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Food Poisoning Follow-up

  • Author: Roberto M Gamarra, MD; Chief Editor: Julian Katz, MD  more...
Updated: Jun 26, 2015

Further Outpatient Care

Because most cases of food poisoning are self-limited, prolonged follow-up care is not required.

Stool cultures should be monitored in individuals working in hospitals, food establishments, and daycare centers and who are infected with E coli O157:H7 or Salmonella or Shigella organisms until they become culture-negative without antibiotics. These people should not return to work until that time.


Patient Education



No vaccine is available that can prevent norovirus infection. An early study conducted in a controlled setting assessed the safety, immunogenicity, and efficacy of an investigational, intranasally delivered norovirus viruslike particle (VLP) vaccine to prevent acute viral gastroenteritis. Results suggest the vaccine protects against illness and infection after exposure to the Norwalk virus and could potentially prevent infection in susceptible, high-risk populations. The vaccine has not been tested in the natural setting, however.[16]

The best way to prevent food poisoning caused by infectious agents is to practice strict personal hygiene, cook all foods adequately, avoid cross-contamination of raw and cooked foods, and keep all foods at appropriate temperatures (ie, < 40°F for refrigerated items and >140°F for hot items).

Avoiding eating wild mushrooms prevents mushroom poisoning.

Prevention of fish poisoning requires avoidance of large tropical fish (ciguatera poisoning) and compliance with seasonal or emergency quarantines of shellfish harvesting areas (shellfish poisoning).

Raw or undercooked milk, poultry, eggs, meat, and seafood are best avoided.

Local health authorities should be notified if an outbreak of food poisoning occurs. This leads to appropriate actions to prevent further spread of food poisoning.

Irradiation of food (ie, the use of ionizing radiation or ionizing energy to treat foods, either packaged or in bulk form) can eliminate food-borne pathogens. Annually, more than half a million tons of food is now irradiated worldwide. Treating raw meat and poultry with irradiation at the slaughter plant could eliminate bacteria, such as E coli O157:H7 and Salmonella and Campylobacter organisms. No evidence of adverse health effects has been found in the well-controlled clinical trials involving irradiated food.

The use of low-temperature gas plasmas in the food industry may potentially reduce the incidence of foodborne disease.[17] The gas plasmas have microbiocidal capabilities and may also aid in degrading undesirable chemical compounds that can be found on food and food-processing equipment (eg, pesticide residues, toxins, allergens).[17]

Prophylaxis for traveler's diarrhea is not recommended routinely because of the risk of adverse effects from the drugs (eg, rash, anaphylaxis, vaginal candidiasis) and the development of resistant gut flora. Possible regimens for prophylaxis include bismuth subsalicylate (Pepto-Bismol, 524 mg PO qid with meals and qhs), doxycycline (100 mg PO qd; resistance documented in many areas of the world), TMP/SMX (160 mg/800 mg 1 double-strength tab qd), or norfloxacin (400 mg PO qd; fluoroquinolones should not be prescribed to children or pregnant women). No significant resistance to the fluoroquinolones has been reported in high-risk areas, and they are the most effective antibiotics in regions where susceptibilities are not known.

Contributor Information and Disclosures

Roberto M Gamarra, MD Consulting Gastroenterologist, Digestive Health Associates, PLC

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, Crohn's and Colitis Foundation of America

Disclosure: Nothing to disclose.


Senthil Nachimuthu, MD, FACP 

Senthil Nachimuthu, MD, FACP is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Michael H Piper, MD 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 is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, Michigan State Medical Society

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.

David Manuel, MD Affiliate Faculty, Department of Medicine, Loyola University Health System; Gastroenterologist, Digestive Health Center

David 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 for Gastrointestinal Endoscopy, Crohn's and Colitis Foundation of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

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 & Ethics, American Trauma Society, Association of American Medical Colleges, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Additional Contributors

Jose A Perez, Jr, MD, MBA, MSEd Residency Director, Internal Medicine Residency Program, Vice Chair of Education, Department of Medicine, Methodist Hospital; Associate Professor of Clinical Medicine, Weill Cornell Medical College

Jose A Perez, Jr, MD, MBA, MSEd is a member of the following medical societies: American Association for Physician Leadership, American College of Physicians, Society of General Internal Medicine, Society of Hospital Medicine

Disclosure: Nothing to disclose.


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.

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Table 1.Causes of Food Poisoning.
Causative Agents Source and

Clinical Features

Pathogenesis Diagnosis and


Staphylococci Improperly stored foods with high salt or sugar content favors growth of staphylococci.

Intense vomiting and watery diarrhea start 1-4 h after ingestion and last as long as 24-48 h

Enterotoxin acts on receptors in the gut that transmit impulses to the medullary centers Symptomatic treatment
B cereus Contaminated fried rice (emetic)

Meatballs (diarrheal)

Emetic: Duration is 9 h, vomiting and cramps

Diarrheal: Lasts for 24 h

Mainly vomiting after 1-6 h and mainly diarrhea after 8-16 h after ingestion; lasts as long as 1 d

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 h after ingestion.

Vomiting is rare. It lasts less than 1 d.

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 d after ingestion, followed by constipation.

Mortality is 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 h after ingestion

Concomitant vomiting and abdominal cramps may be present. It lasts for 1-2 d

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 d after ingestion

Usually progresses from watery to bloody diarrhea. It lasts for 3-8 d

May be complicated by hemolytic-uremic syndrome or thrombotic thrombocytopenic purpura

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

Shigalike 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 h after ingestion. It lasts for 3-5 d

Enterotoxin causes hypersecretion in small intestine

Infective dose usually is 107 -109 organisms

Positive stool culture finding

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 h after ingestion

It lasts for 3-5 d

Enterotoxin causes hypersecretion in small intestine

Hemolytic toxin is lethal

Infective dose is usually 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 (especially 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 d after exposure and recovery is in 5-8 d

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 h after ingestion.

Usually self-limited in 3-7 d

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 dairy 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 h after exposure and lasts 7-12 d

Invasion but no toxin production Positive stool culture finding

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

Polymorphonuclear leukocytes and blood in stool

Positive stool culture finding

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 d 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 diarrhea with nausea and abdominal cramps starts 2-3 d after ingestion; lasts for 1 wk

May become chronic


Highest concentration in the distal duodenum and proximal jejunum

Initial diagnostic test is stool enzyme-linked immunosorbent assay

Duodenal aspiration or small bowel biopsy

Cyst in the stool


Seafood/Shellfish Poisoning Source and

Clinical Features

Pathogenesis Diagnosis and


Paralytic shellfish poisoning Temperate coastal areas

Source - Bivalve mollusks

Onset usually is 30-60 min

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 h

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 h 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


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 min but may be as short as 10 min; 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 min

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 h after ingestion but may be delayed as long as 12 h

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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