Guillain-Barré syndrome (GBS) is an acute immune mediated neuropathy, 
polyradiculoneuritis, characterized by rapid onset of symmetric extremity muscle 
paralysis, areflexia and albuminocytological dissociation in the cerebrospinal 
fluid (CSF). Recently, the heterogeneity of GBS has been noticed with definition 
of several GBS variants. The axonal GBS associated with anti-GM1 antibodies is 
the most important variant with the specific role of Campylobacterjejuni (CJ) in 
the induction of the disease. The role of our study was to determine the 
frequency of antecedent infection with CJ in the population of our patients with 
GBS, the association with anti-GM1 antibodies and the distribution of these 
antibodies within clinical forms of the disease. The diagnosis of GBS has been 
established in 17 patients according to clinical, electrophysiological and 
laboratory (CSF) criteria. The serum antibodies to 63 kDa flagellar protein 
isolated from CJ serotype 0:19 were determined by ELISA and Western blot and 
serum anti-GM1 antibodies by ELISA. In relation to the disability score two 
patients were ambulatory, five were ambulatory with support, seven were 
bedridden and two patients needed respirator. Five (29%) patients had pure 
motor, while 12 (71%) had sensorimotor GBS. The cranial nerves were involved in 
11 (65%) and 9 (53%) patients had autonomic dysfunction. Electromyoneurography 
showed primary axonal, predominantly motor neuropathy in 6 (35%) and 
demyelinating sensorimotor neuropathy in 11 (65%) patients. The CSF protein 
content ranged from 0.47 to 3.88 g/L. The antecedent infection with CJ was shown 
by serum antibodies to CJ flagellar protein in 12 (71%) patients. Fifteen (88%) 
patients had IgG anti-GM1 antibodies. Twelve (71%) patients had both antibodies. 
In relation to the clinical form, anti-CJ antibodies were found in 8 (73%) out 
of 11 patients with demyelinating GBS and in 4 (66.6%) out of 6 patients with 
axonal GBS. The high titer of anti-GM1 antibodies was found in all patients 
(100%) with axonal and in 9 (82%) out of 11 patients with demyelinating GBS. The 
association of IgG anti-CJ and IgG anti-GM1 antibodies was found in 4 (66.6%) 
out of 6 patients with axonal and in 8 (73%) out of 11 patients with 
demyelinating GBS. The main features of our patients with GBS were high 
frequency of antecedent infection with CJ, unusually frequent association with 
anti-GM1 antibodies, and equally frequent association of anti-CJ and anti-GM1 
antibodies in both, axonal and demyelinating GBS.