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Viral Gastroenteritis Clinical Presentation

  • Author: Michael Vincent F Tablang, MD; Chief Editor: Julian Katz, MD  more...
 
Updated: Dec 14, 2014
 

History

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.

  • The history should focus on severity and dehydration. The onset, frequency, quantity, and duration of diarrhea and vomiting are important factors in assessing the status. Oral intake, urine output, and weight loss are important considerations. Viruses are the suspected cause of acute gastroenteritis when vomiting is prominent, when the incubation period is longer than 14 hours, and when the entire illness is over in less than 3 days. Travel history (including cruise ships), eating history, and daycare history are important epidemiological factors.
  • A viral cause should be suspected when the warning signs of bacterial infection (ie, high fever, bloody diarrhea, severe abdominal pain, >6 stools/24 h) are absent and an alternative diagnosis is not suggested by epidemiologic clues from the history (eg, travel, sexual practices, antibiotic use).
  • Factors associated with severe and prolonged disease are immunodeficiency and immune suppression, comorbid disease, and malnutrition.
  • Death results from dehydration and acidosis.
  • Ruling out other diagnoses is important. Mucus or overt blood in the stool almost always indicates bacterial or parasitic infection.

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]

  • Vomiting in 50% of affected persons in the outbreak
  • Mean incubation period of 24-48 hours
  • Mean duration of illness of 12-60 hours
  • Lack of identification of a bacterial pathogen in stool culture
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Physical

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

  • Temperature, blood pressure and pulse, and body weight can provide evidence of severity of the condition.
  • Temperature may be slightly elevated. High fever suggests bacterial infection. Tachycardia, thready pulse, and hypotension suggest severe dehydration.
  • The degree of weight loss may be related to dehydration and the duration of the diarrhea.
  • The mucous membranes and the skin should be examined carefully. Dry mouth, no tears, skin tenting, dry skin, and capillary refill are all signs of dehydration.
  • The mental status in elderly patients and infants may be abnormal, especially when blood pressure and circulation are compromised.
  • The abdominal examination may demonstrate mild tenderness. Severe abdominal pain and tenderness suggest bacterial infection or an abdominal emergency.
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Causes

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.

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Contributor Information and Disclosures
Author

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

Michael Vincent F Tablang, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

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

George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, Association of American Physicians

Disclosure: Received consulting fee from Springer for consulting; Received consulting fee from Gilead for review panel membership; Received honoraria from Vertex for speaking and teaching; Received honoraria from Bristol-Myers Squibb for speaking and teaching; Received royalty from Springer for review panel membership; Received honoraria from Merck for speaking and teaching.

Michael J Grupka, MD Physician, Atlanta Center for Gastroenterology

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Noel Williams, MD, FRCPC FACP, MACG, 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

Noel Williams, MD, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Chief Editor

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

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Additional Contributors

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

John Gunn Lee, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

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