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Acute motor axonal neuropathy after Mycoplasma infection

Evidence of molecular mimicry

From the Department of Neurology (Drs. Susuki, Odaka, Hirata, and Yuki), Dokkyo University School of Medicine, Tochigi; and Department of Neurology (Dr. Mori), Chiba University School of Medicine, Chiba, Japan.

Address correspondence and reprint requests to Dr. Keiichiro Susuki, Department of Neurology, Dokkyo University School of Medicine, Kitakobayashi 880, Mibu, Shimotsuga, Tochigi, 321-0293, Japan; e-mail: ksusuki{at}dokkyomed.ac.jp

Background: Patients with Guillain-Barré syndrome (GBS) after Mycoplasma pneumoniae infection often have antibodies to galactocerebroside (GalC). Electrodiagnosis may show acute inflammatory demyelinating polyneuropathy (AIDP).

Methods: The authors report a patient with acute motor axonal neuropathy (AMAN) after Mycoplasma infection and review seven cases of Mycoplasma-associated GBS. They investigated anti-GalC serology under various conditions associated with Mycoplasma infection.

Results: The patient had immunoglobulin (Ig)G and IgM antibodies against GM1 and GalC, which cross-reacted. During the acute phase, IgM selectively immunostained axons. The cholera toxin B-subunit and rabbit anti-GM1 IgG stained a band in the lipid extract from M pneumoniae, indicative of the presence of a GM1 epitope. Six Mycoplasma-associated GBS patients with anti-GalC antibodies had non-AIDP electrodiagnoses, whereas one with Mycoplasma-associated AIDP had no anti-GalC antibodies. Anti-GalC antibodies were positive in two of five patients who had neurologic diseases other than GBS after Mycoplasma infection and in one of 12 who had acute respiratory disease caused by M pneumoniae not followed by a neurologic disease.

Conclusions: Anti-GalC antibodies in Mycoplasma-associated GBS may be an epiphenomenon. In certain cases, anti-GM1 antibodies induced by molecular mimicry with M pneumoniae may cause acute motor axonal neuropathy.

Received June 3, 2003. Accepted in final form November 18, 2003.

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