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FOODBORNE ILLNESSES

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INTRODUCTION AND EPIDEMIOLOGY

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Foodborne illness occurs after consumption of a food contaminated with bacteria, viruses, parasites, chemicals, or biotoxins. As one example, in 2008, melamine-contaminated dairy products in China affected over 50,000 children. The World Health Organization estimates that more than two million children die every year from exposure to unsafe water or food.1 Outbreaks from contaminated food are often widespread, and foodborne disease is a public health concern. International travel contributes to foodborne illnesses as travelers are exposed to new pathogens, and migrants may introduce diseases.1

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The Centers for Disease Control and Prevention (CDC) estimates that foodborne diseases cause 1 in 6 Americans to get sick, leading to 128,000 hospitalizations and 3000 deaths in the United States each year.2,3 Children have the highest frequency of foodborne illness. Viruses are the most common cause of foodborne disease, with the norovirus causing more than half of all cases and 26% of all admissions.2 Other viral sources of infection include rotavirus, astrovirus, and enteric adenovirus.

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Bacterial causes tend to be more severe, with nontyphoidal Salmonella triggering the most cases requiring admission or resulting in fatality.3 Other common bacterial causes of foodborne illness include Clostridium perfringens, Campylobacter spp., Toxoplasma gondii, Shigella, Staphylococcus aureus, and Shiga toxin–producing Escherichia coli. Over the past decade, there has been little change in the overall incidence of foodborne pathogens aside from Campylobacter, which has been steadily increasing since 2001.3 The most common foods associated with outbreaks reported in the United States are poultry, leafy vegetables, and fruits/nuts.2,3

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PATHOPHYSIOLOGY

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There are three basic mechanisms by which microbes cause illness. First, some pathogens such as S. aureus, Bacillus cereus, and Clostridium botulinum (botulism) produce toxins capable of causing illness. These preformed toxins are present in the food before ingestion and result in the rapid onset (1 to 6 hours) of symptoms. Preformed toxins such as staphylococcal enterotoxin exert their effect by stimulating the host immune system to release inflammatory cytokines within the intestine.4 These cytokines are responsible for the accompanying nausea and vomiting.

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The second method involves toxin production after ingestion, which interacts with intestinal epithelium as seen with Vibrio, Shigella, and Shiga toxin–producing E. coli. These cause diarrhea and lower GI symptoms (cramping and sometimes bloody diarrhea), with onset at approximately 24 hours after exposure. Some toxins produced by Vibrio and enterotoxigenic E. coli alter chloride and sodium transport across intestinal mucosal surfaces without destroying cells.5 The resulting osmotic gradient produces a large fluid shift into the intestinal lumen, which overwhelms the absorptive capacity of the colon, causing watery diarrhea. Other toxins produced after ingestion by organisms such as Shigella and Shiga toxin–producing E. coli disrupt host cell protein production, which causes death of the intestinal ...

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