Brain, Vol. 123, No. 10, 2171-2178,
October 2000
© 2000 Oxford University Press
Haemophilus influenzae infection and Guillain–Barré syndrome
1 Departments of Neurology and 2 Pediatrics, 3 Clinical Laboratory and 4 Second Department of Microbiology, Chiba University School of Medicine, Chiba, Japan
Correspondence to:
Masahiro Mori, MD, Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan E-mail: morim{at}olive.ocn.ne.jp
It has been reported recently that Haemophilus influenzae can elicit an axonal form of Guillain–Barré syndrome. To investigate the incidence and features of H. influenzae-related Guillain–Barré syndrome, anti-H. influenzae antibody titres were measured by enzyme-linked immunosorbent assay (ELISA) in 46 consecutive Japanese patients with Guillain–Barré syndrome, 49 normal controls, 24 patients with multiple sclerosis and 27 patients with amyotrophic lateral sclerosis (ALS). Whole bacteria of non-encapsulated (non-typable) H. influenzae isolated from one of the Guillain–Barré syndrome patients was the antigen used. Elevated anti-H. influenzae antibodies for two or three classes of IgG, IgM and IgA were found in six (13%) Guillain–Barré syndrome patients, but not in the normal controls and patients with multiple sclerosis or ALS. The incidence was significantly higher in patients with Guillain–Barré syndrome than in the normal controls (P = 0.01) and patients with multiple sclerosis or ALS (P = 0.009). Western blot analysis confirmed that the H. influenzae-positive patients' IgG recognized the lipopolysaccharides of H. influenzae. Guillain–Barré syndrome patients with anti-H. influenzae antibodies showed relatively uniform clinical and laboratory features: prodromal respiratory infection, less frequent cranial and sensory nerve involvement, pure motor axonal degeneration on electrophysiology, and positivity for IgG anti-GM1 antibodies. Although the features were similar to those in Guillain–Barré syndrome patients infected by Campylobacter jejuni, the recoveries seemed to be better in patients with H. influenzae-related Guillain–Barré syndrome. It is concluded that a form of Guillain–Barré syndrome occurs after respiratory infection by H. influenzae in the Japanese population. A particular strain of non-typable H. influenzae has a ganglioside GM1-like structure and elicits axonal Guillain–Barré syndrome similar to C. jejuni-related Guillain–Barré syndrome.
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