Intoks Food

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Practice Essentials

Food poisoning is defined as an illness caused by the consumption of food or water contaminatedwith bacteria and/or their toxins, or with parasites, viruses, or chemicals. The most commonpathogens are Norovirus, Salmonella, Clostridium perfringens, Campylobacter, and Staphylococcusaureus.

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

Using data spanning the decade between 1998 and 2008, CDC investigators reported estimates forannual US food-borne illnesses, hospitalizations, and deaths attributable to each of 17 foodcategories.[1, 2]Among their findings: (1) leafy green vegetables were the most common cause of foodpoisoning (22%), primarily due to Norovirus species, followed by E coliO157; (2) poultry was the mostcommon 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 foodborneillnesses (14%) and deaths (10%), with the main factors being contamination by Norovirus from foodhandlers and improper pasteurization resulting in contamination with Campylobacterspecies.[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 suggestunderlying electrolyte loss

Vomiting: Major presenting symptom ofS aureus, B cereus, orNorovirus[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 ifcholera or a similar process

Reactive arthritis: Seen with Salmonella, Shigella, Campylobacter, andYersinia infections

Bloating: May be due to giardiasisMore serious cases of food poisoning can result in life-threatening neurologic, hepatic, and renal

syndromes leading to permanent disability or death.

SeeClinical Presentationfor more detail.

Diagnosis

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

Mild dehydration: A dry mouth, decreased axillary sweat, decreased urine

More severe volume depletion: Orthostasis, tachycardia, hypotension

Salmonellatyphiinfection: Upper abdominal rose spot macules, hepatosplenomegaly

Yersinia infection: Erythema nodosum, exudative pharyngitis

Vibrio vulnificus orV 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 thedegree of dehydration:

CBC with differential

Serum electrolyte assessment

BUN and creatinine levelsOther 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 invasivedisease from noninvasive disease

Microscopic examination of the stool: To detect any ova and parasites
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Bacterial culture for enteric pathogens (eg, Salmonella, Shigella,Campylobacterorganisms):Mandatory when a stool sample shows positive results for WBCs or blood or if patients have feveror 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 inthose with a history of recent antibiotic use

Imaging studies

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

Procedures

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

Sigmoidoscopy/colonoscopy with biopsy

EGD with duodenal aspirate and biopsyIn patients with bloody diarrhea, sigmoidoscopy can be useful in diagnosing inflammatory boweldisease, antibiotic-associated diarrhea, shigellosis, and amebic dysentery.

SeeWorkupfor more detail.

Management

Most food-borne illnesses are mild and improve without any specific treatment. Some patients havesevere 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 electrolytesupplementation, which can be achieved with either an oral rehydration solution or intravenoussolutions in severely dehydrated individuals or those with intractable vomiting (eg, isotonic sodiumchloride solution, lactated Ringer solution).

Patients should avoid milk, dairy products, and other lactose-containing foods during episodes ofacute diarrhea, as these individuals often develop an acquired disaccharidase deficiency due towashout 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, bismuthsubsalicylate); antiperistaltics (eg, opiate derivatives such as diphenoxylate with atropine,loperamide)

Antibiotics (eg, ciprofloxacin, norfloxacin, TMX/SMP, doxycycline, rifaximin): Selection of antibioticdepends 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)SeeTreatmentandMedicationfor more detail.

Background

Food poisoningis 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 indegree and combination, include abdominal pain, vomiting, diarrhea, and headache; more serious
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cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanentdisability or death.

Most of the illnesses are mild and improve without any specific treatment. Some patients have severedisease 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 people2. Evidence of food as the source

Pathophysiology

The pathogenesis of diarrhea in food poisoning is classified broadly into either noninflammatory orinflammatory types.

Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory mechanisms of themucosa of the small intestine, without invasion. This leads to large volume watery stools in theabsence of blood, pus, or severe abdominal pain. Occasionally, profound dehydration may result. Theenterotoxins may be either preformed before ingestion or produced in the gut after ingestion.Examples includeVibrio cholerae, enterotoxicEscherichia coli, Clostridium perfringens, Bacilluscereus,[5]Staphylococcus organisms,Giardia lamblia, Cryptosporidium,rotavirus, norovirus(genus Norovirus, previously calledNorwalk virus), andadenovirus.

Inflammatory diarrhea is caused by the action of cytotoxin on the mucosa, leading to invasion anddestruction. 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 isless likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes ora positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicatecolitis.

Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue,followed by systemic dissemination. Examples includeCampylobacter jejuni, Vibrio

parahaemolyticus, enterohemorrhagic and enteroinvasiveE coli, Yersinia enterocolitica,Clostridiumdifficile,Entamoeba histolytica, andSalmonellaandShigellaspecies.

In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting onthe central nervous system. The clinical syndrome ofbotulismresults from the inhibition ofacetylcholine release in nerve endings by the botulinum.

The pathophysiological mechanisms that result in acute GIsymptoms produced by some of thenoninfectious causes of food poisoning (naturally occurring substances [eg,mushrooms, toadstools]andheavy 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 manyas 9000 deaths each year.[6, 7] However, the change in food supply, the identification of new food-borne diseases, and the availability of new surveillance data have changed the morbidity andmortality 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 suggest128,000 people are hospitalized and 3,000 die.[8] The 31 known pathogens account for an estimated9.4 million annual cases, 55,961 hospitalizations, and 1,351 deaths. Unspecified agents account for38.4 million cases, 71,878 hospitalizations, and 1,686 deaths.[9]

Overall, food-borne diseases appear to cause more illnesses but fewer deaths than previouslyestimated.[10]

The most common pathogens are as follows:[8]

Norovirus 5,461,731 cases
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Salmonella 1,027,561

C perfringens 965,958

Campylobacterspecies 845,024

Staphylococcus aureus 241,148The most common pathogens responsible for hospitalizations are as follows:[8]

Salmonella 19,336 hospitalizations Norovirus 14,663 hospitalizations

Campylobacterspecies 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

Campylobacterspecies 76 deathsIn 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 notpreviously associated with outbreaks. Outbreaks reported to CDCs Foodborne Disease OutbreakSurveillance System from 2005-2010 implicated 39 outbreaks and 2,348 illnesses that were linked toimported food from 15 countries. Within this 5-year period, nearly half (17) occurred in 2009 and2010. Fish (17 outbreaks) were the most common source of implicated imported foodborne diseaseoutbreaks, followed by spices (6 outbreaks including 5 from fresh or dried peppers). Approximately45% 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, andmarketing pose greater risk of cross-border transmission of infectious diseases and food-borneillness.[12]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 coliis 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, andrenal syndromes leading to permanent disability or death.

Age

Morbidity and mortality are higher in elderly individuals. The reasons for this increased susceptibility inelderly populations include age-associated decrease in immunity, decreased production of gastricacid and intestinal motility, malnutrition, lack of exercise, habitation in a nursing home, and excessiveuse 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 coli0157 , Salmonella,Shigella, and Y enterocolitica) caused 291,162 illnesses annually in children younger than 5years.[13] This resulted in 102,746 doctor visits, 7,830 hospitalizations, and 64 deaths. Rates of illnessremain higher in children.

Proceed toClinical Presentation

History
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A detailed history, including the duration of the disease, characteristics and frequency of bowelmovements, and associated abdominal and systemic symptoms, may provide a clue to the underlyingcause. The presence of a common source, types of specific food, travel history, and use of antibioticsalways 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 isclassified 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 mayresult 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, Bcereus, orNorovirus.[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 crampssuggest underlying electrolyte loss, as in severe cholera.

A history of bloating should raise the suspicion ofgiardiasis.

Yersinia enterocolitis may mimic the symptoms of appendicitis.

Proctitis syndrome, seen withshigellosis, is characterized by frequent painful bowel movementcontaining blood, pus, and mucus. Tenesmus and rectal discomfort are prominent features.

Consumption of undercooked meat/poultry is suspicious forSalmonella, Campylobacter, Shigatoxin 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 forCampylobacter, Salmonella, Shigatoxin 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 seenin Salmonella typhi infection.

Erythema nodosum and exudative pharyngitis are suggestive ofYersiniainfection. Patients with Vibrio vulnificus orVibrio 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 casesresult from food prepared at home.[8]

The most common causes are as follows: (1) leaving prepared food at temperatures that allowbacterial growth, (2) inadequate cooking or reheating, (3) cross-contamination, and (4) infection infood handlers. Cross-contamination may occur when raw contaminated food comes in contact withother foods, especially cooked foods, through direct contact or indirect contact on food preparationsurfaces.
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Bacteria are responsible for approximately 75% of the outbreaks of food poisoning and for 80% of thecases with a known cause in the United States.[6]As many as 1 in 10 Americans has diarrhea due tofood-borne infection each year.

Table 1.Causes of Food Poisoning. (Open Table in a new window)

Causative Agents Source and

Clinical Features

Pathogenesis Diagnosis and

Treatment

Staphylococci Improperly stored foods with high salt or sugarcontent favor growth of staphylococci.

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

Enterotoxin acts on receptors in gut thattransmit impulses to 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 hand mainly diarrheaafter 8-16 hafter ingestion; lasts as long as 1 d

Emetic enterotoxin (short incubationand duration) - Poorly understood

Diarrheal enterotoxin (long incubationand duration) - Increasing intestinalsecretion by activation of adenylatecyclase in intestinal epithelium


C perfringens Inadequately cooked meat, poultry, or legumes

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

Vomiting is rare. It lasts less than 1 d.

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

Enterotoxin produced in the gut, andfood causes hypersecretion in the smallintestine

Culture of clostridia in food and stool


C botulinum Canned foods (eg, smoked fish, mushrooms,

vegetables, honey)

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

Mortality is high

Toxin absorbed from the gut blocks the

release of acetylcholine in theneuromuscular junction

Toxin present in food, serum, and

stool.

Respiratory support

Intravenous trivalent antitoxin fromCDC


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Listeria monocytogenes Raw and pasteurized milk, soft cheeses, rawvegetables, shrimp

Systemic disease associated with bacteremia

Intestinal symptoms precede systemic disease

Can seed meninges, heart valves, and otherorgans

Highest mortality among bacterial foodpoisonings

Highly motile, heat-resistant, gram-positive organism

CSF or blood culture

Must treat with antibiotics if

bacteremic

EnterotoxicE coli(eg,traveler's diarrhea)

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

Acute-onset watery diarrhea starts 24-48 hafteringestion

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

Enterotoxin causes hypersecretion insmall and large intestine via guanylatecyclase activation

Supportive treatment

No antibiotics

EnterohemorrhagicE

coli (eg,E coliO157:H7)

Improperly cooked hamburger meat and

previously spinach

Most common isolate pathogen in bloodydiarrhea starts 3-4 dafter ingestion

Usually progresses from watery to bloodydiarrhea. It lasts for 3-8 d

May be complicated by hemolytic-uremicsyndromeor thrombotic thrombocytopenicpurpura

Cytotoxin results in endothelial damage

and leads to platelet aggregation andmicrovascular fibrin thrombi

Diagnosis with stool culture


No antibiotics

EnteroinvasiveE coli Contaminated imported cheese

Usually watery diarrhea (some may presentwith dysentery)

Enterotoxin produces secretion

Shigalike toxin facilitates invasion


No antibiotics

EnteroaggregativeE coli Implicated in traveler's diarrhea in developingcountries

Can cause bloody diarrhea

Bacteria clump on the cell surfaces Ciprofloxacin may shorten durationand eradicate the organism


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V cholera Contaminated water and food

Large amount of nonbloody diarrhea starts 8-24

hafter ingestion. It lasts for 3-5 d

Enterotoxin causes hypersecretion insmall 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 andexcretion ofVibrio

V parahaemolyticus Raw and improperly cooked seafood (ie,mollusks and crustaceans)

Explosive watery diarrhea starts 8-24 hafteringestion

It lasts for 3-5 d

Enterotoxin causes hypersecretion insmall intestine

Hemolytic toxin is lethal

Infective dose is usually 107 -109 organisms

Positive stool culture

Prompt replacement of fluids andelectrolytes

Sensitive to tetracycline, but unclearrole for antibiotics

V vulnificus Wound infection in salt water or consumptionof 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 bullouslesions 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 bybloody diarrhea

Abdominal pain and fever also may bepresent;it starts 1-3 dafter exposure andrecovery is in 5-8 d

Uncertain about endotoxin productionand invasion

Culture in special media at 42C

Erythromycin for invasive disease(fever)

Shigella Potato, egg salad, lettuce, vegetables, milk, icecream, and water

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

Usually self-limited in 3-7 d

Organisms invade epithelial cells andproduce toxins

Infective dose is 102 -103organisms

Enterotoxin-mediated diarrhea followedby 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


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No opiates

Salmonella Beef, poultry, eggs, and dairy products Abruptonset of moderate-to-large amount of diarrhea

with low-grade fever; in some cases, bloodydiarrhea

Abdominal pain and vomiting also present,beginning 6-48 hafter 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 routeor contaminated milk or ice cream

Acute abdominal pain, diarrhea, and fever(enterocolitis)

Incubation period not known Polyarthritis anderythema nodosum in children

May mimic appendicitis

Gastroenteritis and mesenteric adenitis

Direct invasion and enterotoxin

Polymorphonuclear leukocytesandblood in stool

Positive stool culture finding

No evidence that antibiotics alter thecourse but may be used in severeinfections

Aeromonas Untreated well or spring water

Diarrhea may be bloody

May be chronic up to 42 din the United States

Enterotoxin, hemolysin, and cytotoxin Positive stool culture

Fluoroquinolones or TMP/SMX for

chronic diarrhea

Parasitic Food

PoisoningSource 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 iscolonoscopywithbiopsy

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 bloody diarrhea with nausea andabdominal cramps starts 2-3 dafter ingestion;

Unknown

Highest concentration in the distalduodenum and proximal jejunum

Initial diagnostic test is stool enzyme-linked immunosorbent assay

Duodenal aspiration or small bowelbiopsy
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lasts for 1 wk

May become chronic

Cyst in the stool

Metronidazole

Seafood/Shellfish

PoisoningSource and

Clinical Features

Pathogenesis Diagnosis and

Treatment

Paralytic shellfishpoisoning

Temperate costal areas

Source - Bivalve mollusks

Onset usually is 30-60 min

Initial symptoms include perioral and intraoralparesthesia

Other symptoms include paresthesia of theextremities, headache, ataxia, vertigo, cranialnerve palsies, and paralysis of respiratorymuscles, resulting in respiratory arrest

Fish acquires toxin-producingdinoflagellates

General observation for 4-6 h

Maintain patent airway.

Administer oxygen, and assistventilation if necessary

For recent ingestion, charcoal 50-60 gmay 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 hafteringestion and last from days to months

Diarrhea may be accompanied by a variety ofneurologic symptoms including paresthesia,reversal of hot and cold sensation, vertigo,headache, and autonomic disturbances such ashypotension and bradycardia

Chronic symptoms (eg, fatigue, headache) maybe aggravated by caffeine or alcohol

Fish acquires toxin-producingdinoflagellates

Toxin increases intestinal secretion bychanging intracellular calciumconcentration

Symptomatic

Anecdotal reports of successful

treatment of neurologic symptoms withmannitol 1 g/kg IV


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Tetrodotoxin poisoning Japan

Source - Puffer fish

Onset of symptoms usually is 30-40 minbutmay be as short as 10 min;it includes lethargy,paresthesia, emesis, ataxia, weakness, anddysphagia; ascending paralysis occurs in severecases; mortality is high.

Neurotoxin is concentrated in the skinand viscera of puffer fish.

Symptomatic

Scombroid Source - Tuna, mahi-mahi, kingfish

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

Improper preservation of large fishresults in bacterial degradation ofhistidine to histamine

Antihistamines (diphenhydramine 25-50 mg IV)

H2 blockers (cimetidine 300 mg IV)

Severe reactions may requiresubcutaneous epinephrine (0.3-0.5 mLof 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 mucousmembranes, abdominal pain, vomiting,bloody diarrhea, and acute renal failure

Consult a toxicologist

Remove ingested salts by emesis andlavage, and administer activatedcharcoal and a cathartic

Dimercaprol is useful in acuteingestion

Lead Toxicity results from chronic repeated exposure

It is rare after single ingestion

Common symptoms include colickyabdominal pain, constipation, headache,and irritability

Diagnosis is based on lead level (>10mcg/dL)

Other than activated charcoal andcathartic, severe toxicity should betreated with antidotes (edetate calciumdisodium [EDTA] and dimercaprol).

Arsenic Ingestion of pesticide and industrial chemicals Symptoms usually appear within 1hafter ingestion but may be delayed aslong as 12 h

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

Gastric lavage and activated charcoal

Dimercaprol injection 10% solution in

oil (3-5 mg/kg IM q4-6h for 2 d) andoral penicillamine (100 mg/kg/ddivided qid for 1 wk)

Proceed toWorkup

Laboratory Studies
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Gram staining and Loeffler methylene blue staining of the stool for WBCs help to differentiate invasivedisease from noninvasive disease.

Perform microscopic examination of the stool for ova and parasites.

Bacterial culture for enteric pathogens, such as Salmonella, Shigella, andCampylobacterorganisms,becomes mandatory if a stool sample shows positive results for WBCs or blood or if patients havefever 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 forC difficile to help rule out antibiotic-associated diarrhea in patients receiving antibiotics or inthose with a history of recent antibiotic use.

Imaging Studies

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

Other Tests

When a stool examination is nondiagnostic, performing sigmoidoscopy/colonoscopywith biopsy andesophagogastroduodenoscopy (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 toTreatment & 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 isadequate rehydration and electrolyte supplementation. This can be achieved with either an oralrehydration solution (ORS) or intravenous solutions (eg, isotonic sodium chloride solution, lactatedRinger solution). Strict personal hygiene should be practiced during the illness.

Oral rehydration is achieved by administering clear liquids and sodium-containing and glucose-containing solutions. A simple ORS may be composed of 1 level teaspoon of salt and 4 heapingteaspoons 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 lessthan 1%.

ORS also is indicated in other dehydrating diarrheal diseases.

ORS promotes cotransport of glucose, sodium, and water across the gut epithelium, a mechanismunaffected 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 intractablevomiting.

Absorbents (eg, Kaopectate, aluminum hydroxide) help patients have more control over the timing ofdefecation. 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 30mL every 30 minutes, not to exceed 8-10 doses.

Antiperistaltics (opiate derivatives) should not be used in patients with fever, systemic toxicity, orbloody 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 (2.5mg of diphenoxylate/5 mL). The initial dose for adults is 2 tablets 4 times a day (ie, 20 mg/d). Thedose 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 andsecretion. 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 stoolcultures. 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 orsystemic symptoms. Treatment with an agent that covers Shigellaand Campylobacterorganisms is

reasonable in patients with diarrhea (>4 stools/d) for more than 3 days and with fever, abdominalpain, vomiting, headache, or myalgias. A 5-day course of a fluoroquinolone (eg, ciprofloxacin 500 mgPO bid, norfloxacin 400 mg PO bid) is the first-line therapy. TMP/SMX (Bactrim DS 1 tab qd) is analternative therapy, but resistant organisms are common in the tropics. Infection with eitherV

cholerae orV parahaemolyticus can be treated either with a fluoroquinolone or with doxycycline (100mg PO bid).

In the absence of dysentery, do not administer antibiotics until a microbiologic diagnosis is confirmedand E coliO157:H7 is ruled out.

Diet

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

Proceed toMedication

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 achievedwith 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 somedifferences exist between metabolic changes observed with administration of large quantities of eitherfluid, for practical purposes and in most situations, differences are clinically irrelevant. No

demonstrable difference exists in hemodynamic effect, morbidity, or mortality between resuscitationusing either NS or LR.

Oral electrolyte mixtures (Rehydralyte, Pedialyte)

Acts by glucose-facilitated absorption of sodium and water, which is unaffected in diseases such ascholera. 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 sodiumbicarbonate, 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 ofdefecation 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 inpatients with fever, systemic toxicity, bloody diarrhea, or in patients whose condition either shows noimprovement or deteriorates.

View full drug information

Attapulgite (Kaopectate, Diasorb)

Adsorbent and protectant that controls diarrhea.


Aluminum hydroxide (Amphojel, Dialume, ALternaGEL)

Commonly used as an antacid. Adsorbent and protectant that controls diarrhea.
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Bismuth subsalicylate (Pepto-Bismol)

Antisecretory agent that also may have antimicrobial and anti-inflammatory effects.


Diphenoxylate and atropine (Lomotil, Lonox)

Drug combination that consists of diphenoxylate, which is a constipating meperidine congener, andatropine to discourage abuse. Inhibits excessive GI propulsion and motility.

Available in tabs (2.5 mg diphenoxylate) and liquid (2.5 mg diphenoxylate/5 mL).


Loperamide (Imodium)

Acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. Prolongs movement ofelectrolytes 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).

AntibioticsClass Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in thecontext of the clinical setting. Antibiotic selection should be guided by blood culture sensitivity.


Ciprofloxacin (Cipro)

First-line therapy. Fluoroquinolone with activity against pseudomonads, streptococci,MRSA, Staphylococcus epidermidis, and most gram-negative organisms, but no activity againstanaerobes. Inhibits bacterial DNA synthesis, and, consequently, growth.


Norfloxacin (Noroxin)

Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and mostgram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis, and,consequently, growth.


Trimethoprim/sulfamethoxazole (Bactrim DS, Septra DS)

Alternative therapy, but resistant organisms are common in the tropics. Inhibits bacterial growth byinhibiting synthesis of dihydrofolic acid.


Doxycycline (Doryx, Vibramycin, Vibra-Tabs)

For V cholerae or Vparahaemolyticus infections. Inhibits protein synthesis and thus bacterial growth

by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.


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-subunitof bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. Indicated forEcoli(enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.

Proceed toFollow-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, anddaycare centers and who are infected with E coliO157:H7 orSalmonella orShigella organisms untilthey become culture-negative without antibiotics. These people should not return to work until thattime.

Deterrence/Prevention

No vaccine available canprevent norovirus infection. An early study conducted in a controlled settingassessed the safety, immunogenicity, and efficacy of an investigational, intranasally deliverednorovirus viruslike particle (VLP) vaccine to prevent acute viral gastroenteritis. Results suggest thevaccine protects against illness and infection after exposure to the Norwalk virus and could potentiallyprevent infection in susceptible, high-risk populations. The vaccine has not been tested in the naturalsetting, however.[14]

The best way to prevent food poisoning caused by infectious agents is to practice strict personalhygiene, cook all foods adequately, avoid cross-contamination of raw and cooked foods, and keep allfoods 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 (shellfishpoisoning).

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 toappropriate 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 orin bulk form) can eliminate food-borne pathogens. Annually, more than half a million tons of food isnow irradiated worldwide. Treating raw meat and poultry with irradiation at the slaughter plant couldeliminate bacteria, such asE coliO157:H7 and Salmonella and Campylobacterorganisms. Noevidence of adverse health effects is found in the well-controlled clinical trials involving irradiatedfood.

Prophylaxis for traveler's diarrhea is not recommended routinely because of the risk of adverse effectsfrom 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 withmeals 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; fluoroquinolonesshould not be prescribed to children or pregnant women). No significant resistance to thefluoroquinolones has been reported in high-risk areas, and they are the most effective antibiotics inregions 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. Othercomplications include the following:

Guillain-Barr syndrome (Campylobacterinfection)

Reactive arthritis

Hemolytic uremic syndrome (E coliO157:H7)Irritable bowel symptoms may follow acute gastroenteritis.

Patient Education

For excellent patient education resources, visit eMedicineHealth'sDigestive DisordersCenterandHealthy Living Center. Also, see eMedicineHealth's patient education articlesFoodPoisoning,Abdominal Pain in Adults,Vomiting and Nausea,Diarrhea,Traveler's Diarrhea,andForeign Travel.
http://www.emedicinehealth.com/collections/SU307.asphttp://www.emedicinehealth.com/collections/SU307.asphttp://www.emedicinehealth.com/collections/SU307.asphttp://www.emedicinehealth.com/collections/SU307.asphttp://www.emedicinehealth.com/collections/CO1594.asphttp://www.emedicinehealth.com/collections/CO1594.asphttp://www.emedicinehealth.com/collections/CO1594.asphttp://www.emedicinehealth.com/articles/17289-1.asphttp://www.emedicinehealth.com/articles/17289-1.asphttp://www.emedicinehealth.com/articles/17289-1.asphttp://www.emedicinehealth.com/articles/17289-1.asphttp://www.emedicinehealth.com/articles/10377-1.asphttp://www.emedicinehealth.com/articles/10377-1.asphttp://www.emedicinehealth.com/articles/10377-1.asphttp://www.emedicinehealth.com/articles/6029-1.asphttp://www.emedicinehealth.com/articles/6029-1.asphttp://www.emedicinehealth.com/articles/6029-1.asphttp://www.emedicinehealth.com/articles/5917-1.asphttp://www.emedicinehealth.com/articles/5917-1.asphttp://www.emedicinehealth.com/articles/5917-1.asphttp://www.emedicinehealth.com/articles/17577-1.asphttp://www.emedicinehealth.com/articles/17577-1.asphttp://www.emedicinehealth.com/articles/17577-1.asphttp://www.emedicinehealth.com/Articles/11934-1.asphttp://www.emedicinehealth.com/Articles/11934-1.asphttp://www.emedicinehealth.com/Articles/11934-1.asphttp://www.emedicinehealth.com/Articles/11934-1.asphttp://www.emedicinehealth.com/articles/17577-1.asphttp://www.emedicinehealth.com/articles/5917-1.asphttp://www.emedicinehealth.com/articles/6029-1.asphttp://www.emedicinehealth.com/articles/10377-1.asphttp://www.emedicinehealth.com/articles/17289-1.asphttp://www.emedicinehealth.com/articles/17289-1.asphttp://www.emedicinehealth.com/collections/CO1594.asphttp://www.emedicinehealth.com/collections/SU307.asphttp://www.emedicinehealth.com/collections/SU307.asp


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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 ofGastroenterology,American College of Physicians,American Gastroenterological

Association,American Medical Association,American Society for Gastrointestinal Endoscopy,

andCrohns 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 ofGastroenterology,American College of Physicians,American Gastroenterological

Association,American Medical Association,American Society of Gastrointestinal Endoscopy,andCrohns and Colitis Foundation of America


Michael H Piper, MD Clinical Assistant Professor, Department of Internal Medicine, Division ofGastroenterology, 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,AmericanCollege of Gastroenterology,American College of Physicians, andMichigan State Medical Society


Senthil Nachimuthu MD, FACP

Senthil Nachimuthu is a member of the following medical societies:American College of Physicians


Priyankha Balasundaram, MD Director, Kovai Heart Foundation, India; Resident, Department ofSurgery, Tulane University School of Medicine


Specialty Editor Board

Jose A Perez Jr, MD, MBA, MSEd Residency Director, Internal Medicine Residency Program, ViceChair of Education, Department of Medicine, Methodist Hospital; Associate Professor of ClinicalMedicine, Weill Cornell Medical College

Jose A Perez Jr, MD, MBA, MSEd is a member of the following medical societies:American Collegeof Physician Executives,American College of Physicians,Society of General Internal Medicine,andSociety of Hospital Medicine


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

http://www.acg.gi.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.gastro.org/http://www.gastro.org/http://www.gastro.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.asge.org/http://www.asge.org/http://www.asge.org/http://www.ccfa.org/http://www.ccfa.org/http://www.ccfa.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.gastro.org/http://www.gastro.org/http://www.gastro.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.asge.org/http://www.asge.org/http://www.asge.org/http://www.ccfa.org/http://www.ccfa.org/http://www.ccfa.org/http://www.alphaomegaalpha.org/http://www.alphaomegaalpha.org/http://www.alphaomegaalpha.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.msms.org/http://www.msms.org/http://www.msms.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.acpe.org/http://www.acpe.org/http://www.acpe.org/http://www.acpe.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.sgim.org/http://www.sgim.org/http://www.sgim.org/http://www.hospitalmedicine.org/AM/Template.cfm?Section=Homehttp://www.hospitalmedicine.org/AM/Template.cfm?Section=Homehttp://www.hospitalmedicine.org/AM/Template.cfm?Section=Homehttp://www.sgim.org/http://www.acponline.org/http://www.acpe.org/http://www.acpe.org/http://www.acponline.org/http://www.msms.org/http://www.acponline.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.alphaomegaalpha.org/http://www.ccfa.org/http://www.asge.org/http://www.ama-assn.org/http://www.gastro.org/http://www.gastro.org/http://www.acponline.org/http://www.acg.gi.org/http://www.acg.gi.org/http://www.ccfa.org/http://www.asge.org/http://www.ama-assn.org/http://www.gastro.org/http://www.gastro.org/http://www.acponline.org/http://www.acg.gi.org/http://www.acg.gi.org/


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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 OmegaAlpha,American College of Physicians-American Society of Internal Medicine, andSociety of GeneralInternal Medicine


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 ofGastroenterology,American College of Physicians,American Gastroenterological

Association,American Geriatrics Society,American Medical Association,American Society forGastrointestinal Endoscopy,American Society of Law, Medicine & Ethics,American TraumaSociety,Association of American Medical Colleges, andPhysicians for Social Responsibility


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3. Xerry J, Gallimore CI, Iturriza-Gomara M, Gray JJ. Tracking the transmission routes ofgenogroup II noroviruses in suspected food-borne or environmental outbreaks of gastroenteritis

through sequence analysis of the P2 domain. J Med Virol. Jul 2009;81(7):1298-304.[Medline].

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