Gastrointestinal Viral Infections — Questions

A complete answer names the likely agent, the specimens to collect, the assay of choice and its interpretation, and the environmental sampling that links the cases to a source.

The likely agent in a waterborne outbreak affecting all ages is norovirus. Collect stool specimens from several cases early in the illness, when shedding is highest, since a single positive is weak evidence in an outbreak. The method of choice is reverse-transcription polymerase chain reaction (RT-PCR), which is far more sensitive than antigen enzyme immunoassay; norovirus antigen assays have low sensitivity and are useful only for confirming the agent across a group, not for excluding it in an individual. Sequencing the RT-PCR product allows genotyping, which is what ties cases to each other and to the source.

Test in parallel for rotavirus and enteric adenovirus by antigen assay to exclude the endemic childhood agents. Sample the suspected water source, and any implicated food or environmental surfaces, for the same virus. Because norovirus is frequently detected in well people, interpret results against the clinical and epidemiological picture. A single matching strain across cases and the water source confirms the outbreak and its vehicle.

Zinc supplementation reduces the severity, duration and incidence of childhood diarrhoea and is a mainstay of paediatric treatment in low- and middle-income countries.

Antibiotics, vitamin A, antimotility drugs and immunoglobulin are not routine adjuncts for uncomplicated viral gastroenteritis.

Severe dehydration (about a 10% deficit), shock or near-shock, intractable vomiting or failure of oral therapy call for intravenous fluids.

Mild diarrhoea, occasional vomiting, non-bloody stool and low-grade fever are all managed with oral rehydration.

Antibiotics have no role in uncomplicated viral gastroenteritis and may cause harm, including antibiotic-resistant carriage and adverse events.

They neither shorten the illness, prevent dehydration, nor eradicate shedding, and vomiting is not an indication for them.

Norovirus attaches to histo-blood-group antigens on the gut mucosa, so an inactivating FUT2 mutation (the nonsecretor phenotype) confers relative resistance to the dominant GII.4 genotype.

Blood group O, vaccination, IgA deficiency and cystic fibrosis do not confer this genetic resistance.

Rotavirus is a reovirus with 11 segments of double-stranded RNA, the segmentation allowing reassortment and genotype diversity.

The caliciviruses (norovirus, sapovirus) and astroviruses carry single-stranded RNA; the enteric adenoviruses carry double-stranded DNA.

Rotavirus is shed in huge numbers and is easily detected by a rapid, sensitive stool antigen enzyme immunoassay, which is cheap and field-usable.

PCR works but is not required, culture is not routine, and serology and electron microscopy are not first-line for the individual case.

The rotavirus non-structural protein NSP4 acts as a viral enterotoxin, raising intracellular calcium and driving chloride and water secretion, so diarrhoea occurs without tissue invasion.

There is no mucosal invasion or preformed food toxin, and the mechanism is not autoimmune or a cytokine storm.

The enteric adenoviruses, types 40 and 41, cause endemic childhood gastroenteritis.

Types 3 and 7 cause respiratory and conjunctival disease, types 8 and 19 keratoconjunctivitis, type 14 severe respiratory outbreaks, and types 1 and 2 common childhood respiratory infection.

Rotavirus is globally the leading cause of severe childhood gastroenteritis, because it best combines high infectivity with a heavy inoculum and severe fluid loss in the under-fives.

Norovirus dominates outbreaks and, where rotavirus vaccine is used, endemic disease; astrovirus, adenovirus and sapovirus cause milder endemic illness.

Reverse-transcription PCR is the method of choice for norovirus, being highly sensitive; genotyping the product links outbreak cases.

Antigen assays have low sensitivity, the virus is not readily cultured, and electron microscopy and single-sample serology are insensitive or impractical.

Low-osmolarity oral rehydration solution is the mainstay, correcting the fluid and electrolyte loss that causes death; breastfeeding and early refeeding continue.

Antibiotics have no role, antimotility drugs are avoided in young children, intravenous fluids are reserved for severe cases, and no specific antiviral exists.

Norovirus causes most gastroenteritis outbreaks, spreading rapidly in hospitals, care homes, cruise ships and around contaminated food and water.

The other agents cause mainly endemic childhood diarrhoea; group A rotavirus is the endemic paediatric leader rather than an outbreak agent.

Norovirus needs fewer than 100 particles to infect and is a non-enveloped virus that survives on surfaces, so it transmits readily by contact, food, water and aerosolised vomitus.

It is not confined to water or droplets, has a short incubation, and needs no vector.

Blood and mucus in the stool indicate an invasive, inflammatory process such as bacterial dysentery, which is not a feature of viral gastroenteritis.

Watery non-bloody stool, early vomiting, low-grade fever and a three-to-five-day course are all typical of the viral illness.