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 8 Cases of Food Poisoning: Find the Pathogen Responsible, 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
Salmonellatyphi infection: Upper abdominal rose spot macules, hepatosplenomegaly
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)
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:
Similar illness, often GI, in a minimum of 2 people
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.
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.
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.
For patient education resources, visit Digestive Disorders Center and Healthy Living Center, as well as Abdominal Pain in Adults, Vomiting and Nausea, Diarrhea, Traveler's Diarrhea, and Foreign Travel.
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.
A detailed history, including the duration of the disease, characteristics and frequency of bowel movements, and associated abdominal and systemic symptoms, may provide a clue to the underlying cause. The presence of a common source, types of specific food, travel history, and use of antibiotics always should be investigated.
The presenting complaints, typical features and pathogenesis of various causative agents, and diagnosis and treatment information can be found in Table 1 in the Causes section.
The following are some of the salient features of food poisoning:
Acute diarrhea in food poisoning usually lasts less than 2 weeks. Diarrhea lasting 2-4 weeks is classified as persistent. Chronic diarrhea is defined by duration of more than 4 weeks.
The presence of fever suggests an invasive disease. However, sometimes fever and diarrhea may result from infection outside the GI tract, as in malaria.
A stool with blood or mucus indicates invasion of the intestinal or colonic mucosa.
When vomiting is the major presenting symptom, suspect Staphylococcus aureus, B cereus, or Norovirus.[1]
Reactive arthritis can be seen with Salmonella, Shigella, Campylobacter, and Yersinia infections.
A profuse rice-water stool suggests cholera or a similar process.
Abdominal pain is most severe in inflammatory processes. Painful abdominal cramps suggest underlying electrolyte loss, as in severe cholera.
A history of bloating should raise the suspicion of giardiasis.
Yersinia enterocolitis may mimic the symptoms of appendicitis.
Proctitis syndrome, seen with shigellosis, is characterized by frequent painful bowel movements containing blood, pus, and mucus. Tenesmus and rectal discomfort are prominent features.
Consumption of undercooked meat/poultry is suspicious for Salmonella, Campylobacter, Shiga toxin E coli, and C perfringens.
Consumption of raw seafood is suspicious for Norwalk-like virus, Vibrio organism, or hepatitis A.
Consumption of homemade canned foods is associated with C botulinum.
Consumption of unpasteurized soft cheeses is associated with Listeria, Salmonella, Campylobacter, Shiga toxin E coli, and Yersinia.
Consumption of deli meats notoriously is responsible for listeriosis.
Consumption of unpasteurized milk or juice is suspicious for Campylobacter, Salmonella, Shiga toxin E coli, and Yersinia.
Salmonella has been associated with consumption of raw eggs.
The physical examination should focus on assessing the severity of dehydration and include the following evaluation:
A dry mouth, decreased axillary sweat, and decreased urine output indicate mild dehydration, whereas orthostasis, tachycardia, and hypotension indicate more severe volume depletion.
A rectal examination always should be performed to directly visualize the stool, to test occult blood, and to palpate the rectal mucosa for any lesions.
Rose spot macules on the upper abdomen and hepatosplenomegaly may be seen in Salmonella typhi infection.
Erythema nodosum and exudative pharyngitis are suggestive of Yersinia infection.
Patients with Vibrio vulnificus or Vibrio alginolyticus may present with cellulitis and otitis media.
The CDC estimates that 97% of all cases of food poisoning result from improper food handling; 79% of cases result from food prepared in commercial or institutional establishments and 21% of cases result from food prepared at home.[7]
The most common causes are as follows: (1) leaving prepared food at temperatures that allow bacterial growth, (2) inadequate cooking or reheating, (3) cross-contamination, and (4) infection in food handlers. Cross-contamination may occur when raw contaminated food comes in contact with other foods, especially cooked foods, through direct contact or indirect contact on food preparation surfaces.
Bacteria are responsible for approximately 75% of the outbreaks of food poisoning and for 80% of the cases with a known cause in the United States.[5] As many as 1 in 10 Americans has diarrhea due to food-borne infection each year.
Obtain the following laboratory studies in cases of suspected food poisoning:
Gram staining and Loeffler methylene blue staining of the stool for WBCs help to differentiate invasive disease from noninvasive disease.
Perform microscopic examination of the stool for ova and parasites.
Bacterial culture for enteric pathogens, such as Salmonella, Shigella, and Campylobacter organisms, becomes mandatory if a stool sample shows positive results for WBCs or blood or if patients have fever or symptoms persisting for longer than 3-4 days.
Perform blood culture if the patient is notably febrile.
CBC with differential, serum electrolyte assessment, and BUN and creatinine levels help to assess the inflammatory response and the degree of dehydration.
Assay for C difficile to help rule out antibiotic-associated diarrhea in patients receiving antibiotics or in those with a history of recent antibiotic use.
Histamine food poisoning from gram-negative bacteria in fin-fish products is also common, and Morganella morganii and M psychrotolerans are particularly strong histamine producers. The development of real-time quantitative polymerase chain reaction (RTiqPCR) techniques in conjunction with the use of selective primers and a quantitative enrichment step appear to have the potential to identify and quantify these two species in fish products.[15]
Flat and upright abdominal radiographs should be obtained if the patient experiences bloating, severe pain, or obstructive symptoms or if perforation is suggested.
When a stool examination is nondiagnostic, performing sigmoidoscopy/colonoscopy with biopsy and esophagogastroduodenoscopy (EGD) with duodenal aspirate and biopsy may be beneficial. This is especially important in patients who are immunocompromised.
Consider sigmoidoscopy in patients with bloody diarrhea. It can be useful in diagnosing inflammatory bowel disease, antibiotic-associated diarrhea, shigellosis, and amebic dysentery.
Because most cases of acute gastroenteritis are self-limited, specific treatment is not necessary. Strict personal hygiene should be practiced during the illness. 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). Note the following:
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. Note the following:
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.
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.
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).
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.
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.
Clinical Context:
Both fluids are essentially isotonic and have equivalent volume-restorative properties. While some differences exist between metabolic changes observed with the administration of large quantities of either fluid, for practical purposes and in most situations, differences are clinically irrelevant. No demonstrable difference exists in hemodynamic effect, morbidity, or mortality between resuscitation using either NS or LR.
Clinical Context:
Acts by glucose-facilitated absorption of sodium and water, which is unaffected in diseases such as cholera. Oral rehydration is achieved using clear liquids and sodium-containing and glucose-containing solutions. WHO recommends a solution containing 3.5 g of sodium chloride, 2.5 g sodium bicarbonate, 1.5 g potassium chloride, and 20 g glucose per liter of water.
A simple solution may be made using 1 level tsp salt and 4 heaping tsp sugar added to 1 L water.
The main objective is adequate rehydration and electrolyte supplementation. This can be achieved with ORS or intravenous solutions (eg, isotonic sodium chloride solution, lactated Ringer solution).
Clinical Context:
Drug combination that consists of diphenoxylate, which is a constipating meperidine congener, and atropine to discourage abuse. Inhibits excessive GI propulsion and motility.
Available in tabs (2.5 mg diphenoxylate) and liquid (2.5 mg diphenoxylate/5 mL).
Clinical Context:
Acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. Prolongs movement of electrolytes and fluid through bowel and increases viscosity and loss of fluids and electrolytes.
Available over the counter in 2-mg capsules and liquid (1 mg/5 mL).
Adsorbents (eg, attapulgite, aluminum hydroxide) help patients have more control over the timing of defecation but do not alter the course of the disease or reduce fluid loss. Antisecretory agents (eg, bismuth subsalicylate) may be useful. Antiperistaltics (opiate derivatives) should not be used in patients with fever, systemic toxicity, bloody diarrhea, or in patients whose condition either shows no improvement or deteriorates.
Clinical Context:
First-line therapy. Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis, and, consequently, growth.
Clinical Context:
Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis, and, consequently, growth.
Clinical Context:
Alternative therapy, but resistant organisms are common in the tropics. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
Clinical Context:
For V cholerae or V parahaemolyticus infections. Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
Clinical Context:
Nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the GI tract (ie, gram-positive, gram-negative, aerobic, anaerobic). Rifampin structural analog. Binds to beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. Indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Antibiotic selection should be guided by blood culture sensitivity.
How is food poisoning defined?What are the signs and symptoms of food poisoning?Which physical findings are characteristic of food poisoning?What is the role of lab testing in the evaluation of food poisoning?What is the role of imaging studies in the workup of food poisoning?Which procedures are performed in the workup of food poisoning?How is food poisoning treated?What is included in supportive care for patients affected by food poisoning?Which medications are used to treat food poisoning?How is food poisoning prevented?What is food poisoning?How is a food-borne disease outbreak defined?What is the pathophysiology of food poisoning?What is the prevalence of food poisoning in the US?What is the global prevalence of food poisoning?What are the signs and symptoms of food poisoning?How does the prevalence of food poisoning vary by age?Where are patient education resources regarding food poisoning found?What are the possible complications of food poisoning?Which clinical history findings are characteristic of food poisoning?What is included in the physical exam for evaluation of suspected food poisoning?What causes food poisoning?What is the role of lab testing in the workup of food poisoning?What is the role of imaging studies in the workup of food poisoning?Which procedures may be beneficial in the workup of food poisoning?How is food poisoning treated?What is the role of absorbents in the treatment of food poisoning?When is empiric treatment for food poisoning indicated?Which dietary modifications are used in the treatment of food poisoning?How is food poisoning prevented?How are patients with food poisoning monitored?What are the goals of drug treatment for food poisoning?Which medications in the drug class Antibiotics are used in the treatment of Food Poisoning?Which medications in the drug class Antidiarrheals are used in the treatment of Food Poisoning?Which medications in the drug class Rehydration solutions are used in the treatment of Food Poisoning?
Roberto M Gamarra, MD, Consulting Gastroenterologist, Digestive Health Associates, PLC
Disclosure: Nothing to disclose.
Coauthor(s)
David Manuel, MD, Affiliate Faculty, Department of Medicine, Loyola University Health System; Gastroenterologist, Digestive Health Center
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
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.
Senthil Nachimuthu, MD, FACP,
Disclosure: Nothing to disclose.
Specialty Editors
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
Disclosure: Nothing to disclose.
Chief Editor
Praveen K Roy, MD, AGAF, Clinical Assistant Professor of Medicine, University of New Mexico School of Medicine
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
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
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.
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; Accessed: April 6, 2012.
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.
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)
