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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.

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Patient Education

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Deterrence/Prevention

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.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Acknowledgements

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.

References
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  8. Scallan E, Griffin PM, Angulo FJ, Tauxe RV, Hoekstra RM. Foodborne illness acquired in the United States--unspecified agents. Emerg Infect Dis. 2011 Jan. 17(1):16-22. [Medline]. [Full Text].

  9. Preliminary FoodNet Data on the incidence of infection with pathogens transmitted commonly through food--10 States, 2008. MMWR Morb Mortal Wkly Rep. 2009 Apr 10. 58(13):333-7. [Medline].

  10. Doheny K. Most common foods for foodborne illness: CDC report. Medscape Medical News. Available at http://www.medscape.com/viewarticle/778455. January 30, 2013; Accessed: February 6, 2013.

  11. Painter JA, Hoekstra RM, Ayers, et al. Attribution of foodborne illnesses, hospitalizations, and deaths to food commodities by using outbreak data, United States, 1998-2008. Emerg Infect Dis. 2013 March;19:3. [Full Text].

  12. CDC research shows outbreaks linked to imported foods increasing. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/media/releases/2012/p0314_foodborne.html. March 14, 2012;

  13. Jacobs RA. General problems in infectious diseases: acute infectious diarrhea. Tierney LM Jr, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment 2001. 40th ed. New York, NY: McGraw-Hill; 2000. 1215-6.

  14. Scallan E, Mahon BE, Hoekstra RM, Griffin PM. Estimates of Illnesses, Hospitalizations, and Deaths Caused By Major Bacterial Enteric Pathogens in Young Children in the United States. Pediatr Infect Dis J. 2012 Dec 17. [Medline].

  15. Podeur G, Dalgaard P, Leroi F, et al. Development of a real-time PCR method coupled with a selective pre-enrichment step for quantification of Morganella morganii and Morganella psychrotolerans in fish products. Int J Food Microbiol. 2015 Jun 16. 203:55-62. [Medline].

  16. Atmar RL, Bernstein DI, Harro CD, et al. Norovirus vaccine against experimental human Norwalk Virus illness. N Engl J Med. 2011 Dec 8. 365(23):2178-87. [Medline].

  17. Shaw A, Shama G, Iza F. Emerging applications of low temperature gas plasmas in the food industry. Biointerphases. 2015 Jun 16. 10(2):029402. [Medline].

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

  19. Butterton JR, Calderwood SB. Acute infectious diarrheal diseases and bacterial food poisoning. 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.

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

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

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



Clinical Features



Pathogenesis Diagnosis and



Treatment



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



Unknown



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



Metronidazole



Seafood/Shellfish Poisoning Source and



Clinical Features



Pathogenesis Diagnosis and



Treatment



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



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 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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