eMedicine Specialties > Gastroenterology > Systemic Disease

Food Poisoning

Author: Roberto M Gamarra, MD, Fellow, Department of Internal Medicine, Section of Gastroenterology and Hepatology, Providence Hospital and Medical Center
Coauthor(s): David M Manuel, MD, Fellow, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital and Medical Center; Michael H Piper, MD, FACG, FACP, Clinical Assistant Professor, Department of Internal Medicine, Division of Gastroenterology, Wayne State University School of Medicine; Consulting Staff, Digestive Health Associates PLC; Senthil Nachimuthu, MD, FACP, Fellow, Department of Internal Medicine, Heart and Vascular Institute, Tulane University School of Medicine; Priyankha Balasundaram, MD, Director, Kovai Heart Foundation, India; Resident, Department of Surgery, Tulane University School of Medicine
Contributor Information and Disclosures

Updated: Nov 18, 2009

Introduction

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.

A food-borne disease outbreak is defined by the following 2 criteria:

  1. Similar illness, often gastrointestinal, in a minimum of 2 people
  2. 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, 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.

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.1,2 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, 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.3

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.4 (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.5 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 Outbreaks5

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Table
CountryYearDiseaseNumber of Cases
United
Kingdom
1985Salmonellosis1000
United States1985Salmonellosis>168,000
United States1993Salmonellosis224,000
China1988Hepatitis A>310,000
Germany1993Salmonellosis1000
Australia1991Norwalk-like agent>3050
United States1992-1993E coli O157
infection
>500
Japan1996E coli O157
infection
>6000
CountryYearDiseaseNumber of Cases
United
Kingdom
1985Salmonellosis1000
United States1985Salmonellosis>168,000
United States1993Salmonellosis224,000
China1988Hepatitis A>310,000
Germany1993Salmonellosis1000
Australia1991Norwalk-like agent>3050
United States1992-1993E coli O157
infection
>500
Japan1996E 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.

Clinical

History

A detailed history, including the duration of the disease, characteristics and frequency of bowel movements, and associated abdominal and systemic symptoms, may provide a clue to the underlying cause. The presence of a common source, types of specific food, travel history, and use of antibiotics always should be investigated.

The presenting complaints, typical features and pathogenesis of various causative agents, and diagnosis and treatment information can be found in Table 2 in the Causes section.

The following are some of the salient features of food poisoning:

  • Acute diarrhea in food poisoning usually lasts less than 2 weeks. Diarrhea lasting 2-4 weeks is classified as persistent. Chronic diarrhea is defined by duration of more than 4 weeks.
  • The presence of fever suggests an invasive disease. However, sometimes fever and diarrhea may result from infection outside the gastrointestinal tract, as in malaria.
  • A stool with blood or mucus indicates invasion of the intestinal or colonic mucosa.
  • When vomiting is the major presenting symptom, suspect Staphylococcus aureus, B cereus, or Norovirus.6
  • Reactive arthritis can be seen with Salmonella, Shigella, Campylobacter, and Yersinia infections.
  • A profuse rice-water stool suggests cholera or a similar process.
  • Abdominal pain is most severe in inflammatory processes. Painful abdominal muscle cramps suggest underlying electrolyte loss, as in severe cholera.
  • A history of bloating should raise the suspicion of giardiasis.
  • Yersinia enterocolitis may mimic the symptoms of appendicitis.
  • Proctitis syndrome, seen with shigellosis, is characterized by frequent painful bowel movement containing blood, pus, and mucus. Tenesmus and rectal discomfort are prominent features.
  • Consumption of undercooked meat/poultry is suspicious for Salmonella, Campylobacter, Shiga toxin E coli, and C perfringens.
  • Consumption of raw seafood is suspicious for Norwalk-like virus, Vibrio organism, or hepatitis A.
  • Consumption of homemade canned foods is associated with C botulinum.
  • Consumption of unpasteurized soft cheeses is associated with Listeria, Salmonella, Campylobacter, Shiga toxin E coli, and Yersinia.
  • Consumption of deli meats notoriously is responsible for listeriosis.
  • Consumption of unpasteurized milk or juice is suspicious for Campylobacter, Salmonella, Shiga toxin E coli, and Yersinia.
  • Salmonella has been associated with consumption of raw eggs.

Physical

The physical examination should focus on assessing the severity of dehydration.

  • A dry mouth, decreased axillary sweat, and decreased urine output indicate mild dehydration, whereas orthostasis, tachycardia, and hypotension indicate more severe volume depletion.
  • A rectal examination always should be performed to directly visualize the stool, to test occult blood, and to palpate the rectal mucosa for any lesions.
  • Rose spot macules on the upper abdomen and hepatosplenomegaly may be seen in Salmonella typhi infection.
  • Erythema nodosum and exudative pharyngitis are suggestive of Yersinia infection.
  • Patients with Vibrio vulnificus or Vibrio alginolyticus may present with cellulitis and otitis media.

Causes

The CDC estimates that 97% of all cases of food poisoning result from improper food handling; 79% of cases result from food prepared in commercial or institutional establishments7 and 21% of cases result from food prepared at home.

The most common causes are as follows: (1) leaving prepared food at temperatures that allow bacterial growth, (2) inadequate cooking or reheating, (3) cross-contamination, and (4) infection in food handlers. Cross-contamination may occur when raw contaminated food comes in contact with other foods, especially cooked foods, through direct contact or indirect contact on food preparation surfaces.

Bacteria are responsible for approximately 75% of the outbreaks of food poisoning and for 80% of the cases with a known cause in the United States.1 As many as 1 in 10 Americans has diarrhea due to food-borne infection each year.

Table 2. Causes of Food Poisoning

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Table
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)
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)
 

More on Food Poisoning

Overview: Food Poisoning
Differential Diagnoses & Workup: Food Poisoning
Treatment & Medication: Food Poisoning
Follow-up: Food Poisoning
References
Further Reading

References

  1. 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.

  2. Smith JL. Foodborne illness in the elderly. J Food Prot. Sep 1998;61(9):1229-39. [Medline].

  3. 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].

  4. Surveillance for foodborne disease outbreaks - United States, 2006. MMWR Morb Mortal Wkly Rep. Jun 12 2009;58(22):609-15. [Medline][Full Text].

  5. 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.

  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].

  7. 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].

  8. Archer DL. Incidence and cost of foodborne diarrheal disease in the United States. J Food Prot. 1985;48:887-94.

  9. 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.

  10. Gianella RA. Infectious enteritis and proctocolitis and bacterial food poisoning. In: Sleisenger and Fordtran's Gastrointestinal and Liver Disease. Vol 2. 2006:2333-91.

  11. Sherman PM, Wine E. Emerging intestinal infections. Gastroenterology & Hepatology Annual Review. 2006;1:50-54. [Full Text].

Further Reading

Clinical guidelines

Diagnosis and management of foodborne illnesses: a primer for physicians and other health care professionals.
American Medical Association - Medical Specialty Society
Center for Food Safety and Applied Nutrition - Federal Government Agency [U.S.]
Centers for Disease Control and Prevention - Federal Government Agency [U.S.]
Food Safety and Inspection Service - Federal Government Agency [U.S.]. 2001 Jan (revised 2004 Apr 16). 33 pages. NGC:003593

Prevention of rotavirus gastroenteritis among infants and children. Recommendations of the Advisory Committee on Immunization Practices (ACIP).
Centers for Disease Control and Prevention - Federal Government Agency [U.S.].  2006 Aug 11 (revised 2009 Feb 6). 25 pages. NGC:007073


Clinical trial

Study of Human Botulism Immunoglobulin in Infants With Botulism

Related eMedicine topics

Food Poisoning (Pediatrics: General Medicine)

Gastroenteritis, Bacterial

Gastroenteritis, Viral

Botulism

CBRNE - Staphylococcal Enterotoxin B

Keywords

food poisoning, gastroenteritis, botulism, , , cholera, , enterotoxins, , , , , , , , Norwalk virus, foodborne illness, , , , , , , tenesmus, shigellosis

Contributor Information and Disclosures

Author

Roberto M Gamarra, MD, Fellow, Department of Internal Medicine, Section of Gastroenterology and Hepatology, Providence Hospital and Medical Center
Roberto M Gamarra, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America
Disclosure: Nothing to disclose.

Coauthor(s)

David M Manuel, MD, Fellow, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital and Medical Center
David M Manuel, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society of Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America
Disclosure: Nothing to disclose.

Michael H Piper, MD, FACG, FACP, Clinical Assistant Professor, Department of Internal Medicine, Division of Gastroenterology, Wayne State University School of Medicine; Consulting Staff, Digestive Health Associates PLC
Michael H Piper, MD, FACG, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Senthil Nachimuthu, MD, FACP, Fellow, Department of Internal Medicine, Heart and Vascular Institute, Tulane University School of Medicine
Senthil Nachimuthu, MD, FACP is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Priyankha Balasundaram, MD, Director, Kovai Heart Foundation, India; Resident, Department of Surgery, Tulane University School of Medicine
Disclosure: Nothing to disclose.

Medical Editor

Jose A Perez Jr, MD, MSEd, MBA, Consulting Physician, Department of Internal Medicine, Residency Director, Vice Chair of Education Department of Medicine, The Methodist Hospital, Houston; Associate Professor of Clinical Medicine, Weill Cornell Medical College
Jose A Perez Jr, MD, MSEd, MBA is a member of the following medical societies: American College of Physician Executives, American College of Physicians, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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