Acute 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.

Causes 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.
• 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.
• The third is sporadic acute gastroenteritis of adults, which most likely is caused by caliciviruses, rotaviruses, astroviruses, or adenoviruses.

Causes of Sporadic infantile viral gastroenteritis

• Group A rotavirus causes 25-65% of severe infantile gastroenteritis worldwide.
• After rotavirus, the most important cause of acute infantile gastroenteritis probably is calicivirus infection. 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.
• Studies confirm that they cause 2-6% of cases.

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.
• Some viruses, like noroviruses, may be transmitted by an airborne route.
• Rotaviruses attach and enter mature enterocytes at the tips of small intestinal villi.

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

• Rotavirus infections induce maldigestion of carbohydrates, and their accumulation in the intestinal lumen, as well as a malabsorption of nutrients and a concomitant inhibition of water reabsorption, can lead to a malabsorption component of diarrhea.
• Rotavirus secretes an enterotoxin, NSP4, which leads to a Ca2+ -dependent Cl- secretory mechanism.  Mobilization of intracellular calcium associated with NSP4 expressed endogenously or added exogenously is known to induce transient chloride secretion.
• 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.

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.