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Overview of Gastroenteritis
Gastroenteritis is inflammation of the lining of the stomach and small and large intestines. Most cases are infectious, although gastroenteritis may occur after ingestion of drugs and chemical toxins (eg, metals, plant substances). Acquisition may be foodborne, waterborne, or via person-to-person spread. In the US, an estimated 1 in 6 people contracts foodborne illness each year. Symptoms include anorexia, nausea, vomiting, diarrhea, and abdominal discomfort. Diagnosis is clinical or by stool culture, although PCR and immunoassays are increasingly used. Treatment is symptomatic, although some parasitic and some bacterial infections require specific anti-infective therapy.
Gastroenteritis is usually uncomfortable but self-limited. Electrolyte and fluid loss is usually little more than an inconvenience to an otherwise healthy adult but can be grave for people who are very young (see Dehydration in Children), elderly, or immunocompromised or who have serious concomitant illnesses. Worldwide, an estimated 1.5 million children die each year from infectious gastroenteritis; although high, this number represents one half to one quarter of previous mortality. Improvements in water sanitation in many parts of the world and the appropriate use of oral rehydration therapy for infants with diarrhea are likely responsible for this decrease.
Infectious gastroenteritis may be caused by viruses, bacteria, or parasites. Many specific organisms are discussed further in the Infectious Diseases section.
The viruses most commonly implicated are
Viruses are the most common cause of gastroenteritis in the US. They infect enterocytes in the villous epithelium of the small bowel. The result is transudation of fluid and salts into the intestinal lumen; sometimes, malabsorption of carbohydrates worsens symptoms by causing osmotic diarrhea. Diarrhea is watery. Inflammatory diarrhea (dysentery), with fecal WBCs and RBCs or gross blood, is uncommon. Four categories of viruses cause most gastroenteritis: norovirus and rotavirus cause the majority of viral gastroenteritis, followed by astrovirus and enteric adenovirus.
Norovirus infects people of all ages. Since the introduction of rotavirus vaccines, norovirus has become the most common cause of acute gastroenteritis in the US, including in children. Infections occur year-round, but 80% occur from November to April. Norovirus is now the principal cause of sporadic and epidemic viral gastroenteritis in all age groups; however, the peak age is between 6 mo and 18 mo. Large waterborne and foodborne outbreaks occur. Person-to-person transmission also occurs because the virus is highly contagious. This virus causes most cases of gastroenteritis epidemics on cruise ships and in nursing homes. Incubation is 24 to 48 h.
Rotavirus is the most common cause of sporadic, severe, dehydrating diarrhea in young children worldwide (peak incidence, 3 to 15 mo). Its incidence has decreased by about 80% in the US since the introduction of routine rotavirus immunization. Rotavirus is highly contagious; most infections occur by the fecal-oral route. Adults may be infected after close contact with an infected infant. The illness in adults is generally mild. Incubation is 1 to 3 days. In temperate climates, most infections occur in the winter. Each year in the US, a wave of rotavirus illness begins in the Southwest in November and ends in the Northeast in March.
Astrovirus can infect people of all ages but usually infects infants and young children. Infection is most common in winter. Transmission is by the fecal-oral route. Incubation is 3 to 4 days.
Adenoviruses are the 4th most common cause of childhood viral gastroenteritis. Infections occur year-round, with a slight increase in summer. Children < 2 yr are primarily affected. Transmission is by the fecal-oral route. Incubation is 3 to 10 days.
The bacteria most commonly implicated are
Escherichia coli (especially serotype O157:H7)
Bacterial gastroenteritis is less common than viral. Bacteria cause gastroenteritis by several mechanisms.
Enterotoxins are produced by certain species (eg, Vibrio cholerae, enterotoxigenic strains of E. coli) that adhere to intestinal mucosa without invading. These toxins impair intestinal absorption and cause secretion of electrolytes and water by stimulating adenylate cyclase, resulting in watery diarrhea. Clostridium difficile produces a similar toxin.
Exotoxins that are ingested in contaminated food are produced by some bacteria (eg, Staphylococcus aureus,Bacillus cereus,Clostridium perfringens—see Clostridium perfringens Food Poisoning). The exotoxin can cause gastroenteritis without bacterial infection. These toxins generally cause acute nausea, vomiting, and diarrhea within 12 h of ingestion of contaminated food. Symptoms abate within 36 h.
Mucosal invasion occurs with other bacteria (eg, Shigella,Salmonella,Campylobacter, some Escherichia coli subtypes) that invade the mucosa of the small bowel or colon and cause microscopic ulceration, bleeding, exudation of protein-rich fluid, and secretion of electrolytes and water. The invasive process and its results can occur whether or not the organism produces an enterotoxin. The resulting diarrhea contains WBCs and RBCs and sometimes gross blood.
Salmonella and Campylobacter are the most common bacterial causes of diarrheal illness in the US. Both infections are most frequently acquired through undercooked poultry; unpasteurized milk is also a possible source. Campylobacter is occasionally transmitted from dogs or cats with diarrhea. Salmonella can be transmitted by consuming undercooked eggs and by contact with reptiles, birds, or amphibians. Species of Shigella are the 3rd most common bacterial cause of diarrhea in the US and are usually transmitted person to person, although foodborne epidemics occur. Shigella dysenteriae type 1 (not present in the US) produces Shiga toxin, which can cause hemolytic-uremic syndrome.
Several different subtypes of E. coli cause diarrhea. The epidemiology and clinical manifestations vary greatly depending on the subtype:
EnterohemorrhagicE. coli is the most clinically significant subtype in the US. It produces Shiga toxin, which causes bloody diarrhea (hemorrhagic colitis). Thus, these subtypes are sometimes termed Shiga toxin–producing E. coli (STEC). E. coli O157:H7 is the most common strain of this subtype in the US. Undercooked ground beef, unpasteurized milk and juice, and contaminated water are possible sources. Person-to-person transmission is common in the day care setting. Outbreaks associated with exposure to water in recreational settings (eg, pools, lakes, water parks) have also been reported. Hemolytic-uremic syndrome is a serious complication that develops in 5 to 10% of STEC cases (and 10 to 15% of O157:H7), most commonly among the young and old.
EnterotoxigenicE. coli produces two toxins (one similar to cholera toxin) that cause watery diarrhea. This subtype is the most common cause of traveler’s diarrhea in people visiting the developing world.
EnteropathogenicE. coli causes watery diarrhea. Once a common cause of diarrhea outbreaks in nurseries, this subtype is now rare.
EnteroinvasiveE. coli causes bloody or nonbloody diarrhea, primarily in the developing world. It is rare in the US.
EnteroaggregativeE. coli causes diarrhea of lesser severity but longer duration than the other subtypes. As with some of the other subtypes, it is more common in the developing world and can be a cause of traveler's diarrhea.
Each of these E. coli subtypes can be detected in stool by PCR, typically using a multiplex panel. Sometimes more than one organism is detected simultaneously, the clinical significance of which is unclear.
In the past, Clostridium difficile infection occurred almost exclusively in hospitalized patients receiving antibiotics. With the emergence of the hypervirulent NAP1 strain in the US in the late 2000s, many community-associated cases are now occurring.
Several other bacteria cause gastroenteritis, but most are uncommon in the US. Yersinia enterocolitica can cause gastroenteritis or a syndrome that mimics appendicitis. It is transmitted by undercooked pork, unpasteurized milk, or contaminated water. Several Vibrio species (eg, V. parahaemolyticus) cause diarrhea after ingestion of undercooked seafood. V. cholerae sometimes causes severe dehydrating diarrhea in the developing world and is a particular concern after natural disasters or in refugee camps. Listeria can rarely cause food-borne gastroenteritis but more often causes bloodstream infection or meningitis in pregnant women, neonates (see Neonatal Listeriosis), or the elderly. Aeromonas is acquired from swimming in or drinking contaminated fresh or brackish water. Plesiomonas shigelloides can cause diarrhea in patients who have eaten raw shellfish or traveled to tropical regions of the developing world.
The parasites most commonly implicated are
Certain intestinal parasites, notably Giardia intestinalis (G. lamblia), adhere to or invade the intestinal mucosa, causing nausea, vomiting, diarrhea, and general malaise. Giardiasis occurs in every region of the US and throughout the world. The infection can become chronic and cause a malabsorption syndrome. It is usually acquired via person-to-person transmission (often in day care centers) or from contaminated water.
Cryptosporidium parvum causes watery diarrhea sometimes accompanied by abdominal cramps, nausea, and vomiting. In healthy people, the illness is self-limited, lasting about 2 wk. In immunocompromised patients, illness may be severe, causing substantial electrolyte and fluid loss. Cryptosporidium is usually acquired through contaminated water. It is not easily killed by chlorine and is the most common cause of recreational waterborne illness in the US, accounting for about three fourths of outbreaks.
Other parasites that can cause symptoms similar to those of cryptosporidiosis include Cyclospora cayetanensis and, in immunocompromised patients, Cystoisospora (Isospora) belli and a collection of organisms referred to as microsporidia (eg, Enterocytozoon bieneusi, Encephalitozoon intestinalis). Entamoeba histolytica (see amebiasis) is a common cause of subacute bloody diarrhea in the developing world but is rare in the US.
The character and severity of symptoms of gastroenteritis vary. Generally, onset is sudden, with anorexia, nausea, vomiting, abdominal cramps, and diarrhea (with or without blood and mucus). Malaise, myalgias, and prostration may occur. The abdomen may be distended and mildly tender; in severe cases, muscle guarding may be present. Gas-distended intestinal loops may be palpable. Hyperactive bowel sounds are present on auscultation even without diarrhea (an important differential feature from paralytic ileus, in which bowel sounds are absent or decreased). Persistent vomiting and diarrhea can result in intravascular fluid depletion with hypotension and tachycardia. In severe cases, shock, with vascular collapse and oliguric renal failure, occurs.
If vomiting is the main cause of fluid loss, metabolic alkalosis with hypochloremia can occur. If diarrhea is more prominent, acidosis is more likely. Both vomiting and diarrhea can cause hypokalemia. Hyponatremia may develop, particularly if hypotonic fluids are used in replacement therapy.
In viral infections, watery diarrhea is the most common symptom; stools rarely contain mucus or blood.
Rotavirus gastroenteritis in infants and young children may last 5 to 7 days. Vomiting occurs in 90% of patients, and fever > 39° C (>102.2° F) occurs in about 30%.
Norovirus typically causes acute onset of vomiting, abdominal cramps, and diarrhea, with symptoms lasting only 1 to 2 days. In children, vomiting is more prominent than diarrhea, whereas in adults, diarrhea usually predominates. Patients may also have fever, headache, and myalgias.
The hallmark of adenovirus gastroenteritis is diarrhea lasting 1 to 2 wk. Affected infants and children may have mild vomiting that typically starts 1 to 2 days after the onset of diarrhea. Low-grade fever occurs in about 50% of patients. Respiratory symptoms may be present. Symptoms are generally mild but can last longer than with other viral causes of gastroenteritis.
Astrovirus causes a syndrome similar to mild rotavirus infection.
E. coli O157:H7 infection usually begins with watery diarrhea for 1 to 2 days, followed by bloody diarrhea. Fever is absent or low grade.
The spectrum of illness with C. difficile infection ranges from mild abdominal cramps and mucus-filled diarrhea to severe hemorrhagic colitis and shock.
Parasitic infections typically cause subacute or chronic diarrhea. Most cause nonbloody diarrhea; an exception is E. histolytica, which causes amebic dysentery (see Amebiasis). Fatigue and weight loss are common when diarrhea is persistent.
Findings suggestive of gastroenteritis include copious, watery diarrhea; ingestion of potentially contaminated food (particularly during a known outbreak), untreated surface water, or a known GI irritant; recent travel; or contact with certain animals or similarly ill people.
E. coli O157:H7–induced diarrhea is notorious for appearing to be a hemorrhagic rather than an infectious process, manifesting as GI bleeding with little or no stool. Hemolytic-uremic syndrome may follow as evidenced by renal failure and hemolytic anemia.
Recent oral antibiotic use (within 3 mo) must raise suspicion for C. difficile infection. However, about one fourth of patients with community-associated C. difficile infection do not have a history of recent antibiotic use.
Stool testing is guided by clinical findings and the organisms that are suspected based on patient history and epidemiologic factors (eg, immunosuppression, exposure to a known outbreak, recent travel, recent antibiotic use). Cases are typically stratified into
Multiplex PCR platforms that can identify causative organisms in each of these categories are being used more often. However, this testing is expensive, and because the categories are distinguishable clinically, se it is usually more cost-effective to test for specific microorganisms depending on the type and duration of diarrhea.
Acute watery diarrhea is probably viral and testing is not indicated unless the diarrhea persists. Although rotavirus and enteric adenovirus infections can be diagnosed using commercially available rapid assays that detect viral antigen in the stool, these assays are rarely indicated.
Subacute and chronic watery diarrhea require testing for parasitic causes, typically with microscopic stool examination for ova and parasites. Fecal antigen tests are available for Giardia, Cryptosporidia, and Entamoeba histolytica.
Acute inflammatory diarrhea without gross blood can be recognized by the presence of WBCs on stool examination. Patients should have stool culture for typical enteric pathogens (eg, Salmonella, Shigella, Campylobacter, E. coli).
Acute inflammatory diarrhea with gross blood should also prompt testing specifically for E. coli O157:H7, as should nonbloody diarrhea during a known outbreak. Specific cultures must be requested because this organism is not detected on standard stool culture media. Alternatively, a rapid enzyme assay for the detection of Shiga toxin in stool can be done; a positive test indicates infection with E. coli O157:H7 or one of the other serotypes of enterohemorrhagic E. coli. (Note: Shigella species in the US do not produce Shiga toxin.) However, a rapid enzyme assay is not as sensitive as culture. PCR is used to detect Shiga toxin in some centers.
Adults with grossly bloody diarrhea should usually have sigmoidoscopy with cultures and biopsy. Appearance of the colonic mucosa may help diagnose amebic dysentery, shigellosis, and E. coli O157:H7 infection, although ulcerative colitis may cause similar lesions.
Patients with a history of recent antibiotic use or other risk factors for C. difficile infection (eg, inflammatory bowel disease, use of proton pump inhibitors) should have a stool assay for C. difficiletoxin, but testing should also be done in patients with significant illness even when these risk factors are not present because about 25% of cases of C. difficile infection currently occur in people without identified risk factors. Historically, enzyme immunoassays for toxins A and B were used to diagnose C. difficile infection. However, nucleic acid amplification tests targeting one of the C. difficile toxin genes or their regulator have been shown to have higher sensitivity and are now the diagnostic tests of choice.
Serum electrolytes, BUN, and creatinine should be obtained to evaluate hydration and acid-base status in patients who appear seriously ill. CBC is nonspecific, although eosinophilia may indicate parasitic infection. Renal function tests and CBC should be done about a week after the start of symptoms in patients with E. coli O157:H7 to detect early-onset hemolytic-uremic syndrome. It is unclear whether this testing is necessary in patients with non–E. coli O157:H7 Shiga toxin infection.
Supportive treatment is all that is needed for most patients. Bed rest with convenient access to a toilet or bedpan is desirable. Oral glucose-electrolyte solutions, broth, or bouillon may prevent dehydration or treat mild dehydration. Even if vomiting, the patient should take frequent small sips of such fluids; vomiting may abate with volume replacement. For patients with E. coli O157:H7 infection, rehydration with isotonic IV fluids may attenuate the severity of any renal injury should hemolytic-uremic syndrome develop. Children may become dehydrated more quickly and should be given an appropriate rehydration solution (several are available commercially—see Oral Rehydration). Carbonated beverages and sports drinks lack the correct ratio of glucose to sodium and thus are not appropriate, particularly for children < 5 yr. If the child is breastfed, breastfeeding should continue. If vomiting is protracted or if severe dehydration is prominent, IV replacement of volume and electrolytes is necessary (see Intravenous Fluid Resuscitation).
When the patient can tolerate fluids without vomiting and the appetite has begun to return, food may be gradually restarted. There is no demonstrated benefit from restriction to bland food (eg, cereal, gelatin, bananas, toast). Some patients have temporary lactose intolerance.
Antidiarrheal agents are safe for patients > 2 yr with watery diarrhea (as shown by heme-negative stool). However, antidiarrheals may cause deterioration of patients with C. difficile or E. coli O157:H7 infection and thus should not be given to any patient with recent antibiotic use or heme-positive stool, pending specific diagnosis. Effective antidiarrheals include loperamide 4 mg po initially, followed by 2 mg po for each subsequent episode of diarrhea (maximum of 6 doses/day or 16 mg/day), or diphenoxylate 2.5 to 5 mg tid or qid in tablet or liquid form. For children, loperamide is used. The dose for children 13 to 21 kg is 1 mg after the first loose stool then 1 mg after each subsequent loose stool (maximum dose is 3 mg/day); for children 21 to 28 kg, 2 mg after the first loose stool then 1 mg after each subsequent loose stool (maximum dose is 4 mg/day); and for children 27 to 43 kg, up to age 12, 2 mg after the first loose stool followed by 1 mg after each subsequent loose stool (maximum dose is 6 mg/day).
If vomiting is severe and a surgical condition has been excluded, an antiemetic may be beneficial. Drugs useful in adults include prochlorperazine 5 to 10 mg IV tid or qid, or 25 mg per rectum bid and promethazine 12.5 to 25 mg IM tid or qid, or 25 to 50 mg per rectum qid. These drugs are usually avoided in children because of lack of demonstrated efficacy and the high incidence of dystonic reactions. Ondansetron is safe and effective in decreasing nausea and vomiting in children and in adults, including those with gastroenteritis, and is available as a standard tablet, oral disintegrating pill, or IV formulation. The dose for adults is 4 or 8 mg po or IV tid. For children, the IV dose is 0.15 or 0.3 mg/kg (maximum 16 mg) and the oral dose for children 8 to 15 kg is 2 mg, for children > 15 to 30 kg, 4 mg, and for children > 30 kg, 8 mg. A single dose of ondansetron is usually adequate for children, but if needed the dose may be repeated q 8 h for 2 more doses; children still vomiting after 24 h require reevaluation.
Although probiotics appear to briefly shorten the duration of diarrhea, there is insufficient evidence that they affect major clinical outcomes (eg, decrease the need for IV hydration and/or hospitalization) to support their routine use in the treatment or prevention of infectious diarrhea.
Empiric antibiotics are generally not recommended except for certain cases of traveler’s diarrhea or when suspicion of Shigella or Campylobacter infection is high (eg, contact with a known case). Otherwise, antibiotics should not be given until stool culture results are known, particularly in children, who have a higher rate of infection with E. coli O157:H7 (antibiotics increase the risk of hemolytic-uremic syndrome in patients infected with E. coli O157:H7).
In proven bacterial gastroenteritis, antibiotics are not always required. They do not help with Salmonella and prolong the duration of shedding in the stool. Exceptions include immunocompromised patients, neonates, and patients with Salmonella bacteremia. Antibiotics are also ineffective against toxic gastroenteritis (eg, S. aureus,B. cereus,C. perfringens). Indiscriminate use of antibiotics fosters the emergence of drug-resistant organisms. However, certain infections do require antibiotics (see Table: Selected Oral Antibiotics for Infectious Gastroenteritisa).
Initial management of C. difficile colitis involves stopping the causative antibiotic if possible. Mild cases are treated with oral metronidazole. More severe cases should be treated with oral vancomycin. Unfortunately, recurrences are common with either regimen, occurring in about 20% of patients. A newer drug, fidaxomicin, may have a slightly lower relapse rate but is expensive. Many centers are using fecal microbial transplantation for patients with multiple recurrences of C. difficile colitis. This treatment has been shown to be safe and effective in adults and children (see Clostridium difficile –Induced Diarrhea : Treatment).
For cryptosporidiosis, a 3-day course of nitazoxanide may be helpful in immunocompetent patients. The dose is 100 mg po bid for children 1 to 3 yr, 200 mg po bid for children 4 to 11 yr, and 500 mg po bid for children ≥ 12 yr and adults. Giardiasis is treated with metronidazole or nitazoxanide.
Selected Oral Antibiotics for Infectious Gastroenteritisa
Two live-attenuated oral rotavirus vaccines are available that are safe and effective against the majority of strains responsible for disease. Rotavirus immunization is part of the recommended infant vaccination schedule (see Table: Recommended Immunization Schedule for Ages 0–6 yr).
Prevention of infection is complicated by the frequency of asymptomatic infection and the ease with which many agents, particularly viruses, are transmitted from person to person. In general, proper procedures for handling and preparing food must be followed. Travelers should avoid potentially contaminated food and drink.
To prevent recreational waterborne infections, people should not swim if they have diarrhea. Infants and toddlers should have frequent diaper checks and should be changed in a bathroom and not near the water. Swimmers should avoid swallowing water when they swim.
Infants and other immunocompromised people are particularly predisposed to developing severe cases of salmonellosis and should not be exposed to reptiles, birds, or amphibians, which commonly carry Salmonella.
Breastfeeding affords some protection to neonates and infants. Caregivers should wash their hands thoroughly with soap and water after changing diapers, and diaper-changing areas should be disinfected with a freshly prepared solution of 1:64 household bleach (¼ cup diluted in 1 gallon of water). Children with diarrhea should be excluded from child care facilities for the duration of symptoms. Children infected with enterohemorrhagic E. coli or Shigella should also have two negative stool tests before readmission to the facility.
Drug NameSelect Trade
trimethoprimNo US brand name
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