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, medications, and chemical toxins (eg, metals, plant substances). Acquisition may be foodborne, waterborne, person-to-person spread, or occasionally through zoonotic spread. Symptoms include anorexia, nausea, vomiting, diarrhea, and abdominal discomfort. Diagnosis is clinical, by stool culture, polymerase chain reaction testing, or immunoassays. Treatment is supportive and directed at symptoms, but some parasitic and some bacterial infections require specific anti-infective therapy.
Most episodes of gastroenteritis are self-limited but cause uncomfortable symptoms. Electrolyte and fluid loss is usually primarily an inconvenience to an otherwise healthy adult but can be serious or life-threatening for people who are very young (see Dehydration in Children), who are older, or who are immunocompromised or have serious concomitant illnesses. After initial recovery from acute gastroenteritis, affected people can also develop post-infectious irritable bowel syndrome and dyspepsia (1).
Worldwide, an estimated 1.6 million people die each year of infectious gastroenteritis (2); although high, this number represents a significant decrease from 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.
In the United States, each year approximately 48 million, or 1 in 6, people contract a foodborne illness (a major route of transmission for gastroenteritis-causing pathogens) and 3,000 die of one (3).
General references
1. Porcari S, Ingrosso MR, Maida M, et al: Prevalence of irritable bowel syndrome and functional dyspepsia after acute gastroenteritis: systematic review and meta-analysis [published correction appears in Gut 2025 Jan 17;74(2):e12. doi: 10.1136/gutjnl-2023-331835corr1]. Gut 73(9):1431-1440, 2024. doi:10.1136/gutjnl-2023-331835
2. GBD 2016 Diarrhoeal Disease Collaborators: Estimates of the global, regional, and national morbidity, mortality, and aetiologies of diarrhoea in 195 countries: A systematic analysis for the Global Burden of Disease Study 2016. Lancet Infect Dis 18(11):1211–1228, 2018. doi: 10.1016/S1473-3099(18)30362-1
3. Centers for Disease Control and Prevention: About Food Safety. Accessed March 27, 2025.
Etiology of Gastroenteritis
Infectious gastroenteritis may be caused by viruses, bacteria, or parasites. Many specific organisms are discussed further in the Infectious Diseases section.
Viral gastroenteritis
Viruses are the most common cause of gastroenteritis in the United States, and most viral gastroenteritis is caused by:
Norovirus affects people of all ages including infants and toddlers (1, 2). Outbreaks and epidemics occur year-round with a peak in the United States in the winter months of November to April. Transmission is by direct contact, foodborne, or fecal-oral routes. Incubation period is 24 to 48 hours.
Rotavirus affects young children, with a peak age of 3 to 15 months. In areas where vaccine use is (or was) not widespread, rotavirus occurs in a seasonal pattern. In areas where vaccine is commonly used, the overall incidence is lower, with a flattening of the seasonal peak and a biennial pattern with alternating years of higher and lower activity (3, 4). Transmission is primarily by the fecal-oral route. Incubation period is 1 to 3 days.
Most other viral gastroenteritis infections are caused by astrovirus or enteric adenovirus.
Astrovirus can infect people of all ages but usually infects infants and young children. In temperate climates, infection is most common in winter months, and in tropical regions, infection is more common in summer months. Transmission is by the fecal-oral route. Incubation is 3 to 4 days (5).
Adenoviruses are the fourth most common cause of childhood viral gastroenteritis. Infections occur year-round, with a slight increase in summer. Children < 2 years of age are primarily affected. Transmission is by the fecal-oral route as well as by respiratory droplets. Incubation is 3 to 10 days (6).
Viruses infect enterocytes in the villous epithelium of the small bowel. The result is transudation of fluid and electrolytes into the intestinal lumen; sometimes, unabsorbed carbohydrates resulting from malabsorption in the affected bowel subsequently worsen symptoms by causing osmotic diarrhea. Diarrhea is watery. Inflammatory diarrhea (dysentery), with fecal white blood cells (WBCs) and red blood cells (RBCs) or gross blood, is uncommon.
In patients with immunocompromise, additional viruses (eg, cytomegalovirus, enterovirus) can cause gastroenteritis.
Bacterial gastroenteritis
The bacteria most commonly implicated are:
Escherichia coli (especially serotype O157:H7)
Staphylococci, causing staphylococcal food poisoning
Bacterial gastroenteritis is less common than viral. Bacteria cause gastroenteritis by several mechanisms (7).
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. C. difficile produces a similar toxin.
Exotoxins that are ingested in contaminated food are produced by some bacteria (eg, Staphylococcus aureus, Bacillus cereus, Clostridium perfringens). The exotoxin can cause gastroenteritis without bacterial infection. These toxins generally cause acute nausea, vomiting, and diarrhea within 12 hours of ingestion of contaminated food. Symptoms abate within 36 hours.
Mucosal invasion occurs with other bacteria (eg, Shigella, Salmonella, Campylobacter, C. difficile, some E. coli subtypes) that invade the mucosa of the small bowel or colon and cause 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 has evidence of this invasion and inflammation with WBCs and RBCs present on microscopy and sometimes with gross blood.
Salmonella and Campylobacter are common bacterial causes of diarrheal illness in the United States. 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 also common bacterial causes of diarrhea in the United States and are usually transmitted person to person, although foodborne epidemics occur. Shigella dysenteriae type 1, which is rare in the United States (8), produces Shiga toxin, which can cause hemolytic-uremic syndrome.
E. coli gastroenteritis can be caused by several different subtypes of the bacteria. The epidemiology and clinical manifestations vary greatly depending on the subtype.
In the past, Clostridioides difficile infection occurred almost exclusively in hospitalized patients receiving antibiotics. With the emergence of the hypervirulent NAP1 strain in the United States in the late 2000s, many community-associated cases are now occurring. C. difficile is now probably the most common bacterial cause of diarrhea in the United States (9).
Pearls & Pitfalls
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Several other bacteria cause gastroenteritis, but most are uncommon in the United States. Yersinia enterocolitica can cause gastroenteritis or a syndrome that mimics appendicitis because patients may have pain in the right lower quadrant. 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 regions where people lack access to clean drinking water and sanitary disposal of human waste and is a particular concern after natural disasters or in refugee camps. Listeria can rarely cause foodborne gastroenteritis but more often causes bloodstream infection or meningitis in pregnant women, neonates (see Neonatal Listeriosis), or older adults. 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 Southeast Asia and Africa (10).
Parasitic gastroenteritis
The parasites most commonly implicated in high-resource countries are:
Certain intestinal parasites, notably Giardia intestinalis (G. lamblia), adhere to the intestinal mucosa, causing nausea, vomiting, diarrhea, and general malaise. Giardiasis occurs in every region of the United States and throughout the world. The infection can become chronic and may cause a malabsorption syndrome. It is usually acquired via person-to-person transmission (often in day care centers) or from ingestion of cysts in contaminated water or food (11).
Cryptosporidium parvum causes watery diarrhea and can sometimes be accompanied by abdominal cramps, nausea, and vomiting. In healthy people, the illness is self-limited, lasting about 2 weeks. In patients with immunocompromise, illness may be severe and prolonged, 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 United States, accounting for about three-fourths of outbreaks.
Other parasites that can cause symptoms similar to those of cryptosporidiosis include Cyclospora cayetanensis and, in patients with immunocompromise, 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 regions with poor sanitation but is rare in the United States. Amebiasis can cause an ulcerating colitis that mimics ulcerative colitis and must be excluded when that diagnosis is considered.
Etiology references
1. Flynn TG, Olortegui MP, Kosek MN: Viral gastroenteritis. Lancet 403(10429):862-876, 2024. doi:10.1016/S0140-6736(23)02037-8
2. Zhang P, Hao C, Di X, et al: Global prevalence of norovirus gastroenteritis after emergence of the GII.4 Sydney 2012 variant: a systematic review and meta-analysis. Front Public Health 12:1373322, 2024. doi:10.3389/fpubh.2024.1373322
3. Hallowell BD, Parashar UD, Curns A, DeGroote NP, Tate JE: Trends in the Laboratory Detection of Rotavirus Before and After Implementation of Routine Rotavirus Vaccination - United States, 2000-2018. MMWR Morb Mortal Wkly Rep 68(24):539-543, 2019. doi:10.15585/mmwr.mm6824a2
4. Sun ZW, Fu Y, Lu HL, et al: Association of Rotavirus Vaccines With Reduction in Rotavirus Gastroenteritis in Children Younger Than 5 Years: A Systematic Review and Meta-analysis of Randomized Clinical Trials and Observational Studies. JAMA Pediatr 175(7):e210347, 2021. doi:10.1001/jamapediatrics.2021.0347
5. Vu DL, Bosch A, Pintó RM, Guix S: Epidemiology of Classic and Novel Human Astrovirus: Gastroenteritis and Beyond. Viruses 9(2):33, 2017. doi:10.3390/v9020033
6. Shieh WJ: Human adenovirus infections in pediatric population - An update on clinico-pathologic correlation. Biomed J 45(1):38-49, 2022. doi:10.1016/j.bj.2021.08.009
7. Fleckenstein JM, Matthew Kuhlmann F, Sheikh A: Acute Bacterial Gastroenteritis. Gastroenterol Clin North Am 50(2):283-304, 2021. doi:10.1016/j.gtc.2021.02.002
8. Centers for Disease Control and Prevention (CDC): Clinical Overview of Shigellosis. Accessed April 3, 2025.
9. Johnson S, Lavergne V, Skinner AM, et al: Clinical practice guideline by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA): 2021 focused update guidelines on management of Clostridioides difficile infection in adults. Clin Infect Dis ciab549, 2021. doi: 10.1093/cid/ciab549
10. Janda JM, Abbott SL, McIver CJ: Plesiomonas shigelloides Revisited. Clin Microbiol Rev 29(2):349-374, 2016. doi:10.1128/CMR.00103-15
11. Lagunas-Rangel FA, Kameyama-Kawabe LY, Bermúdez-Cruz RM: Giardiavirus: an update. Parasitol Res 120(6):1943-1948, 2021. doi:10.1007/s00436-021-07167-y
Symptoms and Signs of Gastroenteritis
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 and myalgias 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. Hypovolemic shock with vascular collapse and oliguric acute kidney injury or kidney failure may occur in severe cases.
If vomiting is the main cause of fluid loss, metabolic alkalosis with hypochloremia can occur. If diarrhea is more prominent, metabolic acidosis is more likely. Both vomiting and diarrhea can cause hypokalemia. Hyponatremia may develop, particularly if hypotonic fluids are used in replacement therapy.
Viral gastroenteritis
In viral infections, watery diarrhea is the most common symptom; stools rarely contain mucus or blood. For manifestations specific to norovirus and rotavirus, see Norovirus Gastroenteritis and Rotavirus Gastroenteritis.
The hallmark of adenovirus gastroenteritis is diarrhea lasting 1 to 2 weeks. 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 many patients. Respiratory symptoms may be present. Symptoms are generally mild but can last longer than with other viral causes of gastroenteritis (1).
Astrovirus causes a syndrome similar to mild rotavirus infection.
Cytomegalovirus can cause bloody diarrhea in patients with immunocompromise.
Bacterial gastroenteritis
Bacteria that cause invasive disease (eg, Shigella, Salmonella) are more likely to result in fever, prostration, and bloody diarrhea.
E. coli O157:H7 infection usually begins with severe abdominal cramps and 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.
Bacteria that produce an enterotoxin (eg, S. aureus, B. cereus, C. perfringens) usually cause watery diarrhea. S. aureus and some strains of B. cereus predominantly cause vomiting.
Parasitic gastroenteritis
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.
Symptoms and signs reference
1. Shieh WJ: Human adenovirus infections in pediatric population - An update on clinico-pathologic correlation. Biomed J 45(1):38-49, 2022. doi:10.1016/j.bj.2021.08.009
Diagnosis of Gastroenteritis
History and physical examination
Stool testing in select cases
Other gastrointestinal disorders that cause similar symptoms (eg, appendicitis, cholecystitis, ulcerative colitis) must be excluded (see also evaluation of diarrhea).
Findings suggestive of gastroenteritis include the following:
Copious, watery diarrhea
Ingestion of potentially contaminated food (particularly during a known outbreak), untreated surface water, or a known gastrointestinal irritant
Recent travel
Contact with infected people or certain animals
E. coli O157:H7–induced diarrhea is notorious for appearing to be a hemorrhagic rather than an infectious process, manifesting as gastrointestinal bleeding with little or no stool. Hemolytic-uremic syndrome may follow as evidenced by kidney failure and hemolytic anemia.
Recent oral antibiotic use (within 3 months) must raise suspicion for C. difficile infection. However, one-fifth to one-third of patients with community-associated C. difficile infection do not have a history of recent antibiotic use (1, 2, 3).
Stool testing
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) (4). Cases are typically stratified into:
Acute watery diarrhea
Subacute or chronic watery diarrhea
Acute inflammatory diarrhea
Multiplex polymerase chain reaction panels that can identify causative organisms in each of these categories are increasingly used (5). However, this testing is expensive, and because the categories are often distinguishable clinically or the disease courses are self-limiting, it is usually more cost-effective to test for specific microorganisms depending on the type and duration of diarrhea. In addition, polymerase chain reaction testing does not allow for antibiotic susceptibility testing as does a culture.
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 and are more sensitive than microscopic stool examination.
Acute inflammatory diarrhea without gross blood can be recognized by the presence of leukocytes 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 Shiga toxin-producing E. coli O157:H7 or one of the other serotypes of enterohemorrhagic E. coli. However, a rapid enzyme assay is not as sensitive as culture. In some centers, polymerase chain reaction testing is used to detect Shiga toxin.
Adults with grossly bloody diarrhea may require endoscopic evaluation (sigmoidoscopy or colonoscopy) for further evaluation. Candidates for endoscopy include at-risk patients such as those with a history of inflammatory bowel disease or immunocompromise (in the case of suspected cytomegalovirus colitis). Appearance of the colonic mucosa may help diagnose amebic dysentery, shigellosis, and E. coli O157:H7 infection, although ulcerative colitis may cause similar lesions. Biopsy and culture are helpful in making a diagnosis.
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. difficile toxin, but testing should also be done in patients with significant illness even when these risk factors are not present because approximately 25% of cases of C. difficile infection currently occur in people without identified risk factors (1, 2, 6). 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 are the diagnostic tests of choice in most cases.
General tests
Serum electrolytes, blood urea nitrogen (BUN), and creatinine should be obtained to evaluate hydration and acid-base status in patients who appear significantly volume depleted.
Complete blood count (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.
Diagnosis references
1. Chitnis AS, Holzbauer SM, Belflower RM, et al: Epidemiology of community-associated Clostridium difficile infection, 2009 through 2011. JAMA Intern Med 173(14):1359-1367, 2013. doi:10.1001/jamainternmed.2013.7056
2. Guh AY, Adkins SH, Li Q, et al: Risk Factors for Community-Associated Clostridium difficile Infection in Adults: A Case-Control Study. Open Forum Infect Dis 4(4):ofx171, 2017. doi:10.1093/ofid/ofx171
3. Guh AY, Mu Y, Winston LG, et al: Trends in U.S. Burden of Clostridioides difficile Infection and Outcomes. N Engl J Med 382(14):1320-1330, 2020. doi:10.1056/NEJMoa1910215
4. Riddle MS, DuPont HL, Connor BA: ACG Clinical Guideline: Diagnosis, Treatment, and Prevention of Acute Diarrheal Infections in Adults. Am J Gastroenterol 111(5):602-622, 2016. doi:10.1038/ajg.2016.126
5. Torres-Miranda D, Akselrod H, Karsner R, et al: Use of BioFire FilmArray gastrointestinal PCR panel associated with reductions in antibiotic use, time to optimal antibiotics, and length of stay. BMC Gastroenterol 20(1):246, 2020. doi: 10.1186/s12876-020-01394-w
6. Bai M, Guo H, Zheng XY: Inflammatory bowel disease and Clostridium difficile infection: clinical presentation, diagnosis, and management. Therap Adv Gastroenterol 16:17562848231207280, 2023. doi:10.1177/17562848231207280
Treatment of Gastroenteritis
Oral or IV rehydration
Consideration of antidiarrheal (antimotility) agents, unless C. difficile or E. coli O157:H7 infection is suspected
Antibiotics only in select cases
Supportive treatment is all that is needed for most patients. Bed rest with convenient access to a toilet or bedpan is desirable. Rehydration is critical for treatment of dehydration and to prevent unnecessary hospitalization. Antidiarrheal, antiemetic, and probiotic agents may be useful. Antimicrobial agents are used in select cases in which bacterial infection is suspected or documented.
Symptomatic treatment
Antidiarrheal (antimotility) agents are not recommended in children < 18 years of age with acute diarrhea). Use of antidiarrheal agents is contraindicated in children < 2 years of age. These agents are generally safe for adult patients 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, heme-positive or bloody stool, or diarrhea with fever, pending specific diagnosis (1).
Effective antidiarrheals include loperamide or diphenoxylate/atropine. Effective antidiarrheals include loperamide or diphenoxylate/atropine.
If vomiting is severe and a surgical condition (eg, small-bowel obstruction) has been excluded, an antiemetic may be beneficial. Medications useful in adults include ondansetron, prochlorperazine, and promethazine. In children, ondansetron has been shown to reduce the need for intravenous rehydration and to prevent hospitalizations (may be beneficial. Medications useful in adults include ondansetron, prochlorperazine, and promethazine. In children, ondansetron has been shown to reduce the need for intravenous rehydration and to prevent hospitalizations (2).
Pearls & Pitfalls
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Children who are still vomiting after 24 hours 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 (3, 4).
Rehydration
Oral glucose-electrolyte solutions, broth, or bouillon may prevent or treat mild dehydration. In children, if a rehydration solution is not available, either dilute apple juice or another fluid preferred by the child are also reasonable options (5). If the child is breastfed, breastfeeding should continue.
Even patients with vomiting should take frequent small sips of such fluids in between episodes of emesis; 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 kidney dysfunction 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). If vomiting is protracted, severe dehydration is present, or oral rehydration is not tolerated, 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. Although commonly recommended, there is no demonstrated benefit to restricting the diet to bland food (eg, cereal, gelatin, bananas, toast). Some patients have temporary lactose intolerance.
Antimicrobials
Empiric antibiotics are generally not recommended except for certain cases of traveler’s diarrhea, when suspicion of Shigella or Campylobacter infection is high (eg, contact with a known case), or if the patient is developing sepsis following international travel (6). 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 may prolong the duration of shedding in the stool. Exceptions include patients with immunocompromise, 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, increases the risk of adverse effects, and increases the potential for C. difficile infection. However, certain infections do require antibiotics (see table Treatment for Infectious Gastroenteritis).
Initial management of C. difficile colitis involves stopping the causative antibiotic if possible. The medication of choice to treat C. difficile colitis is oral vancomycin, which is superior to metronidazole. Unfortunately, recurrences occur in approximately 20% of patients receiving colitis is oral vancomycin, which is superior to metronidazole. Unfortunately, recurrences occur in approximately 20% of patients receivingvancomycin. Fidaxomicin may have a slightly lower relapse rate than . Fidaxomicin may have a slightly lower relapse rate thanvancomycin or metronidazole. The Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA) 2021 guidelines recommend fidaxomicin as preferred first-line therapy for new and recurrent cases of C. difficile infection (7). Monoclonal antibodies can be administered to patients to prevent risk of recurrence, especially in more severe cases (8). Vaccines for both the prevention and treatment of C. difficile infection are under investigation (9).
Many centers use fecal microbial transplantation (FMT) for patients with multiple recurrences of C. difficile colitis. This treatment generally has been shown to be safe and effective overall. Despite quality control and screening of fecal samples, there is still risk to the recipient from receiving donor stool, and FMT risks and benefits should be considered on a case-by-case basis (see treatment of recurrences of C. difficile-induced diarrhea) (10) (11). Fecal microbiota therapy for patients with recurrent ). Fecal microbiota therapy for patients with recurrentC. difficile infection can be administered either as oral capsules or as enema (12, 13).
For cryptosporidiosis, a course of nitazoxanide may be helpful in patients with immunocompromise. Giardiasis is treated with metronidazole or nitazoxanide. For cryptosporidiosis, a course of nitazoxanide may be helpful in patients with immunocompromise. Giardiasis is treated with metronidazole or nitazoxanide.
Treatment for Infectious Gastroenteritis*
Organism | Antibiotic (or Other Therapy) |
|---|---|
AzithromycinAzithromycin | |
Ciprofloxacin †Ciprofloxacin † | |
CiprofloxacinCiprofloxacin | |
Doxycycline §Doxycycline § | |
AzithromycinAzithromycin | |
Fidaxomicin Fidaxomicin | |
VancomycinVancomycin | |
Metronidazole ‖Metronidazole ‖ | |
Monoclonal antibodies (for severe infection, to prevent recurrence) | |
Fecal microbial transplant | |
Metronidazole ¶Metronidazole ¶ | |
Tinidazole ¶Tinidazole ¶ | |
TinidazoleTinidazole | |
MetronidazoleMetronidazole | |
NitazoxanideNitazoxanide | |
CiprofloxacinCiprofloxacin | |
AzithromycinAzithromycin | |
* Antibiotics are not indicated in most cases but may be used supportively with IV fluids to treat infections caused by specific organisms. | |
† Resistance is increasing. | |
‡ Antibiotic selection should be guided by susceptibility testing when available because resistance to doxycycline, fluoroquinolones, and sulfamethoxazole/trimethoprim (SMX/TMP) is increasing in certain areas and strains. In general, ‡ Antibiotic selection should be guided by susceptibility testing when available because resistance to doxycycline, fluoroquinolones, and sulfamethoxazole/trimethoprim (SMX/TMP) is increasing in certain areas and strains. In general,doxycycline is the recommended first-line antibiotic for non-pregnant adults. Azithromycin is first-line for children and pregnant women and second-line for others. Other recommendations vary, but SMX/TMP is generally a second-line antibiotic for children if the strain in an outbreak is susceptible. Ciprofloxacin is second- or third-line in non-pregnant adults and, although generally avoided in children, can be used as second-line if strains are resistant to SMX/TMP.is the recommended first-line antibiotic for non-pregnant adults. Azithromycin is first-line for children and pregnant women and second-line for others. Other recommendations vary, but SMX/TMP is generally a second-line antibiotic for children if the strain in an outbreak is susceptible. Ciprofloxacin is second- or third-line in non-pregnant adults and, although generally avoided in children, can be used as second-line if strains are resistant to SMX/TMP. | |
§ This antibiotic should not be given to pregnant women. | |
‖ Metronidazole is not recommended but may be used in patients intolerant of vancomycin and fidaxomicin.‖ Metronidazole is not recommended but may be used in patients intolerant of vancomycin and fidaxomicin. | |
¶ Treatment should be followed by a course of iodoquinol for 20 days or paromomycin for 7 days.¶ Treatment should be followed by a course of iodoquinol for 20 days or paromomycin for 7 days. | |
Treatment references
1. Shane AL, Mody RK, Crump JA, et al: 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea. Clin Infect Dis 65(12):e45-e80, 2017. doi:10.1093/cid/cix669
2. Niño-Serna LF, Acosta-Reyes J, Veroniki AA, Florez ID: Antiemetics in Children With Acute Gastroenteritis: A Meta-analysis. Pediatrics 145(4):e20193260, 2020. doi:10.1542/peds.2019-3260
3. Preidis GA, Weizman AV, Kashyap PC, Morgan RL: AGA technical review on the role of probiotics in the management of gastrointestinal disorders. Gastroenterology 159(2):708–738.e4, 2020. doi: 10.1053/j.gastro.2020.05.060
4. Nelwan EJ, Herdiman A, Kalaij AGI, Lauditta RK, Yusuf SM, Suarthana E: Role of probiotic as adjuvant in treating various infections: a systematic review and meta-analysis. BMC Infect Dis 24(1):505, 2024. doi:10.1186/s12879-024-09259-3
5. Freedman SB, Willan AR, Boutis K, Schuh S: Effect of Dilute Apple Juice and Preferred Fluids vs Electrolyte Maintenance Solution on Treatment Failure Among Children With Mild Gastroenteritis: A Randomized Clinical Trial. JAMA 315(18):1966-1974, 2016. doi:10.1001/jama.2016.5352
6. Riddle MS, DuPont HL, Connor BA: ACG Clinical Guideline: Diagnosis, Treatment, and Prevention of Acute Diarrheal Infections in Adults. Am J Gastroenterol 111(5):602-622, 2016. doi:10.1038/ajg.2016.126
7. Johnson S, Lavergne V, Skinner AM, et al: Clinical Practice Guideline by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA): 2021 Focused update guidelines on management of Clostridioides difficile infection in adults. Clin Infect Dis 73(5):e1029–e1044, 2021. doi: 10.1093/cid/ciab549
8. Akiyama S, Yamada A, Komaki Y, Komaki F, Micic D, Sakuraba A: Efficacy and Safety of Monoclonal Antibodies Against Clostridioides difficile Toxins for Prevention of Recurrent Clostridioides difficile Infection: A Systematic Review and Meta-Analysis. J Clin Gastroenterol 55(1):43–51, 2021. doi:10.1097/MCG.0000000000001330
9. Young VB: Vaccinating against Clostridioides difficile Infection. N Engl J Med 392(12):1237–1240, 2025. doi:10.1056/NEJMcibr2413794
10. Perler BK, Chen B, Phelps E, et al: Long-term efficacy and safety of fecal microbiota transplantation for treatment of recurrent : Long-term efficacy and safety of fecal microbiota transplantation for treatment of recurrentClostridioides difficile infection. J Clin Gastroenterol 54(8):701–706, 2020. doi: 10.1097/MCG.0000000000001281
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Prevention of Gastroenteritis
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.
Data are inconclusive regarding whether oral probiotic prevent gastroenteritis (1).
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 people with immunocompromise 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 (one-quarter cup diluted in 1 gallon of water [60 mL in 3.75 liters]). 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 2 negative stool tests before readmission to the facility.
Appropriate infection control measures (gloves, gown, hand hygiene) should be used in the medical care of patients with diarrhea (2, 3, 4).
Prevention references
1. Preidis GA, Weizman AV, Kashyap PC, Morgan RL: AGA Technical Review on the Role of Probiotics in the Management of Gastrointestinal Disorders. Gastroenterology 159(2):708–738.e4, 2020. doi:10.1053/j.gastro.2020.05.060
2. Riddle MS, Connor BA, Beeching NJ, et al: Guidelines for the prevention and treatment of travelers' diarrhea: a graded expert panel report. J Travel Med. 24(suppl_1):S57-S74, 2017. doi:10.1093/jtm/tax026
3. Riddle MS, DuPont HL, Connor BA: ACG Clinical Guideline: Diagnosis, Treatment, and Prevention of Acute Diarrheal Infections in Adults. Am J Gastroenterol 111(5):602-622, 2016. doi:10.1038/ajg.2016.126
4. Shane AL, Mody RK, Crump JA, et al: 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea. Clin Infect Dis 65(12):e45-e80, 2017. doi:10.1093/cid/cix669
Drugs Mentioned In This Article
