Food Poisoning Treatment & Management

  • Author: Roberto M Gamarra, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Dec 20, 2011
 

Medical Care

Because most cases of acute gastroenteritis are self-limited, specific treatment is not necessary. Some studies have quantified that only 10% of cases require antibiotic therapy.

  • The main objective is adequate rehydration and electrolyte supplementation. This can be achieved with either an oral rehydration solution (ORS) or intravenous solutions (eg, isotonic sodium chloride solution, lactated Ringer solution). Strict personal hygiene should be practiced during the illness.
    • Oral rehydration is achieved by administering clear liquids and sodium-containing and glucose-containing solutions. A simple ORS may be composed of 1 level teaspoon of salt and 4 heaping teaspoons of sugar added to 1 liter of water.
    • The use of ORS has reduced the mortality rate associated with cholera from higher than 50% to less than 1%.
    • ORS also is indicated in other dehydrating diarrheal diseases.
    • ORS promotes cotransport of glucose, sodium, and water across the gut epithelium, a mechanism unaffected in cholera.
    • The World Health Organization (WHO) recommends a solution containing 3.5 g of sodium chloride, 2.5 g of sodium bicarbonate, 1.5 g of potassium chloride, and 20 g of glucose per liter of water.
  • Intravenous solutions are indicated in patients who are severely dehydrated or who have intractable vomiting.
  • Absorbents (eg, Kaopectate, aluminum hydroxide) help patients have more control over the timing of defecation. However, they do not alter the course of the disease or reduce fluid loss.
    • An interval of at least 1-2 hours should elapse when using other medications with absorbents.
    • Antisecretory agents, such as bismuth subsalicylate (Pepto-Bismol), may be useful. The dose is 30 mL every 30 minutes, not to exceed 8-10 doses.
    • Antiperistaltics (opiate derivatives) should not be used in patients with fever, systemic toxicity, or bloody diarrhea or in patients whose condition either shows no improvement or deteriorates.
    • Diphenoxylate with atropine (Lomotil) is available in tablets (2.5 mg of diphenoxylate) and liquid (2.5 mg of diphenoxylate/5 mL). The initial dose for adults is 2 tablets 4 times a day (ie, 20 mg/d). The dose is tapered as diarrhea improves.
    • Loperamide (Imodium) is available over the counter as 2-mg capsules and as a liquid (1 mg/5 mL). It increases the intestinal absorption of electrolytes and water and decreases intestinal motility and secretion. The dose in adults is 4 mg initially, followed by 2 mg after each diarrhea stool, not to exceed 16 mg in a 24-hour period.
  • If symptoms persist beyond 3-4 days, the specific etiology should be determined by performing stool cultures.
  • If symptoms persist and the pathogen is isolated, specific treatment should be initiated.
  • Empiric treatment should be initiated in patients with suspected traveler's diarrhea or dysenteric or systemic symptoms. Treatment with an agent that covers Shigella and Campylobacter organisms is reasonable in patients with diarrhea (>4 stools/d) for more than 3 days and with fever, abdominal pain, vomiting, headache, or myalgias. A 5-day course of a fluoroquinolone (eg, ciprofloxacin 500 mg PO bid, norfloxacin 400 mg PO bid) is the first-line therapy.
  • TMP/SMX (Bactrim DS 1 tab qd) is an alternative therapy, but resistant organisms are common in the tropics. Infection with either V cholerae or V parahaemolyticus can be treated either with a fluoroquinolone or with doxycycline (100 mg PO bid).
  • In the absence of dysentery, do not administer antibiotics until a microbiologic diagnosis is confirmed and E coli O157:H7 is ruled out.
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Diet

During episodes of acute diarrhea, patients often develop an acquired disaccharidase deficiency due to washout of the brush-border enzymes. For this reason, avoiding milk, dairy products, and other lactose-containing foods is advisable.

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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, and Crohns and Colitis Foundation of America

Disclosure: Nothing to disclose.

Coauthor(s)

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

David Manuel 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

Senthil Nachimuthu 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.

Specialty Editor Board

Jose A Perez Jr, MD, MBA, MSEd  Consulting Staff, 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 College of Physician Executives, American College of Physicians, Society of General Internal Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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.

Alex J Mechaber, MD, FACP  Senior 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

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, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

References
  1. Logan NA. Summer Meeting 2011: Bacillus and relatives in food-borne illness. J Appl Microbiol. Nov 28 2011;[Medline].

  2. 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].

  3. 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.

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

  5. 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].

  6. 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].

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

  8. 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.

  9. 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].

  10. 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].

  11. 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].

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

  13. 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.

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

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

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Table 1. Examples of Large Food-Borne Disease Outbreaks[8]
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
Table 2. Causes of Food Poisoning
Causative AgentsSource and



Clinical Features



PathogenesisDiagnosis and



Treatment



StaphylococciImproperly 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 cereusContaminated 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 perfringensInadequately 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 botulinumCanned 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 monocytogenesRaw 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 organismCSF 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 thrombiDiagnosis with stool culture



Supportive treatment



No antibiotics



Enteroinvasive E coliContaminated imported cheese



Usually watery diarrhea (some may present with dysentery)



Enterotoxin produces secretion



Shiga-like toxin facilitates invasion.



Supportive treatment



No antibiotics



Enteroaggregative E coliImplicated in traveler's diarrhea in developing countries



Can cause bloody diarrhea



Bacteria clump on the cell surfacesCiprofloxacin may shorten duration and eradicate the organism
V choleraContaminated 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 parahaemolyticusRaw 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 vulnificusWound 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 jejuniDomestic 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 invasionCulture in special media at 42°C



Erythromycin for invasive disease (fever)



ShigellaPotato, 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



SalmonellaBeef, 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 productionPositive stool culture



Antibiotic for systemic infection



YersiniaPets; 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



AeromonasUntreated well or spring water



Diarrhea may be bloody.



May be chronic up to 42 days in the United States



Enterotoxin, hemolysin, and cytotoxinPositive stool culture



Fluoroquinolones or TMP/SMX for chronic diarrhea



Parasitic Food PoisoningSource and Clinical FeaturesPathogenesisDiagnosis and Treatment
E histolyticaContaminated food and water



90% asymptomatic



10% dysentery



Minority may develop liver abscesses



Invasion of the mucosa by the parasitesCriterion 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 lambliaContaminated 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 PoisoningSource and



Clinical Features



PathogenesisDiagnosis and



Treatment



Paralytic shellfish poisoningTemperate 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 dinoflagellatesGeneral 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 poisoningCoastal Florida



Source - Mollusks



Illness is milder than in paralytic shellfish poisoning.



Fish acquires toxin-producing dinoflagellatesSymptomatic
CiguateraHawaii, 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 poisoningJapan



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
ScombroidSource - 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 PoisoningSourceSymptomsTreatment
MercuryIngestion of inorganic mercuric saltsCauses metallic taste, salivation, thirst, discoloration and edema of oral mucous membranes, abdominal pain, vomiting, bloody diarrhea, and acute renal failureConsult a toxicologist.



Remove ingested salts by emesis and lavage, and administer activated charcoal and a cathartic.



Dimercaprol is useful in acute ingestion.



LeadToxicity 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).
ArsenicIngestion of pesticide and industrial chemicalsSymptoms 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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