Guillain‐Barre Syndrome and Influenza Virus Infection
Background. In Western countries, the cause of 60% of all Guillain‐Barre syndrome (GBS) cases remains unidentified. The number of cases of unidentified cause peaks in winter, and these cases are commonly preceded by respiratory tract infection or influenza‐like illness. We investigated the triggering role of influenza virus infection.
Methods. Of 405 patients with GBS who were admitted to a French reference center during 1996–2004, 234 had cases caused by an unidentified agent. We used time‐series methods to study the correlation between the monthly incidence of such cases and influenza‐like illnesses reported by the Sentinelles surveillance network. We analyzed anti‐influenza antibodies using complement fixation testing and hemagglutination‐inhibition assays. We studied etiological subgroups using Wilcoxon and Fisher’s exact tests.
Results. We found a positive association between the monthly incidence of GBS caused by an unidentified agent and reported influenza‐like illnesses. Of 73 patients whose cases occurred during periods in which there was a possible link to influenza, 10 (13.7%) had serological evidence of recent influenza A, and 4 (5.5%) had serological evidence of influenza B. Eight of 10 influenza A–related cases occurred during “major” influenza seasons, and antibodies specific to the current epidemic strain were found in 9 cases. Most patients with influenza A–related cases were aged <65 years, and none had antiganglioside antibodies. Influenza‐related cases differed both from Campylobacter jejuni–related cases, with regard to the lack of need for mechanical ventilation ( P = .0,14), and from the cases caused by an unidentified agent, with regard to the presence of preceding influenza‐like illness or respiratory tract infection ( P = .0,15) and longer time from the infectious event to GBS onset (P = .0,4 ).
Conclusions. Influenza viruses are infrequent triggering agents of GBS but may play a significant role during major influenza outbreaks. Influenza‐related GBS displays specific features and is not associated with antiganglioside antibody response, which suggests the presence of underlying immune mechanisms.