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(searched for: doi:10.1007/978-1-4471-3175-5_5)
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Joachim Schessl, Birgit Luther, , Gottfried Mauff,
Published: 12 May 2006
European Journal of Pediatrics, Volume 165, pp 605-612; https://doi.org/10.1007/s00431-006-0140-1

Abstract:
We performed a prospective, multicentre study in children with Guillain-Barré syndrome (GBS), diagnosed according to international criteria, to investigate the frequency and aetiology of antecedent diseases. All infections and vaccinations occurring within a 6-week period prior to the onset of GBS were documented. Stool cultures, standardised serological investigations and PCR analyses for 24 different infective agents were performed. Serological findings were regarded as significant if specific immunoglobulin (Ig)M or IgA antibodies were detected, if the IgM enzyme immunoassay or immunfluorescence assay findings were confirmed by immunoblot, if complement fixation test titres rose fourfold or if geometric titres were more than threefold higher than in uninfected control persons. Ninety-five children with GBS were included in the study over a 40-month period. Preceding events were reported in 82%. Microbiological studies carried out on 84 patients resulted in a probable diagnosis in 46 (55%). Coxsackieviruses (15%), Chlamydia pneumoniae (8%), cytomegalovirus (7%) and Mycoplasma pneumoniae (7%) were the most frequently involved agents. Serological evidence of a Campylobacter jejuni infection was found in six patients (7%). Eight children had been vaccinated during the 6 weeks preceding the onset of GBS; in six of these children concomitant infectious diseases were reported, and in one child the time between vaccination and GBS was extremely short. We conclude that, in contrast to adults, Campylobacter spp. does not seem to play a major role in childhood GBS in German-speaking countries. The aetiology of antecedent diseases is distributed over a wide spectrum of paediatric infectious diseases. Most of the children who had been vaccinated showed concomitant infectious diseases, thus obscuring the causative role for GBS.
S. Schmidt, A. Cordt-Schlegel, R. Heitmann
Published: 1 January 1993
Journal of Neurology, Volume 240, pp 506-507; https://doi.org/10.1007/bf00874121

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