Retrospective review of children attending our tertiary centre over an 11 year period meeting consensus case definitions for GBS or Fisher syndrome (FS). Data were collected on clinical features of triggering infections, laboratory findings, neurophysiological investigations and outcome.
52 children met case definition for GBS; one child met case definition for FS. 89% met neurophysiological criteria for acute inflammatory demyelinating polyneuropathy (AIDP) and 4% met criteria for acute motor axonal neuropathy (AMAN). Infectious illness in the 6 weeks prior to GBS onset was reported in 81% of cases, including respiratory tract infection in 53% and gastroenteritis in 23%. Onset of infection preceded onset of neurological symptoms by a median 9 days (range 0–25). A suspected triggering organism was identified in 42% of cases, including Mycoplasma pneumoniae in 28%, streptococcal species in 9% and herpes viruses in 8%. 95% of suspected M. pneumoniae cases were categorised as AIDP. In cases where final outcome was known (n=13), M. pneumoniae was associated with full recovery in all cases. Analysis of Health Protection Agency data on M. pneumoniae cases in England and Wales over the period studied revealed significantly greater than expected incidence of GBS in our cohort in M. pneumoniae epidemic seasons (Fisher's exact test, p=0.02).
M. pneumoniae was the most frequently identified triggering organism in our cohort. Our novel observation of a relationship between M. pneumoniae epidemic seasons and incidence of GBS supports the conclusion that M. pneumoniae is an under-recognised trigger of GBS in children. Transient mycoplasma-induced immunosuppression is considered as a possible mechanism mediating the relationship. GBS triggered by suspected M. pneumoniae infection tends to be of the AIDP subtype and associated with a positive outcome.