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Food Poisoning


Food poisoning is defined as an illness caused by the consumption of food contaminated with bacteria, bacterial toxins, parasites, viruses, or chemicals. The percentage of outbreaks for which an etiology is confirmed has increased significantly from 40% in 1998 to 67% in 2002 and has remained consistent to the present. In a report from 2015, bacteria were responsible for 54% of foodborne outbreaks, whereas viruses accounted for 38% and the remainder was attributed to parasites and chemicals. Using data from surveillance networks, the Centers for Disease Control and Prevention (CDC) estimates that each year approximately 48 million Americans get sick, of which 128,000 are hospitalized, and 3,000 die from foodborne illness. In only half of outbreaks is a single-etiology identified, most notably norovirus (37%) and nontyphoidal Salmonella spp. (34%). An additional 38.4 million episodes of domestically acquired foodborne illness are caused by unspecified agents, including bacteria known to cause acute gastroenteritis, agents that may not be recognized as being transmitted in food (e.g., Clostridioides difficile ), and as yet undefined agents.

A foodborne disease outbreak is defined by 2 criteria: similar illness, usually GI, in 2 or more persons; and epidemiologic or laboratory investigation that implicates food as the source. An extensive list of causatve agents has been associated with foodborne illnesses ( Table 111.1 ). Newer stool-testing assays, such as the FilmArray GI Panel that allows for simultaneous detection of 22 enteric pathogens by PCR, will likely make it easier to identify the etiology of GI illness, because the panel is fast, sensitive, specific, and simple to perform. However, other new challenges have emerged. Globalization of the food trade, with centralized processing and wide distribution, provide opportunities for foodborne outbreaks to spread rapidly between countries, and indiscriminate use of antibiotics in the meat industry has led to increasing resistance of organisms to treatment.

TABLE 111.1
Estimated Rates of Foodborne Illnesses and Associated Mortality in the USA, 2006
From Scallan E, Hoekstra RM, Angulo FJ, et al. Foodborne illness acquired in the United States—major pathogens. Emerg Infect Dis 2011; 17:7-15.
Pathogen Estimated Total No. of Cases Foodborne Transmission (%) No. of Deaths Death Rate (%) a
Bacteria

  • Brucella

839 50 1 0.9

  • Campylobacter

845,024 80 76 0.1

  • E. coli

  • O157:H7 (EHEC)

  • 63,153

  • 68

  • 20

  • 0.5

  • Non-O157:H7 (non-EHEC)

  • 112,752

  • 82

  • 0

  • 0.3

  • L. monocytogenes

  • 1,591

  • 99

  • 255

  • 15.9

  • S. typhi

  • 1,821

  • 96

  • 0

  • 0

  • Nontyphoidal Salmonella

  • 1,027,561

  • 94

  • 378

  • 0.5

  • Shigella

  • 131,254

  • 31

  • 10

  • 0.1

  • V. parahaemolyticus

  • 34,664

  • 86

  • 4

  • 0.9

  • V. vulnificus

  • 96

  • 47

  • 36

  • 34.8

  • Y. enterocolitica

  • 97,656

  • 90

  • 29

  • 2

  • B. cereus

  • 63,400

  • 100

  • 0

  • 0

  • C. botulinum (food botulism)

  • 55

  • 100

  • 9

  • 17.3

  • C. perfringens

  • 965,958

  • 100

  • 26

  • <0.1

  • Staphylococcal

  • 241,148

  • 100

  • 6

  • <0.1

  • Streptococcal

  • 11,217

  • 100

  • 0

  • 0

Parasites

  • Cryptosporidium parvum

  • 57,616

  • 8

  • 4

  • 0.3

  • Cyclospora cayetanensis

  • 11,407

  • 99

  • 0

  • 0

  • Giardia lamblia

  • 76,840

  • 7

  • 2

  • 0.1

  • Toxoplasma gondii

  • 86,686

  • 50

  • 327

  • 0.2

  • Trichinella spiralis

  • 156

  • 100

  • 0

  • 0.2

Viruses

  • Astrovirus

  • 15,433

  • <1

  • 0

  • <0.1

  • Norovirus and Norwalk-like viruses

  • 5,461,731

  • 26

  • 149

  • <0.1

  • Rotavirus

  • 15,433

  • <1

  • 0

  • <0.1

  • HAV

  • 1,566

  • 7

  • 7

  • 2.4

  • Sapovirus

  • 15,433

  • <1

  • 0

  • <0.1

TOTAL 9,388,075 — 1,351
EHEC , Enterohemorrhagic E. coli .

a For laboratory-confirmed illnesses.

Approach to the Patient

A thorough history should be obtained on all patients with suspected foodborne illness. Symptoms of foodborne illnesses are similar one to another, but details to be elicited should include the food ingested ( Box 111.1 ); the time period between ingestion and onset of symptoms; the number of people who ingested the food and how many became ill; and the means of preparation and storage of the suspected food (e.g., picnic, home canning, restaurant) ( Table 111.2 ).

BOX 111.1
Organisms and Foodborne Diseases Associated With Specific Foods or Beverages
From Bishai WR, Sears CL. Food poisoning syndromes. Gastroenterol Clin North Am 1993; 22:579-608.
EHEC , Enterohemorrhagic E. coli ; EIEC , enteroinvasive E. coli .

Beef and Pork

  • Salmonella spp.

    • S. aureus

    • C. perfringens

    • EHEC

    • B. cereus

    • Y. enterocolitica

    • L. monocytogenes

    • Brucella spp.

    • Trichinella spiralis

Chinese Food

  • B. cereus (in fried rice)

    • Monosodium glutamate poisoning

Eggs

  • Salmonella spp.

    • S. aureus

Fish

  • C. botulinum

    • Ciguatera poisoning

    • Scombroid poisoning

    • Diphyllobothrium latum

    • Anisakidosis

Honey

  • C. botulinum

Milk and Cheese

  • Salmonella spp.

    • Campylobacter spp.

    • EIEC and EHEC

    • Y. enterocolitica

    • Group A streptococci

    • Brucella spp.

    • L. monocytogenes

Poultry

  • Salmonella spp.

    • S. aureus

    • Campylobacter spp.

    • C. perfringens

    • L. monocytogenes

Shellfish

  • V. parahaemolyticus

    • V. cholerae (O1 and non-O1)

    • Hepatitis A

    • Norovirus and Norwalk-like viruses

    • Paralytic shellfish poisoning

    • Neurotoxic shellfish poisoning

Vegetables

  • C. botulinum

    • Salmonella spp.

    • Shigella spp.

    • B. cereus

    • Norovirus

TABLE 111.2
Features of Bacterial Food Poisoning
From Snydman DR. Food poisoning. In: Gorbach SL, Bartlett JG, Blacklow NR, editors. Infectious diseases. Philadelphia: WB Saunders; 1992. p 771.
Organism Common Vehicles Median Incubation (hr) (Range) Primary Toxin Clinical Features Median Duration, Days (Range) Secondary Attack Rate (%) Sources of Diagnostic Material
B. cereus Fried rice, vanilla sauce, cream, meatballs, boiled beef, barbecued chicken 2 (1-16)
9 (6-14)		 Heat stable
Heat labile		 V, C, D
D, C, V		 0.4 (0.2-0.5)
1 (1-2)		 0 Vomitus, stool, implicated food
C. jejuni Milk, chicken, beef 48 (24-240) Unknown D, F, C, B, H, M, N, V 7 (2-30) 25 Stool, rectal swab
C. perfringens Beef, turkey, chicken 12 (8-22) Heat labile D, C (N, V, F rare) 1 (0.3-3) 0 Stool, rectal swab; food, food-contact surfaces
E. coli spp . Salads, beef 24 (8-44) Heat labile D, C, N, H, F, M 3 (1-4) 0 Stool, rectal swab
96 (24-120) Heat stable F, M, D, C
E. coli O157:H7 Verotoxin B, C, F, hemolytic-uremic syndrome
L. monocytogenes Milk, raw vegetables, coleslaw, dairy products, poultry, beef ? Unknown D, F, C, N, V, B ? 10 Stool, rectal swab
Salmonella spp . Eggs, meat, poultry 24 (5-72) Role of toxin unclear D, C, N, V, F, H, B (rare), enteric fever 3 (0.5-14) 30-50 Stool, rectal swab from patients and food preparers; raw food
Shigella spp. Milk, salads (potato, tuna, turkey) 24 (7-168) Role of toxin unclear C, F, D, B, H, N, V 3 (0.5-14) 40-60 Stool, rectal swab from patients, and food preparers; implicated food
S. aureus Ham, pork, canned beef, cream-filled pastry 3 (1-6) Heat stable V, N, C, D, F (rare) 1 (0.3-1.5) 0 Stool, vomitus; food or food-contact surfaces; nose, hands, purulent lesion on food preparer
V. parahaemolyticus Seafood (rarely saltwater) or salted vegetables 12 (2-48) Role of toxin unclear D, C, N, V, H, F, B (rare) 3 (2-10) 0 Stool, rectal swab; food, food-contact surfaces; seawater
Y. enterocolitica Chocolate milk or raw milk, pork 72 (2-144) Heat stable F, C, D, V, pharyngitis, arthritis, mesenteric adenitis, rash 7 (2-30) 20 Stool from food preparer
B , Bloody diarrhea; C , cramping abdominal pain; D , diarrhea; F , fever; H , headache; M , myalgias; N , nausea; V , vomiting.

Some foodborne illnesses are more common during certain seasons. For example, during the summer months, illnesses due to Salmonella spp., Shigella spp. and Staphylococcus aureus are prevalent. Disease from Campylobacter jejuni is more common in the spring and fall, whereas Clostridium perfringens outbreaks occur least often in the summer. Infections due to Bacillus cereus and Norovirus occur year round.

In addition to considering the culprit organism and its vector, one must also be aware of the susceptibility of the host. For example, persons with liver disease have an annual rate of infection with and death from Vibrio vulnificus that is 80 times and 200 times, respectively, greater than those of adults without liver disease. Patients with compromised immune systems, either from a disease process or medication to manage their disease, as well as patients at the extremes of age or who are pregnant, are at increased risk for infection and mortality related to foodborne illness. For example, 47% patients with common variable immune deficiency were found to have infection with Giardia , Campylobacter , or Salmonella spp. Gastric acidity is a natural defense mechanism against infection that may be compromised by prior gastric surgery or use of PPIs. There is evidence that patients with achlorhydria or those treated with PPIs or H2RAs are more susceptible to infection by Campylobacter spp. , Escherichia coli O157, Listeria monocytogenes, Salmonella spp., Shigella spp., and Vibrio cholerae than healthy controls.

The presenting symptom complex also can give a clue to the causative organism. Symptom complexes may be classified as nausea and vomiting, noninflammatory diarrhea, inflammatory diarrhea, neurologic symptoms, and systemic or miscellaneous symptoms (see Table 111.2 ).

Bacterial Food Poisoning

The following entities are discussed in order of their reported frequencies.

Clostridium perfringens

C. perfringens is a major foodborne pathogen that produces vomiting and diarrhea. The disease is caused by an enterotoxin elaborated by strains of C. perfringens type A. A more severe and often fatal foodborne illness, variably known as enteritis necroticans, darmbrand (German, fire bowels) and pigbel , is caused by C. perfringens type C.

Microbiology

Clostridia are gram-positive, spore-forming, obligate anaerobes that can be found in the normal intestinal flora of humans and animals, and in the soil. Although an anaerobe, C. perfringens is remarkably aerotolerant and survives exposure to oxygen for as long as 72 hours. There are multiple strains of C. perfringens, which produce different toxins; symptoms differ based on the bacterial strain and toxin present. The food-poisoning syndrome of C. perfringens is caused by a heat-labile protein enterotoxin, better termed functionally as a secretory cytotoxin , which is a structural component of the spore coat and is formed during sporulation. Clostridial cytotoxin has its maximum activity in the ileum, inhibits glucose transport, damages the intestinal epithelium, and causes intestinal protein loss.

Epidemiology and Pathogenic Mechanisms

Epidemics of C. perfringens are characterized by high attack rates and a large number of affected persons, usually 40 to 50 per outbreak. The incubation period varies from 8 to 14 hours but can be as long as 22 hours. In almost every outbreak of clostridial food poisoning, poultry or roasted, boiled, stewed, or steamed meat is the vehicle of infection. Usually, the meat is cooked in bulk so that heat gain and internal pressure are insufficient to kill the spores. The implicated food invariably undergoes a period of inadequate cooling, during which the spores can still germinate. The organism proliferates rapidly at temperatures between 15°C and 50°C, and unless the food is reheated to a very high temperature, it will contain many viable organisms. Although largely preventable with proper food handling, large outbreaks, sometimes with fatal outcome, due to C. perfringens food poisoning are still frequently reported.

Clinical Features

C. perfringens type A food poisoning is characterized by watery diarrhea, severe cramping abdominal pain, and, often, vomiting that begins 8 to 24 hours after the incriminating meal. Fever, chills, headache, or other signs of infection usually are absent. The illness is of short duration and usually lasts less than 24 hours. Rare fatalities have been recorded in debilitated or hospitalized patients and are usually caused by dehydration. No specific treatment is required.

Enteritis Necroticans

Enteritis necroticans is a segmental necrotizing infection of the jejunum and ileum caused by the β-toxin of C. perfringens , strain type C, that was originally described in post–World War II Germany, in an outbreak that affected more than 400 people who consumed rancid meat. The β-toxin is normally inactivated by trypsin, but when a low-protein diet is consumed and therefore there is decreased activity of trypsin, or with improper cooking techniques, the disease emerges. Similar outbreaks, associated with the consumption of inadequately cooked pork, have been described in Papua New Guinea and referred to as pigbel, referring to abdominal pain after a pig feast. In malnourished patients, especially like the children in Papua New Guinea, whose diet is composed mostly of sweet potatoes that contain a heat-labile trypsin inhibitor, the toxin cannot be inactivated and transmural intestinal wall necrosis ensues. Fibrin thrombi that occlude superficial arteries and veins of the lamina propria and submucosa are characteristic of this condition, and animal studies suggest that vascular thrombosis initiates the intestinal necrosis typical of C. perfringens type C infections. Enteritis necroticans may rarely be encountered in the US because it is associated with the consumption of chitterlings (prepared pig intestine; a traditional African-American holiday food in the South). Intestinal perforation, sepsis, and hemorrhage result in a 40% mortality rate. Fortunately, this disease is rare. In the uncomplicated case, treatment is symptomatic and supportive.

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