No evidence of an increase of bacterial and viral infections following Measles, Mumps and Rubella vaccine
Section snippets
Background
Addition of a number of new vaccines to the infant vaccination programme in recent years has raised theoretical concerns about the possible adverse effects of multiple immunisations on the developing immune system [1]. One such concern relates to the potential for increasing susceptibility to other infections as a result of “immune overload”. When reviewing this issue in 2002, the US Institute of Medicine concluded that the available epidemiological evidence favoured rejection of a causal
Methods
Children aged 12–23 months were identified from computerised hospital admission records from North, East and South London, Essex, East Anglia, Sussex and Kent, for the period 1st April 1995 to 1st May 2005. Admissions were identified using ICD 9 and 10 codes for bacterial and viral infections (specific codes available on request). Each episode is coded with an ICD code which can be found in any of the seven diagnostic fields, with the first field being the primary diagnosis. Bacterial
Results
A total of 2077 admissions in 2025 children were linked to an MMR record. An admission within 14 days of an earlier admission with the same condition was considered part of the same episode. Of these admissions, 871 were coded as lobar pneumonia and 449 as invasive bacterial infection. Of the children with more than one bacterial infection, 25 had 2 episodes, 3 had 3 episodes and 1 child had 8 episodes.
Of the viral infection admissions, 18 were coded as viral encephalitis/viral meningitis/CNS,
Discussion
Our results show that MMR vaccine administered in the second year of life, either alone or with concomitant MCC vaccine, does not increase the risk of severe infection, bacterial or viral, in various periods up to three months after vaccination. It therefore adds weight to the existing epidemiological evidence that multiple immunisations do not “overload” the immune system and increase susceptibility to heterologous infection [1]. Moreover, there is no scientific rationale for the hypothesis;
Acknowledgement
JS is supported by a Department of Health Research and Development Directorate grant 039/031.
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