Updated: Nov 18, 2009
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:
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 cytotoxin on the mucosa, leading to invasion and destruction. The colon or the distal small bowel commonly is involved. The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicate colitis.
Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigella species.
In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting on the central nervous system. The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum.
The pathophysiological mechanisms that result in acute gastrointestinal 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.
Initially, food-borne diseases were estimated to be responsible for 6-8 million illnesses and as many as 9000 deaths each year.1,2 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. A study from the US Centers for Disease Control and Prevention (CDC) reports that food-borne diseases cause approximately 76 million illnesses, 325,000 hospitalizations, and 5000 deaths in the United States each year. Identified pathogens account for an estimated 14 million illnesses, 60,000 hospitalizations, and 1800 deaths. Salmonella, Listeria, and Toxoplasma organisms are responsible for 1500 deaths. Unidentified pathogens account for the remaining 62 million illnesses, 265,000 hospitalizations, and 3200 deaths. Overall, food-borne diseases appear to cause more illnesses but fewer deaths than previously estimated.3
According to a 2009 CDC study on food-borne disease outbreaks (for the year 2006), there were 1270 such outbreaks, or 27,634 cases, reported within 48 states, with 11 deaths resulting.4 (However, most cases of food poisoning occur sporadically, rather than as part of an outbreak.) The etiologic agent was confirmed for more than 620 outbreaks, with Norovirus accounting for 54% of the outbreaks and a total of 11,879 cases. Salmonella was the second most frequent cause, accounting for 18% of the outbreaks and 3,252 cases. One of the 11 deaths resulted from a mushroom toxin; the rest were associated with bacteria, as follows:
In the 243 outbreaks known to have resulted from a single food commodity, the foods associated with the most cases were poultry (1355 cases), leafy vegetables (1081 cases), and fruits/nuts (1021 cases).
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.5 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.
Table 1. Examples of Large Food-Borne Disease Outbreaks5
| Country | Year | Disease | Number of Cases |
| United Kingdom | 1985 | Salmonellosis | 1000 |
| United States | 1985 | Salmonellosis | >168,000 |
| United States | 1993 | Salmonellosis | 224,000 |
| China | 1988 | Hepatitis A | >310,000 |
| Germany | 1993 | Salmonellosis | 1000 |
| Australia | 1991 | Norwalk-like agent | >3050 |
| United States | 1992-1993 | E coli O157 infection | >500 |
| Japan | 1996 | E coli O157 infection | >6000 |
Symptoms vary in degree and combination. They may include abdominal pain, vomiting, diarrhea, headache, and prostration. More serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
In children younger than 5 years, attacks range from 2-3 illnesses per child per year in developed countries; attacks are at least 5 times more common in developing countries. In underdeveloped countries, acute diarrheal diseases are responsible for 1 billion cases per year and 4-6 million deaths per year.
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.
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 2 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.
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 establishments7 and 21% of cases result from food prepared at home.
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.1 As many as 1 in 10 Americans has diarrhea due to food-borne infection each year.
Table 2. Causes of Food Poisoning
| Causative Agents | Source and Clinical Features | Pathogenesis | Diagnosis and Treatment |
| Staphylococci | Improperly stored foods with high salt or sugar content favor growth of staphylococci Intense vomiting and watery diarrhea start 1-4 hours after ingestion and last as long as 24-48 hours. | Enterotoxin acts on receptors in gut that transmit impulses to medullary centers. | Symptomatic treatment |
| B cereus | Contaminated fried rice (emetic) Meatballs (diarrheal) Emetic: Duration is 9 hours, vomiting and cramps Diarrheal: Lasts for 24 h Mainly vomiting after 1-6 hours and mainly diarrhea after 8-16 hours after ingestion; lasts as long as 1 day | 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 | Symptomatic treatment |
| C perfringens | Inadequately cooked meat, poultry, or legumes Acute onset of abdominal cramps with diarrhea starts 8-24 hours after ingestion. Vomiting is rare. It lasts less than 1 day. 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 treatment |
| C botulinum | Canned foods (eg, smoked fish, mushrooms, vegetables, honey) Descending weakness and paralysis start 1-4 days after ingestion, followed by constipation. Mortality is very high. | Toxin 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 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 hours after ingestion. Concomitant vomiting and abdominal cramps may be present. It lasts for 1-2 days | Enterotoxin causes hypersecretion in small and large intestine via guanylate cyclase activation. | Supportive treatment No antibiotics |
| Enterohemorrhagic E coli (eg, E coli O157:H7) | Improperly cooked hamburger meat and previously spinach Most common isolate pathogen in bloody diarrhea starts 3-4 days after ingestion. Usually progresses from watery to bloody diarrhea. It lasts for 3-8 days May be complicated by HUS or TTP | Cytotoxin results in endothelial damage and leads to platelet aggregation and microvascular fibrin thrombi | Diagnosis with stool culture Supportive treatment No antibiotics |
| Enteroinvasive E coli | Contaminated imported cheese Usually watery diarrhea (some may present with dysentery) | Enterotoxin produces secretion Shiga-like toxin facilitates invasion. | Supportive treatment No antibiotics |
| Enteroaggregative E coli | Implicated in traveler's diarrhea in developing countries Can cause bloody diarrhea | Bacteria clump on the cell surfaces | Ciprofloxacin may shorten duration and eradicate the organism |
| V cholera | Contaminated water and food Large amount of nonbloody diarrhea starts 8-24 hours after ingestion. It lasts for 3-5 days. | Enterotoxin causes hypersecretion in small intestine. Infective dose usually is 107 -109 organisms. | Positive stool culture 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 hours after ingestion. It lasts for 3-5 days. | Enterotoxin causes hypersecretion in small intestine. Hemolytic toxin is lethal. Infective dose usually is 107 -109 organisms. | Positive stool culture Prompt replacement of fluids and electrolytes Sensitive to tetracycline, but unclear role for antibiotics |
| V vulnificus | Wound infection in salt water or consumption of raw oysters Can be lethal in patients with liver disease (50% mortality) | Polysaccharide capsule Growth correlates with availability of iron (esp. 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 days after exposure and recovery is in 5-8 days. | 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 hours after ingestion. Usually self-limited in 3-7 days | Organisms invade epithelial cells and produce toxins. Infective dose is 102 -103 organisms. Enterotoxin-mediated diarrhea followed by invasion (dysentery/colitis) | Polymorphonuclear leukocytes (PMNs), blood, and mucus in stool Positive stool culture Oral rehydration is mainstay. Trimethoprim-sulfamethoxazole (TMP-SMX) or ampicillin for severe cases No opiates |
| Salmonella | Beef, poultry, eggs, and diary 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 hours after exposure and lasts 7-12 days | Invasion but no toxin production | Positive stool culture 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 | PMNs and blood in stool Positive stool culture 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 days in the United States | Enterotoxin, hemolysin, and cytotoxin | Positive stool culture Fluoroquinolones or TMP/SMX for chronic diarrhea |
| Parasitic Food Poisoning | Source and Clinical Features | Pathogenesis | Diagnosis and Treatment |
| E histolytica | Contaminated food and water 90% asymptomatic 10% dysentery Minority may develop liver abscesses | Invasion of the mucosa by the parasites | Criterion standard is colonoscopy with biopsy Ova and parasites may be seen in the stool but has low sensitivity Luminal amebicides (eg, paromomycin) Tissue amebicides (eg, metronidazole) |
| G lamblia | Contaminated ground water Fecal-oral transmission in humans Mild bloody diarrhea with nausea and abdominal cramps starts 2-3 days after ingestion; lasts for 1 week May become chronic | Unknown Highest concentration in the distal duodenum and proximal jejunum | Initial diagnostic test is stool ELISA Duodenal aspiration or small bowel biopsy Cyst in the stool Metronidazole |
| Seafood/Shellfish Poisoning | Source and Clinical Features | Pathogenesis | Diagnosis and Treatment |
| Paralytic shellfish poisoning | Temperate costal areas Source - Bivalve mollusks Onset usually is 30-60 minutes. 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 hours 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 hours after ingestion and last from days to months. Diarrhea may be accompanied by a variety of neurologic symptoms including paresthesia, reversal of hot and cold sensation, vertigo, headache, and autonomic disturbances such as hypotension and bradycardia. Chronic symptoms (eg, fatigue, headache) may be aggravated by caffeine or alcohol | Fish acquires toxin-producing dinoflagellates Toxin increases intestinal secretion by changing intracellular calcium concentration | Symptomatic Anecdotal reports of successful treatment of neurologic symptoms with mannitol 1 g/kg IV |
| Tetrodotoxin poisoning | Japan Source - Puffer fish Onset of symptoms usually is 30-40 minutes but may be as short as 10 minutes. 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 minutes. | 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 hour after ingestion but may be delayed as long as 12 hours. 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) |
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.
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.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
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).
Both fluids are essentially isotonic and have equivalent volume-restorative properties. While some differences exist between metabolic changes observed with administration of large quantities of either fluid, for practical purposes and in most situations, differences are clinically irrelevant. No demonstrable difference exists in hemodynamic effect, morbidity, or mortality between resuscitation using either NS or LR.
Depends on severity of dehydration; should be given until adequately resuscitated and able to take PO fluids
Administer as in adults
None reported
Major complication of isotonic fluid resuscitation is interstitial edema; edema of extremities is unsightly but not a significant complication; edema in brain or lungs is potentially fatal; major contraindication to isotonic fluid resuscitation is pulmonary edema; added fluid promotes more edema and may lead to development of ARDS
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Administering isotonic fluids during resuscitation of septic shock requires close monitoring of cardiovascular and pulmonary function; stop fluids when desired hemodynamic response is observed or pulmonary edema develops
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.
Depends on severity of dehydration; should be given until adequately resuscitated and able to take PO fluids
Administer as in adults
None reported
Intractable vomiting or diarrhea; prolonged shock; anuria; oliguria
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Critical fluid losses require IV therapy
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.
Adsorbent and protectant that controls diarrhea.
1200-1500 mg/dose PO after each loose stool; not to exceed 9000 mg/24h
<3 years: Not recommended
3-6 years: 300 mg/dose PO after each loose stool; not to exceed 2100 mg/24h
6-12 years: 600 mg/dose PO after each loose stool; not to exceed 4200 mg/24h
>12 years: Administer as in adults
Decreases absorption of digoxin, clindamycin, tetracyclines, and penicillamine
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in patients <3 y or >60 y; avoid in presence of high fever; at high doses, may cause constipation; should be an interval of at least 1-2 h when using other medications with adsorbents
Commonly used as an antacid. Adsorbent and protectant that controls diarrhea.
15-45 mL/dose PO q3-6h or 1 and 3 h pc and hs
5-15 mL/dose PO q3-6h or 1 and 3 h pc and hs
Decreases effects of tetracyclines, ranitidine, ketoconazole, benzodiazepines, penicillamine, phenothiazines, digoxin, indomethacin, and isoniazid; corticosteroids decrease effects of aluminum in hyperphosphatemia
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in patients with recent massive upper GI hemorrhage; renal failure may cause aluminum toxicity; should be interval of at least 1-2 h when using other medications with adsorbents
Antisecretory agent that also may have antimicrobial and anti-inflammatory effects.
2 tab or 30 mL PO q30min; not to exceed 8 doses/24 h
3-6 years: One third of tab or 5 mL PO q30min to 1 h prn
6-9 years: Two thirds of tab or 10 mL PO q30min to 1 h prn
9-12 years: 1 tab or 15 mL PO q30min to 1 h prn
Not to exceed 8 doses/24 h
Coadministration with anticoagulants may increase risk of bleeding; may increase toxicity of aspirin and hypoglycemics; decreases effects of tetracyclines and uricosurics
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause temporary and harmless darkening of tongue and/or black stool; alcohol consumption may cause abdominal cramps, nausea, and vomiting
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).
5-20 mg/d of diphenoxylate PO tid/qid
Maintenance dose: 5-15 PO mg/d
<2 years: Not recommended
2-5 years: 2 mg of diphenoxylate PO tid
5-8 years: 2 mg of diphenoxylate PO qid
8-12 years: 2 mg of diphenoxylate PO 5 times/d
>12 years: Administer as in adults
May delay metabolism of drugs in liver; CNS depressants, MAOIs, and antimuscarinic agents may increase toxicity
Documented hypersensitivity; narrow-angle glaucoma; hepatic insufficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In young children, dehydration may influence variability of response and predispose patients to delayed diphenoxylate intoxication; caution in patients with ulcerative colitis; decrease in intestinal motility may be detrimental to patients with diarrhea resulting from Shigella or Salmonella organisms and toxigenic strains of E coli
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).
4 mg PO initially, then 2 mg after each loose stool; not to exceed 16 mg/d
Initial doses
2-6 years: 1 mg PO tid
6-8 years: 2 mg PO bid
8-12 years: 2 mg PO tid
Maintenance
0.1 mg/kg PO after each loose stool, not to exceed initial dose
Chronic diarrhea
0.08-0.24 mg/kg/d PO divided bid/tid; not to exceed 2 mg/dose
Phenothiazines, tricyclic antidepressants, and CNS depressants may increase toxicity
Documented hypersensitivity; diarrhea resulting from infections; pseudomembranous colitis
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue if no clinical improvement in 48 h; because loperamide primarily is metabolized in the liver, monitor for CNS toxicity in patients with hepatic insufficiency; do not use if high fever or blood in stool coincides with 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.
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.
500 mg PO bid for 3 d
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in patients with renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
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.
400 mg PO bid for 3 d; not to exceed 800 mg/d
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in patients with renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Alternative therapy, but resistant organisms are common in the tropics. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
160 mg TMP/800 mg SMX PO qd for 3 d
<2 months: Do not administer
>2 months: 6-10 mg TMP/kg/d PO divided q12h
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, persons with long-term alcoholism, elderly persons, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in individuals who are G-6-PD deficient; patients with AIDS may not tolerate or respond to TMP/SMZ; caution in patients with renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation
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.
200 mg PO/IV immediately and 100 mg hs, followed by 100 mg bid for 3 d
Alternatively, 100-200 mg PO bid for 14 d
<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO/IV qd or divided bid; not to exceed 200 mg/d
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in patients with renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Nonabsorbed (<0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal 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.
200 mg PO tid
<12 years: Not established
>12 years: Administer as in adults
Induces CYP450 3A4 in vitro; limited data exist; no significant interactions shown in single-dose studies with midazolam and oral contraceptives
Documented hypersensitivity to rifaximin or rifamycin antimicrobial agents (eg, rifampin)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May promote intestinal bacterial overgrowth and cause superinfection; discontinue if diarrhea persists >24-48 h or worsens; seek immediate medical care if fever and/or bloody stools emerge (tablets not effective); not effective for travelers' diarrhea due to suspected pathogens other than E coli; postmarketing reports include allergic dermatitis, rash, angioneurotic edema, urticaria, and pruritus
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food poisoning, gastroenteritis, botulism, , , cholera, , enterotoxins, , , , , , , , Norwalk virus, foodborne illness, , , , , , , tenesmus, shigellosis
Roberto M Gamarra, MD, Fellow, Department of Internal Medicine, Section of Gastroenterology and Hepatology, Providence Hospital and Medical Center
Roberto M Gamarra, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America
Disclosure: Nothing to disclose.
David M Manuel, MD, Fellow, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital and Medical Center
David M Manuel, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society of Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America
Disclosure: Nothing to disclose.
Michael H Piper, MD, FACG, FACP, Clinical Assistant Professor, Department of Internal Medicine, Division of Gastroenterology, Wayne State University School of Medicine; Consulting Staff, Digestive Health Associates PLC
Michael H Piper, MD, FACG, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, and Michigan State Medical Society
Disclosure: Nothing to disclose.
Senthil Nachimuthu, MD, FACP, Fellow, Department of Internal Medicine, Heart and Vascular Institute, Tulane University School of Medicine
Senthil Nachimuthu, MD, FACP is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.
Priyankha Balasundaram, MD, Director, Kovai Heart Foundation, India; Resident, Department of Surgery, Tulane University School of Medicine
Disclosure: Nothing to disclose.
Jose A Perez Jr, MD, MSEd, MBA, Consulting Physician, Department of Internal Medicine, Residency Director, Vice Chair of Education Department of Medicine, The Methodist Hospital, Houston; Associate Professor of Clinical Medicine, Weill Cornell Medical College
Jose A Perez Jr, MD, MSEd, MBA is a member of the following medical societies: American College of Physician Executives, American College of Physicians, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.
Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
Clinical guidelines
Diagnosis and management of foodborne illnesses: a primer for physicians and other health care professionals.
American Medical Association - Medical Specialty Society
Center for Food Safety and Applied Nutrition - Federal Government Agency [U.S.]
Centers for Disease Control and Prevention - Federal Government Agency [U.S.]
Food Safety and Inspection Service - Federal Government Agency [U.S.]. 2001 Jan (revised 2004 Apr 16). 33 pages. NGC:003593
Prevention of rotavirus gastroenteritis among infants and children. Recommendations of the Advisory Committee on Immunization Practices (ACIP).
Centers for Disease Control and Prevention - Federal Government Agency [U.S.]. 2006 Aug 11 (revised 2009 Feb 6). 25 pages. NGC:007073
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