Co-infection with two different Campylobacter jejuni strains in a patient with the Guillain-Barré syndrome

Peggy C R Godschalk1, Michel Gilbert, Bart C Jacobs

  • 1Department of Medical Microbiology and Infectious Diseases, Erasmus MC - University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. p.godschalk@erasmusmc.nl

Microbes and Infection
|October 11, 2005
PubMed

Insights

Multiple Campylobacter jejuni strains can co-infect Guillain-Barré syndrome (GBS) patients. Only specific strains, identified by their lipo-oligosaccharides (LOS), trigger GBS through molecular mimicry, even with non-sialylated structures.

Area of Science:

  • Immunology
  • Microbiology
  • Neuroscience

Background:

  • Campylobacter jejuni is a primary cause of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS).
  • The mechanism is thought to involve molecular mimicry between bacterial lipo-oligosaccharides (LOS) and host gangliosides.
  • Previous research focused on single C. jejuni strain infections.

Purpose of the Study:

  • To investigate the occurrence of multiple C. jejuni strains in GBS/MFS patients.
  • To characterize these co-infecting strains and their role in pathogenesis.
  • To explore the molecular mimicry mechanism in GBS/MFS.

Main Methods:

  • Pulsed-field gel electrophoresis (PFGE) for strain typing.
  • Analysis of LOS biosynthesis gene loci.
  • Mass spectrometry for LOS structure determination.
  • Serological assays to detect patient antibody cross-reactivity.

Main Results:

  • Co-infection with two C. jejuni strains was identified in 8% of GBS/MFS patients studied.
  • Only one of the co-infecting strains (GB5.1) possessed a neuropathy-associated LOS gene locus.
  • Patient antibodies cross-reacted with GB5.1 LOS, specifically with anti-asialo-GM2 antibodies.
  • Both co-infecting strains expressed non-sialylated LOS outer core structures.

Conclusions:

  • Co-infections with multiple C. jejuni strains are possible in GBS patients.
  • Not all isolated C. jejuni strains from GBS patients contribute to disease pathogenesis.
  • Molecular mimicry involving non-sialylated LOS structures and anti-asialo-GM2 antibodies is a potential mechanism in GBS pathogenesis.

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