Norwalk virus
Etiology
Norwalk virus is classified as a member of the Caliciviridae.
These are single-strand RNA viruses with 27-38nm naked capsids.
Life cycle of the virus
Clinical manifestations
Nausea, vomiting, diarrhea, anorexia, or abdominal cramps or any combination.
Accompanying clinical manifestations reported in 25-50% of patients include myalgias, low-grade fever, headache, and chills. It is not clear whether these symptoms are due to viremia or due to interferon.
The onset of illness may be abrupt
Usually mild and lasts about 24 to 60 hours.
Stools are characteristically loose and watery; blood, mucus, and leukocytes are not typically present.
Diagnosis
No lab testing for clinical diagnosis
The characteristic absence of fecal leukocytes in Norwalk infection may be helpful for differentiation from Shigella or Salmonella enteritis.
Although a specific clinical diagnosis of infection with Norwalk virus cannot be made in the individual patient, a tentative diagnosis of infection can be made during an outbreak if certain criteria are met:
bacterial or parasitic pathogens are not detected;
vomiting is present in at least 50% of cases;
incubation period is 24 to 48 hours
mean or median duration of illness is 12 to 60 hours.
CDC ivestigation for outbreaks: There is no quick and easy assay for detection of this viral infection. CDC investigates reported outbreaks by analyzing electron microcopy and seroconversion studies.
Epidemilogy
Transmission
Norwalk virus is most likely transmitted via the fecal-oral route; however, it has also been detected in vomitus.
The virus particles are extremely hardy; their infectivity persists after exposure to acid, ether and heat (60 degrees for 30 minutes)
The explosive nature of outbreaks associated with the Norwalk virus group often suggests a common source of infection, such as water or food.
Secondary person-to-person transmission to contacts is relatively common. Infectivity can last as long as 2 days after resolution of symptoms.
Typically occurs as a sharp outbreak affecting adults, school-age children, and family contacts.
Various settings such as schools, camps and recreational areas, nursing homes, swimming facilities, cruise ships, and restaurants.
Norwalk virus outbreaks occur throughout the year without a peak season.
Pathology and pathogenesis
Characterized by a reversible involvement of the upper jejunum.
The jejunal mucosa remains intact with marked broadening and blunting of the villi and shortening of the microvilli, along with mononuclear cell infiltration and cytoplasmic vacuolization.
Functional alterations may include a transient malabsorption of fat, D-xylose, and lactose and a significant decrease in levels of small intestinal brush border enzymes (alkaline phosphatase and trehalase).
Adenylate cyclase activity in the jejunum is not elevated.
Delay in gastric emptying may be responsible for the nausea and vomiting associated with these agents.
In addition, although immunity has been observed in approximately 50% of adults, it appears to correlate inversely with the level of serum or local jejunal antibody.
The nature of resistance and susceptibility is poorly understood.
Prevention
There are no specific methods for preventing illness by the Norwalk virus group.
Careful hand washing and proper disposal of contaminated material should minimize transmission.
Hygienic preparation of food
Measures to decrease contamination of drinking water or swimming facilities should limit the frequency of Norwalk virus outbreaks.
Active immunization against this group of viruses is not yet feasible.
Treatment
Replacement of fluid and electrolyte loss with orally administered isotonic fluids is usually sufficient.
If severe vomiting or diarrhea occurs, parenteral fluid replacement may be necessary.
The American Academy of Pediatrics did not recommend the use of bismuth subsalicylate for relief of cramps associated with acute diarrhea, of infants and young children because of concerns about toxic effects.