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Chapter 13 : Guillain-Barré Syndrome and Infection

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Guillain-Barré Syndrome and Infection, Page 1 of 2

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Abstract:

Guillain-Barré Syndrome (GBS) is currently considered to be a true case of molecular mimicry mediated disease, at least in those patients with a preceding infection. There is convincing evidence from extensive histology, serology, and animal model studies that GBS is caused by an autoimmune response. This parallels the failure of natural immune tolerance in other disorders such as rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis, which are generally classified as autoimmune diseases. GBS is therefore frequently classified as a typical postinfectious disease. Studies based on stool culture alone will therefore underestimate the frequency of infections in GBS. The current trend toward direct DNA sequence-based typing has also penetrated the research field. There appears to be an association between the specific clinical symptoms, GBS variants, and particular characteristics of strains that primarily resides in the lipooligosaccharides (LOS) biosynthesis genes. Two conditions need to be fulfilled to induce a cross-reactive immune response against autologous antigens by molecular mimicry. First, the microbial and autologous antigens need to be sufficiently similar to induce antibodies that can cross-react. Second, the microbial antigen needs to be sufficiently different from the autoantigen to break the tolerance of the immune system and induce a specific immune response. Many studies have reported an association between preceding infections and axonal forms of GBS. Considering the crucial role of antiganglioside antibodies in the pathogenesis of these forms of GBS, patients may profit from selective depletion of antibodies.

Citation: Jacobs B, van Belkum A, Endtz H. 2008. Guillain-Barré Syndrome and Infection, p 245-261. In Nachamkin I, Szymanski C, Blaser M (ed), , Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815554.ch13

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Figure 1.

Sequence of events in a typical case of –related GBS.

Citation: Jacobs B, van Belkum A, Endtz H. 2008. Guillain-Barré Syndrome and Infection, p 245-261. In Nachamkin I, Szymanski C, Blaser M (ed), , Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815554.ch13
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Image of Figure 2.
Figure 2.

genotype and LOS phenotype in relation to serum antiganglioside antibodies and clinical features in GBS and MFS. Two illustrative examples of strains isolated from a patient with a severe, pure motor form of GBS (strain GB2) and from a patient with MFS (strain MF6) ( ). Strain with a class A genotype produces a GM1- and GD1a-like LOS, which induced cross-reactive antibodies to the peripheral nerve ganglioside GM1 and GD1a. Strain MF6 with a class B genotype produces a GM1b- and GD1c-like LOS, which induced cross-reactive antibodies to the peripheral nerve ganglioside GD3 and GQ1b.

Citation: Jacobs B, van Belkum A, Endtz H. 2008. Guillain-Barré Syndrome and Infection, p 245-261. In Nachamkin I, Szymanski C, Blaser M (ed), , Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815554.ch13
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Tables

Generic image for table
Table 1.

Diagnostic criteria for Guillain-Barré syndrome

Citation: Jacobs B, van Belkum A, Endtz H. 2008. Guillain-Barré Syndrome and Infection, p 245-261. In Nachamkin I, Szymanski C, Blaser M (ed), , Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815554.ch13
Generic image for table
Table 2.

Heterogeneity in Guillain-Barré syndrome

Citation: Jacobs B, van Belkum A, Endtz H. 2008. Guillain-Barré Syndrome and Infection, p 245-261. In Nachamkin I, Szymanski C, Blaser M (ed), , Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815554.ch13
Generic image for table
Table 3.

General comparison between classic autoimmune diseases and Guillain-Barré syndrome

Citation: Jacobs B, van Belkum A, Endtz H. 2008. Guillain-Barré Syndrome and Infection, p 245-261. In Nachamkin I, Szymanski C, Blaser M (ed), , Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815554.ch13
Generic image for table
Table 4.

Frequency studies on infections in patients with Guillain-Barré syndrome

Citation: Jacobs B, van Belkum A, Endtz H. 2008. Guillain-Barré Syndrome and Infection, p 245-261. In Nachamkin I, Szymanski C, Blaser M (ed), , Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815554.ch13
Generic image for table
Table 5.

Evidence for a causal role of infections in the pathogenesis of Guillain-Barré syndrome

Citation: Jacobs B, van Belkum A, Endtz H. 2008. Guillain-Barré Syndrome and Infection, p 245-261. In Nachamkin I, Szymanski C, Blaser M (ed), , Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815554.ch13

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