- Author: Roberto M Gamarra, MD; Chief Editor: Julian Katz, MD more...
Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The most common pathogens are Norovirus, Escherichia coli, Salmonella, Clostridium perfringens, Campylobacter, and Staphylococcus aureus.
Signs and symptoms
The symptoms of food poisoning vary in degree and combination. They may include the following:
Abdominal pain: Most severe in inflammatory processes; painful abdominal muscle cramps suggest underlying electrolyte loss
Vomiting: Major presenting symptom of S aureus, B cereus, or Norovirus 
Diarrhea: Usually lasts less than 2 weeks
Fever: May be an invasive disease or an infection outside the GI tract
Stool changes: Bloody or mucousy if invasion of intestinal or colonic mucosa; profuse rice-watery if cholera or a similar process
Reactive arthritis: Seen with Salmonella, Shigella, Campylobacter, and Yersinia infections
Bloating: May be due to giardiasis
More serious cases of food poisoning can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
See Clinical Presentation for more detail.
See 5 Cases of Food Poisoning: Can You Identify the Pathogen?, a Critical Images slideshow, to help identify various pathogens and symptoms related to foodborne disease.
Examination of patients suspected of having food poisoning should focus on assessing the severity of dehydration. General findings may include the following:
Mild dehydration: A dry mouth, decreased axillary sweat, decreased urine
More severe volume depletion: Orthostasis, tachycardia, hypotension
Salmonella typhi infection: Upper abdominal rose spot macules, hepatosplenomegaly
Yersinia infection: Erythema nodosum, exudative pharyngitis
Vibrio vulnificus or V alginolyticus infection: cellulitis, otitis media
Always perform a rectal examination to (1) directly visualize the stool, (2) test occult blood, and (3) palpate the rectal mucosa for any lesions.
The following routine laboratory tests may help to assess the patient’s inflammatory response and the degree of dehydration:
CBC with differential
Serum electrolyte assessment
BUN and creatinine levels
Other laboratory studies can be helpful in cases of food poisoning and include the following:
Stool Gram staining and Loeffler methylene blue staining for WBCs: To help differentiate invasive disease from noninvasive disease
Microscopic examination of the stool: To detect any ova and parasites
Bacterial culture for enteric pathogens (eg, Salmonella, Shigella, Campylobacter organisms): Mandatory when a stool sample shows positive results for WBCs or blood or if patients have fever or symptoms persisting for longer than 3-4 days
Blood culture in febrile patients
C difficile assay: To help rule out antibiotic-associated diarrhea in patients receiving antibiotics or in those with a history of recent antibiotic use
Obtain flat and upright abdominal radiographs if the patient experiences bloating, severe pain, or obstructive symptoms or if the clinical picture suggests perforation.
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.
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.
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.
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
The best ways to prevent food poisoning caused by infectious agents are as follows:
Practice strict personal hygiene
Cook all foods adequately
Avoid cross-contamination of raw and cooked foods
Keep all foods at appropriate temperatures (ie, refrigerated items: < 40°F; hot items: >140°F)
Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The symptoms, varying in degree and combination, include abdominal pain, vomiting, diarrhea, and headache; more serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
Most of the illnesses are mild and improve without any specific treatment. Some patients have severe disease and require hospitalization, aggressive hydration, and antibiotic treatment.
A food-borne disease outbreak is defined by the following 2 criteria:
- Similar illness, often GI, in a minimum of 2 people
- Evidence of food as the source
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, Staphylococcus organisms , Giardia lamblia, Cryptosporidium,rotavirus, norovirus (genus Norovirus, previously called Norwalk virus), and adenovirus.
Inflammatory diarrhea is caused by the action of cytotoxins on the mucosa, leading to invasion and destruction. The colon or the distal small bowel commonly is involved. The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicate colitis.
Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigella species.
In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting on the central nervous system. The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum.
The pathophysiological mechanisms that result in acute GI symptoms produced by some of the noninfectious causes of food poisoning (naturally occurring substances [eg, mushrooms, toadstools] and heavy metals [eg, arsenic, mercury, lead]) are not well known.
A major contributor to seafood contamination with foodborne pathogens appears to be naturally occurring biofilm formation. Vibro and Salmonella species, Aeromonas hydrophila, and Listeria monocytogenes are common seafood bacterial pathogens that form biofilms.
Initially, food-borne diseases were estimated to be responsible for 6-8 million illnesses and as many as 9000 deaths each year.[5, 6] However, the change in food supply, the identification of new food-borne diseases, and the availability of new surveillance data have changed the morbidity and mortality figures. The US Centers for Disease Control and Prevention (CDC) estimates 1 in 6 Americans (48 million people) are affected by foodborne illness annually. The estimates suggest 128,000 people are hospitalized and 3,000 die. 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.
Overall, food-borne diseases appear to cause more illnesses but fewer deaths than previously estimated.
In a 2013 report, CDC investigators used data spanning the decade between 1998 and 2008 to report estimates for annual US food-borne illnesses, hospitalizations, and deaths attributable to each of 17 food categories.[10, 11] The following were among their findings[10, 11] :
Leafy green vegetables were the most common cause of food poisoning (22%), primarily due to Norovirus species, followed by E coli O157.
Poultry was the most common cause of death from food poisoning (19%), with Listeria and Salmonella species being the main infectious organisms.
Dairy items were the second most frequent causes of foodborne illnesses (14%) and deaths (10%), with the main factors being contamination by Norovirus from food handlers and improper pasteurization resulting in contamination with Campylobacter species.
In March 2012, the CDC reported a rise in foodborne disease outbreaks caused by imported food in 2009 and 2011. Nearly 50% of the outbreaks implicated food that was imported from regions not previously associated with outbreaks. Outbreaks reported to CDC’s Foodborne Disease Outbreak Surveillance System from 2005-2010 implicated 39 outbreaks and 2,348 illnesses that were linked to imported food from 15 countries. Within this 5-year period, nearly half (17) occurred in 2009 and 2010. Fish (17 outbreaks) was the most common source of implicated imported foodborne disease outbreaks, followed by spices (6 outbreaks including 5 from fresh or dried peppers). Approximately 45% of the imported foods causing outbreaks came from Asia.
The CDC recognized the following outbreaks and sources in 2012 :
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
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. A travel history should be obtained because traveler's diarrhea is the leading cause of travel-related illness. Onset occurs 3 days to 2 weeks after arrival. Illness is self-limiting within 5 days. Enterotoxigenic E coli is the most common isolate.
Symptoms vary in degree and combination. These may include abdominal pain, vomiting, diarrhea, headache, and prostration. More serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
Morbidity and mortality are higher in elderly individuals. The reasons for this increased susceptibility in elderly populations include age-associated decrease in immunity, decreased production of gastric acid and intestinal motility, malnutrition, lack of exercise, habitation in a nursing home, and excessive use of antibiotics. Elderly persons are more likely to die from infection with C perfringens; E coli O157; and Salmonella, Campylobacter, and Staphylococcus organisms.
The CDC found that 5 bacterial enteric pathogens (Campylobacter, E coli 0157 , Salmonella, Shigella, and Y enterocolitica) caused 291,162 illnesses annually in children younger than 5 years. This resulted in 102,746 doctor visits, 7,830 hospitalizations, and 64 deaths. Rates of illness remain higher in children.
Complications are very rare in healthy hosts, except in cases of botulism or mushroom poisoning. Infants, elderly people, and immunocompromised hosts are more susceptible to complications. Other complications include the following:
Guillain-Barré syndrome ( Campylobacter infection)
Hemolytic uremic syndrome ( E coli O157:H7)
Irritable bowel symptoms may follow acute gastroenteritis.
Xerry J, Gallimore CI, Iturriza-Gomara M, Gray JJ. Tracking the transmission routes of genogroup II noroviruses in suspected food-borne or environmental outbreaks of gastroenteritis through sequence analysis of the P2 domain. J Med Virol. 2009 Jul. 81(7):1298-304. [Medline].
Logan NA. Bacillus and relatives in foodborne illness. J Appl Microbiol. 2012 Mar. 112(3):417-29. [Medline].
Mizan MF, Jahid IK, Ha SD. Microbial biofilms in seafood: A food-hygiene challenge. Food Microbiol. 2015 Aug. 49:41-55. [Medline].
Hughes JM, Angulo FJ. Food borne diseases. Hurst JW, ed. Medicine for the Practicing Physician. 4th ed. Stamford, Conn: Appleton & Lange; 1996. 344-7.
Smith JL. Foodborne illness in the elderly. J Food Prot. 1998 Sep. 61(9):1229-39. [Medline].
Preliminary FoodNet Data on the incidence of infection with pathogens transmitted commonly through food--10 States, 2008. MMWR Morb Mortal Wkly Rep. 2009 Apr 10. 58(13):333-7. [Medline].
Doheny K. Most common foods for foodborne illness: CDC report. Medscape Medical News. Available at http://www.medscape.com/viewarticle/778455. January 30, 2013; Accessed: February 6, 2013.
Painter JA, Hoekstra RM, Ayers, et al. Attribution of foodborne illnesses, hospitalizations, and deaths to food commodities by using outbreak data, United States, 1998-2008. Emerg Infect Dis. 2013 March;19:3. [Full Text].
CDC research shows outbreaks linked to imported foods increasing. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/media/releases/2012/p0314_foodborne.html. March 14, 2012;
Jacobs RA. General problems in infectious diseases: acute infectious diarrhea. Tierney LM Jr, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment 2001. 40th ed. New York, NY: McGraw-Hill; 2000. 1215-6.
Scallan E, Mahon BE, Hoekstra RM, Griffin PM. Estimates of Illnesses, Hospitalizations, and Deaths Caused By Major Bacterial Enteric Pathogens in Young Children in the United States. Pediatr Infect Dis J. 2012 Dec 17. [Medline].
Podeur G, Dalgaard P, Leroi F, et al. Development of a real-time PCR method coupled with a selective pre-enrichment step for quantification of Morganella morganii and Morganella psychrotolerans in fish products. Int J Food Microbiol. 2015 Jun 16. 203:55-62. [Medline].
Atmar RL, Bernstein DI, Harro CD, et al. Norovirus vaccine against experimental human Norwalk Virus illness. N Engl J Med. 2011 Dec 8. 365(23):2178-87. [Medline].
Shaw A, Shama G, Iza F. Emerging applications of low temperature gas plasmas in the food industry. Biointerphases. 2015 Jun 16. 10(2):029402. [Medline].
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Gianella RA. Infectious enteritis and proctocolitis and bacterial food poisoning. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 2006. Vol 2: 2333-91.
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|Causative Agents||Source and
|Staphylococci||Improperly stored foods with high salt or sugar content favors growth of staphylococci.
Intense vomiting and watery diarrhea start 1-4 h after ingestion and last as long as 24-48 h
|Enterotoxin acts on receptors in the gut that transmit impulses to the medullary centers||Symptomatic treatment|
|B cereus||Contaminated fried rice (emetic)
Emetic: Duration is 9 h, vomiting and cramps
Diarrheal: Lasts for 24 h
Mainly vomiting after 1-6 h and mainly diarrhea after 8-16 h after ingestion; lasts as long as 1 d
|Emetic enterotoxin (short incubation and duration) - Poorly understood
Diarrheal enterotoxin (long incubation and duration) - Increasing intestinal secretion by activation of adenylate cyclase in intestinal epithelium
|C perfringens||Inadequately cooked meat, poultry, or legumes
Acute onset of abdominal cramps with diarrhea starts 8-24 h after ingestion.
Vomiting is rare. It lasts less than 1 d.
Enteritis necroticans associated with C perfringens type C in improperly cooked pork (40% mortality)
|Enterotoxin produced in the gut, and food causes hypersecretion in the small intestine||Culture of clostridia in food and stool
|C botulinum||Canned foods (eg, smoked fish, mushrooms, vegetables, honey)
Descending weakness and paralysis start 1-4 d after ingestion, followed by constipation.
Mortality is high
|Toxin absorbed from the gut blocks the release of acetylcholine in the neuromuscular junction||Toxin present in food, serum, and stool.
Intravenous trivalent antitoxin from CDC
|Listeria monocytogenes||Raw and pasteurized milk, soft cheeses, raw vegetables, shrimp
Systemic disease associated with bacteremia
Intestinal symptoms precede systemic disease
Can seed meninges, heart valves, and other organs
Highest mortality among bacterial food poisonings
|Highly motile, heat-resistant, gram-positive organism||CSF or blood culture
Must treat with antibiotics if bacteremic
|Enterotoxic E coli (eg, traveler's diarrhea)||Contaminated water and food (eg, salad, cheese, meat)
Acute-onset watery diarrhea starts 24-48 h after ingestion
Concomitant vomiting and abdominal cramps may be present. It lasts for 1-2 d
|Enterotoxin causes hypersecretion in small and large intestine via guanylate cyclase activation||Supportive treatment
|Enterohemorrhagic E coli (eg, E coli O157:H7)||Improperly cooked hamburger meat and previously spinach
Most common isolate pathogen in bloody diarrhea starts 3-4 d after ingestion
Usually progresses from watery to bloody diarrhea. It lasts for 3-8 d
May be complicated by hemolytic-uremic syndrome or thrombotic thrombocytopenic purpura
|Cytotoxin results in endothelial damage and leads to platelet aggregation and microvascular fibrin thrombi||Diagnosis with stool culture
|Enteroinvasive E coli||Contaminated imported cheese
Usually watery diarrhea (some may present with dysentery)
|Enterotoxin produces secretion
Shigalike toxin facilitates invasion
|Enteroaggregative E coli||Implicated in traveler's diarrhea in developing countries
Can cause bloody diarrhea
|Bacteria clump on the cell surfaces||Ciprofloxacin may shorten duration and eradicate the organism|
|V cholera||Contaminated water and food
Large amount of nonbloody diarrhea starts 8-24 h after ingestion. It lasts for 3-5 d
|Enterotoxin causes hypersecretion in small intestine
Infective dose usually is 107 -109 organisms
|Positive stool culture finding
Prompt replacement of fluids and electrolytes (oral rehydration solution)
Tetracycline (or fluoroquinolones) shortens the duration of symptoms and excretion of Vibrio
|V parahaemolyticus||Raw and improperly cooked seafood (ie, mollusks and crustaceans)
Explosive watery diarrhea starts 8-24 h after ingestion
It lasts for 3-5 d
|Enterotoxin causes hypersecretion in small intestine
Hemolytic toxin is lethal
Infective dose is usually 107 -109 organisms
|Positive stool culture
Prompt replacement of fluids and electrolytes
Sensitive to tetracycline, but unclear role for antibiotics
|V vulnificus||Wound infection in salt water or consumption of raw oysters
Can be lethal in patients with liver disease (50% mortality)
Growth correlates with availability of iron (especially transferrin saturation >70%)
|Culture of characteristic bullous lesions or blood
Immediate antibiotics if suspected (eg, doxycycline and ceftriaxone)
|C jejuni||Domestic animals, cattle, chickens
Fecal-oral transmission in humans
Foul-smelling watery diarrhea followed by bloody diarrhea
Abdominal pain and fever also may be present; it starts 1-3 d after exposure and recovery is in 5-8 d
|Uncertain about endotoxin production and invasion||Culture in special media at 42°C
Erythromycin for invasive disease (fever)
|Shigella||Potato, egg salad, lettuce, vegetables, milk, ice cream, and water
Abrupt onset of bloody diarrhea, cramps, tenesmus, and fever starts 12-30 h after ingestion.
Usually self-limited in 3-7 d
|Organisms invade epithelial cells and produce toxins
Infective dose is 102 -103 organisms
Enterotoxin-mediated diarrhea followed by invasion (dysentery/colitis)
|Polymorphonuclear leukocytes (PMNs), blood, and mucus in stool
Positive stool culture
Oral rehydration is mainstay
Trimethoprim-sulfamethoxazole (TMP-SMX) or ampicillin for severe cases
|Salmonella||Beef, poultry, eggs, and dairy products
Abrupt onset of moderate-to-large amount of diarrhea with low-grade fever; in some cases, bloody diarrhea
Abdominal pain and vomiting also present, beginning 6-48 h after exposure and lasts 7-12 d
|Invasion but no toxin production||Positive stool culture finding
Antibiotic for systemic infection
|Yersinia||Pets; transmission in humans by fecal-oral route or contaminated milk or ice cream
Acute abdominal pain, diarrhea, and fever (enterocolitis)
Incubation period not known Polyarthritis and erythema nodosum in children
May mimic appendicitis
|Gastroenteritis and mesenteric adenitis
Direct invasion and enterotoxin
|Polymorphonuclear leukocytes and blood in stool
Positive stool culture finding
No evidence that antibiotics alter the course but may be used in severe infections
|Aeromonas||Untreated well or spring water
Diarrhea may be bloody
May be chronic up to 42 d in the United States
|Enterotoxin, hemolysin, and cytotoxin||Positive stool culture
Fluoroquinolones or TMP/SMX for chronic diarrhea
|Parasitic Food Poisoning||Source and Clinical Features||Pathogenesis||Diagnosis and Treatment|
|E histolytica||Contaminated food and water
Minority may develop liver abscesses
|Invasion of the mucosa by the parasites||Criterion standard is colonoscopy with biopsy
Ova and parasites may be seen in the stool but has low sensitivity
Luminal amebicides (eg, paromomycin)
Tissue amebicides (eg, metronidazole)
|G lamblia||Contaminated ground water
Fecal-oral transmission in humans
Mild diarrhea with nausea and abdominal cramps starts 2-3 d after ingestion; lasts for 1 wk
May become chronic
Highest concentration in the distal duodenum and proximal jejunum
|Initial diagnostic test is stool enzyme-linked immunosorbent assay
Duodenal aspiration or small bowel biopsy
Cyst in the stool
|Seafood/Shellfish Poisoning||Source and
|Paralytic shellfish poisoning||Temperate coastal areas
Source - Bivalve mollusks
Onset usually is 30-60 min
Initial symptoms include perioral and intraoral paresthesia
Other symptoms include paresthesia of the extremities, headache, ataxia, vertigo, cranial nerve palsies, and paralysis of respiratory muscles, resulting in respiratory arrest
|Fish acquires toxin-producing dinoflagellates||General observation for 4-6 h
Maintain patent airway.
Administer oxygen, and assist ventilation if necessary
For recent ingestion, charcoal 50-60 g may be helpful
|Neurotoxic shellfish poisoning||Coastal Florida
Source - Mollusks
Illness is milder than in paralytic shellfish poisoning
|Fish acquires toxin-producing dinoflagellates||Symptomatic|
|Ciguatera||Hawaii, Florida, and Caribbean
Source - Carnivorous reef fish
Vomiting, diarrhea, and cramps start 1-6 h after ingestion and last from days to months
Diarrhea may be accompanied by a variety of neurologic symptoms including paresthesia, reversal of hot and cold sensation, vertigo, headache, and autonomic disturbances such as hypotension and bradycardia
Chronic symptoms (eg, fatigue, headache) may be aggravated by caffeine or alcohol
|Fish acquires toxin-producing dinoflagellates
Toxin increases intestinal secretion by changing intracellular calcium concentration
Anecdotal reports of successful treatment of neurologic symptoms with mannitol 1 g/kg IV
Source - Puffer fish
Onset of symptoms usually is 30-40 min but may be as short as 10 min; it includes lethargy, paresthesia, emesis, ataxia, weakness, and dysphagia; ascending paralysis occurs in severe cases; mortality is high.
|Neurotoxin is concentrated in the skin and viscera of puffer fish.||Symptomatic|
|Scombroid||Source - Tuna, mahi-mahi, kingfish
Allergic symptoms such as skin flush, urticaria, bronchospasm, and hypotension usually start within 15-90 min
|Improper preservation of large fish results in bacterial degradation of histidine to histamine||Antihistamines (diphenhydramine 25-50 mg IV)
H2 blockers (cimetidine 300 mg IV)
Severe reactions may require subcutaneous epinephrine (0.3-0.5 mL of 1:1000 solution)
|Heavy Metal Poisoning||Source||Symptoms||Treatment|
|Mercury||Ingestion of inorganic mercuric salts||Causes metallic taste, salivation, thirst, discoloration and edema of oral mucous membranes, abdominal pain, vomiting, bloody diarrhea, and acute renal failure||Consult a toxicologist
Remove ingested salts by emesis and lavage, and administer activated charcoal and a cathartic
Dimercaprol is useful in acute ingestion
|Lead||Toxicity results from chronic repeated exposure
It is rare after single ingestion
|Common symptoms include colicky abdominal pain, constipation, headache, and irritability
Diagnosis is based on lead level (>10 mcg/dL)
|Other than activated charcoal and cathartic, severe toxicity should be treated with antidotes (edetate calcium disodium [EDTA] and dimercaprol).|
|Arsenic||Ingestion of pesticide and industrial chemicals||Symptoms usually appear within 1 h after ingestion but may be delayed as long as 12 h
Abdominal pain, watery diarrhea, vomiting, skeletal muscle cramps, profound dehydration, and shock may occur
|Gastric lavage and activated charcoal
Dimercaprol injection 10% solution in oil (3-5 mg/kg IM q4-6h for 2 d) and oral penicillamine (100 mg/kg/d divided qid for 1 wk)