Food Poisoning: A toxicologic and medical review

Details: Published: Wednesday, 30 January 2013 15:04

Food poisoning is relevant to toxicology and public health largely because of adulterant contamination. Food poisoning is usually caused by infectious agents but other ingested toxic compounds can cause diarrhea, vomiting, and abdominal pain as well. It also has direct relevance to community acquired disease, assessments for such diseases, and surveillance. The following review article was recently published online in emedicine #175569.

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.[1]

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,[2]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 Shigellaspecies.

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

The pathophysiological mechanisms that result in acute GIsymptoms produced by some of the noninfectious causes of food poisoning (naturally occurring substances [eg,mushrooms, toadstools] and heavy metals [eg, arsenic, mercury, lead]) are not well known.

Epidemiology: United States

Initially, food-borne diseases were estimated to be responsible for 6-8 million illnesses and as many as 9000 deaths each year.[3, 4] 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.[5] 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.[6]

Overall, food-borne diseases appear to cause more illnesses but fewer deaths than previously estimated.[7]

The most common pathogens are as follows:[5]

Norovirus – 5,461,731 cases
Salmonella – 1,027,561
C perfringens – 965,958
Campylobacter species – 845,024
Staphylococcus aureus – 241,148

The most common pathogens responsible for hospitalizations are as follows:[5]

Salmonella – 19,336 hospitalizations
Norovirus – 14,663 hospitalizations
Campylobacter species – 8,463 hospitalizations
Toxoplasma gondii – 4,428 hospitalizations
E coli – 2,138 hospitalizations
The pathogens most commonly associated with death are as follows:
Salmonella – 378 deaths
T gondii – 327 deaths
Listeria monocytogenes – 255 deaths
Norovirus – 149 deaths
Campylobacter species – 76 deaths

In March 2012, the CDC reported a rise in foodborne disease outbreaks caused by imported food in 2009 and 2011. Nearly 50% of the outbreaks implicated food that was imported from regions not previously associated with outbreaks. Outbreaks reported 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) were the most common source of implicated imported foodborne disease outbreaks, followed by spices (6 outbreaks including 5 from fresh or dried peppers). Approximately 45% percent of the imported foods causing outbreaks came from Asia.[8]

The CDC recognized the following outbreaks and sources in 2012:[5]

E coli – Spinach and spring mix, raw clover sprouts at Jimmy John’s restaurants
Salmonella – Peanut butter, Frescolina Marte brand ricotta salata cheese, mangoes, cantaloupe, ground beef, live poultry, dry dog food, raw scraped ground tuna product, small turtles, raw clover sprouts

International

Transnational trade; travel; and migration and globalization of food production, manufacturing, and marketing pose greater risk of cross-border transmission of infectious diseases and food-borne illness.[9] 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.

Mortality/Morbidity

Symptoms vary in degree and combination. They may include abdominal pain, vomiting, diarrhea, headache, and prostration. More serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.

Age

Morbidity and mortality are higher in elderly individuals. The reasons for this increased susceptibility in elderly populations include age-associated decrease in immunity, decreased production of gastric acid and intestinal motility, malnutrition, lack of exercise, habitation in a nursing home, and excessive use of antibiotics. Elderly persons are more likely to die from infection with C perfringens; E coli O157; and Salmonella, Campylobacter, and Staphylococcus organisms.

Causes:

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.[10] This resulted in 102,746 doctor visits, 7,830 hospitalizations, and 64 deaths. Rates of illness remain higher in children.

History:

A detailed history, including the duration of the disease, characteristics and frequency of bowel movements, and associated abdominal and systemic symptoms, may provide a clue to the underlying cause. The presence of a common source, types of specific food, travel history, and use of antibiotics always should be investigated.

The presenting complaints, typical features and pathogenesis of various causative agents, and diagnosis and treatment information can be found in Table 1 in the Causes section.

The following are some of the salient features of food poisoning:

Acute diarrhea in food poisoning usually lasts less than 2 weeks. Diarrhea lasting 2-4 weeks is classified as persistent. Chronic diarrhea is defined by duration of more than 4 weeks.
The presence of fever suggests an invasive disease. However, sometimes fever and diarrhea may result from infection outside the GI tract, as in malaria.
A stool with blood or mucus indicates invasion of the intestinal or colonic mucosa.
When vomiting is the major presenting symptom, suspect Staphylococcus aureus, B cereus, or Norovirus.[11]
Reactive arthritis can be seen with Salmonella, Shigella, Campylobacter, and Yersinia infections.
A profuse rice-water stool suggests cholera or a similar process.
Abdominal pain is most severe in inflammatory processes. Painful abdominal muscle cramps suggest underlying electrolyte loss, as in severe cholera.
A history of bloating should raise the suspicion of giardiasis.
Yersinia enterocolitis may mimic the symptoms of appendicitis.
Proctitis syndrome, seen with shigellosis, is characterized by frequent painful bowel movement containing blood, pus, and mucus. Tenesmus and rectal discomfort are prominent features.
Consumption of undercooked meat/poultry is suspicious for Salmonella, Campylobacter, Shiga toxin E coli, and C perfringens.
Consumption of raw seafood is suspicious for Norwalk-like virus, Vibrio organism, or hepatitis A.
Consumption of homemade canned foods is associated with C botulinum.
Consumption of unpasteurized soft cheeses is associated with Listeria, Salmonella, Campylobacter, Shiga toxin E coli,and Yersinia.
Consumption of deli meats notoriously is responsible for listeriosis.
Consumption of unpasteurized milk or juice is suspicious for Campylobacter, Salmonella, Shiga toxin E coli,and Yersinia.
Salmonella has been associated with consumption of raw eggs

The physical examination should focus on assessing the severity of dehydration.

A dry mouth, decreased axillary sweat, and decreased urine output indicate mild dehydration, whereas orthostasis, tachycardia, and hypotension indicate more severe volume depletion.
A rectal examination always should be performed to directly visualize the stool, to test occult blood, and to palpate the rectal mucosa for any lesions.
Rose spot macules on the upper abdomen and hepatosplenomegaly may be seen in Salmonella typhi infection.
Erythema nodosum and exudative pharyngitis are suggestive of Yersinia infection.
Patients with Vibrio vulnificus or Vibrio alginolyticus may present with cellulitis and otitis media.

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.[5]

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.[3] As many as 1 in 10 Americans has diarrhea due to food-borne infection each year.

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

Causative Agents		Source and 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 hafter ingestion and last as long as 24-48 h	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 h, vomiting and cramps Diarrheal: Lasts for 24 h Mainly vomiting after 1-6 hand mainly diarrhea after 8-16 hafter ingestion; lasts as long as 1 d	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 hafter 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 treatment
C botulinum		Canned foods (eg, smoked fish, mushrooms, vegetables, honey) Descending weakness and paralysis start 1-4 dafter 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. 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 hafter 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 No antibiotics
EnterohemorrhagicE coli (eg, E coliO157:H7)		Improperly cooked hamburger meat and previously spinach Most common isolate pathogen in bloody diarrhea starts 3-4 dafter ingestion Usually progresses from watery to bloody diarrhea. It lasts for 3-8 d May be complicated by hemolytic-uremic syndromeor thrombotic thrombocytopenic purpura	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 Shigalike toxin facilitates invasion	Supportive treatment No antibiotics
EnteroaggregativeE 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 hafter ingestion. It lasts for 3-5 d	Enterotoxin causes hypersecretion in small intestine Infective dose usually is 10⁷-10⁹organisms	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 hafter ingestion It lasts for 3-5 d	Enterotoxin causes hypersecretion in small intestine Hemolytic toxin is lethal Infective dose is usually 10⁷-10⁹organisms	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 (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 dafter 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 hafter ingestion. Usually self-limited in 3-7 d	Organisms invade epithelial cells and produce toxins Infective dose is 10²-10³organisms 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 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 hafter exposure and lasts 7-12 d	Invasion but no toxin production	Positive stool culture finding Antibiotic for systemic infection
Yersinia		Pets; transmission in humans by fecal-oral 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 leukocytesand 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 din 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 dafter ingestion; lasts for 1 wk May become chronic	Unknown 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 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 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 hafter 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 minbut may be as short as 10 min;it includes lethargy, paresthesia, emesis, ataxia, weakness, and dysphagia; ascending paralysis occurs in severe cases; mortality is high.	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 hafter 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)

EVALUATION:

Gram staining and Loeffler methylene blue staining of the stool for WBCs help to differentiate invasive disease from noninvasive disease.
Perform microscopic examination of the stool for ova and parasites.
Bacterial culture for enteric pathogens, such as Salmonella, Shigella, and Campylobacter organisms, becomes mandatory if a stool sample shows positive results for WBCs or blood or if patients have fever or symptoms persisting for longer than 3-4 days.
Perform blood culture if the patient is notably febrile.
CBC with differential, serum electrolyte assessment, and BUN and creatinine levels help to assess the inflammatory response and the degree of dehydration.
Assay for C difficile to help rule out antibiotic-associated diarrhea in patients receiving antibiotics or in those with a history of recent antibiotic use.

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.

Treatment:

Because most cases of acute gastroenteritis are self-limited, specific treatment is not necessary. Some studies have quantified that only 10% of cases require antibiotic therapy. The main objective is adequate rehydration and electrolyte supplementation. This can be achieved with either an oral rehydration solution (ORS) or intravenous solutions (eg, isotonic sodium chloride solution, lactated Ringer solution). Strict personal hygiene should be practiced during the illness.

Oral rehydration is achieved by administering clear liquids and sodium-containing and glucose-containing solutions. A simple ORS may be composed of 1 level teaspoon of salt and 4 heaping teaspoons of sugar added to 1 liter of water.
The use of ORS has reduced the mortality rate associated with cholera from higher than 50% to less than 1%.
ORS also is indicated in other dehydrating diarrheal diseases.
ORS promotes cotransport of glucose, sodium, and water across the gut epithelium, a mechanism unaffected in cholera.
The World Health Organization (WHO) recommends a solution containing 3.5 g of sodium chloride, 2.5 g of sodium bicarbonate, 1.5 g of potassium chloride, and 20 g of glucose per liter of water.

Intravenous solutions are indicated in patients who are severely dehydrated or who have intractable vomiting.

Absorbents (eg, Kaopectate, aluminum hydroxide) help patients have more control over the timing of defecation. However, they do not alter the course of the disease or reduce fluid loss.

An interval of at least 1-2 hours should elapse when using other medications with absorbents.
Antisecretory agents, such as bismuth subsalicylate (Pepto-Bismol), may be useful. The dose is 30 mL every 30 minutes, not to exceed 8-10 doses.
Antiperistaltics (opiate derivatives) should not be used in patients with fever, systemic toxicity, or bloody diarrhea or in patients whose condition either shows no improvement or deteriorates.
Diphenoxylate with atropine (Lomotil) is available in tablets (2.5 mg of diphenoxylate) and liquid (2.5 mg of diphenoxylate/5 mL). The initial dose for adults is 2 tablets 4 times a day (ie, 20 mg/d). The dose is tapered as diarrhea improves.
Loperamide (Imodium) is available over the counter as 2-mg capsules and as a liquid (1 mg/5 mL). It increases the intestinal absorption of electrolytes and water and decreases intestinal motility and secretion. The dose in adults is 4 mg initially, followed by 2 mg after each diarrhea stool, not to exceed 16 mg in a 24-hour period.

If symptoms persist beyond 3-4 days, the specific etiology should be determined by performing stool cultures. If symptoms persist and the pathogen is isolated, specific treatment should be initiated.

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

Class Summary

The main objective is adequate rehydration and electrolyte supplementation. This can be achieved with ORS or intravenous solutions (eg, isotonic sodium chloride solution, lactated Ringer solution).

Lactated Ringer solution with NS

Both fluids are essentially isotonic and have equivalent volume-restorative properties. While some differences exist between metabolic changes observed with administration of large quantities of either fluid, for practical purposes and in most situations, differences are clinically irrelevant. No demonstrable difference exists in hemodynamic effect, morbidity, or mortality between resuscitation using either NS or LR.

Oral electrolyte mixtures (Rehydralyte, Pedialyte)

Acts by glucose-facilitated absorption of sodium and water, which is unaffected in diseases such as cholera. Oral rehydration is achieved using clear liquids and sodium-containing and 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.

Class Summary

Adsorbents (eg, attapulgite, aluminum hydroxide) help patients have more control over the timing of defecation but do not alter the course of the disease or reduce fluid loss. Antisecretory agents (eg, bismuth subsalicylate) may be useful. Antiperistaltics (opiate derivatives) should not be used in patients with fever, systemic toxicity, bloody diarrhea, or in patients whose condition either shows no improvement or deteriorates.

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Attapulgite (Kaopectate, Diasorb)

Adsorbent and protectant that controls diarrhea.

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Aluminum hydroxide (Amphojel, Dialume, ALternaGEL)

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

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Bismuth subsalicylate (Pepto-Bismol)

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

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Diphenoxylate and atropine (Lomotil, Lonox)

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

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

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Loperamide (Imodium)

Acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. Prolongs movement of electrolytes and fluid through bowel and increases viscosity and loss of fluids and electrolytes.

Available over the counter in 2-mg capsules and liquid (1 mg/5 mL).

Class Summary

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

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Ciprofloxacin (Cipro)

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

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Norfloxacin (Noroxin)

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

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Trimethoprim/sulfamethoxazole (Bactrim DS, Septra DS)

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

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Doxycycline (Doryx, Vibramycin, Vibra-Tabs)

For V cholerae or V parahaemolyticus infections. Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.

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Rifaximin (Xifaxan, RedActiv, Flonorm)

Nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the GI tract (ie, gram-positive, gram-negative, aerobic, anaerobic). Rifampin structural analog. Binds to beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. Indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.

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 orSalmonella or Shigella organisms until they become culture-negative without antibiotics. These people should not return to work until that time.

No vaccine available canprevent norovirus infection. An early study conducted in a controlled setting assessed the safety, immunogenicity, and efficacy of an investigational, intranasally delivered norovirus viruslike particle (VLP) vaccine to prevent acute viral gastroenteritis. Results suggest the vaccine protects against illness and infection after exposure to the Norwalk virus and could potentially prevent infection in susceptible, high-risk populations. The vaccine has not been tested in the natural setting, however.[12]

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 Salmonellaand Campylobacter organisms. No evidence of adverse health effects is found in the well-controlled clinical trials involving irradiated food.

Prophylaxis for traveler's diarrhea is not recommended routinely because of the risk of adverse effects from the drugs (eg, rash, anaphylaxis, vaginal candidiasis) and the development of resistant gut flora. Possible regimens for prophylaxis include bismuth subsalicylate (Pepto-Bismol, 524 mg PO qid with meals and qhs), doxycycline (100 mg PO qd; resistance documented in many areas of the world), TMP/SMX (160 mg/800 mg 1 double-strength tab qd), or norfloxacin (400 mg PO qd; fluoroquinolones should not be prescribed to children or pregnant women). No significant resistance to the fluoroquinolones has been reported in high-risk areas, and they are the most effective antibiotics in regions where susceptibilities are not known.

Complications 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)
Reactive arthritis
Hemolytic uremic syndrome (E coli O157:H7)

Irritable bowel symptoms may follow acute gastroenteritis.