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Food Poisoning

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

Practice Essentials

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 most common pathogens are Norovirus, Escherichia coli, Salmonella, Clostridium perfringens, Campylobacter, and Staphylococcus aureus.

Signs and symptoms

The symptoms of food poisoning vary in degree and combination. They may include the following:

  • Abdominal pain: Most severe in inflammatory processes; painful abdominal muscle cramps suggest underlying electrolyte loss
  • Vomiting: Major presenting symptom of S aureus, B cereus, or Norovirus [1]
  • Diarrhea: Usually lasts less than 2 weeks
  • Headache
  • Fever: May be an invasive disease or an infection outside the GI tract
  • Stool changes: Bloody or mucousy if invasion of intestinal or colonic mucosa; profuse rice-watery if cholera or a similar process
  • Reactive arthritis: Seen with Salmonella, Shigella, Campylobacter, and Yersinia infections
  • Bloating: May be due to giardiasis

More serious cases of food poisoning can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.

See Clinical Presentation for more detail.

See 5 Cases of Food Poisoning: Can You Identify the Pathogen?, a Critical Images slideshow, to help identify various pathogens and symptoms related to foodborne disease.

Diagnosis

Examination of patients suspected of having food poisoning should focus on assessing the severity of dehydration. General findings may include the following:

  • Mild dehydration: A dry mouth, decreased axillary sweat, decreased urine
  • More severe volume depletion: Orthostasis, tachycardia, hypotension
  • Salmonella typhi infection: Upper abdominal rose spot macules, hepatosplenomegaly
  • Yersinia infection: Erythema nodosum, exudative pharyngitis
  • Vibrio vulnificus or V alginolyticus infection: cellulitis, otitis media

Always perform a rectal examination to (1) directly visualize the stool, (2) test occult blood, and (3) palpate the rectal mucosa for any lesions.

Testing

The following routine laboratory tests may help to assess the patient’s inflammatory response and the degree of dehydration:

  • CBC with differential
  • Serum electrolyte assessment
  • BUN and creatinine levels

Other laboratory studies can be helpful in cases of food poisoning and include the following:

  • Stool Gram staining and Loeffler methylene blue staining for WBCs: To help differentiate invasive disease from noninvasive disease
  • Microscopic examination of the stool: To detect any ova and parasites
  • Bacterial culture for enteric pathogens (eg, Salmonella, Shigella, Campylobacter organisms): Mandatory when a stool sample shows positive results for WBCs or blood or if patients have fever or symptoms persisting for longer than 3-4 days
  • Blood culture in febrile patients
  • C difficile assay: To help rule out antibiotic-associated diarrhea in patients receiving antibiotics or in those with a history of recent antibiotic use

Imaging studies

Obtain flat and upright abdominal radiographs if the patient experiences bloating, severe pain, or obstructive symptoms or if the clinical picture suggests perforation.

Procedures

Consider performing the following procedures when a stool examination is nondiagnostic, especially in immunocompromised patients:

  • Sigmoidoscopy/colonoscopy with biopsy
  • EGD with duodenal aspirate and biopsy

In patients with bloody diarrhea, sigmoidoscopy can be useful in diagnosing inflammatory bowel disease, antibiotic-associated diarrhea, shigellosis, and amebic dysentery.

See Workup for more detail.

Management

Most food-borne illnesses are mild and improve without any specific treatment. Some patients have severe disease and require hospitalization, aggressive hydration, and antibiotic treatment.[2]

Supportive care

The main objective in managing patients with food poisoning is adequate rehydration and electrolyte supplementation, which can be achieved with either an oral rehydration solution or intravenous solutions in severely dehydrated individuals or those with intractable vomiting (eg, isotonic sodium chloride solution, lactated Ringer solution).

Patients should avoid milk, dairy products, and other lactose-containing foods during episodes of acute diarrhea, as these individuals often develop an acquired disaccharidase deficiency due to washout of the brush-border enzymes.

Pharmacotherapy

Medications that may be needed to treat patients with food poisoning include the following:

  • Antidiarrheals: Absorbents (eg, attapulgite, aluminum hydroxide); antisecretory agents (eg, bismuth subsalicylate); antiperistaltics (eg, opiate derivatives such as diphenoxylate with atropine, loperamide)
  • Antibiotics (eg, ciprofloxacin, norfloxacin, TMX/SMP, doxycycline, rifaximin): Selection of antibiotic depends on clinical setting and guided by microbiology and blood culture sensitivity results

Prevention

The best ways to prevent food poisoning caused by infectious agents are as follows:

  • Practice strict personal hygiene
  • Cook all foods adequately
  • Avoid cross-contamination of raw and cooked foods
  • Keep all foods at appropriate temperatures (ie, refrigerated items: < 40°F; hot items: >140°F)

See Treatment and Medication for more detail.

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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.[2]

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

  1. Similar illness, often GI, in a minimum of 2 people
  2. Evidence of food as the source
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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,[3] Staphylococcus organisms , Giardia lamblia, Cryptosporidium,rotavirus, norovirus (genus Norovirus, previously called Norwalk virus), and adenovirus.

Inflammatory diarrhea is caused by the action of cytotoxins 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 GI 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.

A major contributor to seafood contamination with foodborne pathogens appears to be naturally occurring biofilm formation.[4] Vibro and Salmonella species, Aeromonas hydrophila, and Listeria monocytogenes are common seafood bacterial pathogens that form biofilms.

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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.[5, 6] 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. The US Centers for Disease Control and Prevention (CDC) estimates 1 in 6 Americans (48 million people) are affected by foodborne illness annually. The estimates suggest 128,000 people are hospitalized and 3,000 die.[7] The 31 known pathogens account for an estimated 9.4 million annual cases, 55,961 hospitalizations, and 1,351 deaths. Unspecified agents account for 38.4 million cases, 71,878 hospitalizations, and 1,686 deaths.[8]

Overall, food-borne diseases appear to cause more illnesses but fewer deaths than previously estimated.[9]

In a 2013 report, CDC investigators used data spanning the decade between 1998 and 2008 to report estimates for annual US food-borne illnesses, hospitalizations, and deaths attributable to each of 17 food categories.[10, 11] The following were among their findings[10, 11] :

  • Leafy green vegetables were the most common cause of food poisoning (22%), primarily due to Norovirus species, followed by E coli O157.
  • Poultry was the most common cause of death from food poisoning (19%), with Listeria and Salmonella species being the main infectious organisms.
  • Dairy items were the second most frequent causes of foodborne illnesses (14%) and deaths (10%), with the main factors being contamination by Norovirus from food handlers and improper pasteurization resulting in contamination with Campylobacter species.

In March 2012, the CDC reported a rise in foodborne disease outbreaks caused by imported food in 2009 and 2011. Nearly 50% of the outbreaks implicated food that was imported from regions not previously associated with outbreaks. Outbreaks reported to CDC’s Foodborne Disease Outbreak Surveillance System from 2005-2010 implicated 39 outbreaks and 2,348 illnesses that were linked to imported food from 15 countries. Within this 5-year period, nearly half (17) occurred in 2009 and 2010. Fish (17 outbreaks) was the most common source of implicated imported foodborne disease outbreaks, followed by spices (6 outbreaks including 5 from fresh or dried peppers). Approximately 45% of the imported foods causing outbreaks came from Asia.[12]

The CDC recognized the following outbreaks and sources in 2012[7] :

  • E coli – Spinach and spring mix, raw clover sprouts at a national chain of restaurants
  • Salmonella – Peanut butter, ricotta salata cheese, mangoes, cantaloupe, ground beef, live poultry, dry dog food, raw scraped ground tuna product, small turtles, raw clover sprouts

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.[13] 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.

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Mortality/Morbidity

Symptoms vary in degree and combination. These 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.

Age-related morbidity/mortality

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.

The CDC found that 5 bacterial enteric pathogens (Campylobacter, E coli 0157 , Salmonella, Shigella, and Y enterocolitica) caused 291,162 illnesses annually in children younger than 5 years.[14] This resulted in 102,746 doctor visits, 7,830 hospitalizations, and 64 deaths. Rates of illness remain higher in children.

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Complications

Complications are very rare in healthy hosts, except in cases of botulism or mushroom poisoning. Infants, elderly people, and immunocompromised hosts are more susceptible to complications. Other complications include the following:

  • Guillain-Barré syndrome ( Campylobacter infection)
  • Reactive arthritis
  • Hemolytic uremic syndrome ( E coli O157:H7)

Irritable bowel symptoms may follow acute gastroenteritis.

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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
  1. Xerry J, Gallimore CI, Iturriza-Gomara 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. 2009 Jul. 81(7):1298-304. [Medline].

  2. Logan NA. Bacillus and relatives in foodborne illness. J Appl Microbiol. 2012 Mar. 112(3):417-29. [Medline].

  3. Lee JH, Shin H, Son B, Ryu S. Complete genome sequence of Bacillus cereus bacteriophage BCP78. J Virol. 2012 Jan. 86(1):637-8. [Medline]. [Full Text].

  4. Mizan MF, Jahid IK, Ha SD. Microbial biofilms in seafood: A food-hygiene challenge. Food Microbiol. 2015 Aug. 49:41-55. [Medline].

  5. Hughes JM, Angulo FJ. Food borne diseases. Hurst JW, ed. Medicine for the Practicing Physician. 4th ed. Stamford, Conn: Appleton & Lange; 1996. 344-7.

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

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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.

  21. Goulet V, Hebert M, Hedberg C, et al. Incidence of listeriosis and related mortality among groups at risk of acquiring listeriosis. Clin Infect Dis. 2012 Mar 1. 54(5):652-60. [Medline].

  22. Malek M, Barzilay E, Kramer A, et al. Outbreak of norovirus infection among river rafters associated with packaged delicatessen meat, Grand Canyon, 2005. Clin Infect Dis. 2009 Jan 1. 48(1):31-7. [Medline].

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

  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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