A 46-year-old Caucasian man, a physician from a town in central Serbia, had nausea, fever, and had suffered watery diarrhea that lasted for one day. The diarrhea was self-limiting and he was treated only with antipyretic drugs. Ten days later, he felt muscle weakness in both upper and lower extremities. Proximal weakness in his arms resulted in difficulty in lifting them above his shoulders, and in his legs in difficulty climbing stairs and rising from a low chair. During the following days weakness also appeared in his distal arm muscles, and gradually increased in his upper and lower leg muscles until our patient became severely disabled. Three days prior to admission, our patient complained of muscular pain in both his legs, low back and shoulders.
On admission, seven days after the first symptoms occurred, our patient's mental status was normal and cranial nerves were not affected. Both nerves innervating the proximal and distal muscle groups were affected in the upper and lower extremities resulting in symmetric proximal and distal muscle weakness which ranged between 3 and 4 on the Medical Research Council (MRC) grading scale. Deep tendon reflexes were normal, with the exception of both triceps brachii reflexes which were abolished. Pathological reflexes were also absent. There was no sensory nerve dysfunction and no sphincter disturbances (Quantitative Sensory Testing, Semmes-Weinstein monofilament, 128 Hz tuning fork).
Electrophysiological investigation was performed three weeks after the beginning of the first symptoms. Electromyography (EMG) revealed polyphasic neuropathic muscle action potentials with reduced interference pattern and compensatory motor unit potentials in the proximal and distal muscles of his upper and lower extremities. The amplitude of motor evoked potentials was slightly reduced for both peroneal and right mediana and for the ulnar nerve. Motor and sensory conduction velocities were normal.
The following laboratory examinations were normal: blood sedimentation rate, complete blood count, blood glucose, serum electrolytes, urea nitrogen, creatinine, serum protein content, cholesterol, triglycerides, and liver and muscle enzymes. The protein level in the cerebrospinal fluid (CSF) was measured seven days after the beginning of muscle weakness and was slightly elevated at 0.59 g/L. According to laboratory standards, a normal upper limit is 0.46 g/L. Cell count was normal with 3 mononuclear cells/mm3. A normal cell value is less than 10 cells/mm3.
In view of a probable diagnosis of AMAN, our patient received from the first day of hospitalization a course of intravenous immunoglobulin (IVIG) at the standard dose of 0.4 g/kg/day: a daily dose of 30 g was administrated over a period of five days (our patient's weight was 75 kg). IVIG resulted in an immediate dramatic improvement. From the 11th day after his admission, in view of the positive stool cultures for C. jejuni (see below), he received 1500 mg of oral erythromycin daily in order to eradicate antigenic stimuli. On his 24th day of hospitalization, our patient's neurological status improved with residual mild weakness of the foot dorsiflexor muscles and minimal weakness of the proximal and distal muscles of his arms. Three weeks later he had no muscle weakness and his tendon reflexes were brisk.
Because of the clinical signs and the history of a preceding gastrointestinal infection, a stool sample was sent to the Republic Institute of Public Health, Belgrade, for microbiological examination. For the detection of thermophilic campylobacters the Columbia agar base was supplemented with 5% sheep blood and antibiotics (cefoperazone 1.5 g/L, colistin 106 U, vancomycin 1 g/L, amphotericin B 0.2 g/L), (bioMérieux, Marcy l'Etoile, France). Culture was incubated at 42°C for 48 hours in a microaerophilic atmosphere (biomérieux). Fortunately, due to a delay in sampling, the primary culture was seen as positive for Campylobacter, and the subculture of solid plate yielded a confluent growth of colonies typical for Campylobacter, which were oxidase- and catalase-positive with a characteristic microscopic appearance, with S-shaped and curved rods. Identification, biotyping and serotyping were performed at the Bacteriology and Enteric Disease Program, National Microbiology Laboratory, Winnipeg, Manitoba, Canada. A strain presumptively identified as Campylobacter was differentiated to the species level by a combination of biotyping tests  and by use of a polymerase chain reaction (PCR)-based restriction fragment length polymorphism (RFLP) test . Heat stable serotyping was performed using Penner's method . The strain was identified as C. jejuni subspecies jejuni biotype II HS O:19, sensitive to erythromycin.
Antibodies to C. jejuni were determined by indirect immunofluorescence assay using as antigen methanol-fixed whole bacteria of the C. jejuni. Five pools, each consisting of 50 sera of healthy blood donors, were used as controls.
Autoantibodies to peripheral nerve gangliosides, including monosialoganglioside (GM1), disialoganglioside (GD1a) and asialoganglioside (ASGM1) were determined by enzyme-linked immunosorbent assay (ELISA), using methanol-fixed antigen-coated 96-well micro-ELISA plates and peroxidase-conjugated secondary anti-immunoglobulin G (IgG) and immunoglobulin M (IgM) goat antibodies.
On the day of the admission, serum antibodies to C. jejuni were positive in a titer of 1:128, while the control sera had titers of up to 1:8. On day 24, the antibody titers were still positive at 1:32. The IgG anti-GM1 antibodies were positive in the first serum sample (day 4) in a significant titer (1:16,000, with negative controls 1:400) and changed to negative (1:400) on days 10 and 19 after admission. There was no serum reactivity against gangliosides GD1a and ASGM1.