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NEUROLOGY 1998;51:371-378
© 1998 American Academy of Neurology

Campylobacter jejuni lipopolysaccharides in Guillain-Barré syndrome

Molecular mimicry and host susceptibility

K. A. Sheikh, MD, I. Nachamkin, DrPH, T. W. Ho, MD, H. J. Willison, MBBS, J. Veitch, FIMLS, H. Ung, BS, M. Nicholson, MS, C. Y. Li, MD, H. S. Wu, MD, B. Q. Shen, MD, D. R. Cornblath, MD, A. K. Asbury, MD, G. M. McKhann, MD and J. W. Griffin, MD

From the Department of Neurology (Drs. Sheikh, Ho, Cornblath, McKhann, and Griffin), Johns Hopkins University School of Medicine, Baltimore; the Johns Hopkins University Zanvyl Krieger Mind-Brain Institute (Dr. McKhann), Baltimore, MD; the Departments of Pathology and Laboratory Medicine (Dr. Nachamkin and H. Ung) and Neurology (Dr. Asbury), University of Pennsylvania School of Medicine, Philadelphia, PA; the Department of Neurology (H.J. Willison and J. Veitch), Institute of Neurological Sciences, University of Glasgow, Scotland, UK; Centers for Disease Control and Prevention (M. Nicholson), Atlanta, GA; the Department of Neurology (Dr. Li), Second Teaching Hospital, Hebei Medical School, Shijiazhuang; Department of Neurology (Dr. Wu), Beijing Children's Hospital, Beijing; and the Department of Infectious Diseases (Dr. Shen), First Teaching Hospital, Beijing Medical University, Beijing, People's Republic of China.

Address correspondence and reprint requests to Dr Sheikh, Department of Neurology, Johns Hopkins University School of Medicine, Pathology 509, 600 N. Wolfe Street, Baltimore, MD 21287.

Objective: This study was designed to determine if the presence of specific ganglioside-like moieties in Campylobacter lipopolysaccharides(LPSs) is related to the development of Guillain-Barré syndrome (GBS), and to discover how frequently such moieties, including GM1, are present in these LPSs.

Methods: We studied Campylobacter isolates and sera from seven patients with GBS (five acute motor axonal neuropathy, one acute inflammatory demyelinating polyneuropathy, and one Fisher's syndrome), and compared them with similar specimens from patients with Campylobacter enteritis alone.

Results: All GBS patients had antiganglioside antibodies. Anti-GM1 and anti-GD1a titers were significantly elevated in post-Campylobacter GBS, both axonal and demyelinating, compared with normal control subjects or those with uncomplicated Campylobacter diarrhea. Campylobacter isolated from patients with GBS and with enteritis alone had similar ganglioside-like moieties.

Conclusions: These results indicate that patients who develop GBS respond differently to the ganglioside-like epitopes on Campylobacter than do non-GBS diarrhea patients. Our findings support a role for host susceptibility as a determinant for the outcome following Campylobacter infection. These findings have important implications for the development of vaccines against Campylobacter jejuni.


Supported in part by National Institutes of Health grants NS-34846 and NS-31528.

Received December 3, 1997. Accepted in final form February 22, 1998.




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