It has long been textbook knowledge that in most patients an infective illness precedes the development of the Guillain-Barré syndrome (GBS). About two thirds of patients report symptoms of an upper respiratory tract or gastrointestinal tract infection predating the disease by 1–4 weeks. Many diverse infectious agents have been incriminated as triggers of this acute polyradiculoneuropathy but only few larger scale and case controlled studies, so important in a disease with a low incidence of 1–2/100 000, have been published.1-3 Based on this evidence, infections with the gram negative enteropathogen Campylobacter jejuni, cytomegalovirus (CMV), Epstein-Barr virus, andMycoplasma pneumoniae are precipitants of GBS whereas other infections occur no more often in this neuropathy than in controls. The agent most commonly associated with GBS isCampylobacter jejuni. In most parts of the western world, the frequency is around 33%, whereas in China and Japan, this figure is around 45-60%.3-5 CMV has been identified as the predominant viral cause of an infective …