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Editorials

Measles in an era of measles control

As measles becomes rare in Australia, clinical diagnosis becomes increasingly inaccurate

MJA 2000; 172: 103-104

It has been a long road to the control of measles in Australia. Live attenuated measles vaccine was licensed in 1968, and included in childhood vaccination schedules in 1971. Even after the first national measles campaign, in 1988, coverage remained too low (85%)1 to achieve herd immunity, as evidenced by major measles outbreaks in many areas in 1993-1994. In 1994, a second dose of measles-mumps-rubella (MMR) vaccine was introduced for all children aged 10-16 years. Although the incidence of measles declined, seroprevalence studies2 indicated that further measles outbreaks were likely.

In response to these findings, the Australian Measles Control Campaign (MCC) was launched in July 1998. The centrepiece of this campaign was administration of a dose of MMR vaccine to all primary school children in the second half of 1998. This "catch-up" dose was needed before lowering the recommended age for the second dose of MMR vaccine to four years in 1999. After the MCC, an estimated 96% of children aged five to 12 years had received two doses of MMR vaccine.3 As a result of this campaign and the continuing efforts to eradicate measles, it is hoped that Australia will soon be shown to have joined other countries, such as the United States,4 the United Kingdom5 and Finland,6 where indigenous measles transmission has been interrupted.

The better the control of measles, the lower the probability that someone presenting with fever and rash will have measles, and the poorer the positive predictive value (PPV) of a clinical diagnosis. Even in 1990-1993, before any major measles control measures, a study of 58 people notified with measles in eastern Sydney found that only 49% of cases were serologically confirmed.7 A case definition of morbilliform rash, cough and fever at rash onset had a PPV of 69%.7 In this issue of the Journal, there is a report of a larger study of enhanced measles surveillance in Victoria from July 1997 to December 1998 (ie, primarily conducted before the MCC) which showed a much lower level of confirmation.8 Only 8% of the 248 notified cases that could be classified on the basis of serological results were confirmed as measles. The PPV of the National Health and Medical Research Council (NHMRC) clinical case definition for considering public health action9 was as low as 5% when secondary cases from clusters were excluded.8 Since the MCC, the proportion of serologically confirmed cases is likely to have fallen even further. In the UK, after a similar school-based MMR program in 1994,5 and in Finland 12 years after high coverage with a two-dose MMR schedule,6 only about 1% of suspected cases were shown to be measles.

These developments necessitate major changes in the approach of medical practitioners to suspected measles, especially in general practice where most cases will be seen. The latest draft of the revised NHMRC guidelines for measles control emphasise that confirmation by detection of measles IgM in a serum specimen is essential when measles is clinically suspected.10 This policy is also recommended by the authors of the Victorian study and by the National Measles Surveillance Strategy.11 Confirmation is particularly important in sporadic cases, where the prior probability of measles is especially low, and should also be obtained from at least two cases during an outbreak. The high level of laboratory testing achieved in Victoria is encouraging. However, overall, only 44% of the 428 cases accepted as measles notifications in Australia between January 1998 and June 1999 were laboratory confirmed (personal communications from State and Territory health departments). It may be possible to improve this percentage -- although teams of venepuncturists are impractical for many areas of Australia, arrangements to bleed patients can usually be made in consultation with local public health authorities.

Considerable interest has also focused on non-invasive diagnostic methods, such as salivary testing. This method has been used in the UK but has technical difficulties,11 making timely testing more difficult than for serological testing. Even when serological testing is done, as measles becomes rare the likelihood of a falsely positive measles IgM will rise, as found in Victoria and elsewhere.4 A positive measles IgM test should therefore be confirmed by a reference laboratory, especially in sporadic cases.

Clinicians should be aware that many viral infections in children may resemble measles clinically, and that measles is more likely in older children and young adults than in infants. After control of measles in Finland,6 37% of 993 children with suspected measles had serological evidence of infection caused by parvovirus, enteroviruses, adenovirus or human herpesvirus type 6 (HHV-6).12 The most common serological diagnoses were parvovirus infection, in children aged four to 15 years, and enterovirus and HHV-6 infection, in children aged under four years. In Sydney, in 1990-1993, the mean age of patients with confirmed measles was 11.3 years,7 and, in Victoria in 1997-1998, more than half (53%) the patients with confirmed measles were aged at least 10 years.8 An outbreak of measles in Victoria in 1999, after the MCC, indicates the likely future pattern of measles in Australia -- 84% of patients were aged 18-30 years and all patients aged one to eight years were unvaccinated.13

Sustained measles control will require further efforts in young adults as well as continued high coverage with two doses of measles vaccine in children. Young adults, especially those attending tertiary institutions or planning travel to areas where measles remains endemic, should be encouraged to have a second dose of MMR or serological confirmation of measles immunity.

Peter B McIntyre
Deputy Director

Heather F Gidding
Epidemiologist
National Centre for Immunisation Research and Surveillance of Vaccine
Preventable Diseases, Royal Alexandra Hospital for Children
and University of Sydney, Sydney, NSW

Gwendolyn L Gilbert
Director, Centre for Infectious Diseases and Microbiology
and University of Sydney, Sydney, NSW

  1. Australian Bureau of Statistics. National health survey. Children's immunisation, Australia, 1989-90. Canberra: ABS, 1992. (Catalogue no. 4379.0.)
  2. Gilbert GL, Chan S-W, Escott R, et al. Seroepidemiology of measles in New South Wales, 1997. Report to the National Centre for Disease Control, Commonwealth Department of Health and Aged Care, 1998 (available from the Department).
  3. National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases. Australian measles control campaign 1998. Evaluation report. Sydney: University of Sydney, Royal Alexandra Hospital for Children, 1999.
  4. Watson JC, Redd SC, Rhodes PH, Hadler SC. The interruption of transmission of indigenous measles in the United States during 1993. Pediatr Infect Dis J 1998; 17: 363-366.
  5. Gay N, Ramsay M, Cohen B, et al. The epidemiology of measles in England and Wales since the 1994 vaccination campaign. Commun Dis Rep CDR Rev 1997; 7: R17-R21.
  6. Peltola H, Hienonen OP, Valle M, et al. The elimination of indigenous measles, mumps, and rubella from Finland by a 12-year, two-dose vaccination program. N Engl J Med 1994; 331: 1397-1402.
  7. Ferson MJ, Young LC, Robertson PW, Whybin LR. Difficulties in clinical diagnosis of measles: proposal for modified clinical case definition. Med J Aust 1995; 163: 364-366.
  8. Lambert SB, Kelly HA, Andrews RM, et al. Enhanced measles surveillance during an interepidemic period in Victoria. Med J Aust 2000; 172: 114-118.
  9. National Health and Medical Research Council. Measles: guidelines for the control of outbreaks in Australia. Canberra: NHMRC, 1996.
  10. National Health and Medical Research Council. Measles: guidelines for the control of outbreaks in Australia [draft]. Canberra: NHMRC, 2000.
  11. Heath T, Burgess M, McIntyre P, Catton M. The national measles surveillance strategy. Commun Dis Intell 1999; 23: 41-49.
  12. Davidkin I, Valle M, Peltola H, et al. Etiology of measles and rubella-like illness in measles, mumps, and rubella-vaccinated children. J Infect Dis 1998; 178: 1567-1570.
  13. Lambert S, Lynch P, Morgan M, Gercovich D. Measles outbreak -- young adults at high risk. Victorian Infect Dis Bull 1999; 2: 21-22.

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