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FOODBORNE ILLNESS-CLOSTRIDIUM PERFRINGENS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Clostridium perfringens food poisoning is generally a mild, self-limiting gastrointestinal illness that usually occurs within 8 to 16 hours of exposure with an average duration of 24 hours.

Specific Substances

    1) C. perfringens (synonym)
    2) Enterotoxin, Clostridium perfringens, type A (synonym)
    3) Clostridium perfringens (welchii) type A enterotoxin (synonym)
    4) Clostridium perfringens beta-toxin (synonym)
    5) Clostridium perfringens exotoxin (synonym)
    6) Clostridium perfringens food poisoning (synonym)
    7) Spoiled food, clostridium perfringens (synonym)
    8) Food poisoning clostridium perfringens (synonym)

Available Forms Sources

    A) SOURCES
    1) MECHANISM: The Clostridium perfringens organism produces heat-stable spores and enterotoxins that cause gastroenteritis(Center for Food Safety and Applied Nutrition (CFSAN), 2012). Food poisoning progresses as a result of survival of the heat-resistant spores of C. perfringens food poisoning isolates in thermally treated foods (Paredes-Sabja & Sarker, 2009). In many cases, because the implicated food is often heat-treated it typically kills off competing flora, while the C. perfringens spores survive (Brynestad & Granum, 2002). Optimal growth occurs between 43 and 45 degrees C (Young et al, 2008). Under optimal conditions, growth is very fast with a generation time of less than 10 minutes (Lindstrom et al, 2011).
    2) FOOD VEHICLES: Meat, meat products, and gravy are the foods most commonly implicated in C. perfringens food poisoning. Outbreaks commonly originate in institutional settings (ie, hospitals, prisons, nursing facilities, and school cafeterias) (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    3) HUMAN RESERVOIR: Healthy individuals have been found to be reservoirs of cpe positive C. perfringens in the gastrointestinal tract and may serve as a source of contamination in people handling food (Lindstrom et al, 2011). In one study, C. perfringens type A enterotoxin was found in the feces of some healthy food handlers. There was a prevalence rate of 18%. Healthy individuals (eg, food handlers) may be a risk factor for the spread of C. perfringens food poisoning (Heikinheimo et al, 2006).
    4) PERSON-TO-PERSON TRANSMISSION: Person-to-person transmission may occur among individuals residing in institutions (ie, nursing facilities, schools, prisons) (Abubakar et al, 2007).
    5) INADEQUATE TEMPERATURE CONTROL: In many outbreaks the cause of poisoning is due to holding prepared food at an inadequate temperature, and/or reheating of prepared foods after the organism is allowed to multiply in the food, and poor hygiene practices (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Hook et al, 1996; Parikh et al, 1997; Tallis et al, 1999).

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) Clostridium perfringens is an anaerobic, Gram-positive, sporeforming rod. It is widely distributed in the environment and frequently occurs in the intestines of humans and many domestic and feral animals. Spores of the organism can persist in soil, sediments and areas subject to human or animal fecal pollution.
    B) TOXINS
    1) There are at least 5 toxinotypes (A through E) associated with C. perfringens; type A typically contains the enterotoxin (cpe gene) that causes food poisoning. Types B through E may sometimes contain this gene. Foodborne illness, caused by C. perfringens, comes in two forms: the gastroenteritis form, a milder and often self-limiting form that is common in the US, and enteritis necroticans ("pig-bel disease"), a more severe form of food poisoning, often fatal, and extremely rare in the U.S. In general, illness occurs after the ingestion of a large number (greater than or equal to 10(5)) of viable, vegetative cells of a C. perfringens enterotoxin (cpe) producing strain, which is followed by sporulation of the organism in the small intestine to produce enterotoxin.
    C) EPIDEMIOLOGY
    1) C. perfringens food poisoning is a common foodborne illness in the US. Outbreaks may go unreported because the implicated food or the patient are not routinely tested for C. perfringens. In most individuals, the illness is mild and self-limited; deaths are rarely reported. It is estimated that approximately 966,000 cases occur annually in the US.
    D) TARGET POPULATION
    1) C. perfringens food poisoning often occurs in institutional settings (eg, schools, hospitals, nursing centers, prisons) where large quantities of food may be improperly refrigerated or stored. The young and elderly are most likely to develop symptoms of poisoning, with the elderly more likely to have prolonged and severe illness (up to 1 to 2 weeks). It is unusual for individuals under the age of 30 to develop significant symptoms, except in the case of pigbel syndrome (a rare illness due to necrotic enteritis).
    E) MECHANISM
    1) The C. perfringens organism can produce heat-stable spores and the enterotoxin produced causes gastroenteritis. If the conditions are ideal, growth is very fast with doubling times of 7 to 10 minutes. Optimal growth occurs between 43 and 45 degrees C.
    F) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) Abdominal pain and watery diarrhea. Other symptoms may include nausea, vomiting (less common), headache and chills. Infrequent events can include: fever, bloody diarrhea, generalized aches, fatigue and necrotizing enterocolitis (rare). Overall, complications are rare.
    2) CHRONIC SYMPTOMS
    a) Less severe symptoms can persist for up to 1 to 2 weeks. In rare cases, complications and death may occur.
    3) ROUTE OF EXPOSURE
    a) C. perfringens is a foodborne illness. Commonly implicated foods: meats, meat products and gravy. Poisoning often develops when prepared food is held at an improper temperature. The organism is often found in small numbers in cooked foods and will multiply rapidly to food poisoning levels, if prepared food is held or stored incorrectly (ie, not held at an optimal temperature). Person-to-person transmission may occur among individuals residing in institutions (ie, nursing facilities, schools, prisons). In addition, healthy individuals have been found to be reservoirs of cpe positive C. perfringens in the gastrointestinal tract and may serve as a source of contamination in people handling food.
    4) TIME TO ONSET
    a) Generally, 8 to 16 hours.
    5) DURATION
    a) Generally, 24 hours.

Laboratory Monitoring

    A) Laboratory analyses of the stool and suspected food source for the organism can be used to confirm the diagnosis, but are not generally required for clinical management.
    B) Monitor fluid volume and electrolytes in patients with severe diarrhea.
    C) Confirmation of C. perfringens foodborne illness can be done by quantitative cultures of the implicated food or enterotoxin-positive stool specimen from the patient.
    D) In a suspected outbreak, isolates from the suspected food and stool of an affected individual to produce enterotoxin needs to be confirmed that the strains are the same, because many healthy individuals (in particular the elderly) commonly have high numbers of C. perfringens spores in their feces.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is primarily symptomatic and supportive. In most cases, C. perfringens food poisoning produces mild, self-limited illness that is likely to be resolved within 24 hours. Patients with mild fluid deficits can be managed with clear liquids or specially formulated electrolyte solutions. Antidiarrheal agents are not usually indicated.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Severe complications are unlikely; however the elderly, immune compromised and the very young may develop persistent symptoms. Treatment is symptomatic and supportive. Assess fluid status and electrolyte balance. Moderate to severe dehydration may require IV fluids and electrolyte replacement. Antidiarrheal agents may be indicated.
    C) DECONTAMINATION
    1) Decontamination is not indicated.
    D) ANTIDOTE
    1) None.
    E) PATIENT DISPOSITION
    1) HOME CRITERIA: Most patients will develop mild, self-limited symptoms that can be managed at home.
    2) ADMISSION CRITERIA: All patients with significant toxicity, severe dehydration, clinical instability, abnormal electrolyte concentrations, or baseline immunocompromised state should be admitted for evaluation, intravenous rehydration and electrolyte replacement.
    3) OBSERVATION CRITERIA: Patients with severe or persistent symptoms should be sent to a healthcare facility for evaluation and treatment.
    4) CONSULT CRITERIA: The local heath department should be notified of any suspected outbreak of C perfringens food poisoning.
    F) PITFALLS
    1) Because early symptoms and signs are nonspecific, they may be attributed to other conditions (ie, other organisms which may produce infection, viral illness).
    G) TOXICOKINETICS
    1) Generally a mild, self-limited illness. C. perfringens type A food poisoning produces illness after ingesting a large number (greater than or equal to 10(5)) of viable, vegetative cells of a C. perfringens enterotoxin-producing strain, which is followed by sporulation of the organism in the small intestine to produce enterotoxin. Incubation period: 8 to 22 hours. Duration: Usually, up to 24 hours.
    H) DIFFERENTIAL DIAGNOSIS
    1) The differential diagnosis includes other bacterial (eg, E. coli) or nonbacterial (eg, viruses, parasites, plants or mushrooms ingestion) causes of acute gastroenteritis; exposure to chemicals (eg, insecticides, pesticides).

Range Of Toxicity

    A) TOXICITY: INFECTIVE DOSE: In type A food poisoning, illness occurs after the ingestion of a large number (greater than or equal to 10(5)) of viable, vegetative cells of a C. perfringens enterotoxin-producing strain, which is followed by sporulation of the organism in the small intestine to produce enterotoxin.

Clinical Effects

Summary Of Exposure

    A) CAUSATIVE ORGANISM
    1) Clostridium perfringens is an anaerobic, Gram-positive, sporeforming rod. It is widely distributed in the environment and frequently occurs in the intestines of humans and many domestic and feral animals. Spores of the organism can persist in soil, sediments and areas subject to human or animal fecal pollution.
    B) TOXINS
    1) There are at least 5 toxinotypes (A through E) associated with C. perfringens; type A typically contains the enterotoxin (cpe gene) that causes food poisoning. Types B through E may sometimes contain this gene. Foodborne illness, caused by C. perfringens, comes in two forms: the gastroenteritis form, a milder and often self-limiting form that is common in the US, and enteritis necroticans ("pig-bel disease"), a more severe form of food poisoning, often fatal, and extremely rare in the U.S. In general, illness occurs after the ingestion of a large number (greater than or equal to 10(5)) of viable, vegetative cells of a C. perfringens enterotoxin (cpe) producing strain, which is followed by sporulation of the organism in the small intestine to produce enterotoxin.
    C) EPIDEMIOLOGY
    1) C. perfringens food poisoning is a common foodborne illness in the US. Outbreaks may go unreported because the implicated food or the patient are not routinely tested for C. perfringens. In most individuals, the illness is mild and self-limited; deaths are rarely reported. It is estimated that approximately 966,000 cases occur annually in the US.
    D) TARGET POPULATION
    1) C. perfringens food poisoning often occurs in institutional settings (eg, schools, hospitals, nursing centers, prisons) where large quantities of food may be improperly refrigerated or stored. The young and elderly are most likely to develop symptoms of poisoning, with the elderly more likely to have prolonged and severe illness (up to 1 to 2 weeks). It is unusual for individuals under the age of 30 to develop significant symptoms, except in the case of pigbel syndrome (a rare illness due to necrotic enteritis).
    E) MECHANISM
    1) The C. perfringens organism can produce heat-stable spores and the enterotoxin produced causes gastroenteritis. If the conditions are ideal, growth is very fast with doubling times of 7 to 10 minutes. Optimal growth occurs between 43 and 45 degrees C.
    F) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) Abdominal pain and watery diarrhea. Other symptoms may include nausea, vomiting (less common), headache and chills. Infrequent events can include: fever, bloody diarrhea, generalized aches, fatigue and necrotizing enterocolitis (rare). Overall, complications are rare.
    2) CHRONIC SYMPTOMS
    a) Less severe symptoms can persist for up to 1 to 2 weeks. In rare cases, complications and death may occur.
    3) ROUTE OF EXPOSURE
    a) C. perfringens is a foodborne illness. Commonly implicated foods: meats, meat products and gravy. Poisoning often develops when prepared food is held at an improper temperature. The organism is often found in small numbers in cooked foods and will multiply rapidly to food poisoning levels, if prepared food is held or stored incorrectly (ie, not held at an optimal temperature). Person-to-person transmission may occur among individuals residing in institutions (ie, nursing facilities, schools, prisons). In addition, healthy individuals have been found to be reservoirs of cpe positive C. perfringens in the gastrointestinal tract and may serve as a source of contamination in people handling food.
    4) TIME TO ONSET
    a) Generally, 8 to 16 hours.
    5) DURATION
    a) Generally, 24 hours.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER
    a) Fever and chills have been reported (Loewenstein, 1972).
    1) INCIDENCE: Fever developed in 19% of 230 patients in one series (Hook et al, 1996).
    2) CHILLS
    a) Chills, with or without fever, have been associated with C. perfringens infection (Centers for Disease Control and Prevention, 2009; Loewenstein, 1972).
    b) INCIDENCE: In an outbreak of C. perfringens food poisoning among inmates (n=200) in a Wisconsin prison, chills were reported in 85 (43%) confirmed and probable (self-reported symptoms) cases (Centers for Disease Control and Prevention, 2009).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may develop (Loewenstein, 1972).
    b) INCIDENCE: In an outbreak of C. perfringens food poisoning among inmates (n=200) in a Wisconsin prison, headache was reported in 94 (47%) confirmed and probable (self-reported symptoms) cases (Centers for Disease Control and Prevention, 2009).
    1) In another series, headache was reported in 42% of 230 patients (Hook et al, 1996).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea (watery) and abdominal cramps are characteristic of C. perfringens food poisoning; symptoms are likely to occur within 8 to 16 hours (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Young et al, 2008). The illness is generally mild and self-limited and rarely lasts more than 24 hours. However, some patients (ie, the elderly) may have symptoms for up to 2 weeks (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Young et al, 2008; McCabe-Sellers & Beattie, 2004; McDonel, 1980). Fatalities are extremely rare and are most often associated with the elderly or debilitated patients (Center for Food Safety and Applied Nutrition (CFSAN), 2012; McDonel, 1980).
    b) INCIDENCE: In an outbreak of C. perfringens food poisoning among inmates (n=200) in a Wisconsin prison, diarrhea was reported in 194 (97%) confirmed and probable (self-reported symptoms) cases (Centers for Disease Control and Prevention, 2009).
    1) In two other C. perfringens outbreaks (82 patients and 230 patients) diarrhea was reported in 100% and 67% respectively, abdominal cramps were reported in 90% and 78% respectively, and nausea developed in 63% and 46%, respectively (Hook et al, 1996; Parikh et al, 1997).
    c) CPE-INDUCED DIARRHEA: There have been reports of patients developing CPE-induced diarrhea following antibiotic therapy, and in the absence of an implicated food. These cases are most often reported in the elderly following a course of antibiotic therapy. These patients are more likely to have more persistent (2 days to 5 weeks) and severe symptoms (ie, bloody diarrhea). This may be seen with increasing frequency due to the rise in immunocompromised patients in the overall population (Meer et al, 1997).
    d) CARRIERS: Some individuals may continue to shed the spore in the feces for a long period and can become carriers (McCabe-Sellers & Beattie, 2004).
    B) ABDOMINAL CRAMPS
    1) WITH POISONING/EXPOSURE
    a) Mild abdominal cramps are a common characteristic of C. perfringens food poisoning (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    b) INCIDENCE: In an outbreak of C. perfringens foodborne illness among inmates (n=200) in a Wisconsin prison, abdominal cramps were reported in 169 (85%) confirmed and probable (self-reported symptoms) cases (Centers for Disease Control and Prevention, 2009).
    C) NAUSEA
    1) WITH POISONING/EXPOSURE
    a) Nausea is a typical symptom of C. perfringens infection (Centers for Disease Control and Prevention, 2009; Young et al, 2008).
    b) INCIDENCE: In an outbreak of C. perfringens foodborne illness among inmates (n=200) in a Wisconsin prison, nausea was reported in 128 (64%) confirmed and probable (self-reported symptoms) cases (Centers for Disease Control and Prevention, 2009).
    D) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting may develop with exposure, but it is not typically associated with C. perfringens infection (Centers for Disease Control and Prevention, 2009; Hobbs, 1974; Granum, 1990).
    b) INCIDENCE: In an outbreak of C. perfringens foodborne illness among inmates (n=200) in a Wisconsin prison, vomiting was reported in 45 (23%) confirmed and probable (self-reported symptoms) cases (Centers for Disease Control and Prevention, 2009).
    1) In other outbreaks, vomiting developed in 13% of 230 patients in one series, and 30% of 82 patients in another series (Hook et al, 1996; Parikh et al, 1997).
    E) ENTEROCOLITIS
    1) WITH POISONING/EXPOSURE
    a) NECROTIZING ENTEROCOLITIS
    1) TYPE C: Necrotizing enterocolitis (pigbel syndrome) has been associated with C. perfringens Type C (beta-toxin) food poisoning. It is rarely observed in the industrialized world. Symptoms can develop within 5 to 6 hours and usually begin as severe abdominal pain and diarrhea (often bloody) followed by necrotic inflammation of the small intestines. The illness can be fatal with a mortality rate of 15% to 25%, even in treated patients. It appears that individuals with reduced levels of proteolytic enzymes in the intestine due to a low protein intake are more likely to become ill (Brynestad & Granum, 2002).
    2) TYPE A: C. perfringens type A is generally a mild illness and NOT usually associated with necrotizing enterocolitis. However, there have been a few reports of this event in the literature (Sobel et al, 2005).
    a) CASE REPORTS: Adult necrotizing enterocolitis was associated with C. perfringens Type A infection in 4 adults. Of the 3 fatalities reported, two were members of the same family. The patient that recovered was a college student and his illness was not associated with any reported foodborne outbreak. C. perfringens type A was isolated from 3 (2 died; 1 survived) of the patients and in the remaining patient (a fatality) an organism was not detected (Sobel et al, 2005).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Generalized aches/pain may be associated with C. perfringens infection (Centers for Disease Control and Prevention, 2009).
    b) INCIDENCE: In an outbreak of C. perfringens food poisoning among inmates (n=200) in a Wisconsin prison, generalized aches were reported in 102 (51%) confirmed and probable (self-reported symptoms) cases (Centers for Disease Control and Prevention, 2009).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Laboratory analyses of the stool and suspected food source for the organism can be used to confirm the diagnosis, but are not generally required for clinical management.
    B) Monitor fluid volume and electrolytes in patients with severe diarrhea.
    C) Confirmation of C. perfringens foodborne illness can be done by quantitative cultures of the implicated food or enterotoxin-positive stool specimen from the patient.
    D) In a suspected outbreak, isolates from the suspected food and stool of an affected individual to produce enterotoxin needs to be confirmed that the strains are the same, because many healthy individuals (in particular the elderly) commonly have high numbers of C. perfringens spores in their feces.
    4.1.2) SERUM/BLOOD
    A) Monitor fluid volume and electrolytes in patients with severe diarrhea or as necessary.
    4.1.4) OTHER
    A) OTHER
    1) A median spore count of equal to or greater than 10(5)/g in a fecal sample is considered consistent with C. perfringens-induced diarrhea (Hook et al, 1996a; Young et al, 2008).

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) SUMMARY
    a) LIMITATIONS: C. perfringens serotyping is only available in a few laboratories worldwide. The organism can lose viability quickly in refrigerated food and fecal counts may be high in the elderly without any signs of illness. Typical diagnostic tests (ie, isolation of sulfite-reducing colonies and confirmed by nitrite reduction, lactose fermentation and motility assays) do not identify the C. perfringens enterotoxin (CPE) and do not identify the particular toxin type. During an outbreak, detection of the enterotoxin may be the only method available to diagnose a C. perfringens exposure. In addition, C. perfringens does not readily produce toxin in vitro and no one standard method has been able to detect all C. perfringens strains. Because of these testing difficulties, isolates are not routinely tested for toxin production (Lindstrom et al, 2011; Abubakar et al, 2007).
    2) CULTURE
    a) Bacteriological cultures can detect the organism in implicated food and the stool of patients (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    3) MOLECULAR TECHNIQUES
    a) Polymerase chain reaction (PCR) can be used to identify the C. perfringens enterotoxin gene (Heikinheimo et al, 2006; Miwa et al, 1999; Arcieri et al, 1999; Miwa et al, 1996; Ridell et al, 1998) and for the identification of toxicogenic C. perfringens isolates (Meer et al, 1997).
    1) The real-time PCR assay can detect the cpa (alpha toxin gene) and cpe (enterotoxin) genes of C. perfringens for rapid identification. This assay can be used to quickly examine the implicated food and stool of patients to determine if a particular strain contains the cpe gene which is responsible for diarrheal illness (Grant et al, 2008).
    4) IMMUNOASSAYS
    a) SUMMARY: Several immunoassays including immunoelectrophoresis, ELISA, and RPLA methods have been used to detect enterotoxin and antienterotoxin antibodies in a variety of specimens (eg, serum, feces and food). Immunoassays have also been used to determine the potency of toxoids (Meer et al, 1997). These procedures may take 1 to 3 days (U.S. Food and Drug Administration, 2009).
    b) ENUMERATION ASSAY: The colony hybridization-based isolation along with the enumeration assay have been able to detect the cpe gene in some colonies and isolation of the C. perfringens food poisoning strain (Lindstrom et al, 2011).
    c) ELISA has been used to identify C. perfringens enterotoxin (CPE) antibodies in human serum (Kim et al, 1998) and the presence of CPE in the stool (Meer et al, 1997).
    5) TYPING METHODS
    a) Plasmid profiling, ribotyping and macrorestriction analysis by pulsed-field gel electrophoresis can be used to classify C. perfringens isolates in an outbreak (Schalch et al, 1999; Schalch et al, 1997).

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) All patients with significant toxicity, severe dehydration, clinical instability, abnormal electrolyte concentrations, or baseline immunocompromised state should be admitted for evaluation, intravenous rehydration and electrolyte replacement.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Most patients will develop mild, self-limited symptoms that can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) The local heath department should be notified of any suspected outbreak of C perfringens food poisoning.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with severe or persistent symptoms should be sent to a healthcare facility for evaluation and treatment.

Monitoring

    A) Laboratory analyses of the stool and suspected food source for the organism can be used to confirm the diagnosis, but are not generally required for clinical management.
    B) Monitor fluid volume and electrolytes in patients with severe diarrhea.
    C) Confirmation of C. perfringens foodborne illness can be done by quantitative cultures of the implicated food or enterotoxin-positive stool specimen from the patient.
    D) In a suspected outbreak, isolates from the suspected food and stool of an affected individual to produce enterotoxin needs to be confirmed that the strains are the same, because many healthy individuals (in particular the elderly) commonly have high numbers of C. perfringens spores in their feces.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Decontamination is not indicated.
    6.5.2) PREVENTION OF ABSORPTION
    A) Gastrointestinal decontamination is NOT indicated.
    6.5.3) TREATMENT
    A) FLUID/ELECTROLYTE BALANCE REGULATION
    1) In most cases, C. perfringens food poisoning produces mild, self-limited illness that is likely to be resolved within 24 hours. Patients with mild fluid deficits can be managed with clear liquids or specially formulated electrolyte solutions.
    2) Monitor fluid status and electrolyte balance, as necessary. IV fluids may be needed if the patient develops moderate to severe dehydration.
    3) Antidiarrheal agents are not usually indicated.
    B) MONITORING OF PATIENT
    1) Laboratory analyses of the stool and suspected food source for the organism can be used to confirm the diagnosis in an outbreak, but are not generally required for clinical management.
    2) Confirmation of C. perfringens foodborne illness can be done by quantitative cultures of the implicated food or enterotoxin-positive stool specimen from the patient.
    3) In a suspected outbreak, isolates from the implicated food and stool of an affected individual to produce enterotoxin needs to be confirmed that the strains are the same, because many healthy individuals (in particular the elderly) commonly have high numbers of C. perfringens spores in their feces.
    C) ANTIEMETIC
    1) Vomiting is not a typical characteristic of C. perfringens food poisoning. Antiemetics may be of use, if vomiting is severe.
    D) ANTIBIOTIC
    1) The illness is usually self-limited, NO specific antibiotic treatment is indicated (Shandera et al, 1983).
    E) ISCHEMIC COLITIS
    1) Necrotizing enterocolitis is a very rare complication of C. perfringens infection. Patients typically have severe abdominal pain, appear acutely ill and may have evidence of sepsis (Sobel et al, 2005). These patients require emergent abdominal CT scans and surgical consultation.

Range Of Toxicity

Summary

    A) TOXICITY: INFECTIVE DOSE: In type A food poisoning, illness occurs after the ingestion of a large number (greater than or equal to 10(5)) of viable, vegetative cells of a C. perfringens enterotoxin-producing strain, which is followed by sporulation of the organism in the small intestine to produce enterotoxin.

Minimum Lethal Exposure

    A) TYPE A: C. perfringens type A foodborne illness can be life-threatening in the elderly or patients with a debilitating condition (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Meer et al, 1997).
    B) TYPE C: Necrotizing enterocolitis (pigbel syndrome) has been associated with C. perfringens Type C (beta-toxin) food poisoning. It is rarely observed in the industrialized world. Symptoms can develop within 5 to 6 hours and usually begin as severe abdominal pain and diarrhea (often bloody) followed by necrotic inflammation of the small intestines. The illness can be fatal with a mortality rate of 15% to 20%, even in treated patients. It appears that individuals with reduced levels of proteolytic enzymes in the intestine due to a low protein intake are more likely to become ill (Brynestad & Granum, 2002).
    1) C. perfringens type A is generally NOT associated with necrotizing enterocolitis. However, there have been a few reports of this event in the literature (Sobel et al, 2005).
    2) CASE REPORTS: Adult necrotizing enterocolitis was associated with C. perfringens Type A infection in 4 adults. Of the 3 fatalities reported, two were members of the same family. The patient that recovered was a college student and his illness was not associated with any reported foodborne outbreak. C. perfringens type A was isolated from 3 (2 died; 1 survived) of the patients and in the remaining patient (a fatality) an organism was not detected (Sobel et al, 2005).

Maximum Tolerated Exposure

    A) INFECTIVE DOSE: In type A food poisoning, illness occurs after the ingestion of a large number (greater than or equal to 10(5)) of viable, vegetative cells of a C. perfringens enterotoxin-producing strain, which is followed by sporulation of the organism in the small intestine to produce enterotoxin (Lindstrom et al, 2011; Meer et al, 1997).
    B) SELF-LIMITED DISEASE: C. perfringens type A foodborne illness usually produces a mild, self-limiting disease that results in diarrhea and abdominal cramps (Meer et al, 1997).
    C) CONTRIBUTING FACTORS: Foodborne transmission accounts for most cases of C. perfringens illness. Improper holding time and temperature of food were found to be frequent contributing factors of C. perfringens outbreaks and improper holding was frequently seen with diarrhea-toxin and vomiting-toxin clinical profiles (Hedberg & Osterholm, 1993).

Pharmacology Toxicology

Toxicologic Mechanism

    A) INCUBATION PERIOD
    1) The incubation period can range from 8 to 24 hours (in some cases it maybe 6 to 12 hours) (Young et al, 2008; Meer et al, 1997). Symptoms generally last 12 to 24 hours; milder symptoms may persist for up to 1 to 2 weeks in some cases (ie, elderly, debilitated patients) (U.S. Food and Drug Administration, 2009).
    B) GENERAL
    1) C. perfringens is a sporeforming, anaerobic bacterium and the isolates are classified into 1 of 5 types (types A through E) and are able to produce the 4 major lethal toxins (alpha, beta, epsilon, and iota). Type A produces C. perfringens enterotoxin (CPE) that is commonly responsible for producing food poisoning (Paredes-Sabja & Sarker, 2009). Although all types of C. perfringens can produce food poisoning, type A is primarily seen in foodborne illness associated with this organism in the US and other industrialized countries (Lindstrom et al, 2011; U.S. Food and Drug Administration, 2009; Meer et al, 1997).
    C) TYPE A FOOD POISONING
    1) The progression of food poisoning is likely due to the survival of the heat resistant spores of C. perfringens in heat-treated foods (ie, meat, meat products, gravy) that are typically associated with illness (Paredes-Sabja & Sarker, 2009; U.S. Food and Drug Administration, 2009). Anaerobic conditions of food cause bacteria spores to germinate into a vegetative form, multiply and produce toxin which causes illness when eaten (McDonel, 1980).
    a) Type A produces an enterotoxin (CPE), which is responsible for most of the foodborne illness that occurs with this organism in the US. The production of the enterotoxin is typically associated with spore formation in the gut, however, in patients that develop symptoms quickly (less than 2 hours) it may be due to the presence of enterotoxin in the implicated food (ie, meat, poultry) (Meer et al, 1997).
    b) ENTEROTOXIN: C perfringens enterotoxin binds to a mammalian protein receptor, causing a conformational change. This protein receptor then forms a large complex within the membrane that breaks down the normal membrane permeability properties for small (molecular weight: less than 200,000 daltons) molecules (McClane, 1996). It typically requires the ingestion of a large number (equal to or greater than 10(5)) of viable, vegetative cells of a CPE-producing strain, following the sporulation of the organism in the small intestine to produce enterotoxin (Lindstrom et al, 2011; Meer et al, 1997). In the ileum, the enterotoxin causes secretion of fluid, sodium, and chloride, and sloughing of epithelial cells (McDonel & Duncan, 1975).
    c) MECHANISM: The C. perfringens enterotoxin (CPE) can cause disruption of villus integrity producing fluid loss (ie, diarrhea) associated with the illness (Meer et al, 1997)
    D) TYPE C FOOD POISONING
    1) Type C C. perfringens has been associated with a severe illness, with a high mortality rate, known as enteritis necroticans, "Darmbrand" (Germany), and "pigbel" (New Guinea). Hemorrhagic enteritis and spontaneous gangrene of the small intestine has occurred (Shandera et al, 1983; Granum, 1990).
    2) C. perfringens type C food poisoning is due to the beta-toxin, which causes necrosis of the small intestine. Beta-toxin is produced during vegetative growth and in greater quantities if the pH is fairly constant around 7.5; pH of the small intestine averages about 7 (Granum, 1990).
    3) Beta-toxins are degraded by proteolytic enzymes, such as trypsin, in the intestinal tract. Individuals with normal pancreatic trypsin activity that avoid foods containing powerful trypsin inhibitors, such as sweet potatoes, are at minimal risk of developing necrotic enteritis (Granum, 1990).

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