Emergent Treatment of Gastroenteritis

Updated: Oct 27, 2023
  • Author: Arthur Diskin, MD; Chief Editor: Steven C Dronen, MD, FAAEM  more...
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Gastroenteritis is a nonspecific term for various pathologic states of the gastrointestinal tract. The primary manifestation is diarrhea, but it may be accompanied by nausea, vomiting, and abdominal pain. A universal definition of diarrhea does not exist, although patients seem to have no difficulty defining their own situation. Although most definitions center on the frequency, consistency, and water content of stools, the author prefers defining diarrhea as stools that take the shape of their container.

The severity of illness may vary from mild and inconvenient to severe and life-threatening. Appropriate management requires extensive history and assessment; appropriate, general supportive treatment is often etiology-specific. Diarrhea associated with nausea and vomiting is referred to as gastroenteritis.

Diarrhea is one of the most common reasons patients seek medical care. In the developed world, it is one of the most common reasons for missing work, while in the developing world, it is a leading cause of death. In developing countries, diarrhea is a seasonal scourge usually worsened by natural phenomena, as evidenced by monsoon floods in Bangladesh in 1998,  Hurricane Katrina in 2005, or the earthquake in Haiti in 2010. [1] Prior to the coronavirus disease 2019 (COVID-19) pandemic, an estimated 179 million cases of acute gastroenteritis occurred every year in the United States. [2] Of these patients, 80-85% did not seek medical attention, and only 1-2% require hospital admission. [3] Diarrheal diseases can quickly reach epidemic proportions, rapidly overwhelming public health systems in even the most advanced societies.

A sharp decline in the incidence of norovirus outbreaks was observed in early 2020 owing to COVID-19–related measures, including limiting travel, physical distancing, mask-wearing, handwashing, and surface disinfection. [4, 5] As such measures are increasingly relaxed, an uptick in cases has occurred, and it is projected that norovirus cases will return to pre-pandemic levels by 2026. [6]



Infectious agents are the usual cause of acute gastroenteritis. These agents cause diarrhea by several mechanisms, including adherence, mucosal invasion, enterotoxin production, and/or cytotoxin production.

These mechanisms result in increased fluid secretion and/or decreased absorption. This produces an increased luminal fluid content that cannot be adequately reabsorbed, leading to dehydration and the loss of electrolytes and nutrients.

Diarrheal illnesses may be classified as follows:

  • Osmotic, due to an increase in the osmotic load presented to the intestinal lumen, either through excessive intake or diminished absorption

  • Inflammatory (or mucosal), when the mucosal lining of the intestine is inflamed

  • Secretory, when increased secretory activity occurs

  • Motile, caused by intestinal motility disorders

The small intestine is the prime absorptive surface of the gastrointestinal tract. The colon then absorbs additional fluid, transforming a relatively liquid fecal stream in the cecum to well-formed solid stool in the rectosigmoid.

Disorders of the small intestine result in increased amounts of diarrheal fluid with a concomitantly greater loss of electrolytes and nutrients.

Microorganisms may produce toxins that facilitate infection. Enterotoxins, generated by some bacteria (ie, enterotoxigenic Escherichia coli, Vibrio cholera) act directly on secretory mechanisms and produce a typical, copious watery (rice water) diarrhea. No mucosal invasion occurs. The small intestines are primarily affected, and an elevation of the adenosine monophosphate (AMP) levels is the common pathogenic mechanism.

Cytotoxin production by other bacteria (ie, Shigella dysenteriae, Vibrio parahaemolyticus, Clostridium difficile, enterohemorrhagic E coli) results in mucosal cell destruction that leads to bloody stools with inflammatory cells. A resulting decreased absorptive ability occurs.

Enterocyte invasion is the preferred method by which microbes such as Shigella and Campylobacter organisms and enteroinvasive E coli cause destruction and inflammatory diarrhea. Similarly, Salmonella and Yersinia species also invade cells but do not cause cell death. Hence, dysentery does not usually occur. However, these bacteria invade the bloodstream across the lamina propria and can cause enteric fevers such as typhoid.

Diarrheal illness occurs when microbial virulence overwhelms the normal host defenses. A large inoculum may overwhelm the host capacity to mount an effective defense. Normally, more than 100,000 E coli are required to cause disease, while only 10 Entamoeba,Giardia cysts, or norovirus particles may suffice to do the same. Some organisms (eg, V cholera, enterotoxigenic E coli) produce proteins that aid their adherence to the intestinal wall, thereby displacing the normal flora and colonizing the intestinal lumen.

In addition to the ingestion of pathogenic organisms or toxins, other intrinsic factors can lead to infection. An alteration of the normal bowel flora can create a biologic void that is filled by pathogens. This occurs most commonly after antibiotic administration, but infants are also at risk prior to the colonization with normal bowel flora.

The normally acidic pH of the stomach and colon is an effective antimicrobial defense. In achlorhydric states (ie, caused by antacids, histamine-2 [H2] blockers, proton pump inhibitors [PPIs], gastric surgery, decreased colonic anaerobic flora), this defense is weakened.

Hypomotility states may result in colonization by pathogens, especially in the proximal small bowel, where motility is the major mechanism for the removal of organisms. Hypomotility may be induced by antiperistaltic agents (eg, opiates, diphenoxylate and atropine [Lomotil], loperamide) or anomalous anatomy (eg, fistulae, diverticula, antiperistaltic afferent loops) and is inherent in disorders such as diabetes mellitus or scleroderma.

The immunocompromised host is more susceptible to infection, as evidenced by the wide spectrum of diarrheal pathogens in patients with acquired immunodeficiency syndrome (AIDS).

The exact mechanism of vomiting in acute diarrheal illness is not known, although serotonin release has been postulated as a cause, stimulating visceral afferent input to the chemoreceptor trigger zone in the lower brainstem. Preformed neurotoxins produced by Staphylococcus aureus and Bacillus cereus, when ingested, can cause severe vomiting.



Viral (50-70%) causes of gastroenteritis


Norovirus is the leading cause of viral gastroenteritis in the United States. Noroviruses (formerly known as Norwalk virus in the United States and as small, round structured virus [SRSV] in the United Kingdom), along with the sapoviruses (formerly known as Sapporo-like viruses), are members of the Caliciviridae family of viruses. The norovirus is a small, 26-40 nm, nonenveloped, single-stranded RNA virus classified as a Calicivirus. Sapoviruses, a cause of gastroenteritis, predominantly in children, are also in the Caliciviridae family. Five norovirus genogroups have been identified: GI, GII, GIII, GIV, and GV; many clusters (genotypes) have also been identified. In 2010, the land-based experience was far busier than usual. The dominating strain was GII-4 (New Orleans). Norovirus is often called the "winter vomiting disease" in Britain and the incidence seems to be higher in colder weather.

It is a highly infectious virus—with as few as 10-100 particles necessary for transmission—and is quite resistant to quaternary ammonia compounds, alcohol, detergent-based compounds, freezing, and heat (to 60o C). It is a very difficult virus to culture and measure; thus, studies on norovirus are limited, with researchers using a "surrogate," nonenveloped virus, Feline calicivirus (FCV), to assess the efficacy of disinfectants and other mitigation strategies. Some researchers have questioned the use of FCV as a surrogate since FCV is a respiratory virus and norovirus is a gastrointestinal (GI) virus and likely is more resilient than FCV due to the need for norovirus to survive in the hostile environment of the gut. Therefore, the results of testing performed to validate the efficacy of disinfectants and hand sanitizers possibly overestimate the actual effectiveness of these products on human norovirus.

It has been suggested that murine norovirus (MNV) can serve as a useful tool in assessing the risk of infection with human norovirus. It has been used as a surrogate to evaluate the resistance of human norovirus to disinfectants due to its similar characteristics (ie, resistance to basic and acidic pHs, capsid structure, genomic organization, and replication cycle) to human norovirus. [7]

Various modes of transmission exist including fecal-oral transmission (predominant), person to person, fecal contamination of food and/or water, fomite transmission, and airborne spread when in close proximity to someone vomiting, as the virus is easily aerosolized.

Between January 1996 and November 2000, 348 outbreaks of norovirus were reported to the Centers for Disease Control and Prevention (CDC). Of these, 39% of patients were contaminated by food, 12% by person to person, 3% by water, and 18% by unidentified sources. [8] Most of the food sources responsible were identified as oysters, salads, salad dressing, sandwiches, deli meats, cake and frosting, raspberries, drinking water, and ice. Shellfish have been implicated in some outbreaks, but it is not a frequent source on cruise ships, where the predominant mode of infection is believed to be fecal-oral and person-to-person from individuals who come onto the ships ill and do not report the illness or quarantine themselves in their cabins. [9]

Public vomiting episodes with aerosolization of the virus is likely a major source of spread in congested public locations such as cruise ships, schools, and casinos. The same study reveals that 39% contracted the disease in restaurants, 30% in nursing homes, 12% at school, 10% on vacation, and 9% remain unidentified. [9]

The CDC launched the National Outbreak Reporting System (NORS), a web-based platform for reporting waterborne, foodborne, and enteric disease outbreaks in 2009. Between 2009 and 2013, 10,756 acute gastroenteritis outbreaks were reported, with primary transmission modes of person-to-person contact, environmental contamination, and unknown. Norovirus accounted for largest percentage of cases (84$). [2]

The incubation period for the norovirus is between 12 and 48 hours. Some of the early symptoms include nausea, a sudden onset of vomiting, moderate diarrhea, headache, fever (~50%), chills, and myalgia and will last 12-60 hours. The clinical features suggestive of norovirus include the patient's presentation and the sudden onset of symptoms, with uncontrolled vomiting being a classic sign. Usually, more vomiting than diarrhea occurs. The virus is noninvasive of the colon; therefore, white blood cells (WBCs) are not seen in the stool, and hematochezia is rare. The severity and length of illness seen is often related to the then current predominant strain.

The natural course of this illness usually provides resolution within 36 hours. Unless the patient is very young, very old, debilitated with severe underlying disease, or immunocompromised, they usually do very well with this self-limited illness responding to oral rehydration and a rapid return to a normal diet once the vomiting has ceased. The only therapy is oral and/or intravenous hydration with occasional need for antiemetics. The usual cautions concerning the use of antiemetics in very young patients apply. Although viral shedding has been reported for up to 2 weeks or more, the polymerase chain reaction (PCR) testing used to determine this may just be detecting inactivated RNA. The length of viral shedding, the large number of viruses shed in stool (millions) relative to the number required for infection (10-100) explains the communicability and the need for education as to meticulous hand hygiene.

There are many norovirus strains with no cross-immunity, so repeat infections are possible throughout one's lifetime.


Various caliciviruses, other than norovirus, are likely responsible for many outbreaks of previously unidentified viral gastroenteritis.


Rotavirus may cause severe dehydration. (See Pediatric Gastroenteritis.)

Rotavirus is a nonenveloped, double-stranded RNA virus of the Reoviridae family with a wheel-like appearance under electron microscopy—hence the name. The virus is extremely contagious. Nearly all children are infected with rotavirus at some point before age 5 years, unless immunized. There are two commercially available vaccines in the United States, each with antibodies to multiple strains. Prior to this, there were 55,000–70,000 hospitalizations per year in United States. [10] The illness lasts 3-8 days and usually starts with some vomiting, followed by severe foul-smelling (distinctive) diarrhea, potentially leading to severe dehydration.

Adults can be infected with rotavirus, although symptoms are usually not as severe. Those adults most likely to be infected include people with children affected by the virus, elderly persons, and the immunocompromised. There are multiple strains (4 are common in the United States), so people can be infected with rotavirus multiple times. Usually, the first infection is the most severe. Most initial infections occur by age 2 years. Rotavirus is considered the most significant etiological agent for acute GI illness in children worldwide, with up to 500,000 deaths annually worldwide. [10] The peak rotavirus season is November to April (cooler weather) in temperate weather and year-round in tropical climates.

Other viruses that can also cause gastroenteritis include the following:

Bacterial (15-20%) causes of gastroenteritis


Salmonella appears as the second most common agent among outbreaks with known pathogens. It is manifested by acute enterocolitis, with abdominal pain, diarrhea, nausea, headache, sometimes vomiting, and almost always fever. Infected persons may develop a localized infection or septicemia. Salmonellosis is predominantly foodborne, and, on average, the onset of symptoms occurs 12-36 hours after ingestion of the contaminated source. It is estimated that Salmonella is responsible for approximately 1.35 million infections in the United States each year, with 26,500 hospitalizations and 420 deaths. [11] Over 2,500 serotypes of Salmonella have been described, but S typhimurium and S enteritidis are the most commonly detected in infected persons.

The incidence of S typhimurium has increased since 1997, and it was the cause of a multistate outbreak associated with peanut butter and other peanut-containing products that resulted in 714 cases across 46 states. The outbreak began in the summer of 2008; however, the epidemiologic investigation was initiated in November due to the inherent time lag in reporting (stool sample results may take 2 wk). The problem became evident when there was a growing cluster of Salmonella serotype typhimurium isolates with the same pulsed-field gel electrophoresis (PFGE) pattern in several states.

Review of detailed epidemiologic questionnaires, assessment of foods, and results of case-control studies in industrialized settings where clusters appeared led to the assumption of peanut butter being the common source of the outbreak. The FDA inspected the facility where the peanut butter was produced and positive test results from finished peanut butter obtained on site confirmed the presence of the outbreak strain. Being an ingredient-driven outbreak, many products distributed through various channels had the potential of being contaminated. As a result of the findings, recalls of peanut butter and peanut-containing foods were issued for products dated as far back as January 2007. In addition, the producing facility was directed to stop production and distribution of all products. [12]

C difficile

Clostridium difficile, often referred to as “C diff,” is a gram-positive, spore-forming, toxin-producing bacillus that typically affects patients receiving antibiotic treatment, especially with broad-spectrum drugs (eg, cephalosporins, clindamycin, fluoroquinolones). Clinical symptoms of C difficile infection include watery diarrhea, fever, nausea, loss of appetite, and abdominal pain or tenderness. Complications that may result from infection include pseudomembranous colitis, toxic megacolon, perforations of the colon, sepsis, and even death, although it is rare. In some cases, infection resolves within 2-3 days of discontinuing the offending antibiotic. However, there are cases that require a full course of an appropriate antibiotic; several antibiotics are effective against C difficile. Severe cases may require surgery to remove the infected portion of the intestine.

Incidence and severity have increased during recent years due to the emergence of a more virulent epidemic strain. It is the leading cause of hospital-acquired gastrointestinal illness in the United States, with costs of 3.2 billion dollars annually. [13] A recent study reported that of 320 patients admitted to a tertiary care center, 31 (9.7%) tested positive for C difficile but had no symptoms of infection. [14] Host susceptibility is greater in hospitalized persons and those with underlying medical conditions. The bacterium is shed in feces and can be acquired from contact with contaminated surfaces, devices, or hands; it is considered to be a healthcare-associated infection.

Elderly individuals are more commonly affected; however, infection may occur at any age and over the last few years its appearance in populations considered low risk has increased (ie, healthy outpatients, children, and people with no recent history of taking antibiotics). In cases of community-acquired infection, obesity has been reported to be a possible risk factor. [15] The use and application of evidence-based management and prevention strategies are important factors in the collaboration to reduce incidence of C difficile. New treatment strategies are currently under study.

Other bacterial causes include the following:

Parasitic (10-15%) causes of gastroenteritis


Giardia lamblia (also called Giardia intestinalis), a flagellate protozoan parasite, lives primarily in the upper part of the small intestine of an organism. Some infected individuals present with symptoms including diarrhea, bloating, greasy stools that tend to float, abdominal cramps, nausea/vomiting, and dehydration, while others may be asymptomatic. The average incubation period is 7-10 days, and symptoms may persist for 1-2 weeks. Most infections occur in children aged 1-9 years, but predominantly in those younger than 5 years. It is also seen in adults aged 25-44 years.

Infected persons may excrete cysts intermittently, making it difficult to diagnose. Several stool samples should be collected on various days and enzyme-linked immunosorbent assay (ELISA) or direct fluorescent antibody methods are usually performed to identify the parasite.

Transmission occurs from person to person or even from animals to humans via the fecal-oral route, through the ingestion of contaminated water. For example, it can be acquired from drinking downstream where a cow or other animal(s) may have contaminated the water. The risk of becoming infected is higher for travelers around the world, persons participating in outdoor activities/recreational water facilities, and those who consume unfiltered/untreated water (ie, hikers, campers).

The majority of cases are observed during the months of June to October, coinciding with the months of increased travel and outdoor/recreational water activities. There is increased risk in daycare centers and for close contacts of infected persons as well. Giardiasis occurs worldwide, with higher prevalence in areas where there is poor hygiene and sanitation. However, it is the most common intestinal parasitic disease in the United States, with an excess of 19,000 infections reported each year.

It has two stages, cyst and trophozoite. Both forms are passed in feces; however, the cyst is the infective stage and the one that can survive outside of a host and in the environment for weeks or months. It has moderate tolerance to chlorine and is capable of living in cold water for significant periods. Individuals infected with Giardia may shed 1 to 10 billion cysts daily, while the infectious dose is approximately 10 cysts, sometimes even as few as 1 or 2.

Other parasitic causes include the following:

Food-borne toxigenic diarrhea

Preformed toxins include S aureus and B cereus

Postcolonization toxins include V cholera, C perfringens, enterotoxigenic E coli, and Aeromonas.

Shellfish poisoningand poisoning from other marine animals

Shellfish and marine animal poisoning include the following:

  • Paralytic shellfish poisoning (PSP) - Saxitoxin

  • Neurologic shellfish poisoning (NSP) - Brevetoxin

  • Diarrheal shellfish poisoning (DSP) - Okadaic acid

  • Amnesic shellfish poisoning - Domoic acid

  • Ciguatera (ciguatoxins)

  • Scombroid (conversion of histidine to histamine)

Drug-associated diarrhea

Medications associated with diarrhea include the following:

  • Antibiotics, due to alteration of normal flora

  • Laxatives, including magnesium-containing antacids

  • Colchicine

  • Quinidine

  • Cholinergics

  • Sorbitol

  • Proton pump inhibitors (PPIs): In a prospective population-based study of 38,109 middle-aged and older Australian adults, there was an association between use of PPIs and a significantly higher risk of hospitalization for infectious gastroenteritis, regardless of the PPI used. [16] There was a dose-response relationship noted.

Pseudomembranous colitis

Pseudomembranous colitis occurs as an overgrowth of C difficile.C difficile assay findings are positive.

Other causes

Other causes of diarrhea include the following:

  • Unknown agents, especially in developing countries

  • Ischemic colitis

  • Ulcerative colitis

  • Crohn disease

  • Carcinoid tumor or vasoactive intestinal peptide tumor (VIPoma)

  • Acquired immunodeficiency syndrome (AIDS)

  • Dumping or short bowel syndrome

  • Radiation or chemotherapy



United States data

Frequency is difficult to determine because of underreporting, especially of mild illness, resulting in wide variations of estimated numbers of cases, hospitalizations, and deaths. As many as 179 million cases occur per year with several million healthcare visits and thousands of hospitalizations; children account for more than 1.5 million outpatient visits of which nearly 1 million are associated with norovirus. [17]

It is estimated that the norovirus is responsible for a large percentage of gastrointestinal (GI) illnesses in the United States and possibly worldwide. One contributing factor to its frequency is the mutability of its genome [18] and another is the low minimal infective dose. According to the Centers for Disease Control and Prevention (CDC), 19 to 21 million cases a year and more than 50% of foodborne outbreaks are confirmed to be caused by norovirus or norovirus was the only suspected etiology. [19] In Great Britain, it has been known as "winter vomiting disease." Whether the increased incidence of norovirus is real or simply a result of increased awareness, surveillance, and reporting is unclear.

Acute gastroenteritis outbreaks have been associated with many modes of transmission, including foodborne, waterborne, person-to-person, animal contact, and environmental. Food and water represent important vehicles for pathogens and are linked to several illnesses that cause gastroenteritis. In 2009 alone, foodborne agents were responsible for 13,497 illnesses from 668 reported outbreaks in the United States. There were 2,259 reported acute gastroenteritis outbreaks attributed to person-to-person transmission in the United States between 2009 and 2010. Among the reported settings, nursing homes and other long-term care facilities ranked most common, followed by childcare settings, hospitals, and schools. [3]

Public vomit incidents have also been known to be a source of transmission of acute gastroenteritis in outbreaks, in particular those caused by norovirus. In fact, studies demonstrate that norovirus particles can travel up to 3 meters during such incidents.

The following are examples of outbreaks that have occurred over the years:

  • Gastroenteritis associated with V parahaemolyticus infection from Gulf Coast oysters has been reported.

  • A religious cult in Oregon intentionally contaminated salad with Salmonella typhimurium, which resulted in 751 victims who developed acute gastroenteritis.

  • From 1981-1994, 333 cases of Vibrio vulnificus infection associated with raw oyster consumption were reported in Florida. Two persons died from gastroenteritis, and 50 persons died from septicemia.

  • In 1993, E coli O157:H7–contaminated fast-food hamburger meat in the Pacific Northwest infected 500 persons, 4 of whom died.

  • In April 1994, 96 cases of Campylobacter infection were reported in Florida. The common source was contaminated commercial ice cubes.

  • In January 1995, 322 cases of norovirus, formerly known as Norwalk virus (calicivirus), infection–associated acute gastroenteritis resulted from the consumption of raw oysters in Florida.

  • In July 1995, 77 cases of cryptosporidiosis at a day camp in Florida were reported, most likely secondary to contamination involving a water hose.

  • In 1996, norovirus–associated gastroenteritis resulted from the ingestion of raw oysters in Louisiana.

  • From May 1996 to June 1996, E coli O157:H7 infections secondary to consumption of mesclun lettuce from a single producer were reported in multiple states (first identified in Connecticut and Illinois).

  • In October 1996, 629 children and staff members at one elementary school in Florida were infected in a point-source outbreak of norovirus.

  • In July 1998, more than 60 persons in Wyoming were infected with E coli O157:H7 from a contaminated water supply.

  • In August and September of 1999, E coli O157:H7 infections secondary to contaminated well water at the Washington County Fair (New York) were reported.

  • In 2005, E coli O157:H7 infections secondary to contaminated animals were reported at Florida fairs.

  • After Hurricane Katrina struck the Gulf Coast in September 2005, an evacuation site in Houston, Texas reported 1,169 cases of acute gastroenteritis; of 44 stool samples tested by reverse transcription-polymerase chain reaction, norovirus was confirmed in 22.

  • In September 2006, there were 4 cases of botulism associated with commercial carrot juice; all 4 patients were hospitalized. Three individuals were in Georgia and 1 in Florida.

  • In 2008, there were 1,442 infections, 286 hospitalizations, and 2 possible deaths distributed among 43 states and Canada, caused by the uncommonly detected serotype Salmonellasaintpaul. The outbreak was associated with multiple raw produce items, including jalapeño pepper, Serrano pepper, and possibly tomatoes.

  • Between April and August of 2008, an E coli (O157:H7) multistate outbreak associated with contaminated bagged spinach resulted in 205 confirmed illnesses and 3 deaths.

  • Between November 2008 and April 2009, there were 714 cases (9 deaths) of Salmonellatyphimurium reported in 46 states due to contaminated peanut products, such as peanut butter and peanut-containing products, precipitating a major recall of affected products.

  • From May to November 2010, there were approximately 1,939 infections of Salmonellaenteritidis associated with shell eggs among 11 states.

  • In 2010, there were 9 individuals infected with Salmonella typhi as a result of consuming contaminated frozen mamey fruit pulp in California and Nevada. The product was voluntarily recalled by 2 companies.

  • From November 2010 to February 2011, 140 individuals from 26 states became infected with Salmonella serotype I 4,[5],12:I, linked to the consumption of tiny green alfalfa sprouts or spicy sprouts from a chain restaurant.

  • As of October 2011, 147 people had become ill (including 28 deaths) in multiple states as a result of becoming infected with 4 strains of Listeria monocytogenes from contaminated cantaloupes.

  • In April 2012, 14 individuals became ill with norovirus after consuming contaminated oysters in a restaurant in New Orleans. Oysters were harvested off the Louisiana coast; the shellfish harvesting zone was closed for 3 weeks.

  • One individual spread norovirus to 7 others through contamination of a reusable grocery bag in Washington state.

  • In January 2012, 90 individuals in Indiana became ill with norovirus after eating at a chain restaurant where an infected food handler reported to work. All 6 stool samples collected from employees resulted positive for norovirus. Of the 90 ill, 3 were hospitalized and 2 were treated in an emergency department.

  • In February 2012, 242 persons attending a boy's basketball tournament became ill with acute gastroenteritis; tests confirmed the cause was norovirus GII.7, which is a rare strain. No common source was determined, but there was a public vomit incident where many individuals were exposed.

  • In July 2012, over 200 became ill after eating salad or salsa in a Mexican self-service restaurant.

  • A chain restaurant in Indiana was reported to be the source of norovirus illness for 20 individuals who attended a Red Cross event for rescue workers; an additional 40 close contacts were infected via person-to-person transmission.

  • Data for selected foodborne disease outbreaks by year (from 2006 forward) and by pathogen are available at the CDC site for foodborne outbreaks.

Although norovirus-associated outbreaks of acute gastroenteritis gain the most publicity when they occur on board cruise ships, these actually occur most commonly in long-term care facilities such as nursing homes, schools, and daycare centers. The CDC has established the Vessel Sanitation Program, which monitors GI illness on board cruise ships that carry more than 13 passengers and have a foreign itinerary and US port. [20] The Health Protection Agency, which is a division of Public Health England, has published evidence-based practice parameters for health professionals and ship crew members on the identification and management of norovirus outbreaks aboard cruise ships at sea and on sanitation procedures after ships return to port. [21]

The CDC posts outbreaks as occurring on voyages from 3-21 days, on ships carrying 100 or more passengers in which 3% or more of passengers or crew reported symptoms of diarrheal disease to the ships medical staff during the voyage, and are GI illness outbreaks of public health significance.

Amongst all cruise ship voyages under the auspices of the CDC's Vessel Sanitation Program, the number of reported outbreaks occurred as follows: 14 each in 2010 and 2011, 16 in 2012, 9 each in 2013 and 2014, 12 in 2015, 13 in 2016, 11 each in 2017 and 2018, 10 in 2019, 4 in 2020, 1 in 2021, 4 in 2022, and 13 in the first three quarters of 2023. [22]

International data

There are an estimated 2 billion cases of diarrhea that occur yearly, and it is the leading cause of death in many underdeveloped countries. It is the second leading cause of death in children younger than 5 years, taking the lives of approximately 1.9 million children each year. [23, 24] Approximately 30-50% of visitors to developing countries return with diarrhea.

In May 2011, a shiga-toxin–producing E coli (O104:H4), eventually classified as enteroaggregative pathotype, started in Germany and affected 3000 or more individuals, with 900 (30%) or more developing hemolytic–uremic syndrome (a very high percentage) and with an unusual number of adults affected and a high mortality rate compared with prior shiga-producing E coli strains. The German outbreak is unique as horizontal genetic exchange appears to have resulted in this unique O104:H4 strain, which has a prophage encoding shiga toxin 2 and additional virulence and antibiotic-resistance factors. Fieldwork suggested the source was fresh vegetables. [25]

In a systematic review and meta-analysis of data on the prevalence or incidence of norovirus and acute gastroenteritis in Latin America, the overall prevalence of norovirus in acute gastroenteritis cases was 15%, and 37%-100% of cases were associated with GII.4 strains (but only 7% of asymptomatic norovirus patients were affected with this strain). [26]

In a 2017 report that estimated the healthcare costs of acute gastroenteritis and human Campylobacter infection in Switzerland, investigators reported an annual cost of approximately 29-45 million euros, of which about 9 to 24.2 million euros related to physician visits without a stool diagnostic test being obtained; about 12.3 million euros for patients with negative Campylobacter species stool tests and 1.8 million euros for those with positive Campylobacter species stool tests; and 6.5 million euros for inpatients with Campylobacter infection. [27]

Race-, sex-, and age-related demographics

Significantly higher mortality is observed among women and non-Hispanic white individuals. [28]

Gastroenteritis may occur at any age. Morbidity and mortality are much higher in the very young and the very old. It is a major cause of mortality among children younger than 5 years in developing countries, and persons aged 65 years or older account for the majority of hospitalizations and deaths in the United States. [28]

Norovirus has become the leading cause of acute gastroenteritis in children younger than 5 years seeking medical attention in the United States since the introduction of the rotavirus vaccine. [17]

Pediatric gastroenteritis is discussed in the Medscape Drugs & Diseases article Pediatric Gastroenteritis.




Most cases of gastroenteritis are self-limited with an excellent prognosis.

Estimates for mortality and morbidity widely vary. In the United States, approximately 900,000, including 200,000 pediatric, hospitalizations occur yearly, with an average of 11,255 deaths. [28] Internationally, the mortality rate is 1.4-2.5 million deaths each year.

The Centers for Disease Control and Prevention (CDC) reported that enteritis deaths more than doubled in the United States, an increase to 17,000 in 2007 from about 7,000 in 1999. Adults older than 65 years accounted for 83% of deaths and the majority of hospitalizations. C difficile and norovirus were the most common infectious causes of gastroenteritis-associated deaths. C difficile was associated with 14,500 of these deaths, up from 2,700 in 1999. Norovirus was associated with an estimated 797 deaths annually, causing the majority of gastroenteritis outbreaks, [28] although 50% more deaths occurred in years when epidemics were caused by new strains of the virus. [29]


Complications of gastroenteritis include the following:

  • Dehydration

  • Malabsorption

  • Transient lactose intolerance

  • Chronic diarrhea

  • Systemic infection (meningitis, arthritis, pneumonia) especially with Salmonella infections

  • Sepsis (Salmonella, Yersinia, Campylobacter organisms)

  • Hemolytic-uremic syndrome (much more common in children, especially with E coli O157:H7)

  • Reactive arthritides (Salmonella, Shigella, Yersinia, Campylobacter, Giardia organisms)

  • Persistent diarrhea

  • Thrombotic thrombocytopenic purpura or TTP (E coli O157:H7)

  • Guillain-Barré syndrome (Campylobacter organisms)


Patient Education

Patients should be educated on the importance and proper methods of oral rehydration and early appropriate feeding.

All patients, especially the parents of infants and young children, must be extensively educated about the signs and symptoms of dehydration.

Patients with food-borne exposures should be educated on deterrence.

Immunocompromised patients and individuals with liver disease should be educated not to consume raw shellfish, especially oysters.

Travelers to underdeveloped areas should be made aware of proper avoidance measures, appropriate treatment, and current endemic illnesses.