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Food Poisoning: Toxic Syndromes
Once away from home, travelers are especially vulnerable to food-borne illness since with regard to food, they rely on the sourcing, processing, and culinary skills of others. Toxic syndromes due to food poisoning may occur after ingestion of foods that have been inadequately cooked, stored, or preserved. Knowledge of common food associations and clinical syndromes can help travelers to select safe foods or prompt them to seek help if they are stricken. Humans become intoxicated in two ways: after ingesting pre-formed toxins produced by bacteria present in the foods or by ingesting bacterial forms that proliferate in the gut and produce enterotoxins that are absorbed within the small intestine (the latter mechanism is also called a “toxical infection”). The bacteria commonly recognized as causes of food poisoning are ubiquitous in the environment and include Clostridium perfringens , Staphylococcus aureus , Bacillus cereus , and Clostridium botulinum (types A, B, and E).
Disease caused by pre-formed enterotoxins of S. aureus and B. cereus typically present as acute gastrointestinal illness. C. perfringens type A food poisoning also presents as acute gastrointestinal illness, but enterotoxin production occurs in the host following ingestion of the bacteria. Pigbel or necrotizing enteritis is a serious illness caused by C. perfringens type C. Botulism occurs when foods contain pre-formed toxins produced by C. botulinum ; however, the clinical presentation usually involves neurological rather than gastrointestinal symptoms. Infant botulism is similar to C. perfringens in that toxin is produced after ingestion of contaminated food when C. botulinum spores germinate to produce bacteria that release intraluminal toxin during vegetative multiplication in the gut.
Table 33.1 summarizes the agents of food poisoning, including the incubation periods, clinical syndromes, and characteristic food associations. Websites providing reports of major outbreaks and information on food safety are given in Table 33.2 .
TABLE 33.1
Common Pathogens Causing Food Poisoning
Adapted from: CDC-EIS, 2003. Compendium of Acute Foodborne and Waterborne Diseases. http://www.cdc.gov (accessed July 9, 2009).
| Pathogen | Incubation | Characteristic Foods | Major Symptoms | Pathophysiology |
|---|---|---|---|---|
| Clostridium perfringens | 6-24 h | Meat, poultry | Cramping abdominal pain, a diarrhea; vomiting and fever uncommon | Enterotoxin formed in vivo |
| Staphylococcus aureus | 30 min to 8 h; usually 2-4 h | Creamy desserts, custards, salads, chopped hams, meats, baked goods | Vomiting, a cramping abdominal pain, diarrhea | Preformed enterotoxin |
| Bacillus cereus (emetic syndrome) |
1-6 h | Rice, vegetables, meat (“fried rice syndrome”) | Vomiting, a diarrhea; fever uncommon | ? Preformed enterotoxin |
| Bacillus cereus (diarrheal syndrome) |
6-24 h | Custards, cereals, puddings, sauces, meat loaf | Diarrhea a , abdominal cramps, and vomiting; fever uncommon | ? Preformed enterotoxin similar to ETEC LT toxin |
| Clostridium botulinum | 2 h to 8 days; usually 12-48 h | Types A and B: improperly canned or preserved (pickled, cured, smoked) meats and vegetables; type E: smoked or preserved fish | Diplopia, a blurred vision, a photophobia a ; dysphonia, dysarthria, weakness of tongue; nausea and vomiting; symmetric descending paralysis of motor and respiratory muscles that may progress rapidly | Preformed toxin |
ETEC, Enterotoxigenic Escherichia coli ; LT, heat-labile.
TABLE 33.2
Web Sites for Food Safety and Outbreak Information
| Centers for Disease Control and Prevention | http://www.cdc.gov/foodsafety |
| http://www.cdc.gov/botulism | |
| US Dept. of Agriculture Food Safety and Inspection Service | http://www.fsis.usda.gov |
| US Food and Drug Administration | http://www.cfsan.fda.gov |
| World Health Organization, Regional Food Safety Newsletter | http://www.who.int |
Food Poisoning Presenting as Gastrointestinal Illness
The onset of symptoms is usually within hours after ingestion of contaminated food. In mild cases of food poisoning, vomiting, diarrhea, and abdominal cramping may be of short duration and resolve before the afflicted person seeks medical attention.
Etiology
C. perfringens type A infection has been identified as a common cause of food-borne disease in industrialized countries and is a leading cause of food poisoning cases in the United States, responsible for approximately 10% of food-borne illness associated with a known pathogen. C. perfringens spores germinate during cooking in stews, soups, gravies, and other meat or poultry dishes, and then if the food is allowed to cool at room temperature for a prolonged period (e.g., 12-14 hours) the C. perfringens bacteria proliferate. After ingestion, the actively growing (vegetative stage) bacteria multiply and then sporulate in the small intestine. C. perfringens bacteria entering the sporulation stage produce enterotoxin, which is then absorbed by the host.
Rare cases of fatal adult necrotizing enterocolitis have been reported in association with food-borne C. perfringens type A infections. Cases reported included previously healthy adults, although some reported cases had drug-induced constipation and fecal impaction that may have led to prolonged exposure of the colonic mucosal tissue to C. perfringens type A toxins and contributed to the development of illness.
S. aureus strains producing enterotoxin are usually inoculated from hands of infected human carriers into proteinaceous food products (e.g., creamy desserts and pastries, salads, meats) served or stored at room or refrigerator temperatures, conditions allowing staphylococcal proliferation and toxin production. Staphylococcal enterotoxins (A, B, C, D, and E) are relatively heat stable, so subsequent cooking of contaminated foods will not necessarily destroy them.
B. cereus is a ubiquitous soil bacterium present on rice, vegetables, and some meats. The illness ensuing from ingestion of B. cereus -contaminated food has been given the nickname “fried rice syndrome”, as ingestion of fried rice was associated with the first recognized outbreaks. The ingredients and the cooking technique for this dish are especially conducive to illness-producing situations when fried rice is stored for prolonged periods at room temperature after cooking. The heat of cooking stimulates the B. cereus spores to germinate, and bacterial proliferation takes place in the food at room temperature, liberating enterotoxins. Flash cooking or brief reheating of the contaminated food before serving is not sufficient to inactivate the toxin nor kill the bacteria.
A short-incubation syndrome, with onset 2-9 hours after ingestion, is associated with the pre-formed toxin in the food. There is a long-incubation syndrome, with onset 6-14 hours after ingestion of contaminated food, associated with toxin elaborated by B. cereus bacteria proliferating within the gastrointestinal tract.
Diagnosis
A gastrointestinal illness characterized by a relatively rapid onset of symptoms after eating, and limited to 1 or 2 days, is likely to be food poisoning. Cramping abdominal pain is the hallmark of food poisoning caused by C. perfringens , and severe vomiting is the hallmark of food poisoning caused by S. aureus . B. cereus has two toxins, one causing a gastrointestinal illness with prominent vomiting (like S. aureus toxin) and one causing watery diarrhea (like the heat-labile toxin of enterotoxigenic E. coli ). The diagnosis can be best confirmed if some of the original questionable food is available for laboratory testing. Laboratory testing of patient stool specimens, vomitus, and serum is laborious and is customarily performed by state public health department laboratories during large outbreaks. Commercially available enterotoxin kits available for B. perfringens , S. aureus , and B. cereus allow for rapid diagnosis, often before culture results are available.
Treatment
Antibiotics are of no known value in food poisoning, since onset of symptoms is related to a certain level of the given enterotoxin being present in the gut; once formed, the toxin can exert its biologic effect independently of the continued viability of the bacterial source.
Treatment is directed toward symptomatic relief of the nausea and vomiting and replacement of fluids and electrolytes lost in watery stools and emesis. Oral rehydration is described in Chapter 8 . Rarely, nausea, vomiting, and diarrhea will be so severe that parenteral rehydration is necessary. Infants, the elderly, and the debilitated are most susceptible to complications from common food poisoning.
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