Background
Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The symptoms, varying in degree and combination, include abdominal pain, vomiting, diarrhea, and headache; more serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
Most of the illnesses are mild and improve without any specific treatment. Some patients have severe disease and require hospitalization, aggressive hydration, and antibiotic treatment.[1]
A food-borne disease outbreak is defined by the following 2 criteria:
- Similar illness, often gastrointestinal, in a minimum of 2 people
- Evidence of food as the source
Pathophysiology
The pathogenesis of diarrhea in food poisoning is classified broadly into either noninflammatory or inflammatory types.
Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory mechanisms of the mucosa of the small intestine, without invasion. This leads to large volume watery stools in the absence of blood, pus, or severe abdominal pain. Occasionally, profound dehydration may result. The enterotoxins may be either preformed before ingestion or produced in the gut after ingestion. Examples include Vibrio cholerae, enterotoxic Escherichia coli, Clostridium perfringens, Bacillus cereus,[2] Staphylococcus organisms , Giardia lamblia, Cryptosporidium,rotavirus, norovirus (genus Norovirus, previously called Norwalk virus), and adenovirus.
Inflammatory diarrhea is caused by the action of cytotoxin on the mucosa, leading to invasion and destruction. The colon or the distal small bowel commonly is involved. The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicate colitis.
Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigella species.
In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting on the central nervous system. The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum.
The pathophysiological mechanisms that result in acute gastrointestinal symptoms produced by some of the noninfectious causes of food poisoning (naturally occurring substances [eg, mushrooms, toadstools] and heavy metals [eg, arsenic, mercury, lead]) are not well known.
Epidemiology
Frequency
United States
Initially, food-borne diseases were estimated to be responsible for 6-8 million illnesses and as many as 9000 deaths each year.[3, 4] However, the change in food supply, the identification of new food-borne diseases, and the availability of new surveillance data have changed the morbidity and mortality figures. A study from the US Centers for Disease Control and Prevention (CDC) reports that food-borne diseases cause approximately 76 million illnesses, 325,000 hospitalizations, and 5000 deaths in the United States each year. Identified pathogens account for an estimated 14 million illnesses, 60,000 hospitalizations, and 1800 deaths. Salmonella, Listeria,[5] and Toxoplasma organisms are responsible for 1500 deaths. Unidentified pathogens account for the remaining 62 million illnesses, 265,000 hospitalizations, and 3200 deaths. Overall, food-borne diseases appear to cause more illnesses but fewer deaths than previously estimated.[6]
According to a 2009 CDC study on food-borne disease outbreaks (for the year 2006), there were 1270 such outbreaks, or 27,634 cases, reported within 48 states, with 11 deaths resulting.[7] (However, most cases of food poisoning occur sporadically, rather than as part of an outbreak.) The etiologic agent was confirmed for more than 620 outbreaks, with Norovirus accounting for 54% of the outbreaks and a total of 11,879 cases. Salmonella was the second most frequent cause, accounting for 18% of the outbreaks and 3,252 cases. One of the 11 deaths resulted from a mushroom toxin; the rest were associated with bacteria, as follows:
- E coli O157:H7 - 6 deaths
- Listeria monocytogenes - 2 deaths
- Salmonella serotype Enteritidis - 1 death
- Clostridium botulinum - 1 death
In the 243 outbreaks known to have resulted from a single food commodity, the foods associated with the most cases were poultry (1355 cases), leafy vegetables (1081 cases), and fruits/nuts (1021 cases).
International
Transnational trade; travel; and migration and globalization of food production, manufacturing, and marketing pose greater risk of cross-border transmission of infectious diseases and food-borne illness.[8] A travel history should be obtained because traveler's diarrhea is the leading cause of travel-related illness. Onset occurs 3 days to 2 weeks after arrival. Illness is self-limiting within 5 days. Enterotoxigenic E coli is the most common isolate.
Table 1. Examples of Large Food-Borne Disease Outbreaks[8] (Open Table in a new window)
| Country | Year | Disease | Number of Cases |
| United Kingdom | 1985 | Salmonellosis | 1000 |
| United States | 1985 | Salmonellosis | >168,000 |
| United States | 1993 | Salmonellosis | 224,000 |
| China | 1988 | Hepatitis A | >310,000 |
| Germany | 1993 | Salmonellosis | 1000 |
| Australia | 1991 | Norwalk-like agent | >3050 |
| United States | 1992-1993 | E coli O157 infection | >500 |
| Japan | 1996 | E coli O157 infection | >6000 |
Mortality/Morbidity
Symptoms vary in degree and combination. They may include abdominal pain, vomiting, diarrhea, headache, and prostration. More serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
In children younger than 5 years, attacks range from 2-3 illnesses per child per year in developed countries; attacks are at least 5 times more common in developing countries. In underdeveloped countries, acute diarrheal diseases are responsible for 1 billion cases per year and 4-6 million deaths per year.
Age
Morbidity and mortality are higher in elderly individuals. The reasons for this increased susceptibility in elderly populations include age-associated decrease in immunity, decreased production of gastric acid and intestinal motility, malnutrition, lack of exercise, habitation in a nursing home, and excessive use of antibiotics. Elderly persons are more likely to die from infection with C perfringens; E coli O157; and Salmonella, Campylobacter, and Staphylococcus organisms.
Logan NA. Summer Meeting 2011: Bacillus and relatives in food-borne illness. J Appl Microbiol. Nov 28 2011;[Medline].
Lee JH, Shin H, Son B, Ryu S. Complete Genome Sequence of Bacillus cereus Bacteriophage BCP78. J Virol. Jan 2012;86(1):637-8. [Medline].
Hughes JM, Angulo FJ. Food borne diseases. In: Hurst JW, ed. Medicine for the Practicing Physician. 4th ed. Appleton & Lange: Stamford, Conn; 1996:344-7.
Smith JL. Foodborne illness in the elderly. J Food Prot. Sep 1998;61(9):1229-39. [Medline].
Goulet V, Hebert M, Hedberg C, Laurent E, Vaillant V, De Valk H, et al. Incidence of Listeriosis and Related Mortality Among Groups at Risk of Acquiring Listeriosis. Clin Infect Dis. Dec 14 2011;[Medline].
Preliminary FoodNet Data on the incidence of infection with pathogens transmitted commonly through food--10 States, 2008. MMWR Morb Mortal Wkly Rep. Apr 10 2009;58(13):333-7. [Medline]. [Full Text].
Surveillance for foodborne disease outbreaks - United States, 2006. MMWR Morb Mortal Wkly Rep. Jun 12 2009;58(22):609-15. [Medline]. [Full Text].
Jacobs RA. General problems in infectious diseases: acute infectious diarrhea. In: Tierney LM Jr, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment 2001. 40th ed. New York, NY: McGraw-Hill; 2000:1215-6.
Xerry J, Gallimore CI, Iturriza-Gómara M, Gray JJ. Tracking the transmission routes of genogroup II noroviruses in suspected food-borne or environmental outbreaks of gastroenteritis through sequence analysis of the P2 domain. J Med Virol. Jul 2009;81(7):1298-304. [Medline].
Malek M, Barzilay E, Kramer A, Camp B, Jaykus LA, Escudero-Abarca B, et al. Outbreak of norovirus infection among river rafters associated with packaged delicatessen meat, Grand Canyon, 2005. Clin Infect Dis. Jan 1 2009;48(1):31-7. [Medline].
Atmar RL, Bernstein DI, Harro CD, Al-Ibrahim MS, Chen WH, Ferreira J, et al. Norovirus vaccine against experimental human Norwalk Virus illness. N Engl J Med. Dec 8 2011;365(23):2178-87. [Medline].
Archer DL. Incidence and cost of foodborne diarrheal disease in the United States. J Food Prot. 1985;48:887-94.
Butterton JR, Calderwood SB. Acute infectious diarrheal diseases and bacterial food poisoning. In: Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, eds. Harrison's Principles of Internal Medicine. 15th ed. New York, NY: McGraw-Hill; 2001:834-9.
Gianella RA. Infectious enteritis and proctocolitis and bacterial food poisoning. In: Sleisenger and Fordtran's Gastrointestinal and Liver Disease. Vol 2. 2006:2333-91.
Sherman PM, Wine E. Emerging intestinal infections. Gastroenterology & Hepatology Annual Review. 2006;1:50-54. [Full Text].
| Country | Year | Disease | Number of Cases |
| United Kingdom | 1985 | Salmonellosis | 1000 |
| United States | 1985 | Salmonellosis | >168,000 |
| United States | 1993 | Salmonellosis | 224,000 |
| China | 1988 | Hepatitis A | >310,000 |
| Germany | 1993 | Salmonellosis | 1000 |
| Australia | 1991 | Norwalk-like agent | >3050 |
| United States | 1992-1993 | E coli O157 infection | >500 |
| Japan | 1996 | E coli O157 infection | >6000 |
| Causative Agents | Source and Clinical Features | Pathogenesis | Diagnosis and Treatment |
| Staphylococci | Improperly stored foods with high salt or sugar content favor growth of staphylococci Intense vomiting and watery diarrhea start 1-4 hours after ingestion and last as long as 24-48 hours. | Enterotoxin acts on receptors in gut that transmit impulses to medullary centers. | Symptomatic treatment |
| B cereus | Contaminated fried rice (emetic) Meatballs (diarrheal) Emetic: Duration is 9 hours, vomiting and cramps Diarrheal: Lasts for 24 h Mainly vomiting after 1-6 hours and mainly diarrhea after 8-16 hours after ingestion; lasts as long as 1 day | Emetic enterotoxin (short incubation and duration) - Poorly understood Diarrheal enterotoxin (long incubation and duration) - Increasing intestinal secretion by activation of adenylate cyclase in intestinal epithelium | Symptomatic treatment |
| C perfringens | Inadequately cooked meat, poultry, or legumes Acute onset of abdominal cramps with diarrhea starts 8-24 hours after ingestion. Vomiting is rare. It lasts less than 1 day. Enteritis necroticans associated with C perfringens type C in improperly cooked pork (40% mortality) | Enterotoxin produced in the gut, and food causes hypersecretion in the small intestine. | Culture of clostridia in food and stool Symptomatic treatment |
| C botulinum | Canned foods (eg, smoked fish, mushrooms, vegetables, honey) Descending weakness and paralysis start 1-4 days after ingestion, followed by constipation. Mortality is very high. | Toxin absorbed from the gut blocks the release of acetylcholine in the neuromuscular junction. | Toxin present in food, serum, and stool. Respiratory support Intravenous trivalent antitoxin from CDC |
| Listeria monocytogenes | Raw and pasteurized milk, soft cheeses, raw vegetables, shrimp Systemic disease associated with bacteremia Intestinal symptoms precede systemic disease Can seed meninges, heart valves, and other organs Highest mortality among bacterial food poisonings | Highly motile, heat-resistant, gram-positive organism | CSF or blood culture Must treat with antibiotics if bacteremic |
| Enterotoxic E coli (eg, traveler's diarrhea) | Contaminated water and food (eg, salad, cheese, meat) Acute-onset watery diarrhea starts 24-48 hours after ingestion. Concomitant vomiting and abdominal cramps may be present. It lasts for 1-2 days | Enterotoxin causes hypersecretion in small and large intestine via guanylate cyclase activation. | Supportive treatment No antibiotics |
| Enterohemorrhagic E coli (eg, E coli O157:H7) | Improperly cooked hamburger meat and previously spinach Most common isolate pathogen in bloody diarrhea starts 3-4 days after ingestion. Usually progresses from watery to bloody diarrhea. It lasts for 3-8 days May be complicated by HUS or TTP | Cytotoxin results in endothelial damage and leads to platelet aggregation and microvascular fibrin thrombi | Diagnosis with stool culture Supportive treatment No antibiotics |
| Enteroinvasive E coli | Contaminated imported cheese Usually watery diarrhea (some may present with dysentery) | Enterotoxin produces secretion Shiga-like toxin facilitates invasion. | Supportive treatment No antibiotics |
| Enteroaggregative E coli | Implicated in traveler's diarrhea in developing countries Can cause bloody diarrhea | Bacteria clump on the cell surfaces | Ciprofloxacin may shorten duration and eradicate the organism |
| V cholera | Contaminated water and food Large amount of nonbloody diarrhea starts 8-24 hours after ingestion. It lasts for 3-5 days. | Enterotoxin causes hypersecretion in small intestine. Infective dose usually is 107 -109 organisms. | Positive stool culture Prompt replacement of fluids and electrolytes (oral rehydration solution) Tetracycline (or fluoroquinolones) shortens the duration of symptoms and excretion of Vibrio. |
| V parahaemolyticus | Raw and improperly cooked seafood (ie, mollusks and crustaceans) Explosive watery diarrhea starts 8-24 hours after ingestion. It lasts for 3-5 days. | Enterotoxin causes hypersecretion in small intestine. Hemolytic toxin is lethal. Infective dose usually is 107 -109 organisms. | Positive stool culture Prompt replacement of fluids and electrolytes Sensitive to tetracycline, but unclear role for antibiotics |
| V vulnificus | Wound infection in salt water or consumption of raw oysters Can be lethal in patients with liver disease (50% mortality) | Polysaccharide capsule Growth correlates with availability of iron (esp. transferrin saturation >70%) | Culture of characteristic bullous lesions or blood Immediate antibiotics if suspected (eg, doxycycline and ceftriaxone) |
| C jejuni | Domestic animals, cattle, chickens Fecal-oral transmission in humans Foul-smelling watery diarrhea followed by bloody diarrhea Abdominal pain and fever also may be present. It starts 1-3 days after exposure and recovery is in 5-8 days. | Uncertain about endotoxin production and invasion | Culture in special media at 42°C Erythromycin for invasive disease (fever) |
| Shigella | Potato, egg salad, lettuce, vegetables, milk, ice cream, and water Abrupt onset of bloody diarrhea, cramps, tenesmus, and fever starts 12-30 hours after ingestion. Usually self-limited in 3-7 days | Organisms invade epithelial cells and produce toxins. Infective dose is 102 -103 organisms. Enterotoxin-mediated diarrhea followed by invasion (dysentery/colitis) | Polymorphonuclear leukocytes (PMNs), blood, and mucus in stool Positive stool culture Oral rehydration is mainstay. Trimethoprim-sulfamethoxazole (TMP-SMX) or ampicillin for severe cases No opiates |
| Salmonella | Beef, poultry, eggs, and diary products Abrupt onset of moderate-to-large amount of diarrhea with low-grade fever; in some cases, bloody diarrhea Abdominal pain and vomiting also present, beginning 6-48 hours after exposure and lasts 7-12 days | Invasion but no toxin production | Positive stool culture Antibiotic for systemic infection |
| Yersinia | Pets; transmission in humans by fecal-oral route or contaminated milk or ice cream Acute abdominal pain, diarrhea, and fever (enterocolitis) Incubation period not known Polyarthritis and erythema nodosum in children May mimic appendicitis | Gastroenteritis and mesenteric adenitis Direct invasion and enterotoxin | PMNs and blood in stool Positive stool culture No evidence that antibiotics alter the course but may be used in severe infections |
| Aeromonas | Untreated well or spring water Diarrhea may be bloody. May be chronic up to 42 days in the United States | Enterotoxin, hemolysin, and cytotoxin | Positive stool culture Fluoroquinolones or TMP/SMX for chronic diarrhea |
| Parasitic Food Poisoning | Source and Clinical Features | Pathogenesis | Diagnosis and Treatment |
| E histolytica | Contaminated food and water 90% asymptomatic 10% dysentery Minority may develop liver abscesses | Invasion of the mucosa by the parasites | Criterion standard is colonoscopy with biopsy Ova and parasites may be seen in the stool but has low sensitivity Luminal amebicides (eg, paromomycin) Tissue amebicides (eg, metronidazole) |
| G lamblia | Contaminated ground water Fecal-oral transmission in humans Mild bloody diarrhea with nausea and abdominal cramps starts 2-3 days after ingestion; lasts for 1 week May become chronic | Unknown Highest concentration in the distal duodenum and proximal jejunum | Initial diagnostic test is stool ELISA Duodenal aspiration or small bowel biopsy Cyst in the stool Metronidazole |
| Seafood/Shellfish Poisoning | Source and Clinical Features | Pathogenesis | Diagnosis and Treatment |
| Paralytic shellfish poisoning | Temperate costal areas Source - Bivalve mollusks Onset usually is 30-60 minutes. Initial symptoms include perioral and intraoral paresthesia. Other symptoms include paresthesia of the extremities, headache, ataxia, vertigo, cranial nerve palsies, and paralysis of respiratory muscles, resulting in respiratory arrest. | Fish acquires toxin-producing dinoflagellates | General observation for 4-6 hours Maintain patent airway. Administer oxygen, and assist ventilation if necessary. For recent ingestion, charcoal 50-60 g may be helpful. |
| Neurotoxic shellfish poisoning | Coastal Florida Source - Mollusks Illness is milder than in paralytic shellfish poisoning. | Fish acquires toxin-producing dinoflagellates | Symptomatic |
| Ciguatera | Hawaii, Florida, and Caribbean Source - Carnivorous reef fish Vomiting, diarrhea, and cramps start 1-6 hours after ingestion and last from days to months. Diarrhea may be accompanied by a variety of neurologic symptoms including paresthesia, reversal of hot and cold sensation, vertigo, headache, and autonomic disturbances such as hypotension and bradycardia. Chronic symptoms (eg, fatigue, headache) may be aggravated by caffeine or alcohol | Fish acquires toxin-producing dinoflagellates Toxin increases intestinal secretion by changing intracellular calcium concentration | Symptomatic Anecdotal reports of successful treatment of neurologic symptoms with mannitol 1 g/kg IV |
| Tetrodotoxin poisoning | Japan Source - Puffer fish Onset of symptoms usually is 30-40 minutes but may be as short as 10 minutes. It includes lethargy, paresthesia, emesis, ataxia, weakness, and dysphagia. Ascending paralysis occurs in severe cases. Mortality is high. | Neurotoxin is concentrated in the skin and viscera of puffer fish. | Symptomatic |
| Scombroid | Source - Tuna, mahi-mahi, kingfish Allergic symptoms such as skin flush, urticaria, bronchospasm, and hypotension usually start within 15-90 minutes. | Improper preservation of large fish results in bacterial degradation of histidine to histamine. | Antihistamines (diphenhydramine 25-50 mg IV) H2 blockers (cimetidine 300 mg IV) Severe reactions may require subcutaneous epinephrine (0.3-0.5 mL of 1:1000 solution). |
| Heavy Metal Poisoning | Source | Symptoms | Treatment |
| Mercury | Ingestion of inorganic mercuric salts | Causes metallic taste, salivation, thirst, discoloration and edema of oral mucous membranes, abdominal pain, vomiting, bloody diarrhea, and acute renal failure | Consult a toxicologist. Remove ingested salts by emesis and lavage, and administer activated charcoal and a cathartic. Dimercaprol is useful in acute ingestion. |
| Lead | Toxicity results from chronic repeated exposure. It is rare after single ingestion. | Common symptoms include colicky abdominal pain, constipation, headache, and irritability. Diagnosis is based on lead level (>10 mcg/dL) | Other than activated charcoal and cathartic, severe toxicity should be treated with antidotes (edetate calcium disodium [EDTA] and dimercaprol). |
| Arsenic | Ingestion of pesticide and industrial chemicals | Symptoms usually appear within 1 hour after ingestion but may be delayed as long as 12 hours. Abdominal pain, watery diarrhea, vomiting, skeletal muscle cramps, profound dehydration, and shock may occur. | Gastric lavage and activated charcoal Dimercaprol injection 10% solution in oil (3-5 mg/kg IM q4-6h for 2 d) and oral penicillamine (100 mg/kg/d divided qid for 1 wk) |
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