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While we await a preventive vaccine, we should concentrate on appropriate management, which means avoiding medications and giving dilute fluids to counter dehydration
MJA 1998; 169: 241-242
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Rotavirus is a
major cause of gastroenteritis affecting young
children worldwide. In this issue of the Journal,
Carlin and colleagues present data which suggest that, of the
approximately 20 000 children under five years admitted to hospital
with acute gastroenteritis in Australia annually (a rate of 15/1000
per year), rotavirus is responsible in 50%.1 This accords with a recent New South
Wales study suggesting that 56% of hospitalisations for acute
gastroenteritis in this age group could be attributed to
rotavirus.2
The virus was first identified in 1973 by Bishop and coworkers at the Royal Children's Hospital, Melbourne, when they used electron microscopy to examine duodenal biopsies from infants admitted to hospital with severe acute non-bacterial gastroenteritis.3 Since that time, rotavirus has also been shown to be a cause of acute gastroenteritis in the young of a wide range of wild and domestic mammals. The virus, a member of the family Reoviridae, can be classified into serogroups A-G, and most human infections are caused by serogroup A. Routine diagnosis is based on rapid detection of group A antigen in faeces, generally by latex agglutination or enzyme immunoassay. In temperate climates, rotavirus infection occurs all year round, with very pronounced annual winter-spring peaks in incidence. The major epitope associated with a protective immune response is the viral outer capsid glycoprotein VP7. In mammalian rotavirus strains, monoclonal antibodies can be used to differentiate this protein into 10 serotypes, of which four, G1 to G4, are responsible for most cases of severe disease in young children. The rotavirus genome comprises 11 segments of double-stranded RNA, which readily allows genetic reassortment when coinfection is induced in vitro with strains of differing serotypes from one or more species.4 Approaches to vaccine development have concentrated on G1 rhesus strains, strains of human neonatal origin and tetravalent rhesus-human reassortants expressing G1-G4 serotypes. Large-scale clinical trials to date have shown advantages in the tetravalent vaccine candidates in protective efficacy,4 and it is likely that an oral tetravalent rhesus-human reassortant rotavirus vaccine will be approved in Australia in the next 1-2 years. Randomised controlled trials of this vaccine given as three oral doses between six weeks and six months of age were conducted among both urban and Native American populations in the United States, and in Finland. These trials showed protective efficacies of 49%-66% against any rotavirus gastroenteritis and 69%-100% against very severe infection.5-7 The vaccine was found to be relatively safe, with adverse reactions largely limited to fever and irritability after the first dose -- one-third of children had fever over 38oC, while 3% had fever over 39oC.8 Another approach to preventing rotavirus gastroenteritis is passive immunisation -- giving oral preparations containing high-titre rotavirus antibodies derived from the colostrum of immunised cows. One study showed a marked reduction in the incidence of hospital-acquired rotavirus infection when hospitalised children were given a hyperimmune bovine colostrum preparation,9 and further trials are under way to assess the value of community use. Use of either active or passive immunisation may be of particular value in children aged under three years attending long- daycare, as rotavirus infection in this group causes substantial morbidity and family disruption.10 Although preventing rotavirus gastroenteritis has obvious appeal, our medium-term focus will continue to be on managing children with acute gastroenteritis. Carlin et al note substantial differences in hospital admission rates between Australian States and raise the possibility that there are variations in hospital admission policies or practices.1 Other local data have shown that most children admitted to two NSW children's hospitals have only a minor degree of dehydration.11,12 In an editorial comment on one of these NSW studies, Barnes indicated "continuing concern as to why so many mildly dehydrated children are admitted to Australian hospitals and why so many of them receive intravenous therapy".13 We have limited information on the management of gastroenteritis in the community and in hospital emergency departments. Most of the data are based on extrapolation from children who have been admitted to hospital. Preadmission management is suboptimal -- antibiotics, antiemetics or antidiarrhoeals are prescribed for more than 20%.11,12 The use of oral rehydration solution in the community is low, although most children are offered appropriately diluted clear fluids.11,12 While hospitalised children with gastroenteritis may not accurately reflect treatment practices in the community, there remains a disparity between management guidelines14 and actual practice. Treatment of gastroenteritis in the community should include continued breastfeeding in infants or increased fluids in older children. Either oral rehydration solution or appropriately diluted fluids are acceptable. Children should be allowed to return to their usual diet if they are hungry. Regular review of the child's progress, with particular focus on fluid balance, should be regarded as good clinical practice and not as overservicing. By contrast, medications are rarely required, may be harmful and should be avoided. Undiluted cordial, fruit juice or carbonated drinks (such as flat lemonade) are hyperosmolar solutions and pose the danger of exacerbating the diarrhoea. The prospect that a future rotavirus vaccine, if widely used, will have a major beneficial impact is exciting. Coupled with this is the need to deliver more effective clinical management of acute gastroenteritis in the community. Mark J Ferson Richard Henry
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