Relationship of bacterial strains to clinical syndromes of
            <i>Campylobacter</i>
            -associated neuropathies

Kimoto, Kazuhito; Koga, Michiaki; Odaka, Masaaki; Hirata, Koichi; Takahashi, Masaki; Li, J.; Gilbert, Michel; Yuki, Nobuhiro

doi:10.1212/01.wnl.0000244468.22377.6b

Cited by 73 publications

(72 citation statements)

References 35 publications

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“…65 GD1c-like LOS, which mimics GQ1b, also was identified in C. jejuni isolates from FS. 54,94 GM2/GD2 synthase knockout mice, which lack GQ1b and GT1a, are immune-naive hosts that can be used to obtain high anti-ganglioside antibody responses. Immunization of these mice with C. jejuni (CF93-6) LOS generated monoclonal IgG antibodies that reacted with GQ1b and GT1a.…”

Section: Campylobacter Genes As the Determinant Of Neuropathy Developmentioning

confidence: 99%

“…Over a 9-year period, 139 patients were found, from whom C. jejuni had been isolated and who had medical histories available for clinical analysis, 54 even though the latent period between preceding intestinal infection and neuropathy onset often exceeded the excretion period of viable C. jejuni cells in stools. Diagnoses for the other 139 patients were GBS (n ϭ 90, 65%), FS (n ϭ 22, 16%), atypical GBS with preserved muscle stretch reflexes (MSR; n ϭ 10, 7%), FS overlapping GBS (FS/GBS; n ϭ 6, 4%), Bickerstaff's brainstem encephalitis (BBE; n ϭ 1, 0.7%), BBE overlapping GBS (BBE/ GBS; n ϭ 2, 1.4%), acute ophthalmoparesis without ataxia (AO; n ϭ 3, 2.1%), ataxic GBS (n ϭ 1, 0.7%), acute oropharyngeal palsy (n ϭ 3, 2.1%), and chronic inflammatory demyelinating polyneuropathy (CIDP; n ϭ 1, 0.7%).…”

Section: Campylobacter Genes As the Determinant Of Neuropathy Developmentioning

confidence: 99%

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Ganglioside mimicry and peripheral nerve disease

Yuki

2007

Muscle and Nerve

124

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Four criteria must be satisfied to conclude that a given microorganism causes Guillain-Barré (GBS) or Fisher (FS) syndrome associated with anti-ganglioside antibodies: (1) an epidemiological association between the infecting microbe and GBS or FS; (2) isolation in the acute progressive phase of illness of that microorganism from GBS or FS patients with associated anti-ganglioside IgG antibodies; (3) identification of a microbial ganglioside mimic; and (4) a GBS or FS with associated anti-ganglioside antibodies model produced by sensitization with the microbe itself or its component, as well as with ganglioside. Campylobacter jejuni is a definitive causative microorganism of acute motor axonal neuropathy and may cause FS and related conditions. Haemophilus influenzae and Mycoplasma pneumoniae are possible causative microorganisms of acute motor axonal neuropathy or FS. Acute and chronic inflammatory demyelinating polyneuropathies may be produced by mechanisms other than ganglioside mimicry.

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Section: Campylobacter Genes As the Determinant Of Neuropathy Developmentioning

confidence: 99%

Section: Campylobacter Genes As the Determinant Of Neuropathy Developmentioning

confidence: 99%

Ganglioside mimicry and peripheral nerve disease

Yuki

2007

Muscle and Nerve

124

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“…In most cases the infections are self-limiting; however, in rare cases, some patients with C. jejuni enteritis later develop neurological conditions such as Guillain-Barré or Fisher syndrome (34). Most strains of C. jejuni isolated from patients with various neurological conditions synthesize lipooligosaccharides (LOS) exhibiting molecular mimicry with the carbohydrate moieties of gangliosides enriched in peripheral nerves (20). Ganglioside mimicry by C. jejuni LOS, therefore, could induce the production of autoantibodies against gangliosides and the development of neurological disease (36).…”

mentioning

confidence: 99%

Characterization of Lipooligosaccharide-Biosynthetic Loci ofCampylobacter jejuniReveals New Lipooligosaccharide Classes: Evidence of Mosaic Organizations

Parker

Gilbert

Yuki³

et al. 2008

J Bacteriol

123

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The lipooligosaccharide (LOS) biosynthesis region is one of the more variable genomic regions between strains of Campylobacter jejuni. Indeed, eight classes of LOS biosynthesis loci have been established previously based on gene content and organization. In this study, we characterize additional classes of LOS biosynthesis loci and analyze various mechanisms that result in changes to LOS structures. To gain further insights into the genomic diversity of C. jejuni LOS biosynthesis region, we sequenced the LOS biosynthesis loci of 15 strains that possessed gene content that was distinct from the eight classes. This analysis identified 11 new classes of LOS loci that exhibited examples of deletions and insertions of genes and cassettes of genes found in other LOS classes or capsular biosynthesis loci leading to mosaic LOS loci. The sequence analysis also revealed both missense mutations leading to "allelic" glycosyltransferases and phase-variable and non-phase-variable gene inactivation by the deletion or insertion of bases. Specifically, we demonstrated that gene inactivation is an important mechanism for altering the LOS structures of strains possessing the same class of LOS biosynthesis locus. Together, these observations suggest that LOS biosynthesis region is a hotspot for genetic exchange and variability, often leading to changes in the LOS produced.

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“…15 Immunological studies have shown that some patients develop MFS after Campylobacter jejuni infection, including those with GBS/MFS overlap. 16,17 These findings suggest that AMAN and MFS are part of the same spectrum of disease. In our study, facial weakness was more common in AIDP than MFS or AMAN, whereas delayed facial weakness occurred at the same frequency in AIDP, AMAN, and MFS.…”

Section: Discussionmentioning

confidence: 79%