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Introduction

Food-borne bacteria and bacterial toxins are a common cause of epidemic gastroenteritis. In general, the illness is relatively mild and self-limited, with recovery within 24 hours. However, severe and even fatal poisoning may occur with listeriosis, salmonellosis, or botulism and with certain strains of Escherichia coli. Poisoning after the consumption of fish and shellfish is discussed on. Mushroom poisoning is discussed. Viruses such as the Norwalk virus and Norwalk-like caliciviruses, enteroviruses, and rotaviruses are the causative agent in as many as 80% of food-related illness. Other microbes that can cause food-borne illness include Cryptosporidium and Cyclospora, which can cause serious illness in immunocompromised patients. However, in over half of reported food-borne outbreaks, no microbiological pathogens are identified.

Centers for Disease Control and Prevention website on food-related illnesses: http://emergency.cdc.gov/agent/food

U.S. Food and Drug Administration foodborne illness website: https://www.fda.gov/food/recalls-outbreaks-emergencies/outbreaks-foodborne-illness.

Mechanism of Toxicity

Gastroenteritis may be caused by invasive bacterial infection of the intestinal mucosa or by a toxin elaborated by bacteria. Bacterial toxins may be preformed in food that is improperly prepared or stored before use, or may be produced in the gut by the bacteria after ingestion (Table II-27).

TABLE II-27. BACTERIAL FOOD POISONING

OrganismIncubation PeriodCommon Symptomsa and MechanismCommon Foods
Bacillus cereus

1-6 h (emetic)

8-16 h (diarrheal)

V > D, S; toxins produced in food and gutReheated fried rice, improperly refrigerated meats.
Campylobacter jejuni1-8 dD+, F; invasive and possibly toxin produced in gutPoultry, water, milk; direct contact (eg, food handlers).
Clostridium perfringens6-16 hD > V; toxin produced in food and gutMeats, gravy, dairy products.
E. coli, enterotoxigenic12-72 hD > V; toxin produced in gut“Traveler's diarrhea”: water, various foods; direct contact (eg, food handlers).
E. coli, enteroinvasive24-72 hD+; invasive infectionWater, various foods; direct contact (eg, food handlers).
E. coli, enterohemorrhagic (STEC, eg, 0157:H7)1-8 dD+, S; toxin produced in gutWater, ground beef, salami and other meats, unpasteurized milk and juice, contaminated lettuce and sprouts; direct contact (eg, food handlers).
E. coli, enteropathogenic4 hD; non-invasiveWater, raw meat, fecal contamination
Listeria monocytogenesVariesD+, S; invasive infectionMilk, soft cheeses, raw meat.
Salmonella spp12-36 hD+, F; invasive infectionMeat, dairy, eggs, water, sprouts; direct contact (eg, food handlers).
Shigella spp1-7 dD+, S; invasive infectionWater, fruits, vegetables; direct contact (eg, food handlers, contact with contaminated reptiles/frogs).
Staphylococcus aureus1-6 hV > D; toxin preformed in food; heat-resistantVery common: meats, dairy, bakery foods; direct contact (eg, food handlers).
Vibrio parahemolyticus8-30 hV, D+; invasive and toxin produced in gutShellfish, water.
Yersinia enterocolitica3-7 dD+; invasive infectionWater, meats, dairy.

aD, diarrhea; D+, diarrhea with blood and/or fecal leukocytes; F, fever; S, systemic manifestations; V, vomiting.

Toxic Dose

The toxic dose depends on the type of bacteria or toxin and its concentration in the ingested food as well as individual susceptibility or resistance. Some of the preformed toxins (eg, staphylococcal toxin) are heat resistant and are not removed by cooking or boiling.

Clinical Presentation

Commonly, a delay or “incubation period” of 2 hours to 3 days precedes the onset of symptoms (see Table II-27).

  1. Gastroenteritis is the most common finding, with nausea, vomiting, abdominal cramps, and diarrhea. Vomiting is more common with preformed toxins. Significant fluid and electrolyte abnormalities may occur, especially in young children or elderly patients.
  2. Fever, bloody stools, and fecal leukocytosis are common with invasive bacterial infections.
  3. Systemic infection can result from Bacillus cereus, Campylobacter, E. coli, Listeria, Salmonella, or Shigella.
    1. Rapid onset of fulminant hepatic failure and severe rhabdomyolysis has been reported with ingestion of B. cereus emetic toxin.
    2. Campylobacter infections sometimes are followed by Guillain-Barré syndrome or reactive arthritis.
    3. Listeriosis can cause sepsis and meningitis in high-risk individuals, including children, the elderly, and immunocompromised persons, with an estimated fatality rate of 20-30%. Infection during pregnancy produces a mild flulike illness in the mother but serious intrauterine infection resulting in fetal death, neonatal sepsis, or meningitis.
    4. Salmonella infection can lead to rhabdomyolysis and acute renal failure, and can also trigger acute reactive arthritis.
    5. Shigella and Shiga toxin-producing E. coli (STEC) strains (eg, O157:H7, O154:H4) may cause acute hemorrhagic colitis complicated by hemolytic-uremic syndrome, renal failure, and death, especially in children and immunocompromised adults. Seizures are reported in 10-45% of pediatric patients with shigellosis.

Diagnosis

Bacterial food poisoning is often difficult to distinguish from common viral gastroenteritis unless the incubation period is short and there are multiple victims who ate similar foods at one large gathering. The presence of many white blood cells in a stool smear suggests invasive bacterial infection. With any epidemic gastroenteritis, consider other food-borne illnesses, such as those caused by viruses or parasites, illnesses associated with seafood, botulism, and ingestions of certain mushrooms.

  1. Specific levels
    1. In most laboratories, routine stool cultures may differentiate E. coli, Salmonella, Shigella, and Campylobacter infections. Recent advances provide more accurate and faster detection of enteric pathogens or their toxins, using enzyme immunoassay (EIA), polymerase chain reaction (PCR), and other methods. They can detect many different pathogens in human stool samples, including viruses and protozoa, and yield results in 3 hours or less, compared to 2 or more days required for conventional stool cultures.
    2. Blood and cerebrospinal fluid (CSF) may grow invasive organisms, especially Listeria (and rarely Salmonella or Shigella).
    3. Food samples should be saved for bacterial culture and toxin analysis, primarily for use by public health investigators.
  2. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, and creatinine.

Treatment

  1. Emergency and supportive measures
    1. Replace fluid and electrolyte losses with IV saline or other crystalloid solutions (patients with mild illness may tolerate oral rehydration). Patients with hypotension may require large-volume IV fluid resuscitation.
    2. Use antiemetic agents for symptomatic treatment, but avoid strong antidiarrheal agents such as Lomotil (diphenoxylate plus atropine) in patients with suspected invasive bacterial infection (fever and bloody stools).
  2. Specific drugs and antidotes. There are no specific antidotes.
    1. In patients with invasive bacterial infection, antibiotics may be used once the stool testing reveals the specific bacteria responsible. However, antibiotics do not always shorten the course of illness. In fact, quinolones can prolong the carrier state in salmonellosis, and antibiotics may increase the risk for hemolytic-uremic syndrome from E. coli 0157:H7 infection. Empiric treatment with trimethoprim-sulfamethoxazole (TMP/SMX) or quinolones is often initiated while awaiting culture results; however, antimicrobial resistance is an increasing problem.
    2. Pregnant women who have eaten Listeria-contaminated foods should be treated empirically, even if they are only mildly symptomatic, to prevent serious intrauterine infection. The antibiotic of choice is IV ampicillin, with gentamicin added for severe infection.
  3. Decontamination procedures are not indicated in most cases.
  4. Enhanced elimination. There is no role for enhanced removal procedures.