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.
The symptoms of food poisoning vary in degree and combination. They may include the following:
More serious cases of food poisoning can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
See Clinical Presentation for more detail.
See 8 Cases of Food Poisoning: Find the Pathogen Responsible, a Critical Images slideshow, to help identify various pathogens and symptoms related to foodborne disease.
Examination of patients suspected of having food poisoning should focus on assessing the severity of dehydration. General findings may include the following:
Always perform a rectal examination to (1) directly visualize the stool, (2) test occult blood, and (3) palpate the rectal mucosa for any lesions.
Testing
The following routine laboratory tests may help to assess the patient’s inflammatory response and the degree of dehydration:
Other laboratory studies can be helpful in cases of food poisoning and include the following:
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:
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.[2]
Supportive care
The main objective in managing patients with food poisoning is adequate rehydration and electrolyte supplementation, which can be achieved with either an oral rehydration solution or intravenous solutions in severely dehydrated individuals or those with intractable vomiting (eg, isotonic sodium chloride solution, lactated Ringer solution).
Patients should avoid milk, dairy products, and other lactose-containing foods during episodes of acute diarrhea, as these individuals often develop an acquired disaccharidase deficiency due to washout of the brush-border enzymes.
Pharmacotherapy
Medications that may be needed to treat patients with food poisoning include the following:
Prevention
The best ways to prevent food poisoning caused by infectious agents are as follows:
See Treatment and Medication for more detail.
Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The symptoms, varying in degree and combination, include abdominal pain, vomiting, diarrhea, and headache; more serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
Most of the illnesses are mild and improve without any specific treatment. Some patients have severe disease and require hospitalization, aggressive hydration, and antibiotic treatment.[2]
A food-borne disease outbreak is defined by the following 2 criteria:
The pathogenesis of diarrhea in food poisoning is classified broadly into either noninflammatory or inflammatory types.
Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory mechanisms of the mucosa of the small intestine, without invasion. This leads to large volume watery stools in the absence of blood, pus, or severe abdominal pain. Occasionally, profound dehydration may result. The enterotoxins may be either preformed before ingestion or produced in the gut after ingestion. Examples include Vibrio cholerae, enterotoxic Escherichia coli, Clostridium perfringens, Bacillus cereus,[3] Staphylococcus organisms, Giardia lamblia, Cryptosporidium, rotavirus, norovirus (genus Norovirus, previously called Norwalk virus), and adenovirus.
Inflammatory diarrhea is caused by the action of cytotoxins on the mucosa, leading to invasion and destruction. The colon or the distal small bowel commonly is involved. The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicate colitis.
Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigella species.
In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting on the central nervous system. The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum.
The pathophysiological mechanisms that result in acute GI symptoms produced by some of the noninfectious causes of food poisoning (naturally occurring substances [eg, mushrooms, toadstools] and heavy metals [eg, arsenic, mercury, lead]) are not well known.
A major contributor to seafood contamination with foodborne pathogens appears to be naturally occurring biofilm formation.[4] Vibro and Salmonella species, Aeromonas hydrophila, and Listeria monocytogenes are common seafood bacterial pathogens that form biofilms.
Initially, food-borne diseases were estimated to be responsible for 6-8 million illnesses and as many as 9000 deaths each year.[5, 6] However, the change in food supply, the identification of new food-borne diseases, and the availability of new surveillance data have changed the morbidity and mortality figures. The US Centers for Disease Control and Prevention (CDC) estimates 1 in 6 Americans (48 million people) are affected by foodborne illness annually. The estimates suggest 128,000 people are hospitalized and 3,000 die.[7] The 31 known pathogens account for an estimated 9.4 million annual cases, 55,961 hospitalizations, and 1,351 deaths. Unspecified agents account for 38.4 million cases, 71,878 hospitalizations, and 1,686 deaths.[8]
Overall, food-borne diseases appear to cause more illnesses but fewer deaths than previously estimated.[9]
In a 2013 report, CDC investigators used data spanning the decade between 1998 and 2008 to report estimates for annual US food-borne illnesses, hospitalizations, and deaths attributable to each of 17 food categories.[10, 11] The following were among their findings[10, 11] :
In March 2012, the CDC reported a rise in foodborne disease outbreaks caused by imported food in 2009 and 2011. Nearly 50% of the outbreaks implicated food that was imported from regions not previously associated with outbreaks. Outbreaks reported to CDC’s Foodborne Disease Outbreak Surveillance System from 2005-2010 implicated 39 outbreaks and 2,348 illnesses that were linked to imported food from 15 countries. Within this 5-year period, nearly half (17) occurred in 2009 and 2010. Fish (17 outbreaks) was the most common source of implicated imported foodborne disease outbreaks, followed by spices (6 outbreaks including 5 from fresh or dried peppers). Approximately 45% of the imported foods causing outbreaks came from Asia.[12]
The CDC recognized the following outbreaks and sources in 2012[7] :
Transnational trade; travel; and migration and globalization of food production, manufacturing, and marketing pose greater risk of cross-border transmission of infectious diseases and food-borne illness.[13] A travel history should be obtained because traveler's diarrhea is the leading cause of travel-related illness. Onset occurs 3 days to 2 weeks after arrival. Illness is self-limiting within 5 days. Enterotoxigenic E coli is the most common isolate.
Symptoms vary in degree and combination. These may include abdominal pain, vomiting, diarrhea, headache, and prostration. More serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
Morbidity and mortality are higher in elderly individuals. The reasons for this increased susceptibility in elderly populations include age-associated decrease in immunity, decreased production of gastric acid and intestinal motility, malnutrition, lack of exercise, habitation in a nursing home, and excessive use of antibiotics. Elderly persons are more likely to die from infection with C perfringens; E coli O157; and Salmonella, Campylobacter, and Staphylococcus organisms.
The CDC found that 5 bacterial enteric pathogens (Campylobacter, E coli 0157 , Salmonella, Shigella, and Y enterocolitica) caused 291,162 illnesses annually in children younger than 5 years.[14] This resulted in 102,746 doctor visits, 7,830 hospitalizations, and 64 deaths. Rates of illness remain higher in children.
For patient education resources, visit Digestive Disorders Center and Healthy Living Center, as well as Abdominal Pain in Adults, Vomiting and Nausea, Diarrhea, Traveler's Diarrhea, and Foreign Travel.
Complications are very rare in healthy hosts, except in cases of botulism or mushroom poisoning. Infants, elderly people, and immunocompromised hosts are more susceptible to complications. Other complications include the following:
Irritable bowel symptoms may follow acute gastroenteritis.
A detailed history, including the duration of the disease, characteristics and frequency of bowel movements, and associated abdominal and systemic symptoms, may provide a clue to the underlying cause. The presence of a common source, types of specific food, travel history, and use of antibiotics always should be investigated.
The presenting complaints, typical features and pathogenesis of various causative agents, and diagnosis and treatment information can be found in Table 1 in the Causes section.
The following are some of the salient features of food poisoning:
The physical examination should focus on assessing the severity of dehydration and include the following evaluation:
The CDC estimates that 97% of all cases of food poisoning result from improper food handling; 79% of cases result from food prepared in commercial or institutional establishments and 21% of cases result from food prepared at home.[7]
The most common causes are as follows: (1) leaving prepared food at temperatures that allow bacterial growth, (2) inadequate cooking or reheating, (3) cross-contamination, and (4) infection in food handlers. Cross-contamination may occur when raw contaminated food comes in contact with other foods, especially cooked foods, through direct contact or indirect contact on food preparation surfaces.
Bacteria are responsible for approximately 75% of the outbreaks of food poisoning and for 80% of the cases with a known cause in the United States.[5] As many as 1 in 10 Americans has diarrhea due to food-borne infection each year.
Table 1.Causes of Food Poisoning.
View Table | See Table |
Obtain the following laboratory studies in cases of suspected food poisoning:
Histamine food poisoning from gram-negative bacteria in fin-fish products is also common, and Morganella morganii and M psychrotolerans are particularly strong histamine producers. The development of real-time quantitative polymerase chain reaction (RTiqPCR) techniques in conjunction with the use of selective primers and a quantitative enrichment step appear to have the potential to identify and quantify these two species in fish products.[15]
Flat and upright abdominal radiographs should be obtained if the patient experiences bloating, severe pain, or obstructive symptoms or if perforation is suggested.
When a stool examination is nondiagnostic, performing sigmoidoscopy/colonoscopy with biopsy and esophagogastroduodenoscopy (EGD) with duodenal aspirate and biopsy may be beneficial. This is especially important in patients who are immunocompromised.
Consider sigmoidoscopy in patients with bloody diarrhea. It can be useful in diagnosing inflammatory bowel disease, antibiotic-associated diarrhea, shigellosis, and amebic dysentery.
Because most cases of acute gastroenteritis are self-limited, specific treatment is not necessary. Strict personal hygiene should be practiced during the illness. Some studies have quantified that only 10% of cases require antibiotic therapy.
The main objective is adequate rehydration and electrolyte supplementation. This can be achieved with either an oral rehydration solution (ORS) or intravenous solutions (eg, isotonic sodium chloride solution, lactated Ringer solution). Note the following:
Intravenous solutions are indicated in patients who are severely dehydrated or who have intractable vomiting.
Absorbents (eg, Kaopectate, aluminum hydroxide) help patients have more control over the timing of defecation. However, they do not alter the course of the disease or reduce fluid loss. Note the following:
If symptoms persist beyond 3-4 days, the specific etiology should be determined by performing stool cultures. If symptoms persist and the pathogen is isolated, specific treatment should be initiated.
Empiric treatment should be initiated in patients with suspected traveler's diarrhea or dysenteric or systemic symptoms. Treatment with an agent that covers Shigella and Campylobacter organisms is reasonable in patients with diarrhea (>4 stools/d) for more than 3 days and with fever, abdominal pain, vomiting, headache, or myalgias. A 5-day course of a fluoroquinolone (eg, ciprofloxacin 500 mg PO bid, norfloxacin 400 mg PO bid) is the first-line therapy. TMP/SMX (Bactrim DS 1 tab qd) is an alternative therapy, but resistant organisms are common in the tropics. Infection with either V cholerae or V parahaemolyticus can be treated either with a fluoroquinolone or with doxycycline (100 mg PO bid).
In the absence of dysentery, do not administer antibiotics until a microbiologic diagnosis is confirmed and E coli O157:H7 is ruled out.
During episodes of acute diarrhea, patients often develop an acquired disaccharidase deficiency due to washout of the brush-border enzymes. For this reason, avoiding milk, dairy products, and other lactose-containing foods is advisable.
No vaccine is available that can prevent norovirus infection. An early study conducted in a controlled setting assessed the safety, immunogenicity, and efficacy of an investigational, intranasally delivered norovirus viruslike particle (VLP) vaccine to prevent acute viral gastroenteritis. Results suggest the vaccine protects against illness and infection after exposure to the Norwalk virus and could potentially prevent infection in susceptible, high-risk populations. The vaccine has not been tested in the natural setting, however.[16]
The best way to prevent food poisoning caused by infectious agents is to practice strict personal hygiene, cook all foods adequately, avoid cross-contamination of raw and cooked foods, and keep all foods at appropriate temperatures (ie, < 40°F for refrigerated items and >140°F for hot items).
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 as E coli O157:H7 and Salmonella and Campylobacter organisms. No evidence of adverse health effects has been found in the well-controlled clinical trials involving irradiated food.
The use of low-temperature gas plasmas in the food industry may potentially reduce the incidence of foodborne disease.[17] The gas plasmas have microbiocidal capabilities and may also aid in degrading undesirable chemical compounds that can be found on food and food-processing equipment (eg, pesticide residues, toxins, allergens).[17]
Prophylaxis for traveler's diarrhea is not recommended routinely because of the risk of adverse effects from the drugs (eg, rash, anaphylaxis, vaginal candidiasis) and the development of resistant gut flora. Possible regimens for prophylaxis include bismuth subsalicylate (Pepto-Bismol, 524 mg PO qid with meals and qhs), doxycycline (100 mg PO qd; resistance documented in many areas of the world), TMP/SMX (160 mg/800 mg 1 double-strength tab qd), or norfloxacin (400 mg PO qd; fluoroquinolones should not be prescribed to children or pregnant women). No significant resistance to the fluoroquinolones has been reported in high-risk areas, and they are the most effective antibiotics in regions where susceptibilities are not known.
Because most cases of food poisoning are self-limited, prolonged follow-up care is not required.
Stool cultures should be monitored in individuals working in hospitals, food establishments, and daycare centers and who are infected with E coli O157:H7 or Salmonella or Shigella organisms until they become culture-negative without antibiotics. These people should not return to work until that time.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Clinical Context: Both fluids are essentially isotonic and have equivalent volume-restorative properties. While some differences exist between metabolic changes observed with the administration of large quantities of either fluid, for practical purposes and in most situations, differences are clinically irrelevant. No demonstrable difference exists in hemodynamic effect, morbidity, or mortality between resuscitation using either NS or LR.
Clinical Context: Acts by glucose-facilitated absorption of sodium and water, which is unaffected in diseases such as cholera. Oral rehydration is achieved using clear liquids and sodium-containing and glucose-containing solutions. WHO recommends a solution containing 3.5 g of sodium chloride, 2.5 g sodium bicarbonate, 1.5 g potassium chloride, and 20 g glucose per liter of water.
A simple solution may be made using 1 level tsp salt and 4 heaping tsp sugar added to 1 L water.
The main objective is adequate rehydration and electrolyte supplementation. This can be achieved with ORS or intravenous solutions (eg, isotonic sodium chloride solution, lactated Ringer solution).
Clinical Context: Adsorbent and protectant that controls diarrhea.
Clinical Context: Commonly used as an antacid. Adsorbent and protectant that controls diarrhea.
Clinical Context: Antisecretory agent that also may have antimicrobial and anti-inflammatory effects.
Clinical Context: Drug combination that consists of diphenoxylate, which is a constipating meperidine congener, and atropine to discourage abuse. Inhibits excessive GI propulsion and motility.
Available in tabs (2.5 mg diphenoxylate) and liquid (2.5 mg diphenoxylate/5 mL).
Clinical Context: Acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. Prolongs movement of electrolytes and fluid through bowel and increases viscosity and loss of fluids and electrolytes.
Available over the counter in 2-mg capsules and liquid (1 mg/5 mL).
Adsorbents (eg, attapulgite, aluminum hydroxide) help patients have more control over the timing of defecation but do not alter the course of the disease or reduce fluid loss. Antisecretory agents (eg, bismuth subsalicylate) may be useful. Antiperistaltics (opiate derivatives) should not be used in patients with fever, systemic toxicity, bloody diarrhea, or in patients whose condition either shows no improvement or deteriorates.
Clinical Context: First-line therapy. Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis, and, consequently, growth.
Clinical Context: Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis, and, consequently, growth.
Clinical Context: Alternative therapy, but resistant organisms are common in the tropics. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
Clinical Context: For V cholerae or V parahaemolyticus infections. Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
Clinical Context: Nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the GI tract (ie, gram-positive, gram-negative, aerobic, anaerobic). Rifampin structural analog. Binds to beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. Indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Antibiotic selection should be guided by blood culture sensitivity.
Causative Agents Source and
Clinical FeaturesPathogenesis Diagnosis and
TreatmentStaphylococci 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 hEnterotoxin acts on receptors in the gut that transmit impulses to the medullary centers Symptomatic treatment B cereus Contaminated fried rice (emetic)
Meatballs (diarrheal)
Emetic: Duration is 9 h, vomiting and cramps
Diarrheal: Lasts for 24 h
Mainly vomiting after 1-6 h and mainly diarrhea after 8-16 h after ingestion; lasts as long as 1 dEmetic enterotoxin (short incubation and duration) - Poorly understood
Diarrheal enterotoxin (long incubation and duration) - Increasing intestinal secretion by activation of adenylate cyclase in intestinal epitheliumSymptomatic treatment C perfringens Inadequately cooked meat, poultry, or legumes
Acute onset of abdominal cramps with diarrhea starts 8-24 h after ingestion.
Vomiting is rare. It lasts less than 1 d.
Enteritis necroticans associated with C perfringens type C in improperly cooked pork (40% mortality)Enterotoxin produced in the gut, and food causes hypersecretion in the small intestine Culture of clostridia in food and stool
Symptomatic treatmentC botulinum Canned foods (eg, smoked fish, mushrooms, vegetables, honey)
Descending weakness and paralysis start 1-4 d after ingestion, followed by constipation.
Mortality is highToxin absorbed from the gut blocks the release of acetylcholine in the neuromuscular junction Toxin present in food, serum, and stool.
Respiratory support
Intravenous trivalent antitoxin from CDCListeria 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 poisoningsHighly motile, heat-resistant, gram-positive organism CSF or blood culture
Must treat with antibiotics if bacteremicEnterotoxic 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 dEnterotoxin causes hypersecretion in small and large intestine via guanylate cyclase activation Supportive treatment
No antibioticsEnterohemorrhagic 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 purpuraCytotoxin results in endothelial damage and leads to platelet aggregation and microvascular fibrin thrombi Diagnosis with stool culture
Supportive treatment
No antibioticsEnteroinvasive E coli Contaminated imported cheese
Usually watery diarrhea (some may present with dysentery)Enterotoxin produces secretion
Shigalike toxin facilitates invasionSupportive treatment
No antibioticsEnteroaggregative E coli Implicated in traveler's diarrhea in developing countries
Can cause bloody diarrheaBacteria 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 dEnterotoxin causes hypersecretion in small intestine
Infective dose usually is 107 -109 organismsPositive stool culture finding
Prompt replacement of fluids and electrolytes (oral rehydration solution)
Tetracycline (or fluoroquinolones) shortens the duration of symptoms and excretion of VibrioV parahaemolyticus Raw and improperly cooked seafood (ie, mollusks and crustaceans)
Explosive watery diarrhea starts 8-24 h after ingestion
It lasts for 3-5 dEnterotoxin causes hypersecretion in small intestine
Hemolytic toxin is lethal
Infective dose is usually 107 -109 organismsPositive stool culture
Prompt replacement of fluids and electrolytes
Sensitive to tetracycline, but unclear role for antibioticsV vulnificus Wound infection in salt water or consumption of raw oysters
Can be lethal in patients with liver disease (50% mortality)Polysaccharide capsule
Growth correlates with availability of iron (especially transferrin saturation >70%)Culture of characteristic bullous lesions or blood
Immediate antibiotics if suspected (eg, doxycycline and ceftriaxone)C jejuni Domestic animals, cattle, chickens
Fecal-oral transmission in humans
Foul-smelling watery diarrhea followed by bloody diarrhea
Abdominal pain and fever also may be present; it starts 1-3 d after exposure and recovery is in 5-8 dUncertain 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 dOrganisms invade epithelial cells and produce toxins
Infective dose is 102 -103 organisms
Enterotoxin-mediated diarrhea followed by invasion (dysentery/colitis)Polymorphonuclear leukocytes (PMNs), blood, and mucus in stool
Positive stool culture
Oral rehydration is mainstay
Trimethoprim-sulfamethoxazole (TMP-SMX) or ampicillin for severe cases
No opiatesSalmonella 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 dInvasion but no toxin production Positive stool culture finding
Antibiotic for systemic infectionYersinia 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 appendicitisGastroenteritis and mesenteric adenitis
Direct invasion and enterotoxinPolymorphonuclear leukocytes and blood in stool
Positive stool culture finding
No evidence that antibiotics alter the course but may be used in severe infectionsAeromonas Untreated well or spring water
Diarrhea may be bloody
May be chronic up to 42 d in the United StatesEnterotoxin, hemolysin, and cytotoxin Positive stool culture
Fluoroquinolones or TMP/SMX for chronic diarrheaParasitic Food Poisoning Source and Clinical Features Pathogenesis Diagnosis and Treatment E histolytica Contaminated food and water
90% asymptomatic
10% dysentery
Minority may develop liver abscessesInvasion 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 chronicUnknown
Highest concentration in the distal duodenum and proximal jejunumInitial diagnostic test is stool enzyme-linked immunosorbent assay
Duodenal aspiration or small bowel biopsy
Cyst in the stool
MetronidazoleSeafood/Shellfish Poisoning Source and
Clinical FeaturesPathogenesis Diagnosis and
TreatmentParalytic 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 arrestFish 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 helpfulNeurotoxic shellfish poisoning Coastal Florida
Source - Mollusks
Illness is milder than in paralytic shellfish poisoningFish 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 alcoholFish acquires toxin-producing dinoflagellates
Toxin increases intestinal secretion by changing intracellular calcium concentrationSymptomatic
Anecdotal reports of successful treatment of neurologic symptoms with mannitol 1 g/kg IVTetrodotoxin poisoning Japan
Source - Puffer fish
Onset of symptoms usually is 30-40 min but may be as short as 10 min; it includes lethargy, paresthesia, emesis, ataxia, weakness, and dysphagia; ascending paralysis occurs in severe cases; mortality is high.Neurotoxin is concentrated in the skin and viscera of puffer fish. Symptomatic Scombroid Source - Tuna, mahi-mahi, kingfish
Allergic symptoms such as skin flush, urticaria, bronchospasm, and hypotension usually start within 15-90 minImproper 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 ingestionLead Toxicity results from chronic repeated exposure
It is rare after single ingestionCommon 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 occurGastric 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)