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. 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.
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.
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 Ca 2+ -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.
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
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.
The investigators evaluated data for July 2000 through June 2008 and found not only was the onset of the 2007-2008 rotavirus season (right after the development of a vaccine) 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).
Rotavirus is the most common etiologic agent of health care–acquired diarrhea in *pediatric* patients.
Noroviruses are the most common cause of gastroenteritis in nursing homes
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
General laboratory evaluation
In most cases that fit the clinical features of viral gastroenteritis, lab tests are not indicated.
If bacterial or protozoal infection is suspected, stool studies for occult blood, WBC count, microscopy for protozoa, Clostridium difficile toxin, Giardia lamblia by enzyme immunoassay (EIA), or bacterial culture may be indicated.
Consider investigating patients with low-grade fever, nausea, vomiting, abdominal pain, and extreme dehydration by evaluating serum electrolytes, urea, creatinine, amylase, CBC count, and abdominal imaging studies.
Diagnosis of rotavirus
Rapid antigen testing of the stool, either by EIA (>98% sensitivity and specificity) or latex agglutination tests (less sensitive and specific as compared to EIA), is used to aid in the diagnosis of rotavirus infection.
Expect antirotavirus antibodies (ie, immunoglobulin M, immunoglobulin A) to be excreted in the stool after the first day of illness. Antibody tests can remain positive for 10 days after primary infection and longer after reinfection; therefore, they can be used as an adjunct to diagnosis
Diagnosis of calicivirus infection
In epidemics, save stool and emesis specimens for evaluation by public health officials. Polymerase chain reaction is valuable in both the outbreak setting and the sporadic case setting.
Researchers have cloned several of the caliciviruses and placed the genome in a baculovirus that produces unlimited amounts of recombinant calicivirus capsid protein. Enzyme immunoassays for serum antibody and stool antigen have been developed using this antigen source.
A modification to the polymerase chain reaction has allowed many of the different strains of caliciviruses to be recognized with just a few primers (broadly reactive reverse-transcription polymerase chain reaction). These primers are directed at a region of the genome that is common to many of the strains of calicivirus. This has been an important tool for identifying caliciviruses as the most common cause of epidemic viral gastroenteritis.
Fecal viral concentration of norovirus correlates with duration of illness. As in most viral infections, active viral replication determines clinical disease. High fecal viral concentrations suggest the need for both aggressive fluid replacement and stringent infection control measures