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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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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 epithelium, resulting in bloody diarrhea and extraintestinal symptoms.6
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Finally, direct invasion of the intestinal epithelium is a common mechanism for the enteric viruses, Salmonella, enteroinvasive E. coli, and Campylobacter. These pathogens enter host cells and destroy intestinal epithelium.7 This causes diarrhea due to transient malabsorption that is frequently bloody and accompanied by systemic symptoms such as fever. These viruses require ingestion of just a few viral particles to cause disease. The upper and lower GI symptoms from invasive organisms last from 24 hours to weeks (Table 159-1).
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The normal human digestive tract has physiologic defenses against foodborne diseases. The low gastric pH of 1 to 3 kills many ingested pathogens, while the normal intestinal flora competitively inhibits pathogens and secretes bactericidal fatty acids and other chemicals.8,9 Normal intestinal motility prevents pathogens from having prolonged contact with mucosal surfaces and mixes organisms with mucous-containing protective glycoproteins. Immunologic tissues are also present in the GI tract to directly attack pathogens attempting transmural migration.9
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Alteration of these protective mechanisms can increase susceptibility to foodborne disease. For example, proton pump inhibitors, histamine-2 (H2) blockers, and antacids reduce gastric acid production. Recent antibiotic use, chemotherapy or radiation therapy, and recent surgery alter the intestinal flora. Decreased intestinal motility from narcotics, antiperistaltic drugs, and surgery may encourage pathogen growth and migration.9
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Suspect a foodborne disease when two or more people in a household or close association (e.g., the same workplace or communal eating arrangement) simultaneously develop GI symptoms. The most common symptoms are nausea, vomiting, diarrhea, and abdominal cramping. Systemic symptoms of fever, dehydration, and malaise are also common in patients with severe foodborne infections.
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Question patients about the types of food they have recently ingested, frequency of restaurant meals, consumption of public-vended or street-vended foods, ingestion of seafood, and consumption of raw foods. Additional questions include recent travel or camping, contact with food handlers, and diaper changing. Children who attend day care centers and residents of long-term care facilities are at increased risk for foodborne diseases. People working in the food industry are also frequent victims or sources; ask them about their personal hygiene and food-handling practices. Finally, seek a history of comorbidities or influencing therapies, including human immunodeficiency virus (HIV) infection or immunosuppressive drug use.
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On exam, look for dehydration and a toxic appearance. Another priority is the identification of blood in the stool and the exclusion of alternative causes of symptoms such as appendicitis. The clinical features of specific foodborne infections are summarized in Table 159-2.
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Most patients with foodborne diseases do not require diagnostic testing; illnesses are often self-limited. Routine testing for stool ova and parasites or cultures is not indicated.10 However, electrolytes and a CBC are helpful in toxic patients or those with prolonged symptoms. Stool tests are obtained in the following clinical situations10,11:
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Watery diarrhea with signs of hypovolemia
Bloody diarrhea
Fever ≥38.5oC (101.3oF)
Prolonged duration of illness >1 week
Severe abdominal pain or tenderness
Hospitalized patients or recent antibiotic use
Elderly (≥70 years of age) or the immunocompromised
Pregnant women or those with comorbidities such as inflammatory bowel disease
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Routine stool cultures will identify Salmonella, Campylobacter, and Shigella. A single sample is usually sufficient, but be aware of local laboratory limitations. For example, most laboratories do not routinely culture enterotoxigenic E. coli, vibrios, and viruses. In 2009, the Centers for Disease Control and Prevention recommended that clinical laboratories culture all submitted stool specimens for Shiga toxin–producing E. coli and perform toxin assays for Shiga toxin.12
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Testing for ova and parasites is indicated for the immunocompromised, patients with symptoms lasting longer than 2 weeks, community waterborne outbreaks, or men who have sex with men.10,13 Because parasite excretion may not be continuous, three specimens separated by at least 24 hours may be needed to identify the causative pathogen.
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Testing for fecal leukocytes has historically been performed to predict the presence of an invasive cause for acute diarrhea and increase stool culture yield. Unfortunately, several studies have shown that fecal leukocytes are neither sensitive nor specific for invasive disease, and they are a poor a predictor of response to antimicrobial therapy.14,15 The neutrophil marker lactoferrin is a more sensitive, but less widely available, screening test for inflammatory cells in stool. If positive, fecal lactoferrin also increases the likelihood of positive stool cultures.16,17 Direct antigen detection panels are available for specific viruses such as rotavirus, bacteria, and parasitic pathogens in many clinical laboratories.
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Most episodes of acute gastroenteritis require only adequate hydration and supportive care. The World Health Organization recommends initial therapy with a glucose-containing fluid (i.e., Pedialyte or equivalent) for oral rehydration.18 Parenteral rehydration is recommended for patients with severe dehydration or continued vomiting and inability to tolerate oral fluids. Antiemetics may reduce vomiting, emergency department length of stay, and need for admission.19,20 Antimotility medications, such as loperamide, may decrease illness duration for mild to moderate nonbloody diarrhea in adults without fever but are generally avoided in young children and patients with dysentery (fever and bloody diarrhea) due to concerns of prolonging the illness.21
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Empiric antibiotics do not appear to dramatically alter the course of illness since most cases are viral or self-limited bacterial in origin. The 2001 Infectious Diseases Society of America guidelines recommend empiric treatment for patients with moderate to severe traveler's diarrhea, those with symptoms for more than 1 week, patients requiring hospitalization due to volume depletion, and immunocompromised hosts.10 A common bacterial enteritis regimen is oral ciprofloxacin 500 milligrams twice daily or levofloxacin 500 milligrams once a day, each for 3 to 5 days. Azithromycin 500 milligrams once daily for 3 days is an alternative regimen.10 Antibiotics and antimotility agents are contraindicated in patients with Shiga toxin–producing E. coli O157:H7 infection due to increased risk of hemolytic-uremic syndrome, especially in children and the elderly.22 See Tables 159-3, 159-4, 159-5, and 159-6 for more detailed treatment recommendations.
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DISPOSITION AND FOLLOW-UP
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Patients who appear toxic or have systemic symptoms, significant comorbidities, or severe dehydration with inability to tolerate oral fluids are admitted. Discharged patients should receive instructions on proper hygiene, notably frequent hand washing, to protect family members and contacts who are not ill. Patients discharged with pending stool culture or other studies should have a clear plan for follow-up.
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Elderly patients, young children, and the immunocompromised are more likely to have severe illness, atypical presentations, and long-term sequelae. Patients with human immunodeficiency virus or other immunocompromised states can rapidly develop life-threatening symptoms. Thus, test more liberally and admit at a lower threshold. Pregnant patients have increased risk of complications, especially with Listeria infection, and may require further monitoring.10
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SPECIAL CONSIDERATIONS
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Enterohemorrhagic E. coli and Hemolytic-Uremic Syndrome Enterohemorrhagic E. coli that produces Shiga toxin is the most common cause of hemolytic-uremic syndrome in the United States.22 The Shiga toxin–producing E. coli strain O157:H7 is most commonly associated with pediatric hemolytic-uremic syndrome, but other strains such as O104:H4 and O111 are associated with adult hemolytic-uremic syndrome–like illnesses. The Shiga toxin produced by these organisms halts protein synthesis in renal glomerular cells as the precipitating event in hemolytic-uremic syndrome. Toxin binding to the glomerular endothelium produces a thrombogenic environment leading to microangiopathic hemolysis through multiple cellular mechanisms.23,24 Antibiotics may promote Shiga toxin release, which increases the incidence of hemolytic-uremic syndrome, and are avoided when this is suspected or identified. In addition, avoid antimotility agents. Treatment of hemolytic-uremic syndrome is supportive, with plasma infusion and exchange therapy showing some benefit. Approximately 50% of pediatric patients with hemolytic-uremic syndrome will require dialysis, and dehydration at the time of admission increases the frequency and duration of renal support.25
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Scombroid and Ciguatera Poisoning Scombroid fish poisoning occurs after ingestion of fish of the family Scombridae (tuna, mackerel, and bonito). Other non-Scombridae fish such as mahi-mahi, bluefish, herring, and sardines are also implicated. The disease occurs when histidine is metabolized by bacteria into histamine and other bioactive amines. Improper temperature control allows high concentrations of these substances to accumulate in the fish. Symptoms usually begin 30 minutes to 24 hours after ingestion and include flushing, headache, abdominal cramping, vomiting, and diarrhea. Symptoms are usually self-limited for 12 to 48 hours. However, severe cardiac and respiratory symptoms may occur in the elderly or patients with comorbid conditions. Treatment is with antihistamines (H1 and H2 blockers) such as diphenhydramine and cimetidine. Laboratory testing is not needed in most cases.26
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Ciguatera poisoning is caused by eating reef fish contaminated with the dinoflagellate Gambierdiscus toxicus, which produces ciguatoxin. The toxin is heat resistant and accumulates in large predatory fish such as grouper, snapper, amberjack, and barracuda. Ciguatoxin acts on sodium channels resulting in membrane depolarization. Nausea, vomiting, and diarrhea occur 1 to 24 hours after ingestion, followed by hypesthesias, paresthesias, numbness, malaise, generalized weakness, and sensitivity to temperature extremes. The latter is often described as a reversal of heat and cold sensation. Bradycardia and hypotension are also described.27 The GI symptoms typically resolve over a few days, whereas the neurologic symptoms may persist in a waxing and waning pattern for 3 months to years.28 Acute treatment is supportive. Mannitol has been used to treat severe cases, but the evidence is conflicting.29,30
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Chronic Sequelae of Foodborne Illness About 2% to 3% of patients with foodborne diseases have chronic sequelae thought to be related to autoimmunity.31,32 Protein virulence factors (superantigens) present in a number of foodborne pathogens can initiate extreme immune responses. Salmonella, Shigella, and Campylobacter have been associated with a seronegative reactive arthritis in about 2% of those infected.33 Campylobacter infection is associated with Guillain-Barré syndrome with a reported rate as high as 30.4 per 100,000 cases.32 Symptoms of Guillain-Barré syndrome typically occur 7 to 21 days after the GI symptoms resolve.31,32 Other autoimmune disorders thought to be associated with superantigens from foodborne pathogens include multiple sclerosis, rheumatoid arthritis, psoriasis, and Graves' disease.32 Infections with Salmonella, Yersenia, and Campylobacter may increase short- and long-term risk of death even after accounting for comorbid diseases.33
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Prevention and Surveillance The Centers for Disease Control and Prevention tracks foodborne infections in the United States through FoodNet. The U.S. Food and Drug Administration and U.S. Department of Agriculture provide the Centers for Disease Control and Prevention with data about the origin and distribution of food products, which allows investigators to determine the source of a foodborne outbreak.
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The Food Safety Modernization Act was passed into law in 2011 to address the rise in foodborne diseases by preventing, rather than responding to, outbreaks of foodborne illness. The law gives the U.S. Food and Drug Administration broad regulatory authority to oversee how food is harvested and processed.34