Viral Gastroenteritis



Acute gastroenteritis is a common cause of morbidity and mortality worldwide. Conservative estimates put diarrhea in the top 5 causes of deaths worldwide, with most occurring in young children in nonindustrialized countries. In industrialized countries, diarrheal diseases are a significant cause for morbidity across all age groups. Etiologies include bacteria, viruses, parasites, toxins, and drugs. Viruses are responsible for a significant percentage of cases affecting patients of all ages. Viral gastroenteritis ranges from a self-limited watery diarrheal illness (usually < 1 wk) associated with symptoms of nausea, vomiting, anorexia, malaise, or fever, to severe dehydration resulting in hospitalization or even death.

The clinician encounters acute viral gastroenteritis in 3 settings. The first is sporadic gastroenteritis in infants, which most frequently is caused by rotavirus.[1] The second is epidemic gastroenteritis, which occurs either in semiclosed communities (eg, families, institutions, ships, vacation spots) or as a result of classic food-borne or water-borne pathogens.[2] Most of these infections are caused by caliciviruses. The third is sporadic acute gastroenteritis of adults, which most likely is caused by caliciviruses, rotaviruses, astroviruses, or adenoviruses.

For excellent patient education resources, visit eMedicineHealth's Digestive Disorders Center. Also, see eMedicineHealth's patient education article Gastroenteritis.


Viral spread from person to person occurs by fecal-oral transmission of contaminated food and water. Some viruses, like noroviruses, may be transmitted by an airborne route. Clinical manifestations are related to intestinal infection, but the exact mechanism of the induction of diarrhea is not clear.

The most extensive studies have been done with rotavirus. Rotaviruses attach and enter mature enterocytes at the tips of small intestinal villi. They cause structural changes to the small bowel mucosa, including villus shortening and mononuclear inflammatory infiltrate in the lamina propria.

The current knowledge on the mechanisms leading to diarrheal disease by rotavirus is as follows:[3]

Morphologic abnormalities can be minimal, and studies demonstrate that rotavirus can be released from infected epithelial cells without destroying them. Viral attachment and entry into the epithelial cell without cell death may be enough to initiate diarrhea. The epithelial cell synthesizes and secretes numerous cytokines and chemokines, which can direct the host immune response and potentially regulate cell morphology and function. Studies also suggest that one of the nonstructural viral proteins may act as an enterotoxin, promoting active chloride secretion mediated through increases in intracellular calcium concentration. Toxin-mediated diarrhea would explain the observation that villus injury is not necessarily linked to diarrhea.



United States

Each year, more than 3.5 million infants develop acute viral gastroenteritis, resulting in more than 500,000 office visits, 55,000 hospitalizations, and 30 deaths. Statistics on sporadic cases of adult viral gastroenteritis are not known; however, food- and water-borne epidemics of viral gastroenteritis are monitored by the US Centers for Disease Control and Prevention (CDC) surveillance programs. The CDC estimates that viruses cause 9.2 million cases of food-related illness each year (out of a total of 13.8 million cases from all causes).

Noroviruses cause approximately 23 million cases of acute gastroenteritis each year and are the leading cause of outbreaks of gastroenteritis. They are responsible for 68-80% of all outbreaks in industrialized countries. The genus Norovirus, formerly called the Norwalk-like virus, is a member of the family Caliciviridae.

Noroviruses are now recognized to be a common cause of gastroenteritis in new settings, including nursing homes and other health care settings, cruise ships, in other travelers, and in immunocompromised patients.[4] In 2010-2011, norovirus was transmitted among players and staff of the National Basketball Association.[5]

In March 2012, the CDC reported a rise in foodborne disease outbreaks caused by imported food in 2009 and 2011. Nearly 50% of the outbreaks implicated food that was imported from regions not previously associated with outbreaks (mostly fish and peppers). Approximately 45% percent of the imported foods causing outbreaks came from Asia.[6]

The frequency is seasonal. The highest incidence of rotavirus cases occurs during the months from November to April. Cruise ship outbreaks of noroviruses are more common during the summer months. However, a CDC study by Tate et al demonstrated a decline in the seasonality of rotavirus following the 2006 introduction of the rotavirus vaccine.[7]

The investigators evaluated data for July 2000 through June 2008 to assess national, regional, and local trends in rotavirus testing and detection and found not only was the onset of the 2007-2008 rotavirus season delayed 15 weeks and the peak delayed 8 weeks relative to the prevaccine rotavirus season from 2000 to 2006, but the 2007-2008 season also lasted a little over half (14 wk) of the median prevaccine seasons (26 weeks).[7] Moreover, there was a 67% decline in the number and a 69% decline in the proportion of 2007-2008 rotavirus-positive test results compared with the median in 2000-2006.

Rotavirus is the most common etiologic agent of health care–acquired diarrhea in pediatric patients. Community- and health care–acquired infections have similar temporal distributions; they are caused by the same viral subtypes; and they affect children of the same age groups. All of the health care–acquired infections with known viral subtypes occurred while the same subtype was still active in the community, suggesting that health care–acquired infections arise from repeated introduction of the community-acquired rotavirus into the hospital setting.[8]


Acute viral gastroenteritis is a leading cause of infant mortality throughout the world. By age 3 years, virtually all children become infected with the most common agents. Rotavirus causes 2 million hospitalizations and 600,000-875,000 deaths per year.

Noroviruses were attributed to 9 out of the 21 outbreaks of acute gastroenteritis on cruise ships reported to the CDC's Vessel Sanitation Program from January 1, 2002, to December 2, 2002. The occurrence of noroviruses on cruise ships has led to the use of the term "the cruise ship virus" as another name for these viruses. Some illnesses previously attributed to sea sickness are now recognized to be caused by norovirus infections.[4]


Severe cases are seen in the elderly, infant, and immunosuppressed populations, including transplant patients.

Rotavirus infantile gastroenteritis is an important cause of infant mortality in the developing world.

In the United States, elderly persons have the highest risk of death from gastroenteritis.

Caliciviruses may kill more people in the United States than do rotaviruses.

Noroviruses are the most common cause of gastroenteritis in nursing homes, and several such outbreaks have resulted in deaths due to aspiration or exacerbation of another chronic disease. Norovirus infections in hospitalized patients are more severe than those seen in otherwise healthy persons.[4]

The CDC reported enteritis deaths more than doubled in the United States, an increase to 17,000 in 2007 from about 7,000 in 1999. Adults over 65 years old accounted for 83% of deaths. Clostridium difficile (C difficile) and norovirus were the most common infectious causes of gastroenteritis-associated deaths. Norovirus was associated with about 800 deaths annually, though there were 50% more deaths in years when epidemics were caused by new strains of the virus.[9]



The clinical spectrum of acute viral gastroenteritis ranges from asymptomatic infection to severe dehydration and death. Viral gastroenteritis typically presents with short prodrome, with mild fever and vomiting, followed by 1-4 days of nonbloody, watery diarrhea. Viral gastroenteritis is usually self-limited.

In 1982, the Kaplan criteria were established to distinguish outbreaks due to norovirus from outbreaks of bacterial etiology. The criteria are highly specific (99%) and moderately sensitive (68%). The 4 criteria indicative of an outbreak due to norovirus are as follows:[11]


The physical examination can be helpful in determining the etiology of gastroenteritis and in assessing the presence and degree of dehydration.


Sporadic infantile viral gastroenteritis

Group A rotavirus causes 25-65% of severe infantile gastroenteritis worldwide. Acute infections with group C are quite frequent in the United States and worldwide.

After rotavirus, the most important cause of acute infantile gastroenteritis probably is calicivirus infection. Seroepidemiologic studies have shown that antibodies to caliciviruses are present in 50-90% of children younger than 2 years in Kuwait, Italy, Kenya, China, London, and South Africa. Using broadly reactive reverse-transcription polymerase chain reaction for calicivirus to study stool specimens from children with acute gastroenteritis, studies have found these viruses in 7-22% of cases.

Astrovirus infection is associated with 2-9% of cases of infantile gastroenteritis worldwide, making it the third most frequent cause after rotavirus and calicivirus. The burden of astrovirus disease in developing countries might be especially high.

Researchers have recognized for a long time that certain enteric adenoviruses are an important cause of infantile gastroenteritis. Studies confirm that they cause 2-6% of cases.

A study by Chhabra et al indicated that in addition to rotavirus and norovirus, frequent causes of acute gastroenteritis in US children include adenovirus, sapovirus, and astrovirus. The study, which included patients from hospitals, emergency departments, and primary care clinics in three US counties, found that stool specimens from 22.1% of children under age 5 years who presented with acute gastroenteritis and who tested negative for rotavirus and norovirus, tested positive for adenovirus (11.8%), sapovirus (5.4%), and astrovirus (4.9%).[12]

Epidemic viral gastroenteritis

Most cases of epidemic viral gastroenteritis in adults and children are caused by the caliciviruses. Some examples include Norovirus (formerly called Norwalk-like viruses), genogroup I (eg, Norwalk, Southampton, Desert Shield, Cruise Ship); Norovirus (formerly Norwalk-like viruses), genogroup II (eg, Snow Mountain, Mexico, White River, Lordsdale, Bristol, Camberwell, Toronto, Hawaii, Melksham); and Sapovirus (formerly Sapporo-like viruses), which sometimes are referred to as genogroup III, although they are not like Norwalk (eg, Sapporo, Parkville, Manchester, Houston, London).

Modern molecular diagnostic techniques, such as broadly reactive reverse-transcription polymerase chain reaction, have linked these viruses to epidemics associated with oysters, contaminated community water supplies, restaurant food, hospital patients and staff, day care facilities, nursing homes, college dormitories, military ships, cruise ships, and vacation spots. Rotavirus and astrovirus also may cause epidemics of viral gastroenteritis.

Sporadic adult viral gastroenteritis

Few studies have examined the causes of sporadic cases of adult viral gastroenteritis. Seroepidemiologic evidence suggests that the etiologies are (in descending order of frequency) caliciviruses, non–group A rotavirus, astrovirus, and adenovirus.

Laboratory Studies

In a systematic literature review, Lee et al used pooled data to calculate median incubation periods for astrovirus (4.5 days), norovirus genogroups I and II (1.2 days), sapovirus (1.7 days), and rotavirus (2.0 days).[14]

Medical Care

In 1996, the American Academy of Pediatrics formulated and published practice guidelines for the management of acute gastroenteritis in children. Use the following parameters to assess the degree of dehydration: blood pressure, pulse, heart rate, skin turgor, fontanelle, mucous membranes, eyes, extremities, mental status, urine output, and thirst.

Probiotics are nonpathogenic live microorganisms that provide beneficial effects on the health of the host. In recent years, probiotics have entered mainstream medical practice, as a decrease in the severity and duration of infectious gastroenteritis has been shown in some strains.[15]



Michael Vincent F Tablang, MD, Resident Physician, Department of Internal Medicine, University of Connecticut Health Center

Disclosure: Nothing to disclose.


George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine

Disclosure: Springer Consulting fee Consulting; Gilead Consulting fee Review panel membership; Vertex Honoraria Speaking and teaching; Bristol-Myers Squibb Honoraria Speaking and teaching; Springer Royalty Review panel membership; Merck Honoraria Speaking and teaching

Michael J Grupka, MD, Physician, Atlanta Center for Gastroenterology

Disclosure: Nothing to disclose.

Specialty Editors

John Gunn Lee, MD, Director of Pancreaticobiliary Service, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of California at Irvine School of Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Noel Williams, MD, Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP, Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine

Disclosure: Nothing to disclose.


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