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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, Salmonella, Clostridium perfringens, Campylobacter, and Staphylococcus aureus.

Essential update: CDC reports most common sources of food-borne illnesses


Using data spanning the decade between 1998 and 2008, CDC investigators reported estimates for annual US food-borne illnesses, hospitalizations, and deaths attributable to each of 17 food categories.[1, 2] Among their findings: (1) leafy green vegetables were the most common cause of food poisoning (22%), primarily due to Norovirus species, followed by E coli O157; (2) poultry was the most common cause of death from food poisoning (19%), with Listeria andSalmonella species being the main infectious organisms; and (3) 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.[1, 2]

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[3] 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, andYersinia 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.

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 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 patients 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 notably 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. [4] 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: < 40F; hot items: >140F) See Treatment and Medication for more detail.

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. [4] 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

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,[5] Staphylococcus organisms , Giardia lamblia, Cryptosporidium,rotavirus, norovirus (genus Norovirus, previously calledNorwalk virus), and adenovirus. Inflammatory diarrhea is caused by the action of cytotoxin 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 botulismresults from the inhibition of acetylcholine release in nerve endings by the botulinum. The pathophysiological mechanisms that result in acute GIsymptoms 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.

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.[6, 7] However, the change in food supply, the identification of new foodborne 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.[8] 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.[9] Overall, food-borne diseases appear to cause more illnesses but fewer deaths than previously estimated.[10] The most common pathogens are as follows:[8] Norovirus 5,461,731 cases

Salmonella 1,027,561 C perfringens 965,958 Campylobacter species 845,024 Staphylococcus aureus 241,148 The most common pathogens responsible for hospitalizations are as follows:[8] Salmonella 19,336 hospitalizations Norovirus 14,663 hospitalizations Campylobacter species 8,463 hospitalizations Toxoplasma gondii 4,428 hospitalizations E coli 2,138 hospitalizations The pathogens most commonly associated with death are as follows: Salmonella 378 deaths T gondii 327 deaths Listeria monocytogenes 255 deaths Norovirus 149 deaths Campylobacter species 76 deaths 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 t o CDCs 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) were the most common source of implicated imported foodborne disease outbreaks, followed by spices (6 outbreaks including 5 from fresh or dried peppers). Approximately 45% percent of the imported foods causing outbreaks came from Asia. [11] The CDC recognized the following outbreaks and sources in 2012:[8]

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.[12] A travel history should be obtained because traveler's diarrhea is the leading cause of travelrelated 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.

Mortality/Morbidity
Symptoms vary in degree and combination. They 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
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 coliO157; 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.[13] This resulted in 102,746 doctor visits, 7,830 hospitalizations, and 64 deaths. Rates of illness remain higher in children. Proceed to Clinical Presentation

History

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.[3] Reactive arthritis can be seen with Salmonella, Shigella, Campylobacter, andYersinia infections. A profuse rice-water stool suggests cholera or a similar process. Abdominal pain is most severe in inflammatory processes. Painful abdominal muscle 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 movement 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, Vibrioorganism, 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.

Physical
The physical examination should focus on assessing the severity of dehydration. 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 Yersiniainfection. Patients with Vibrio vulnificus or Vibrio alginolyticus may present with cellulitis and otitis media.

Causes
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.[8] 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.[6] As many as 1 in 10 Americans has diarrhea due to food-borne infection each year. Table 1.Causes of Food Poisoning. (Open Table in a new window)
Causative Agents Source and Pathogenesis Diagnosis and

Clinical Features

Treatment

Staphylococci

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

Enterotoxin acts on receptors in gut that transmit impulses to medullary centers

Symptomatic treatment

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

B cereus

Contaminated fried rice (emetic)

Emetic enterotoxin (short incubation and duration) - Poorly understood

Symptomatic treatment

Meatballs (diarrheal) Diarrheal enterotoxin (long incubation and duration) - Increasing intestinal secretion by activation of adenylate cyclase in intestinal epithelium

Emetic: Duration is 9 h, vomiting and cramps

Diarrheal: Lasts for 24 h

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

C perfringens

Inadequately cooked meat, poultry, or legumes

Enterotoxin produced in the gut, and food causes hypersecretion in the small intestine

Culture of clostridia in food and stool

Acute onset of abdominal cramps with diarrhea starts 8-24 hafter ingestion.

Symptomatic treatment

Vomiting is rare. It lasts less than 1 d.

Enteritis necroticans associated withC perfringens type C in improperly cooked pork (40% mortality)

C botulinum

Canned foods (eg, smoked fish, mushrooms, vegetables, honey)

Toxin absorbed from the gut blocks the release of acetylcholine in the neuromuscular junction

Toxin present in food, serum, and stool.

Descending weakness and paralysis start 1-4 dafter ingestion, followed by constipation.

Respiratory support

Mortality is high

Intravenous trivalent antitoxin from CDC

Listeria monocytogenes

Raw and pasteurized milk, soft cheeses, raw vegetables, shrimp

Highly motile, heat-resistant, grampositive organism

CSF or blood culture

Systemic disease associated with bacteremia

Must treat with antibiotics if bacteremic

Intestinal symptoms precede systemic disease

Can seed meninges, heart valves, and other organs

Highest mortality among bacterial food poisonings

Enterotoxic E coli(eg, traveler's diarrhea)

Contaminated water and food (eg, salad, cheese, meat)

Enterotoxin causes hypersecretion in small and large intestine via guanylate cyclase activation

Supportive treatment

No antibiotics Acute-onset watery diarrhea starts 24-48 hafter ingestion

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

EnterohemorrhagicE coli (eg, E coliO157:H7)

Improperly cooked hamburger meat and previously spinach

Cytotoxin results in endothelial damage and leads to platelet aggregation and microvascular fibrin thrombi

Diagnosis with stool culture

Supportive treatment Most common isolate pathogen in bloody diarrhea starts 3-4 dafter ingestion No antibiotics Usually progresses from watery to bloody diarrhea. It lasts for 3-8 d

May be complicated by hemolytic-uremic syndromeor thrombotic thrombocytopenic purpura

Enteroinvasive E coli

Contaminated imported cheese

Enterotoxin produces secretion

Supportive treatment

Usually watery diarrhea (some may present with dysentery)

Shigalike toxin facilitates invasion

No antibiotics

EnteroaggregativeE coli

Implicated in traveler's diarrhea in developing countries

Bacteria clump on the cell surfaces

Ciprofloxacin may shorten duration and eradicate the organism

Can cause bloody diarrhea

V cholera

Contaminated water and food

Enterotoxin causes hypersecretion in small intestine

Positive stool culture finding

Large amount of nonbloody diarrhea starts 8-24 hafter ingestion. It lasts for 3-5 d

Infective dose usually is 107 109 organisms

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)

Enterotoxin causes hypersecretion in small intestine

Positive stool culture

Explosive watery diarrhea starts 8-24 hafter ingestion

Hemolytic toxin is lethal

Prompt replacement of fluids and electrolytes

It lasts for 3-5 d

Infective dose is usually 107 109 organisms

Sensitive to tetracycline, but unclear role for antibiotics

V vulnificus

Wound infection in salt water or consumption of raw oysters

Polysaccharide capsule

Culture of characteristic bullous lesions or blood

Can be lethal in patients with liver disease (50% mortality)

Growth correlates with availability of iron (especially transferrin saturation >70%)

Immediate antibiotics if suspected (eg, doxycycline and ceftriaxone)

C jejuni

Domestic animals, cattle, chickens

Uncertain about endotoxin production and invasion

Culture in special media at 42C

Fecal-oral transmission in humans

Erythromycin for invasive disease (fever)

Foul-smelling watery diarrhea followed by bloody diarrhea

Abdominal pain and fever also may be present;it starts 1-3 dafter exposure and recovery is in 5-8 d

Shigella

Potato, egg salad, lettuce, vegetables, milk, ice cream, and water

Organisms invade epithelial cells and produce toxins

Polymorphonuclear leukocytes (PMNs), blood, and mucus in stool

Abrupt onset of bloody diarrhea, cramps, tenesmus, and fever starts 12-30 hafter ingestion.

Infective dose is 102 -103organisms

Positive stool culture

Enterotoxin-mediated diarrhea followed by invasion (dysentery/colitis) Usually self-limited in 3-7 d

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

Invasion but no toxin production

Positive stool culture finding

Antibiotic for systemic infection

Abdominal pain and vomiting also present, beginning 6-48 hafter exposure and lasts 7-12 d

Yersinia

Pets; transmission in humans by fecal-oral route or contaminated milk or ice cream

Gastroenteritis and mesenteric adenitis

Polymorphonuclear leukocytesand blood in stool

Direct invasion and enterotoxin Acute abdominal pain, diarrhea, and fever (enterocolitis) Positive stool culture finding

Incubation period not known Polyarthritis and erythema nodosum in children

No evidence that antibiotics alter the course but may be used in severe infections

May mimic appendicitis

Aeromonas

Untreated well or spring water

Enterotoxin, hemolysin, and cytotoxin

Positive stool culture

Diarrhea may be bloody

Fluoroquinolones or TMP/SMX for chronic diarrhea

May be chronic up to 42 din the United States

Parasitic Food Poisoning E histolytica

Source and Clinical Features

Pathogenesis

Diagnosis and Treatment

Contaminated food and water

Invasion of the mucosa by the parasites

Criterion standard iscolonoscopy with biopsy

90% asymptomatic Ova and parasites may be seen in the stool but has low sensitivity 10% dysentery Luminal amebicides (eg, paromomycin) Tissue amebicides (eg, metronidazole)

Minority may develop liver abscesses

G lamblia

Contaminated ground water

Unknown

Initial diagnostic test is stool enzymelinked immunosorbent assay

Fecal-oral transmission in humans

Highest concentration in the distal duodenum and proximal jejunum

Duodenal aspiration or small bowel biopsy

Mild bloody diarrhea with nausea and abdominal cramps starts 2-3 dafter ingestion;

lasts for 1 wk

Cyst in the stool

May become chronic

Metronidazole

Seafood/Shellfish Poisoning

Source and

Pathogenesis

Diagnosis and

Clinical Features

Treatment

Paralytic shellfish poisoning

Temperate costal areas

Fish acquires toxin-producing dinoflagellates

General observation for 4-6 h

Source - Bivalve mollusks

Maintain patent airway.

Onset usually is 30-60 min

Administer oxygen, and assist ventilation if necessary

Initial symptoms include perioral and intraoral paresthesia

For recent ingestion, charcoal 50-60 g may be helpful

Other symptoms include paresthesia of the extremities, headache, ataxia, vertigo, cranial nerve palsies, and paralysis of respiratory muscles, resulting in respiratory arrest

Neurotoxic shellfish poisoning

Coastal Florida

Fish acquires toxin-producing dinoflagellates

Symptomatic

Source - Mollusks

Illness is milder than in paralytic shellfish poisoning

Ciguatera

Hawaii, Florida, and Caribbean

Fish acquires toxin-producing dinoflagellates

Symptomatic

Source - Carnivorous reef fish Toxin increases intestinal secretion by changing intracellular calcium concentration Vomiting, diarrhea, and cramps start 1-6 hafter ingestion and last from days to months

Anecdotal reports of successful treatment of neurologic symptoms with mannitol 1 g/kg IV

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

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Tetrodotoxin poisoning

Japan

Neurotoxin is concentrated in the skin and viscera of puffer fish.

Symptomatic

Source - Puffer fish

Onset of symptoms usually is 30-40 minbut 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.

Scombroid

Source - Tuna, mahi-mahi, kingfish

Improper preservation of large fish results in bacterial degradation of histidine to histamine

Antihistamines (diphenhydramine 2550 mg IV)

Allergic symptoms such as skin flush, urticaria, bronchospasm, and hypotension usually start within 15-90 min

H2 blockers (cimetidine 300 mg IV)

Severe reactions may require subcutaneous epinephrine (0.3-0.5 mL of 1:1000 solution)

Heavy Metal Poisoning Mercury

Source Ingestion of inorganic mercuric salts

Symptoms Causes metallic taste, salivation, thirst, discoloration and edema of oral mucous membranes, abdominal pain, vomiting, bloody diarrhea, and acute renal failure

Treatment 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

Common symptoms include colicky abdominal pain, constipation, headache, and irritability

Other than activated charcoal and cathartic, severe toxicity should be treated with antidotes (edetate calcium disodium [EDTA] and dimercaprol).

It is rare after single ingestion Diagnosis is based on lead level (>10 mcg/dL)

Arsenic

Ingestion of pesticide and industrial chemicals

Symptoms usually appear within 1 hafter ingestion but may be delayed as long as 12 h

Gastric lavage and activated charcoal

Abdominal pain, watery diarrhea, vomiting, skeletal muscle cramps, profound dehydration, and shock may occur

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)

Proceed to Workup

Laboratory Studies

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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, andCampylobacter 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.

Imaging Studies
Flat and upright abdominal radiographs should be obtained if the patient experiences bloating, severe pain, or obstructive symptoms or if perforation is suggested.

Other Tests
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. Proceed to Treatment & Management

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 glucosecontaining 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.

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Empiric treatment should be initiated in patients with suspected traveler's diarrhea or dysenteric or systemic symptoms. Treatment with an agent that covers Shigellaand 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.

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. Proceed to Medication

Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Rehydration solutions
Class Summary
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).

Lactated Ringer solution with NS


Both fluids are essentially isotonic and have equivalent volume-restorative properties. While some differences exist between metabolic changes observed with 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.

Oral electrolyte mixtures (Rehydralyte, Pedialyte)


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 glucosecontaining 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.

Antidiarrheals
Class Summary
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.
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Attapulgite (Kaopectate, Diasorb)


Adsorbent and protectant that controls diarrhea.
View full drug information

Aluminum hydroxide (Amphojel, Dialume, ALternaGEL)


Commonly used as an antacid. Adsorbent and protectant that controls diarrhea.

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View full drug information

Bismuth subsalicylate (Pepto-Bismol)


Antisecretory agent that also may have antimicrobial and anti-inflammatory effects.
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Diphenoxylate and atropine (Lomotil, Lonox)


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).
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Loperamide (Imodium)
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).

Antibiotics
Class Summary
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.
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Ciprofloxacin (Cipro)
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.
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Norfloxacin (Noroxin)
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.
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Trimethoprim/sulfamethoxazole (Bactrim DS, Septra DS)


Alternative therapy, but resistant organisms are common in the tropics. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
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Doxycycline (Doryx, Vibramycin, Vibra-Tabs)


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.
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Rifaximin (Xifaxan, RedActiv, Flonorm)


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. Proceed to Follow-up

Further Outpatient Care


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

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

Deterrence/Prevention
No vaccine available canprevent 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.[14] 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, < 40F for refrigerated items and >140F for hot items). Avoiding eating wild mushrooms prevents mushroom poisoning. Prevention of fish poisoning requires avoidance of large tropical fish (ciguatera poisoning) and compliance with seasonal or emergency quarantines of shellfish harvesting areas (shellfish poisoning). Raw or undercooked milk, poultry, eggs, meat, and seafood are best avoided. Local health authorities should be notified if an outbreak of food poisoning occurs. This leads to appropriate actions to prevent further spread of food poisoning. Irradiation of food (ie, the use of ionizing radiation or ionizing energy to treat foods, either packaged or in bulk form) can eliminate food-borne pathogens. Annually, more than half a million tons of food is now irradiated worldwide. Treating raw meat and poultry with irradiation at the slaughter plant could eliminate bacteria, such asE coli O157:H7 and Salmonella and Campylobacter organisms. No evidence of adverse health effects is found in the well-controlled clinical trials involving irradiated food. 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.

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-Barr syndrome (Campylobacter infection) Reactive arthritis Hemolytic uremic syndrome (E coli O157:H7) Irritable bowel symptoms may follow acute gastroenteritis.

Patient Education
For excellent patient education resources, visit eMedicineHealth's Digestive Disorders Center and Healthy Living Center. Also, see eMedicineHealth's patient education articles Food Poisoning, Abdominal Pain in Adults, Vomiting and Nausea, Diarrhea, Traveler's Diarrhea, and Foreign Travel.

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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, 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 of Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America 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, 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 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 College of Physician Executives, American College of Physicians, Society of General Internal Medicine, andSociety 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.

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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
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8. Scallan E, Hoekstra RM, Angulo FJ, et al. Foodborne illness acquired in the United States-major pathogens. Emerg Infect Dis. Jan 2011;17(1):7-15. [Medline]. [Full Text]. 9. Scallan E, Griffin PM, Angulo FJ, Tauxe RV, Hoekstra RM. Foodborne illness acquired in the United States--unspecified agents. Emerg Infect Dis. Jan 2011;17(1):16-22. [Medline]. [Full Text]. 10. 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]. 11. CDC research shows outbreaks linked to imported foods increasing. Available athttp://www.cdc.gov/media/releases/2012/p0314_foodborne.html. Accessed March 14, 2012. 12. 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.

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13. 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. Dec 17 2012;[Medline]. 14. Atmar RL, Bernstein DI, Harro CD, et al. Norovirus vaccine against experimental human Norwalk Virus illness. N Engl J Med. Dec 8 2011;365(23):2178-87. [Medline]. 15. Archer DL. Incidence and cost of foodborne diarrheal disease in the United States. J Food Prot. 1985;48:887-94. 16. 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. 17. Gianella RA. Infectious enteritis and proctocolitis and bacterial food poisoning. In: Sleisenger and Fordtran's Gastrointestinal and Liver Disease. Vol 2. 2006:2333-91. 18. Goulet V, Hebert M, Hedberg C, et al. Incidence of listeriosis and related mortality among groups at risk of acquiring listeriosis. Clin Infect Dis. Mar 1 2012;54(5):652-60. [Medline]. 19. 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. Jan 1 2009;48(1):31-7. [Medline]. 20. Sherman PM, Wine E. Emerging intestinal infections. Gastroenterology & Hepatology Annual Review. 2006;1:50-54. [Full Text]. 21. Surveillance for foodborne disease outbreaks - United States, 2006. MMWR Morb Mortal Wkly Rep. Jun 12 2009;58(22):609-15. [Medline].

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