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FOODBORNE ILLNESS-STAPHYLOCOCCUS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) The majority of classic enterotoxin serotypes include: Staphylococcus aureus enterotoxin A (SEA); other enterotoxins include SEB, SEC 1,2,3, SED and SEE. Several newly described enterotoxins include: SEG, SEH, and SEI. All of these enterotoxins have emetic activity. Other enterotoxin-like serotypes include: SEIJ-SEIU, and have no apparent emetic activity. Staphylococcal food poisoning is a common cause of foodborne illness in the US
    B) Staphylococcus aureus enterotoxin B (SEB), a pyrogenic toxin, commonly causes food poisoning after ingestion of improperly handled foodstuffs. It causes a markedly different clinical syndrome when inhaled than it characteristically produces when ingested. The toxin is extremely potent and stable and may be used as a bioterrorist agent.

Specific Substances

    A) STAPHYLOCOCCUS AUREUS ENTEROTOXIN A (synonym)
    1) SEA
    STAPHYLOCOCCUS AUREUS ENTEROTOXIN B (synonym)
    1) SEB
    STAPHYLOCOCCUS AUREUS ENTEROTOXIN C (synonym)
    1) SEC
    STAPHYLOCOCCUS AUREUS ENTEROTOXIN D (synonym)
    1) SED
    STAPHYLOCOCCUS AUREUS ENTEROTOXIN E (synonym)
    1) SEE
    FOOD POISONING STAPHYLOCOCCUS (synonym)
    1) Staphylococcus food poisoning (synonym)

Available Forms Sources

    A) FORMS
    1) The majority of classic enterotoxin serotypes include: Staphylococcus aureus enterotoxin A (SEA); other enterotoxins include SEB, SEC 1,2,3, SED and SEE. Several newly described enterotoxins include: SEG, SEH, and SEI. All of these enterotoxins have emetic activity. Other enterotoxin-like serotypes include: SEIJ-SEIU, and have no apparent emetic activity (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) Staphylococcal food poisoning is a common cause of foodborne illness in the US (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    3) Common carriers of staphylococcus aureus include humans (food handlers), their purulent secretions, nasal discharge, and normal skin. Staphylococcus aureus enterotoxin B (SEB), a pyrogenic toxin, commonly causes food poisoning after ingestion of improperly handled foodstuffs. It causes a markedly different clinical syndrome when inhaled than it characteristically produces when ingested. Extreme potency and stability, along with its low incapacitating-lethality ratio, make SEB a likely candidate as incapacitating bioterrorist agent (Franz & Zajtchuk, 2000; Eitzen, 1999a).
    B) SOURCES
    1) Staphylococcal toxins can be formed within a few hours when foods are kept at room temperature. Most foods (particularly those high in protein) will support staphylococcal growth, especially custard-filled pastries, mayonnaise, ham, poultry, and potato and egg salad (CDC, 1986). Foods that are frequently handled or require an extended period of preparation may result in staphylococcal food poisoning (Center for Food Safety and Applied Nutrition (CFSAN), 2012). Other sources have included canned mushrooms, rice, noodles, salads, egg products, cream filling and cooked food that has been left at room temperature (Michino & Otsuki, 2000; Miwa et al, 2001; Anunciacao et al, 1995; Levine et al, 1996).
    2) Staphylococcus aureus is often found in meat and meat products; poultry and egg products; salads (eg, egg, tuna, chicken, potato, and macaroni), dairy products, and bakery products (eg, cream puffs, Boston cream pie, chocolate eclairs) (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    3) Common carriers of staphylococcus aureus include humans (food handlers), their purulent secretions, nasal discharge, and normal skin. Dairy animals with Staphylococcal mastitis may be sources (Bone et al, 1989).
    4) Turkey is a common vehicle of staphylococcal food poisoning accounting for 10% of 131 outbreaks from 1977-1981(Holmberg & Blake, 1984). In 1982, Staphylococcus aureus was responsible for 27% of turkey-related food poisoning outbreaks (CDC, 1985).
    5) An epidemic of 300 cases of staphylococcal food poisoning was associated with hard boiled eggs in 850 children attending an Easter egg hunt (Merrill et al, 1984).
    6) Ham was the most frequently implicated food in a series of 2992 cases (131 outbreaks) of staphylococcal food poisoning, accounting for 24% of the outbreaks (Holmberg & Blake, 1984).
    7) The staphylococcal enterotoxins are highly heat stable and will remain biologically active (Center for Food Safety and Applied Nutrition (CFSAN), 2012). Pasteurizing milk will kill the Staphylococcus bacteria but not inactivate the toxins (Bone et al, 1989).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) CAUSATIVE ORGANISM
    1) Staphylococcus aureus commonly causes food poisoning after ingestion of improperly handled food products especially dairy, meat, eggs, and salads. TOXIN: The majority of classic enterotoxin serotypes include: Staphylococcus aureus enterotoxin A (SEA); other enterotoxins include SEB, SEC 1,2,3, SED and SEE. Several newly described enterotoxins include: SEG, SEH, and SEI. All of these enterotoxins have emetic activity. Staphylococcus aureus enterotoxin B (SBE) is a heat-stable toxin. It causes a markedly different clinical syndrome when inhaled (respiratory symptoms) than it does when ingested (gastrointestinal symptoms). The toxin is extremely potent and stable and may be used as a bioterrorist agent. Other enterotoxin-like serotypes: SEIJ-SEIU, and have no apparent emetic activity.
    B) EPIDEMIOLOGY
    1) Food poisoning from staphylococcus is common and usually self-limited, rarely requiring hospitalization. Fatalities are rare and generally associated with extremes of age and underlying disability.
    C) TARGET POPULATION
    1) All persons are at risk.
    D) MECHANISM
    1) Staphylococcus aureus is gram positive spherical bacterium that appears in pairs or bunched in grape-like clusters. Some strains of S. aureus can produce a highly heat-stable protein toxin (enterotoxin) that can cause Staphylococcal food poisoning (ie, staphyloenterotoxicosis; staphyloenterotoxemia).
    E) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) MILD TO MODERATE TOXICITY: Patients often present within 1 to 7 hours after ingestion of the agent with violent nausea, vomiting, nonbloody diarrhea, crampy abdominal pain, headache and general malaise. Patients are usually afebrile. Symptoms are generally mild and can last a few hours; usually completely resolved within 24 hours. After inhalational exposure patients often present within 3 to 12 hours with fever, headache, chills, myalgia, nonproductive cough, dyspnea and retrosternal chest pain. Gastrointestinal symptoms such as nausea, vomiting, and diarrhea may develop as a result of accidental swallowing of the toxin. Conjunctival injection may also occur. Symptoms usually resolve after 1 to 2 weeks in more severe cases of inhalational exposure.
    b) SEVERE TOXICITY: Severe toxicity rarely results from ingestion, but may present as severe hypotension secondary to fluid loss or in the case of inhalational exposure severe respiratory distress requiring aggressive airway management.
    2) ROUTE OF EXPOSURE
    a) About 50% of people carry staphylococcus in their nasal passages, throat, skin or hair. Contamination of food most commonly results from food handlers, but may come from environmental surfaces or equipment. Staphylococcus then replicates and produces toxin, most often in food that has not been kept hot enough (greater than 45 degrees C) or cold enough (less than 10 degrees C). Illness results from ingestion of toxin. Most common sources are meat and meat products, poultry and egg products, salads (eg, egg, tuna, chicken, potato, and macaroni), bakery products (eg, cream-filled pastries, cream pies, and chocolate eclairs), milk and dairy products.
    3) TIME TO ONSET
    a) 1 to 7 hours after ingestion; 3 to 12 hours after inhalation.
    4) DURATION
    a) Usually mild symptoms last only a few hours up to 24 hours after ingestion; 1 to 2 weeks after inhalation.

Laboratory Monitoring

    A) Routine laboratory evaluation is usually not necessary.
    B) Monitor serum electrolytes in patients with severe vomiting and diarrhea.
    C) Monitor chest radiograph in patients with respiratory symptoms.
    D) Several serological methods are available to detect the toxin in food, but they are usually obtained to evaluate outbreaks, not to direct clinical management.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Symptomatic and supportive care is the mainstay of treatment for mild disease including intravenous fluids, antiemetics and antidiarrheal agents. Replace electrolytes and fluids, if needed.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treat hypotension with intravenous fluids and pressors, if necessary. Treat respiratory distress with beta agonists, steroids, and aggressive airway management for severe distress.
    C) DECONTAMINATION
    1) GI decontamination is not necessary.
    D) AIRWAY MANAGEMENT
    1) Airway management is rarely necessary, but should be considered in patients with severe respiratory symptoms.
    E) ANTIDOTE
    1) There is no specific antidote, the illness is induced by a preformed toxin.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: Most cases can be managed at home, if symptoms are tolerable and the patient is able to tolerate fluids.
    2) OBSERVATION CRITERIA: Patients who are unable to keep down fluids at home should be referred to a healthcare facility. Continued nausea and vomiting; may require IV hydration.
    3) ADMISSION CRITERIA: A patient with hypotension, severe electrolyte abnormalities or respiratory distress should be admitted.
    4) CONSULT CRITERIA: Consult an infectious disease physician, if there is any clinical uncertainty. Consult the local or state health department, if an outbreak is suspected.
    G) PITFALLS
    1) Consider closer observation periods for the elderly, very young, chronically ill, immunosuppressed, or those who might be predisposed to dehydration. Inform patients that reheating food will not destroy the toxin. Contact your local public health department so that they may monitor for other possible outbreaks, especially if multiple patients are involved.
    H) DIFFERENTIAL DIAGNOSIS
    1) Acute onset of vomiting is usually a result of a preformed toxin like B. cereus, but various viral agents, or chemical irritants should also be in the differential diagnosis.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.

Range Of Toxicity

    A) TOXICITY: INFECTIVE DOSE: INGESTION: A toxin dose of less than 1.0 microgram in contaminated food will produce symptoms of staphylococcal intoxication. This is usually reached when S. aureus organism exceeds 100,000 per gram of food. INHALATION: (Aerosol) Incapacitating dose is 30 ng/person; lethal dose is approximately 1.7 mcg/person.

Clinical Effects

Summary Of Exposure

    A) CAUSATIVE ORGANISM
    1) Staphylococcus aureus commonly causes food poisoning after ingestion of improperly handled food products especially dairy, meat, eggs, and salads. TOXIN: The majority of classic enterotoxin serotypes include: Staphylococcus aureus enterotoxin A (SEA); other enterotoxins include SEB, SEC 1,2,3, SED and SEE. Several newly described enterotoxins include: SEG, SEH, and SEI. All of these enterotoxins have emetic activity. Staphylococcus aureus enterotoxin B (SBE) is a heat-stable toxin. It causes a markedly different clinical syndrome when inhaled (respiratory symptoms) than it does when ingested (gastrointestinal symptoms). The toxin is extremely potent and stable and may be used as a bioterrorist agent. Other enterotoxin-like serotypes: SEIJ-SEIU, and have no apparent emetic activity.
    B) EPIDEMIOLOGY
    1) Food poisoning from staphylococcus is common and usually self-limited, rarely requiring hospitalization. Fatalities are rare and generally associated with extremes of age and underlying disability.
    C) TARGET POPULATION
    1) All persons are at risk.
    D) MECHANISM
    1) Staphylococcus aureus is gram positive spherical bacterium that appears in pairs or bunched in grape-like clusters. Some strains of S. aureus can produce a highly heat-stable protein toxin (enterotoxin) that can cause Staphylococcal food poisoning (ie, staphyloenterotoxicosis; staphyloenterotoxemia).
    E) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) MILD TO MODERATE TOXICITY: Patients often present within 1 to 7 hours after ingestion of the agent with violent nausea, vomiting, nonbloody diarrhea, crampy abdominal pain, headache and general malaise. Patients are usually afebrile. Symptoms are generally mild and can last a few hours; usually completely resolved within 24 hours. After inhalational exposure patients often present within 3 to 12 hours with fever, headache, chills, myalgia, nonproductive cough, dyspnea and retrosternal chest pain. Gastrointestinal symptoms such as nausea, vomiting, and diarrhea may develop as a result of accidental swallowing of the toxin. Conjunctival injection may also occur. Symptoms usually resolve after 1 to 2 weeks in more severe cases of inhalational exposure.
    b) SEVERE TOXICITY: Severe toxicity rarely results from ingestion, but may present as severe hypotension secondary to fluid loss or in the case of inhalational exposure severe respiratory distress requiring aggressive airway management.
    2) ROUTE OF EXPOSURE
    a) About 50% of people carry staphylococcus in their nasal passages, throat, skin or hair. Contamination of food most commonly results from food handlers, but may come from environmental surfaces or equipment. Staphylococcus then replicates and produces toxin, most often in food that has not been kept hot enough (greater than 45 degrees C) or cold enough (less than 10 degrees C). Illness results from ingestion of toxin. Most common sources are meat and meat products, poultry and egg products, salads (eg, egg, tuna, chicken, potato, and macaroni), bakery products (eg, cream-filled pastries, cream pies, and chocolate eclairs), milk and dairy products.
    3) TIME TO ONSET
    a) 1 to 7 hours after ingestion; 3 to 12 hours after inhalation.
    4) DURATION
    a) Usually mild symptoms last only a few hours up to 24 hours after ingestion; 1 to 2 weeks after inhalation.

Vital Signs

    3.3.3) TEMPERATURE
    A) FEVER: Temperature elevation is generally absent (Cunha, 1988), but was present in 16 of 67 (24%) patients in one outbreak (CDC, 1986), and in 16% of 2,992 cases during 131 outbreaks (Holmberg & Blake, 1984).
    B) INHALATION: Sudden onset of fever and chills may be observed (Franz & Zajtchuk, 2000; Eitzen, 1999a).

Heent

    3.4.3) EYES
    A) INHALATION: Conjunctival injection may be present (Franz & Zajtchuk, 2000; Eitzen, 1999a).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HEART FAILURE
    1) WITH POISONING/EXPOSURE
    a) CONGESTIVE HEART FAILURE was the cause of death in a previously healthy 20-year-old woman who apparently aspirated vomitus while suffering from staphylococcal food poisoning. Aspiration led to development of staphylococcal bronchopneumonia, sepsis, and congestive heart failure during septic shock. The same strain of S. aureus was cultured from the lungs, tonsils, and ileal loop contents (Duben et al, 1988).
    B) CHEST PAIN
    1) WITH POISONING/EXPOSURE
    a) INHALATION: Retrosternal chest pain may develop in more severe cases (Franz & Zajtchuk, 2000; Eitzen, 1999a).
    C) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) INHALATION: Postural hypotension may develop due to fluid losses (Franz & Zajtchuk, 2000; Eitzen, 1999a).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) INHALATION: Dyspnea may occur in severe cases (Franz & Zajtchuk, 2000; Eitzen, 1999a).
    B) COUGH
    1) WITH POISONING/EXPOSURE
    a) INHALATION: Unproductive cough may occur (Franz & Zajtchuk, 2000; Eitzen, 1999a).
    C) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) CONGESTIVE HEART FAILURE was the cause of death in a previously healthy 20-year-old woman who apparently aspirated vomitus while suffering from staphylococcal food poisoning. Aspiration led to development of staphylococcal bronchopneumonia, sepsis, and congestive heart failure during septic shock. The same strain of S. aureus was cultured from the lungs, tonsils, and ileal loop contents (Duben et al, 1988).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache was reported in 45% of patients in one outbreak of 67 cases (CDC, 1986), and in 11% of 2,992 cases in 131 outbreaks (Holmberg & Blake, 1984).
    b) INHALATION: Headache may be observed (Franz & Zajtchuk, 2000; Eitzen, 1999a).
    B) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Weakness was reported in 8% of 2,992 cases (Holmberg & Blake, 1984).
    C) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Dizziness was reported in 4% of 2,992 cases (Holmberg & Blake, 1984).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Abrupt onset of nausea, vomiting, and abdominal cramping (Center for Food Safety and Applied Nutrition (CFSAN), 2012). In none of 131 outbreaks was diarrhea reported in the absence of vomiting (Holmberg & Blake, 1984). Vomiting was reported in 82% of 2,992 cases.
    b) INHALATION: Nausea, vomiting, and diarrhea may occur as a result of inadvertent swallowing of toxin (Franz & Zajtchuk, 2000; Eitzen, 1999a).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain was reported in 64% of 2,992 cases during 1977 to 1981 (Holmberg & Blake, 1984).
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) The enterotoxin may produce an abrupt onset of gastrointestinal symptoms including diarrhea (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    b) Diarrhea occurred in 68% of 2,992 cases (Holmberg & Blake, 1984). In no case was diarrhea reported in the absence of vomiting.
    c) INHALATION: Nausea, vomiting, and diarrhea may occur as a result of inadvertent swallowing of toxin (Franz & Zajtchuk, 2000; Eitzen, 1999a).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) INHALATION: Myalgia may occur (Franz & Zajtchuk, 2000; Eitzen, 1999a).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Routine laboratory evaluation is usually not necessary.
    B) Monitor serum electrolytes in patients with severe vomiting and diarrhea.
    C) Monitor chest radiograph in patients with respiratory symptoms.
    D) Several serological methods are available to detect the toxin in food, but they are usually obtained to evaluate outbreaks, not to direct clinical management.

Methods

    A) FOOD ANALYSIS
    1) A number of serological methods can be used to determine the enterotoxigenicity of S. aureus from a suspected food source (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) ELISA: During a potential foodborne outbreak, ELISA-based methods are commonly used to identify staphylococcal enterotoxins in foods; several commercial tests use both monoclonal and polyclonal antibodies (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    B) MULTIPLE ANALYTICAL METHODS
    1) Staphylococcal enterotoxins have been detected in foods and biologic fluids using a sandwich ELISA method (Mukhin & Chatterjee, 1997; Wieneke & Gilbert, 1985) or gel diffusion method. Results can be obtained within 2 days using the ELISA method and 5 days using the gel diffusion method (Wieneke & Gilbert, 1985). Other methods that may be used to detect enterotoxin include latex agglutination and DNA probe (Jackson, 1990).
    2) METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS (MRSA): An outbreak of community-acquired foodborne illness caused by methicillin-resistant Staphylococcus aureus (MRSA) has been reported. Pulsed-field gel electrophoresis (PFGE) with Sma I-digested chromosomal DNA were used to perform molecular typing of all S. aureus isolates (Jones et al, 2002).

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) A patient with hypotension, severe electrolyte abnormalities or respiratory distress should be admitted. Patients at risk for dehydration who cannot be relied upon for compliance and/or adequate follow-up treatment should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Most cases can be managed at home, if symptoms are tolerable and the patient is taking adequate fluids; close follow-up care is needed.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult an infectious disease physician, if there is any clinical uncertainty. Consult the local or state health department, if an outbreak is suspected.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients who are unable to keep down fluids at home should be referred to a healthcare facility. Continued nausea and vomiting; may require hydration.

Monitoring

    A) Routine laboratory evaluation is usually not necessary.
    B) Monitor serum electrolytes in patients with severe vomiting and diarrhea.
    C) Monitor chest radiograph in patients with respiratory symptoms.
    D) Several serological methods are available to detect the toxin in food, but they are usually obtained to evaluate outbreaks, not to direct clinical management.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Emetics and purgatives are NOT indicated as the toxin is eliminated by vomiting and diarrhea.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) GI decontamination is not necessary.
    6.5.3) TREATMENT
    A) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Initial assessment must determine and treat the magnitude and type of dehydration. Rapid correction of deficits and careful monitoring of intake and output are essential.
    2) Appropriate fluid therapy may need to be implemented prior to receiving the results of laboratory evaluation.
    a) Patients with mild fluid deficits can often be managed with oral fluid therapy consisting of clear liquids or specially formulated glucose and electrolyte solutions.
    b) Patients with moderate to severe dehydration are generally treated with IV fluids.
    B) MONITORING OF PATIENT
    1) Routine laboratory evaluation is usually not necessary.
    2) Monitor serum electrolytes in patients with severe vomiting and diarrhea.
    3) Monitor chest radiograph in patients with respiratory symptoms.
    4) Several serological methods are available to detect the toxin in food, but they are usually obtained to evaluate outbreaks, not to direct clinical management.
    C) ANTIEMETIC
    1) INDICATIONS: Significant nausea and vomiting in adults may be controlled with an antiemetic agent. This is often the only type of treatment indicated for staphylococcal food poisoning. Antiemetics are not usually required, if alteration of the diet is successful.
    2) Serotonin receptor antagonists such as ondansetron and granisetron offer powerful alternatives, particularly in cases of refractory vomiting.
    3) DOSES
    a) PROMETHAZINE (ADULTS ONLY): 25 to 50 mg IM or IV.
    b) PROCHLORPERAZINE (ADULTS): 10 mg IM or IV; 25 mg rectally twice a day.
    D) ANTIDIARRHEAL
    1) ATROPINE SULFATE/DIPHENOXYLATE (Lomotil(R) (adults only): Effective in controlling pain and tenesmus and may decrease the number of stools. Dose: 2 tablets or 10 mL solution orally 4 times daily (20 mg/day of diphenoxylate) until initial control achieved; maximum dose 20 mg/day (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005). NOTE: Evidence suggests that Lomotil may prolong the symptoms and duration of some bacterial infections. It is not recommended for use in infants or young children.
    E) SUPPORT
    1) There is no specific antidote or treatment as illness is induced by a preformed toxin.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Range Of Toxicity

Summary

    A) TOXICITY: INFECTIVE DOSE: INGESTION: A toxin dose of less than 1.0 microgram in contaminated food will produce symptoms of staphylococcal intoxication. This is usually reached when S. aureus organism exceeds 100,000 per gram of food. INHALATION: (Aerosol) Incapacitating dose is 30 ng/person; lethal dose is approximately 1.7 mcg/person.

Minimum Lethal Exposure

    A) SUMMARY
    1) Fatalities from Staphylococcal food poisoning are reported rarely and generally occur in the very young, the elderly, or severely debilitated individuals (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Anon, 1971).
    B) CASE REPORTS
    1) Death was reported in a previously healthy 57-year-old woman with severe gastroenteritis and shock (Currier et al, 1973). In a series of 2,992 cases reported from 1977 to 1981 there were 2 fatalities, both in patients older than 80 years (Holmberg & Blake, 1984).
    2) A death in a previously healthy 20-year-old woman has been reported. Cause of death was congestive heart failure secondary to staphylococcal sepsis; 4 hours after eating a meal, she aspirated while vomiting and developed respiratory distress, then progressed to heart failure and death within 36 hours (Duben et al, 1988).
    C) SUMMARY
    1) INHALATION: Aerosol-incapacitating dose, 30 ng/person; lethal dose, approximately 1.7 mcg/person (Franz & Zajtchuk, 2000; Eitzen, 1999a).

Maximum Tolerated Exposure

    A) SUMMARY
    1) All individuals are susceptible to this type of infection; however, symptoms can vary widely. A toxin dose of less than 1.0 microgram in contaminated food will produce symptoms of staphylococcal intoxication. This is usually reached when S. aureus organism exceeds 100,000 per gram in food (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    B) CASE REPORTS
    1) In an outbreak due to contaminated chocolate milk, the concentration of staphylococcal enterotoxin A in milk was 0.5 ng/mL for a total dose of 200 ng/container (Balaban & Rasooly, 2000).

Pharmacology Toxicology

Toxicologic Mechanism

    A) SUMMARY
    1) Heat sensitive bacteria, heat resistant toxin (enterotoxin: A,B,C,D, E) and more recently several more toxins have been added and include: SEG, SEH and SEI; all exhibit emetic activity (Center for Food Safety and Applied Nutrition (CFSAN), 2012). Type A toxin is the most common one in the US. Toxins are low-molecular weight proteins (around 28,000) and water soluble. Organism multiplies producing enterotoxin in food when allowed to sit at room temperature (10 to 45 degrees C).
    a) In addition, there are SE-like enterotoxin serotypes: SEIJ-SEIU. Currently, they do not appear to produce emetic activity (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) The ingested enterotoxins indirectly stimulate an enteric-vagus nerve reflex, which results in emesis and bowel hypermotility (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Todd, 1985).
    3) While enterotoxin A is most commonly implicated, type B may be associated with more severe illness. In a study of 2,992 cases, 46% of 80 patients with type B toxin were seen in a hospital compared to 5% of 1,813 patients with type A toxin (Holmberg & Blake, 1984).
    4) While most Staphylococcus aureus strains implicated in food poisoning have been coagulase-positive, outbreaks with coagulase-negative species have been reported (Breckinridge & Bergdoll, 1971; Holmberg & Blake, 1984; Udo et al, 1999).
    5) Methicillin-resistant staphylococcus aureus infection has rarely been caused by contaminated food (Jones et al, 2002; Kluytmans et al, 1995).

References

General Bibliography

    1) Anon: Death from Staphylococcal food poisoning. Br Med J 1971; 4:244.
    2) Anunciacao LLC, Linardi WR, & do Carmo LS: Production of staphylococcal enterotoxin A in cream-filled cake. Int J Food Microbiology 1995; 26:259-263.
    3) Balaban N & Rasooly A: Staphylococcal enterotoxins. Int J Food Microbiology 2000; 61:1-10.
    4) Bone FJ, Bogie D, & Morgan-Jones SC: Staphylococcal food poisoning from sheep milk cheese. Epidem Inf 1989; 103:449-458.
    5) Breckinridge JC & Bergdoll MS: Outbreak in food-borne gastroenteritis due to coagulase negative enterotoxin producing staphylococcus. N Engl J Med 1971; 284:541-543.
    6) CDC: Annual Summary 1982. Foodborne disease outbreaks surveillance, Public Health Service, DHHS Publication no.CDC 85-8185, CDC, Atlanta, GA, 1985.
    7) CDC: Staphyloccal food poisoning from Turkey at a country club buffet - New Mexico. CDC: MMWR 1986; 35:715-722.
    8) Center for Food Safety and Applied Nutrition (CFSAN): Staphylococcus aureus. In: Bad Bug Book Foodborne Pathogenic Microorganisms and Natural Toxins Handbook Second Edition. U.S. Food and Drug Administration (FDA). College Park, MD. 2012. Available from URL: http://www.fda.gov/downloads/Food/FoodSafety/FoodborneIllness/FoodborneIllnessFoodbornePathogensNaturalToxins/BadBugBook/UCM297627.pdf. As accessed 2013-03-06.
    9) Cunha BA: Staphylococcal food poisoning. Emerg Med 1988; 20:117-126.
    10) Currier RW, Taylor A, & Wolf FS: Fatal staphylococcal food poisoning. Southern Med J 1973; 66:703-705.
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