Cause Of Guillain-Barré Syndrome Research Articles

An Unusual Neurological Complication of Multiple Wasp Stings: AIDP

Background and Aims: Wasp stings often result in vascular problems and local irritation. Rarely neurological difficulties result from a delayed immune response, which causes acute inflammatory demyelinating polyradiculopathy, stroke and Parkinson’s disease. Patient’s Concern: Here we are describing a young male, who presented to us with ascending paralysis a few days after being stung by multiple wasps. The patient did not have any infection or recent vaccination. Nerve conduction velocity (NCV) suggested increased latencies in peripheral nerves. Hence, a temporality between Guillain–Barré syndrome (GBS) and the wasp sting was hypothesised. Intervention: After establishing a diagnosis, the patient received standard treatment for acute inflammatory demyelinating polyneuropathy (AIDP). Intravenous immunoglobulins were given over 5 days in divided doses. The patient had gross improvement in the weakness by day 7 and fully recovered in 2 months. Conclusion: This case study highlights the possibility of acute demyelinating polyradiculopathy, a serious neurological consequence that can arise from wasp stings. Nevertheless, the pathophysiology of the same is not well recognised in the literature. This emphasises the importance of identifying uncommon causes of GBS and comprehending the mechanism and curative measures.

Recurrence of a Rare Subtype of Guillain-Barré Syndrome Following a Second Dose of the Shingles Vaccine

Guillain-Barré Syndrome (GBS) is an acute, immune-mediated polyneuropathy. The exact cause of GBS remains unknown, however, it commonly develops post-infection. Since the 1950s, various vaccines have been attributed to causing the syndrome, yet no definitive relationship has ever been determined. In 2021, the Food and Drug Administration (FDA) placed a black-box warning for Shingrix, a non-live recombinant vaccine against the varicella-zoster virus, regarding a possible risk of acquiring GBS post-vaccination in adults aged 65 and older. We report the recurrence of a rare subtype of GBS in a 61-year-old patient following the second dose of Shingrix. This case highlights the difficulty of diagnosing and treating recurrent GBS. It also raises awareness that Shingrix may be related to the development of GBS in younger patients. This case also emphasizes the importance of differentiating GBS from other polyneuropathies.

Guillain-Barré Syndrome Associated with Shiga Toxin-Producing and Enterotoxigenic Escherichia coli Infection

GuillainBarré syndrome (GBS) is the inflammatory neuropathy that affects the myelin and nodal or paranodal areas of peripheral nerves. Immunoglobulin G GM1 antibody is well known as the cause of GBS associated with Campylobacter jejuni infection. However, the relationship between other specific infectious agents and autoantibodies is not yet well elucidated in patients with GBS. Recently we have experienced a case with GBS associated with antiGM1 and phosphatidic acid complex antibody that occurred after Shiga toxinproducing and enterotoxigenic Escherichia coli enteritis.

Causality Assessment Guidelines for Adverse Events Following Immunization with a Focus on Guillain-Barré Syndrome.

South Korea operates a National Vaccine Injury Compensation Program (VICP) for people who experience adverse events following immunization (AEFI). To run this program rationally, it is a prerequisite to confirm whether adverse events were caused by immunization. Guillain–Barré syndrome (GBS), a severe neurological disease with limb pain and muscle weakness as cardinal symptoms, is attracting attention as an AEFI. However, algorithm or guidelines for assessing the causality between vaccination and the incidence of GBS are lacking. We aimed to develop guidelines for causality assessment of GBS as an AEFI and suggest using these guidelines in alignment with the VICP. We systematically searched for other previously published algorithms or guidelines and found a WHO-AEFI guideline used worldwide; however, it only provides general instructions and is not tailored to specific adverse events. We translated and locally adapted the structure of this guideline and then added contents related to GBS. The GBS-specific guideline consists of four steps: case ascertainment of GBS, checklist (including (1) order of incidence, (2) temporal proximity, (3) evidence for other causes and (4) published evidence), an algorithm, and final classification. We listed key information on confirming GBS and whether any other causes of GBS were present. For real world application of the guideline along with the VICP, we collaborated with a panel of neurologists, epidemiologic investigators, and committee members from the VICP. To ensure transparency and a scientific approach, regular updates and collaboration with neurologists are essential. We expect that this guideline will contribute to logical causality assessment and compensation decisions for GBS and will provide the basic structure for causality assessment of other AEFIs.

Dissecting the Role of Anti-ganglioside Antibodies in Guillain-Barré Syndrome: an Animal Model Approach.

Guillain-Barré syndrome (GBS) is an autoimmune polyneuropathy disease affecting the peripheral nervous system (PNS). Most of the GBS patients experienced neurological symptoms such as paresthesia, weakness, pain, and areflexia. There are also combinations of non-neurological symptoms which include upper respiratory tract infection and diarrhea. One of the major causes of GBS is due largely to the autoantibodies against gangliosides located on the peripheral nerves. Gangliosides are sialic acid-bearing glycosphingolipids consisting of a ceramide lipid anchor with one or more sialic acids attached to a neutral sugar backbone. Molecular mimicry between the outer components of oligosaccharide of gangliosides on nerve membrane and lipo-oligosaccharide of microbes is thought to trigger the autoimmunity. Intra-peritoneal implantation of monoclonal ganglioside antibodies secreting hybridoma into animals induced peripheral neuropathy. Recent studies demonstrated that injection of synthesized anti-ganglioside antibodies raised by hybridoma cells into mice initiates immune response against peripheral nerves, and eventually failure in peripheral nerve regeneration. Accumulating evidences indicate that the conjugation of anti-ganglioside monoclonal antibodies to activating FcγRIII present on the circulating macrophages inhibits axonal regeneration. The activation of RhoA signaling pathways is also involved in neurite outgrowth inhibition. However, the link between these two molecular events remains unresolved and requires further investigation. Development of anti-ganglioside antagonists can serve as targeted therapy for the treatment of GBS and will open a new approach of drug development with maximum efficacy and specificity.

Guillain-Barré syndrome.

The term Guillain-Barré syndrome (GBS), the most frequent cause of acute paralytic neuropathy, covers a number of recognisably distinct variants. The exact cause of GBS is unknown, but 50-70% of cases appear 1-2weeks after a respiratory or gastrointestinal infection, or another immune stimulus that induces an aberrant autoimmune response targeting peripheral nerves and their spinal roots. The interplay between the microbial and host factors that dictate whether and how the immune response shifts towards autoreactivity is still unclear, and nothing is known about the genetic and environmental factors that affect an individual's susceptibility to the disease. All patients with GBS need meticulous monitoring, and can benefit from supportive care and the early start of specific treatment. This review summarises the clinical features and diagnostic criteria of GBS and proposes an algorithm for its management. An analysis of the literature showed that, about one century after it was first described, new information concerning its etiopathogenesis has allowed the development of new treatment strategies that should be started immediately after diagnosis; however, the available therapies are not sufficient in many patients, especially in the presence of the acute inflammatory demyelinating polyneuropathy. New post-infectious forms, such as those caused by Zika virus and enterovirus D68, need to be carefully analysed and, in order to improve patient outcomes, research should continue to aim at identifying new biomarkers of disease severity and better means of avoiding axonal injury.

Guillain–Barré Syndrome—A Classical Autoimmune Disease Triggered by Infection or Vaccination

Guillain-Barré syndrome (GBS) is a rare autoimmune disorder, the incidence of which is estimated to be 0.6-4/100,000 person/year worldwide. Often, GBS occurs a few days or weeks after the patient has had symptoms of a respiratory or gastrointestinal microbial infection. The disorder is sub-acute developing over the course of hours or days up to 3 to 4weeks. About a third of all cases of Guillain-Barré syndrome are preceded by Campylobacter jejuni infection. C. jejuni strains isolated from GBS patients have a lipooligosaccharide (LOS) with a GM1-like structure. Molecular mimicry between LOS and the peripheral nerves as a cause of GBS was demonstrated in animal models of human GBS. Following the "swine flu" virus vaccine program in the USA in 1976, an increase in incidence of GBS was observed and the calculated relative risk was 6.2. Later studies have found that influenza vaccines contained structures that can induce anti-GM1 (ganglioside) antibodies after inoculation into mice. More recent information has suggested that the occurrence of GBS after currently used influenza and other vaccines is rare. GBS involves genetic and environmental factors, may be triggered by infections or vaccinations, and predisposition can be predicted by analyzing some of these factors.

Antiganglioside antibodies and their pathophysiological effects on Guillain-Barre syndrome and related disorders--A review

Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy which can cause acute quadriplegia. Infection with micro-organisms, including Campylobacter jejuni (C. jejuni), Haemophilus influenzae, and Cytomegalovirus (CMV), is recognized as a main triggering event for the disease. Lipooligosaccharide (LOS) genes are responsible for the formation of human ganglioside-like LOS structures in infectious micro-organisms that can induce GBS. Molecular mimicry of LOSs on the surface of infectious agents and of ganglioside antigens on neural cells is thought to induce cross-reactive humoral and cellular immune responses. Patients with GBS develop antibodies against those gangliosides, resulting in autoimmune targeting of peripheral nerve sites, leading to neural damage. Heterogeneity of ganglioside expression in the peripheral nervous system (PNS) may underlie the differential clinical manifestation of the GBS variants. Recent studies demonstrate that some GBS sera react with ganglioside complexes consisting of two different gangliosides, such as GD1a and GD1b, or GM1 and GD1a, but not with each constituent ganglioside alone. The discovery of antiganglioside complex antibodies not only improves the detection rate of autoantibodies in GBS, but also provides a new concept in the antibody-antigen interaction through clustered carbohydrate epitopes. Although ganglioside mimicry is one of the possible etiological causes of GBS, unidentified factors may also contribute to the pathogenesis of GBS. While GBS is not considered a genetic disease, host factors, particularly human lymphocyte antigen type, appear to have a role in the pathogenesis of GBS following C. jejuni infection.

Campylobacter coli enteritis and Guillain–Barré syndrome: No evidence of molecular mimicry and serological relationship

Campylobacter coli was isolated from two Guillain–Barré syndrome (GBS) patients who had anti-GM1 and anti-GD1 IgG antibodies. Although both this bacteria and Campylobacter jejuni are common causes of diarrheal illness, previous studies have focused only on C. jejuni as the causal agent of GBS. To determine whether C. coli also is a causative agent, we examined the hypothesis that production of anti-ganglioside antibodies is induced by ganglioside-mimics on that bacterial lipo-oligosaccharide (LOS), as in C. jejuni-associated GBS. LOSs of both C. coli isolates had very weak reactivities with anti-GM1 and anti-GD1a IgG monoclonal antibodies, whereas those of some GBS-related C. jejuni isolates had strong reactivities. Anti-GM1 and anti-GD1a IgG antibodies from the two patients were not absorbed as much by the LOSs of their isolates as were those of GBS-related C. jejuni strains. These findings do not support the hypothesis of ganglioside mimicry on C. coli isolates' LOSs. We next made a serological assay of recent C. coli infection in 74 patients with GBS, 26 with Fisher syndrome (FS), 49 with other neurological diseases (OND), and 37 normal controls (NC) using the bacterial outer membrane protein as antigen. Eight (11%) GBS and two (8%) FS patients had two or three classes of IgG, IgM, and IgA anti- C. coli antibodies. Anti- C. jejuni IgG and IgA antibody titers were significantly higher than those of anti- C. coli (respectively, p = 0.03 and 0.01). This suggests that anti- C. coli antibodies cross-react with C. jejuni protein. We concluded that a C. coli infection was not the cause of GBS in our patients. Both isolation of a microorganism from, and the positive infectious serology of, GBS patients do not always indicate the causal agent.

Microbiologic approaches for studying Campylobacter species in patients with Guillain-Barré syndrome.

Campylobacter jejuni is now considered to be the most common cause of bacterial diarrheal disease in the United States. Sufficient evidence exists to support the hypothesis that C. jejuni induces Guillain-Barré syndrome (GBS); however, many questions about the biology of the organism and host factors need to be answered. In order to study the role of C. jejuni and other Campylobacter species as a cause of GBS, isolates from patients with different forms of GBS and appropriate control populations must be obtained. To continue to study this association, research teams must have laboratory support for isolating and characterizing Campylobacter strains. This review summarizes current knowledge about the laboratory aspects of Campylobacter infection that may be pertinent to studies on GBS.

Clinical and epidemiologic features of Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is defined clinically as a peripheral neuropathy causing limb weakness that progresses for up to 4 weeks before reaching a plateau. The symptoms may be caused by inflammatory demyelination, axonal degeneration, or both. GBS occurs throughout the world, with a median incidence of 1.3 cases/100,000 population (range, 0.4-4.0). Males are more commonly affected than females, and there are peaks in young adults and the elderly. There is no clear seasonal association in Western countries, although this may be because the most frequent antecedent events, respiratory and enteric infections, have opposite seasonality. The most frequently identified cause of GBS is Campylobacter jejuni infection, which has been identified in up to 41% of patients and is associated with more severe disease and prolonged disability. Summer epidemics of GBS occur among children and young adults in Northern China and are particularly likely to be associated with C. jejuni infection.