100 mg/dose; maximum daily dose: 400 mg/day (Prod Info diphenhydramine hcl injection, 2006).
    3) DIPHENHYDRAMINE/PEDIATRIC
    a) DOSE: 5 mg/kg/day or 150 mg/m(2)/day intravenously divided into 4 doses at a rate not exceeding 25 mg/minute, or deep intramuscularly; maximum daily dose: 300 mg/day. Not recommended in premature infants and neonates (Prod Info diphenhydramine hcl injection, 2006).
    4) INTRAMUSCULAR: Diphenhydramine has also been administered in similar doses with good results (Nosanchuk et al, 1982; Kim, 1979).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Patients generally do not present until they are symptomatic, so there is usually little role for GI decontamination. Activated charcoal could theoretically decrease toxin absorption if administered shortly after ingestion.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) No laboratory tests are indicated in the evaluation of patients with scombroid toxicity.
    2) If laboratory confirmation is desired, quantitation of histamine in the implicated fish flesh may be performed by a health department or reference laboratory. Normal fish has less than 1 mg of histamine/100 g of flesh. Illness is usually associated with 100 mg of histamine/100 g of flesh, but 20 mg of histamine/100 g of flesh may cause illness in susceptible individuals.
    B) ANTIHISTAMINE
    1) SUMMARY: Scombroid poisoning generally resolves within 12 hr without treatment; however, antihistamines (H1 and H2 {cimetidine, famotidine}), can ease symptoms quickly (Kerr & Parke, 1998; Bedry et al, 2000; Lehane, 2000). Response to an antihistamine is rapid. Diphenhydramine and chlorpheniramine are commonly used. Steroids and epinephrine are rarely indicated. Serious complications are rare (Lehane, 2000). Since exposure is based on an exogenous histamine release, symptoms would not be anticipated with future consumption of the same fresher fish species (Bedry et al, 2000).
    2) DIPHENHYDRAMINE
    a) DIPHENHYDRAMINE/ADULT
    1) DOSE: 10 to 50 mg intravenously at a rate not exceeding 25 mg/minute or deep intramuscularly; maximum dose: 100 mg/dose; maximum daily dose: 400 mg/day (Prod Info diphenhydramine hcl injection, 2006).
    b) DIPHENHYDRAMINE/PEDIATRIC
    1) DOSE: 5 mg/kg/day or 150 mg/m(2)/day intravenously divided into 4 doses at a rate not exceeding 25 mg/minute, or deep intramuscularly; maximum daily dose: 300 mg/day. Not recommended in premature infants and neonates (Prod Info diphenhydramine hcl injection, 2006).
    c) INTRAMUSCULAR: Diphenhydramine has also been administered IM in similar doses with good results (Nosanchuk et al, 1982; Kim, 1979).
    3) CHLORPHENIRAMINE
    a) CHLORPHENIRAMINE MALEATE: 10 mg IM has been given to adults with good results (Dickinson, 1982) (Waring, 1978) .
    4) PROMETHAZINE
    a) ADULT: 50 mg IM was successful in relieving symptoms in some cases, 180 mg (2 doses) over a 4 hour period was required in a more severe case (Smart, 1992).
    C) CORTICOSTEROID
    1) SUMMARY: The place of steroids in scombroid poisoning has NOT been established, but should be considered in patients with severe toxicity.
    2) METHYLPREDNISOLONE: 40 mg IM was administered with diphenhydramine in a reported case of scombroid poisoning with rapid resolution of symptoms (Pugno et al, 1983).
    D) EPINEPHRINE
    1) SUMMARY: (Subcutaneous epinephrine): 0.2 to 0.3 mg subQ has been administered (Dickinson, 1982; Blakesley, 1983) but has questionable efficacy in the absence of bronchospasm.
    2) ADULT DOSE: (Auto-injector): Usual adult dose for anaphylaxis is 0.3 mg (0.3 mL of a 1:1000 solution [1 mg/mL]) for adults weighing 30 kg or greater, given IM or subQ. The dose may be repeated if severe anaphylaxis persists (Prod Info EPIPEN(R) intramuscular, subcutaneous auto injector, 2008).
    3) PEDIATRIC DOSE: (Injectable solution) 0.01 mg/kg, MAX 0.3 mg (0.3 mL of a 1:1000 solution [1 mg/mL]) IM or subQ every 5 min as needed (guidelines dosing) (Lieberman et al, 2010).
    E) CIMETIDINE
    1) Cimetidine has been used successfully in patients refractory to antihistamines. It has also been used successfully as a first-line treatment (Guss, 1998; Lehane, 2000).
    2) ADULT DOSE: Cimetidine 300 mg IV or ranitidine 50 mg IV when rapid relief is necessary. Cimetidine orally may be useful for refractory borborygmus and headache (Auerbach & Geehr, 1989).
    3) CAUTION: Hypotension may occur with combined H1 and H2 blockers.
    4) CASE REPORT: A 32-year-old man with a presumptive diagnosis of scombroid poisoning (symptoms: a raised, pruritic rash) was treated with a 300 mg IV infusion of cimetidine (Guss, 1998). Pruritus subsided within 10 min of administration with all symptoms resolved by 30 min.
    5) CASE STUDY: Four patients who had poor clinical responses to antihistamine, steroids, or subQ epinephrine were treated with IV cimetidine. All 4 patients had clinical improvement, but 1 developed significant hypotension (Blakesley, 1983).
    F) FAMOTIDINE
    1) INTRAVENOUS: ADULT DOSE: 20 mg IV every 12 hr; PEDIATRIC DOSE: Patients 1 to 16 years of age: 0.25 mg/kg IV (injected over at least 2 minutes or as a 15 minute infusion) every 12 hr up to 40 mg/day. (NOTE: The use of IV famotidine has not been adequately studied in children less than 1 year of age) (Prod Info PEPCID(R) IV injection, 2006).
    2) ORAL: ADULT DOSE: 20 mg every 6 hr as needed; individual adjustment may be indicated. PEDIATRIC DOSE: Patients 1 to 16 years of age: 0.5 mg/kg/day; maximum 40 mg/day (Prod Info PEPCID(R) oral tablets, 2010).
    G) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    H) BRADYCARDIA
    1) ATROPINE: ADULT DOSE: BRADYCARDIA: BOLUS: 0.5 mg IV may repeat every 3 to 5 min. Maximum: 3 mg. PEDIATRIC DOSE: 0.02 mg/kg IV/IO (0.04 to 0.06 mg/kg ET). Repeat once, if needed. Minimum dose: 0.1 mg. Maximum single dose: Child: 0.5 mg; Adolescent: 1 mg. Maximum total dose: Child: 1 mg; Adolescent: 2 mg.
    I) IMPLANTATION OF VENTRICULAR ASSIST DEVICE
    1) CASE REPORT - A 36-year-old woman developed severe myocardial dysfunction, unresponsive to dobutamine and epinephrine administration, and resulting from suspected scombroid poisoning following ingestion of cooked fresh tuna. The patient's ECG, 3 days postingestion, showed supraventricular tachycardia (150 bpm) and a transesophageal echocardiography showed severe biventricular hypokinesia without heart dilation, valvular lesions, or pericardial effusion. On hospital day 3, the patient was implanted with a biventricular assist device that consisted of 2 paracorporeal pneumatic pumps, providing mechanical circulatory support, and set at a rate of 70 bpm corresponding to an output of 5.6 L/min. Dobutamine and epinephrine were discontinued on postoperative days 0 and 3, respectively. On day 7, despite anticoagulation with heparin, a stroke, with left hemiplegia, occurred; however a repeat transesophageal echocardiography showed almost complete recovery of myocardial function, resulting in the explantation of the device on day 8 (11 days postingestion). Follow-up of the patient over the next 3 years showed complete resolution of myocardial dysfunction without cardiac or neurologic sequelae (Grinda et al, 2004).

Enhanced Elimination

    A) SUMMARY
    1) There is no role for enhanced elimination techniques in scombroid toxicity.

Abstracts

Case Reports

    A) CASE REPORT
    1) A moderately severe, throbbing bitemporal headache was the initial symptom seen in one case. This progressed to a warm facial feeling, mild nasal congestion, flushing of face and ears, nausea, and abdominal cramping (Christman, 1991).
    B) CASE SERIES
    1) In a retrospective review of 46 patients with scombroid fish poisoning, tuna was the most common fish consumed. Most exposures occurred among adults with only 4 children under the age of 18 exposed. The majority of cases were mild to moderate with only 2 severe cases reported. Most patients developed symptoms within 20 minutes. The most common events included: rash (41%), flushing (37%), gastrointestinal complaints (37%) and headache (30.4%). All patients recovered within several hours of exposure with no permanent sequelae with most responding to H1-antagonists; 14 patients required no treatment (Lavon et al, 2008).

Range Of Toxicity

Summary

    A) TOXICITY: A bite of spoiled fish may result in symptoms; individual variation to scombroid fish poisoning exists. The recognized toxic concentration of histamine in fish is greater than 100 mg/100 g of meat.

Maximum Tolerated Exposure

    A) ACUTE
    1) HISTAMINE CONCENTRATION IN FISH
    a) NORMAL CONCENTRATIONS: Concentrations are usually under 0.1 mg/100 g of fish (Smart, 1992).
    b) SPOILAGE CONCENTRATION: Greater than 20 mg/100 g (Smart, 1992).
    2) TOXIC CONCENTRATION
    a) SUMMARY: Based on human exposure to histamine in different foods, histamine-induced poisoning occurs at the following rates: a total dose of 8 to 40 mg produces slight symptoms; greater than 40 mg produces moderate symptoms, and severe symptoms occur at concentrations of greater than 100 mg (Lehane, 2000).
    b) INDIVIDUAL VARIABILITY: There is considerable individual variation in sensitivity to scombrotoxic fish poisoning. Amounts of fish eaten by victims have not been well documented.
    c) The FDA considers over 50 mg of histamine/100 g of tuna to be toxic (Taylor et al, 1989).
    d) Most individuals will NOT develop illness unless fish containing 100 mg of histamine/100 g of flesh is eaten. However, cases of illness from implicated fish with 20 mg or less of histamine/100 g of flesh have been reported (Gilbert et al, 1980).
    e) Consumption of fish containing 400 mg of histamine/100 g of flesh has not produced poisoning in some cases (Russell & Maretic, 1986).
    f) POISONING OUTBREAKS: Histamine concentrations from implicated fish have contained the following: 200 mg/100 g, 250 mg/100 g, 500 mg/100 g, and 600 mg/100 g of flesh (Mitchell, 1984; Russell & Maretic, 1986; Etkind et al, 1987).
    B) CASE REPORTS
    1) LITERATURE REVIEW: The following guidelines have been suggested following a literature review of 250 cases of histamine poisoning (Bartholomew et al, 1987):
    1) Less than 5 mg histamine/100 g of fish: considered safe
    2) 5 to 10 mg histamine/ 100 g of fish: possibly toxic
    3) 20 to 100 mg histamine/100 g of fish: probably toxic
    4) Greater than 100 mg histamine/100 g of fish: toxic
    C) ROUTE OF EXPOSURE
    1) PERMISSIBLE CONCENTRATIONS
    a) UNITED STATES: The US Food and Drug Administration action level for histamine in tuna: 50 mg/100 g of meat (Etkind et al, 1987).
    1) Unofficial US maximum allowable histamine concentration in fish: 10 mg/100 g of meat (Russell & Maretic, 1986).
    b) AUSTRALIA: The maximum allowable level for histamine in fish based on the Australian Food Standards Code is 100 mg/kg (10 mg/100 g). It has been proposed to increase this level to 200 mg/kg (20 mg/100 g) (Lehane, 2000).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) BLOOD HISTAMINE CONCENTRATION: A patient had a concentration of 30 mcg/dL (normal: 0.7 to 1.5 mcg/dL) (Kim, 1979).

Pharmacology Toxicology

Toxicologic Mechanism

    A) HISTIDINE
    1) Fishes implicated in scombroid fish poisoning contain large amounts of free histidine (an amino acid) in their musculature.
    2) With improper refrigeration, histamine-forming bacteria can develop and usually belong to the Enterobacteriaceae family (Becker et al, 2001). Thus, normal surface marine microflora containing the enzyme histidine decarboxylase (ie, Proteus morganii, some Salmonella species, Shigella dysenteriae, Clostridium perfringens, E. coli, and Aerobacter aerogenes) convert the histidine to histamine and saurine, a salt of histamine (Foo, 1977; Russell & Maretic, 1986; Etkind et al, 1987).
    3) Histamine development is more likely to occur in raw, unfrozen fish (Becker et al, 2001). Histidine can be readily decarboxylated to histamine at storage conditions of 20 to 30 degrees C (Etkind et al, 1987).
    4) Histamine itself is not toxic when taken orally, because it is converted to inactive N-acetyl histamine in the gut (Lange, 1988; Lerke et al, 1978).
    5) The clinical syndrome is definitely associated with food containing high levels of histamine, which may exert a direct effect if it is absorbed across mucous membranes; and other types of toxins and potentiators of histamine absorption (ie, scombrotoxin, saurine) (Lange, 1988).
    6) Levels of N-methylhistamine were 15 to 20 times the normal mean in patients with clinical signs, suggesting the presence of abnormally high levels of histamine and its metabolites in the body (Morrow et al, 1991).
    B) OTHER TOXINS
    1) Histamine poisoning has been reported after consuming fish that had low levels of histamine; therefore, other vasoactive amines present in the fish (eg, putrescine and cadaverine) might have a synergistic effect with histamine to lower the toxic dose threshold. These amines have been shown to potentiate histamine toxicity through inhibition of metabolizing enzymes that detoxify histamine (Becker et al, 2001).
    a) These aliphatic amines (putrescine and cadaverine) were identified in suspect fish from one outbreak (Etkind et al, 1987).
    C) EPIDEMIOLOGY/IMPLICATED FISH
    1) In one study of exposure, tuna prepared in the form of burgers (ie, ground) and served in pieces for salads were the only cases reported. The authors suggested, that belly meat used for the ground tuna and salad might have an increased susceptibility to bacterial contamination during the evisceration process due to its proximity to the fish gut cavity, where histamine-forming bacteria resides. In addition, pieces of fish used in this manner may be more vulnerable to temperature fluctuations than thicker tuna filets (Becker et al, 2001).

Physicochemical

Physical Characteristics

    A) These fish may have a "sharp" or "peppery" taste when eaten, but may taste completely normal (Dickinson, 1982).

Molecular Weight

    A) Not applicable

References

General Bibliography

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    40) Product Information: EPIPEN(R) intramuscular, subcutaneous auto injector, epinephrine intramuscular, subcutaneous auto-injector. Dey, Napa, CA, 2008.
    41) Product Information: PEPCID(R) IV injection, famotidine IV injection. Merck & Co,Inc, Whitehouse Station, NJ, 2006.
    42) Product Information: PEPCID(R) oral tablets, famotidine oral tablets. MERCK & CO, INC, Whitehouse Station, NJ, 2010.
    43) Product Information: diphenhydramine hcl injection, diphenhydramine hcl injection. Bioniche Pharma USA,LLC, Lake Forest, IL, 2006.
    44) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    45) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
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