A case of Guillain-Barré syndrome following a family outbreak of Campylobacter jejuni enteritis

Ang, C. Wim; Doorn, Pieter A. van; Endtz, Hubert P.; Merkies, Ingemar S.J.; Jacobs, Bart C.; Klerk, M. A. de; Koningsveld, Rinske van; Meché, F. G. A. Van Der

doi:10.1016/s0165-5728(00)00369-6

Cited by 38 publications

(27 citation statements)

References 16 publications

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“…AFLP fingerprints of strains GB13 and GB14, obtained from family members of a GBS patient, were indistinguishable. Both strains were obtained in 1995; unfortunately, no strain was obtained from the GBS patient (2).…”

Section: Resultsmentioning

confidence: 99%

Amplified Fragment Length Polymorphism Analysis of Campylobacter jejuni Strains Isolated from Chickens and from Patients with Gastroenteritis or Guillain-Barré or Miller Fisher Syndrome

Duim¹,

Ang²,

Belkum

et al. 2000

Appl Environ Microbiol

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The high-resolution genotyping method of amplified fragment length polymorphism (AFLP) analysis was used to study the genetic relationships between Campylobacter jejuni strains infecting chickens (n ‫؍‬ 54) and those causing gastroenteritis in humans (n ‫؍‬ 53). In addition, C. jejuni strains associated with the development of Guillain-Barré syndrome (GBS) (n ‫؍‬ 14) and Miller Fisher syndrome (MFS) (n ‫؍‬ 4), two related acute paralytic syndromes in human, were included. Strains were isolated between 1989 and 1998 in The Netherlands. The AFLP banding patterns were analyzed with correlation-based and band-based similarity coefficients and UPGMA (unweighted pair group method using average linkages) cluster analysis. All C. jejuni strains showed highly heterogeneous fingerprints, and no fingerprints exclusive for chicken strains or for human strains were obtained. All strains were separated in two distinct genetic groups. In group A the percentage of human strains was significantly higher and may be an indication that genotypes of this group are more frequently associated with human diseases. We conclude that C. jejuni from chickens cannot be distinguished from human strains and that GBS or MFS related strains do not belong to a distinct genetic group.

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Section: Resultsmentioning

confidence: 99%

Amplified Fragment Length Polymorphism Analysis of Campylobacter jejuni Strains Isolated from Chickens and from Patients with Gastroenteritis or Guillain-Barré or Miller Fisher Syndrome

Duim¹,

Ang²,

Belkum

et al. 2000

Appl Environ Microbiol

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“…The bacterial strains utilized in the present study comprise (i) a group of eight Penner serotype reference strains (3, 35) (see Table S1A in the supplemental material), (ii) 29 well-characterized GBS-or MFS-associated C. jejuni strains isolated from GBS and MFS patient stool samples (GB13, GB14, GB26, and GB27 were cultured from the diarrheal stools of family members of two GBS patients after a family outbreak of C. jejuni enteritis) (4,21,27) (see Table S1B in the supplemental material), (iii) 54 ageand sex-matched enteritis-associated C. jejuni strains isolated from Dutch patients with active diarrhea, and (iv) a sialic acid transferase (cstII) knockout mutant of a GBS-associated strain (GB11⌬cstII) (20).…”

Section: Methodsmentioning

confidence: 99%

Characterization of the Specific Interaction between Sialoadhesin and Sialylated Campylobacter jejuni Lipooligosaccharides

Heikema¹,

Bergman

Richards

et al. 2010

Infect Immun

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In Campylobacter jejuni-induced Guillain-Barré syndrome (GBS), molecular mimicry between C. jejuni lipooligosaccharide (LOS) and host gangliosides leads to the production of cross-reactive antibodies directed against the peripheral nerves of the host. Currently, the presence of surface exposed sialylated LOS in C. jejuni is the single known bacterial pathogenesis factor associated with the development of GBS. Using a unique, well-characterized strain collection, we demonstrate that GBS-associated C. jejuni strains bind preferentially to sialoadhesin (Sn, Siglec-1, or CD169), a sialic acid receptor found on a subset of macrophages. In addition, using a whole-cell enzyme-linked immunosorbent assay (ELISA), C. jejuni strains with sialylated LOS bound exclusively to soluble Sn. Mass spectrometry revealed that binding was sialic acid-linkage specific with a preference for ␣(2,3)-linked sialic acid attached to the terminal galactose of the LOS chain as seen in the gangliosides GD1a, GM1b, and GM3. This molecular interaction was also related to functional consequences as a GBS-associated C. jejuni strain that bound Sn in a whole-cell ELISA adhered to surface-expressed Sn of Sn-transfected CHO cells but was unable to adhere to wild-type CHO cells. Moreover, a sialic acid-negative mutant of the same C. jejuni strain was unable to bind Sn-transfected CHO cells. This is the first report of the preferential binding of GBS-associated C. jejuni strains to the Sn immune receptor (P ‫؍‬ 0.014). Moreover, because this binding is dependent on sialylated LOS, the main pathogenic factor in GBS progression, the present findings bring us closer to unraveling the mechanisms that lead to formation of cross-reactive antibodies in GBS disease.

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“…Seventeen GBS-associated and 4 MFS-associated C. jejuni strains used in this study were isolated from GBS/MFS patients from The Netherlands and Belgium between 1991 and 1999 (10). GB13 and GB26 were cultured from the diarrheal stools of family members of 2 GBS patients (31). Twenty-one control C. jejuni strains were isolated from sporadic Dutch enteritis patients without neurological symptoms between 1990 and 1999 (8).…”

Section: Methodsmentioning

confidence: 99%

The crucial role of Campylobacter jejuni genes in anti-ganglioside antibody induction in Guillain-Barré syndrome

Godschalk¹,

Heikema²,

Gilbert³

et al. 2004

J. Clin. Invest.

123

165

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Molecular mimicry of Campylobacter jejuni lipo-oligosaccharides (LOS) with gangliosides in nervous tissueis considered to induce cross-reactive antibodies that lead to Guillain-Barré syndrome (GBS), an acute polyneuropathy. To determine whether specific bacterial genes are crucial for the biosynthesis of ganglioside-like structures and the induction of anti-ganglioside antibodies, we characterized the C. jejuni LOS biosynthesis gene locus in GBS-associated and control strains. We demonstrated that specific types of the LOS biosynthesis gene locus are associated with GBS and with the expression of ganglioside-mimicking structures. Campylobacter knockout mutants of 2 potential GBS marker genes, both involved in LOS sialylation, expressed truncated LOS structures without sialic acid, showed reduced reactivity with GBS patient serum, and failed to induce an anti-ganglioside antibody response in mice. We demonstrate, for the first time, to our knowledge, that specific bacterial genes are crucial for the induction of anti-ganglioside antibodies.

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A case of Guillain-Barré syndrome following a family outbreak of Campylobacter jejuni enteritis

Cited by 38 publications

References 16 publications

Amplified Fragment Length Polymorphism Analysis of Campylobacter jejuni Strains Isolated from Chickens and from Patients with Gastroenteritis or Guillain-Barré or Miller Fisher Syndrome

Amplified Fragment Length Polymorphism Analysis of Campylobacter jejuni Strains Isolated from Chickens and from Patients with Gastroenteritis or Guillain-Barré or Miller Fisher Syndrome

Characterization of the Specific Interaction between Sialoadhesin and Sialylated Campylobacter jejuni Lipooligosaccharides

The crucial role of Campylobacter jejuni genes in anti-ganglioside antibody induction in Guillain-Barré syndrome

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