Guillain-Barré Syndrome and Campylobacter jejuni Infection: A Review (original) (raw)
Related papers
PLoS ONE, 2012
Background: Campylobacter jejuni is the predominant antecedent infection in Guillain-Barré syndrome (GBS). Molecular mimicry and cross-reactive immune responses to C. jejuni lipo-oligosaccharides (LOS) precipitate the development of GBS, although this mechanism has not been established in patients from developing countries. We determined the carbohydrate mimicry between C. jejuni LOS and gangliosides, and the cross-reactive antibody response in patients with GBS in Bangladesh. Methodology: Sera from 97 GBS patients, and 120 neurological and family controls were tested for antibody reactivity against LOS from C. jejuni isolates from GBS patients in Bangladesh (BD-07, BD-39, BD-10, BD-67 and BD-94) by enzymelinked immunosorbent assay (ELISA). Cross-reactivity to LOS was determined by ELISA. The LOS outer core structures of C. jejuni strains associated with GBS/MFS were determined by mass spectrometry.
Journal of Clinical Investigation, 2004
Molecular mimicry of Campylobacter jejuni lipo-oligosaccharides (LOS) with gangliosides in nervous tissue is 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. Nonstandard abbreviations used: Cm r , chloramphenicol resistance; cst-II, campylobacter sialic acid transferase-II; GBS, Guillain-Barré syndrome; LOS, lipo-oligosaccharides; MFS, Miller Fisher syndrome; orf, open reading frame.
Guillain-Barré Syndrome Induced by Campylobacter jejuni
British Microbiology Research Journal, 2015
Purpose of Review: Guillain-Barré syndrome (GBS) is a neurologic disease that produces ascending paralysis that affects people all over the world. Several infectious agents have been associated with GBS and many reports suggest that infection with Campylobacter jejuni, a common enteric pathogen, may cause GBS by triggering demyelination of peripheral nerves. This review provides an update on the C. jejuni infections engaged in the developing of GBS. Summary and Results: Guillain-Barré syndrome is the most common cause of acute neuromuscular paralysis, yet its cause and pathogenesis are unknown. In approximately two thirds of patients, neuropathic symptoms follow an infection-often a mild, undiagnosed respiratory or gastrointestinal illness. The organism that has most frequently been described in association with GBS is C. jejuni, a gram-negative rod that is now the most common cause of bacterial gastroenteritis in developed countries. Although there has been a plethora of case reports and studies documenting the association, the specific clinical and epidemiologic features are not well Review Article Honarmand and Moghadam; BMRJ, 6(2): 71-83, 2015; Article no.BMRJ.2015.060 72 known. In addition, there is controversy about whether those with preceding C. jejuni infection have a more severe form of the GBS. C. jejuni can cause the disease by a mechanism called molecular mimicry. C. jejuni contains ganglioside-like epitopes in the lipopolysaccharide (LPS) moiety that elicit autoantibodies which can react with peripheral nerve targets. It seems that heterogeneity in the LPS structure determines the specificity of the antiglycolipid response and thereby the clinical features in patients with a post-campylobacter infection neuropathy.
Campylobacter Species and Guillain-Barré Syndrome
Clinical Microbiology Reviews, 1998
SUMMARY Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated w...
Campylobacter infections and Guillain Barré syndrome
Journal of Gastrointestinal Infections
Guillain Barré syndrome (GBS) is a serious disorder of the peripheral nerves preceded by a recognized acute infectious illness. Campylobacter jejuni has been recognized as an important pathogen precipitating GBS and the structure of C. jejuni lipooligosaccharide (LOS) might have a role in the outcome of infection. The development of GBS and Miller Fisher syndrome has been reported to be due to expression of a GM1 like LOS in class A strains and GQ1b like LOS in class B strains of C. jejuni respectively. Virulence of C. jejuni, subtle differences in the interaction between different strains with the host T lymphocyte receptor and MHC class II and host susceptibility may have a role to play in the development of GBS. A humoral immunopathogenic mechanism for GBS has been envisaged as the disease develops 1 to 3 weeks after C. jejuni infection. Antibodies to C. jejuni may remain elevated for several weeks after acute infection. Host susceptibility factors are also important in the pathogenesis of GBS as this disease occurs within families. Association between the occurrence of GBS and a particular HLA type has been envisaged, but studies to prove it are inconclusive. Despite our increasing understanding of the pathophysiology of GBS, the triggering event leading to the disease is still indeed a great puzzle. This review describes the in-depth association of Campylobacter infections with GBS.
Infection and …, 1994
Three Campylobacter jejuni, biotype 2, serotype O:41 strains that were isolated from patients who developed Guillain-Barré syndrome (GBS) and one C. jejuni isolate from a patient who developed enteritis only were examined. The aim of the study was to determine the structure of the core oligosaccharide (OS) of the lipopolysaccharide (LPS) of C. jejuni serotype O:41, a serotype rarely associated with the development of GBS, and to determine if the LPS shares similar epitopes with any of the major human gangliosides. Electrophoretic analysis with silver staining or immunoblotting demonstrated that the strains had LPS profiles characteristic of low-molecular-weight LPS. Colorimetric analysis detected N-acetylneuraminic (sialic) acid in the core OSs of all the strains. Thin-layer chromatography with immunostaining showed that antisera raised against the GBS strains reacted with the GM 1 ganglioside, suggesting that C. jejuni serotype O:41 LPSs and the GM 1 ganglioside have similar epitopes. Furthermore, polyclonal anti-GM 1 and anti-asialoGM 1 antibodies cross-reacted with each C. jejuni O:41 LPS tested, suggesting that the serotype O:41 core OS has a GM 1-and asialoGM 1-like structure. LPSs extracted from C. jejuni serostrains O:2, O:3, and O:19 were also used in the study. Cholera toxin (a GM 1 ligand) and peanut agglutinin (a Gal1-3GalNAc ligand) recognized all serotype O:41 LPSs and the serostrain O:2 LPS. Immunoadsorption results confirmed GM 1 relatedness. Moreover, the core OS was isolated from a GBS-associated C. jejuni O:41 LPS by gel permeation chromatography. An analysis by gasliquid chromatography (GLC), GLC-mass spectrometry, and nuclear magnetic resonance showed the core OS of one of the C. jejuni O:41 GBS isolates to have a tetrasaccharide structure consistent with GM 1 mimicry.
2012
Guillain-Barre syndrome (GBS) is an autoimmune disease in which body’s immune system attacks the nervous system that leads to nerve inflammation causing muscle weakness. This syndrome affects people of both sexes between ages 25 and 50 years. It is not clear what exactly triggers GBS. However, Campylobacter jejuni is found to be the most common pathogenic factor that is found to trigger GBS and this is widely reported. Several of these studies have shown that surface lipopolysaccharide (LPS) present in C. jejuni may act as an antigenic factor that induces GBS. In addition, some of these reports have also suggested that in addition to the host cell and bacterial antigenic factor interactions, the molecular mimicry between C. jejuni LPS and peripheral nerve gangliosides may play a significant role in the development of GBS. Although LPS was recognized as a potent antigen by different studies, nevertheless, the antigenic diversity and the lack of clearly defined protective epitopes are...
Ganglioside GM1 Mimicry inCampylobacterStrains from Sporadic Infections in the United States
The Journal of Infectious Diseases, 1999
To determine whether GM1-like epitopes in Campylobacter species are specific to O serotypes associated with Guillain-Barré syndrome (GBS) or whether they are frequent among random Campylobacter isolates causing enteritis, 275 random enteritis-associated isolates of Campylobacter jejuni were analyzed. The isolates were collected in the United States using a cholera toxin-binding assay. Overall, 26.2% of the isolates were positive for the GM1-like epitope. Of the 36 different O serotypes in the sample, 21 (58.3%) contained no strains positive for GM1, whereas in 6 serotypes (16.7%), 150% of isolates were positive for GM1. GBSassociated serotypes were more likely to contain strains positive for GM1 than were non-GBSassociated serotypes (37.8% vs. 15.1%,). The results suggest that humans are fre-P ϭ .0116 quently exposed to strains exhibiting GM1-like mimicry and, while certain serotypes may be more likely to possess GM1-like epitopes, the presence of GM1-like epitopes on Campylobacter strains does not itself trigger GBS. Campylobacter jejuni subspecies jejuni (referred to as C. jejuni) is one of the most common causes of bacterial gastrointestinal infection in the United States (US), United Kingdom (UK), and worldwide [1]. One recognized complication of campylobacter infection is the development of Guillain-Barré syndrome (GBS), an acute paralytic disease affecting the peripheral nervous system. In the postpolio era, GBS is the most common cause of acute flaccid paralysis [2]. In recent years, C. jejuni infection has been recognized as the most common identifiable event preceding GBS and has been identified in up to 41% of GBS patients in the West [3]. GBS is a heterogenous disorder based on clinical, electrophysiologic, and pathologic findings [2]. In North America, Europe, and Australia, acute inflammatory demyelinating polyneuropathy (AIDP) is the major subtype and is characterized by demyelination of motor and sensory nerves with lymphocytic infiltration [4-6]. The axonal forms, represented primarily by acute motor axonal neuropathy (AMAN), are frequently seen in northern China [7-9] and other countries, such as Mexico [10] and Japan [11]. In contrast to AIDP, the AMAN form
Infection and Immunity, 2007
Molecular mimicry between lipooligosaccharides (LOS) of Campylobacter jejuni and gangliosides in peripheral nerves plays a crucial role in the pathogenesis of C. jejuni -related Guillain-Barré syndrome (GBS). We have analyzed the LOS outer core structures of 26 C. jejuni strains associated with GBS and its variant, Miller Fisher syndrome (MFS), by capillary electrophoresis coupled with electrospray ionization mass spectrometry. Sixteen out of 22 (73%) GBS-associated and all 4 (100%) MFS-associated strains expressed LOS with ganglioside mimics. GM1a was the most prevalent ganglioside mimic in GBS-associated strains (10/22, 45%), and in eight of these strains, GM1a was found in combination with GD1a mimics. All seven strains isolated from patients with ophthalmoplegia (GBS or MFS) expressed disialylated (GD3 or GD1c) mimics. Three out of 22 GBS-associated strains (14%) did not express sialylated ganglioside mimics because their LOS locus lacked the genes necessary for sialylation. Th...