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From the Department of Neurology (Drs. Koga, Yuki, and Hirata), Dokkyo University School of Medicine, Tochigi; and Department of Tumor Immunology (Dr. Tai), Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Address correspondence and reprint requests to Dr. Michiaki Koga, Department of Neurology, Yamaguchi University School of Medicine, Minami-Kogushi 1-1-1, Ube, Yamaguchi 755-8505, Japan; e-mail: kogamrk{at}par.odn.ne.jp
Objective: To examine the association between Miller Fisher syndrome (MFS) and antecedent Haemophilus influenzae infection.
Background: Little is known about agents in prior respiratory tract infection of MFS, whereas antecedent upper respiratory symptoms are frequent. H. influenzae is a major pathogen that can cause human respiratory tract infection.
Methods: The authors used ELISA to detect serum antibody against the bacterium in 70 consecutive patients with MFS and 110 with GuillainBarré syndrome (GBS).
Results: Serum antiH. influenzae IgG and IgM antibody activities were significantly higher in the MFS group than in age- and sex-matched patients with other neurologic diseases (n = 62) and normal control subjects (n = 82). The GBS group showed no significant increase in any class of antibody activities compared with control groups. Serologic evidence of recent infection was found in five (7%) of the patients with MFS and two (2%) of 110 patients with GBS, all of whom had a history of antecedent respiratory tract infection. They frequently showed ophthalmoplegia, but other neurologic features were not remarkable. Serum anti-GQ1b IgG antibody that had cross-reactivity with GT1a ganglioside was detected in six of these seven patients. Thin-layer chromatography with immunostaining showed that serum IgG from H. influenzaeseropositive patients with high anti-GQ1b and anti-GT1a IgG antibody titers bound to the lipopolysaccharide fraction extracted from the type b H. influenzae serostrain. These bands were also stained by anti-GT1a monoclonal antibody (GMR11), indicating that the lipopolysaccharide bears the GT1a epitope.
Conclusions: These findings point to H. influenzae being an agent associated with MFS. Epitopic overlap between H. influenzae and human nerve tissue may be involved in the development of MFS much as GBS is associated with Campylobacter jejuni enteritis.
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