Serum Antibodies To Campylobacter Jejuni In Multifocal Motor Neuropathy

Abstract

Multifocal motor neuropathy (MMN) has been frequently associated with high titers of anti‐ganglioside antibodies but the cause of this immune response is not known. Recently a possible association with an antecedent Campylobacter jejuni (CJ) infection has been reported in three patients who developed MMN and high titers of anti‐GM1 antibodies after CJ enteritis. Furthermore reactivity with the lipopolysaccharides (LPS) of CJ have been reported in some patients with chronic motor neuropathies and high anti‐ganglioside antibodies. To determine whether CJ may be involved in the pathogenesis of MMN we examined 22 patients with MMN, including 6 with anti‐ganglioside reactivity (2 GM1, 2 GD1a, 1 GM1+GD1a, 1 GM1+GM2), for the presence of anti‐CJ antibodies by Covalink ELISA and immunoblot, and correlated their presence with that of anti‐ganglioside antibodies. As controls we examined 17 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 23 with amyotrophic lateral sclerosis (ALS), 43 with other neurological diseases (OND) and 23 normal subjects (NS). By ELISA we found high titers (1/640) of anti‐CJ in 8 patients (36%) with MMN (4 IgM, 2 IgA, 1 IgM+IgA, 1 IgM+IgG+IgA), 2 each with CIDP (12%; 1 IgA and 1 IgM) and ALS (9%; 1 IgM and 1 IgG), one with OND (2%; IgG) and none in NS (MMN vs. neurological controls p < 0.0005; MMN vs. NS p < 0.005). By immunoblot, 5 patients with MMN (23%), one of whom was also positive by ELISA, had a very intense reactivity (3 IgG, 1 IgA, 1 IgG+IgA) with a 14 kD band corresponding to the lipopolysaccharides (LPS) of CJ, as compared to two patients with ALS (9%; 1 IgG and 1 IgM), one each with CIDP (6%; IgG) and NS (4%), while no reactivity was found in OND (MMN vs. neurological controls p < 0.01). Overall anti‐CJ antibodies were detected by at least one method in 12 MMN patients (55%), 3 CIDP (18%), 4 SLA (17%), 1 OND (2%) and 1 NS (4%) (MMN vs. neurological controls p < 0.0005; MMN vs. NS p < 0.0005). Anti‐ganglioside antibodies were similarly frequent in patients with (33%) or without (20%) anti‐CJ reactivity. The high frequency of anti‐CJ antibodies in MMN patients supports the hypothesis of an association between MMN and CJ even if it is still unclear whether this reflects a concurrent or previous CJ infection possibly involved in the pathogenesis of MMN. If this is the case, the lack of association with anti‐ganglioside antibodies suggests that these antibodies might not be the only anti‐neuronal antigens induced by CJ.