Sir: The role of Mycoplasma pneumoniae in the pathophysiology of Guillain-Barre syndrome (GBS) is unknown. Direct invasion of CSF by the micro-organism in GBS has been proved both by immuno¯uorescence [1] and culture [3] although an auto-immune mechanism is the most supported theory, with the key role of a demyelinating process.A 3-year-old boy was admitted to our hospital with a 6-day history of progressive weakness in his lower limbs, frequent falls and diculty in walking. Previously, he had mild respiratory tract symptoms. The most remarkable ®ndings were muscle weakness, absence of tendon re¯exes in the lower limbs and clumsy gait. Haemoglobin was 8.7 g/dl, haematocrit 25.8%, the ESR 25 mm/h and he had positive IgM anticardiolipin antibodies. Cold agglutinins were negative. CSF (lumbar puncture) revealed 1 leucocyte/ mm 3 , protein, 72 mg/dl, glucose, 54 mg/dl, IgG, 7.4 mg/dl (952 mg/dl in serum), and albumin, 44 mg/dl (3,920 mg/dl in serum). The CSF specimen was inadequate to culture for M. pneumoniae. Serological investigations for respiratory viruses (adenovirus, in¯uenza A, and B, para-in¯uenza 1, 2, and 3, cytomegalovirus, respiratory syncytial), and Epstein Barr viruses as well as stool culture for Campylobacter jejuni were negative. Based on conduction velocities in both right and left peroneal nerves of 24 and 17.9 m/s respectively, (normal range: 41±64 m/s), decreased amplitude of the compound muscle action potentials, and absence of sensory sural nerve responses, a diagnosis of GBS was made.Two serum specimens (days 5 and 21) revealed positive IgM and a four-fold increase in IgG antibodies (ELISA Virotech, Germany, and ELISA Bio Whittaker, Walkersville, USA, respectively) to M. pneumoniae. M. pneumoniae antigen was directly detected by a monoclonal antibody ELISA (Pneumofast Ag, International Microbio. Signes, France), in a throat swab and aspirated respiratory secretions.Intravenous immunoglobulins were administered (0.4 g/kg per day for 5 days) with no clinical improvement. A 10-day oral clarythromycin (15 mg/kg per day) course followed, with rapid improvement 2 days after initiating therapy. Tendon re¯exes became normal on day 21.