INTRODUCTION AND EPIDEMIOLOGY

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

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.

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

PATHOPHYSIOLOGY

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.

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

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).

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

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

CLINICAL FEATURES

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.

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.

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.

DIAGNOSIS

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 situations^10,11:

• 
  

  Watery diarrhea with signs of hypovolemia

  
  
• 
  

  Bloody diarrhea

  
  
• 
  

  Fever ≥38.5^oC (101.3^oF)

  
  
• 
  

  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

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

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.

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.

TREATMENT

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

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.