Recent Campylobacter Jejuni Infection Research Articles

Association of mannose-binding lectin\xa02 gene\xa0polymorphisms with Guillain-Barr\xe9 syndrome

Complement activation plays a critical role in the pathogenesis of Guillain-Barré syndrome (GBS), a debilitating immune-mediated neuropathy. Mannose-binding lectin (MBL) is a complement activation factor of lectin pathway which as genetic host factor may influence the susceptibility or severity of GBS. We investigated the frequency of MBL2 promoter (− 550H/L and − 221X/Y) and functional region (exon 1 A/O) polymorphisms and their association with disease susceptibility, clinical features and serum MBL among GBS patients (n = 300) and healthy controls (n = 300) in Bangladesh. The median patient age was 30 years (IQR: 18–42; males, 68%). MBL2 polymorphisms were not significantly associated with GBS susceptibility compared to healthy controls. HL heterozygosity in GBS patients was significantly associated with mild functional disability at enrolment (P = 0.0145, OR, 95% CI 2.1, 1.17–3.82). The HY, YA, HA and HYA heterozygous haplotypes were more common among mildly affected (P = 0.0067, P = 0.0086, P = 0.0075, P = 0.0032, respectively) than severely affected patients with GBS. Reduced serum MBL was significantly associated with the LL, OO and no HYA variants and GBS disease severity. No significant association was observed between MBL2 polymorphisms and electrophysiological variants, recent Campylobacter jejuni infection or anti-ganglioside (GM1) antibody responses in GBS. In conclusion, MBL2 gene polymorphisms are related to reduced serum MBL and associated with the severity of GBS.

Guillain-Barré syndrome after SARS-CoV-2 infection in an international prospective cohort study.

In the wake of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, an increasing number of patients with neurological disorders, including Guillain-Barré syndrome (GBS), have been reported following this infection. It remains unclear, however, if these cases are coincidental or not, as most publications were case reports or small regional retrospective cohort studies. The International GBS Outcome Study is an ongoing prospective observational cohort study enrolling patients with GBS within 2 weeks from onset of weakness. Data from patients included in this study, between 30 January 2020 and 30 May 2020, were used to investigate clinical and laboratory signs of a preceding or concurrent SARS-CoV-2 infection and to describe the associated clinical phenotype and disease course. Patients were classified according to the SARS-CoV-2 case definitions of the European Centre for Disease Prevention and Control and laboratory recommendations of the World Health Organization. Forty-nine patients with GBS were included, of whom eight (16%) had a confirmed and three (6%) a probable SARS-CoV-2 infection. Nine of these 11 patients had no serological evidence of other recent preceding infections associated with GBS, whereas two had serological evidence of a recent Campylobacter jejuni infection. Patients with a confirmed or probable SARS-CoV-2 infection frequently had a sensorimotor variant 8/11 (73%) and facial palsy 7/11 (64%). The eight patients who underwent electrophysiological examination all had a demyelinating subtype, which was more prevalent than the other patients included in the same time window [14/30 (47%), P = 0.012] as well as historical region and age-matched control subjects included in the International GBS Outcome Study before the pandemic [23/44 (52%), P = 0.016]. The median time from the onset of infection to neurological symptoms was 16 days (interquartile range 12–22). Patients with SARS-CoV-2 infection shared uniform neurological features, similar to those previously described in other post-viral GBS patients. The frequency (22%) of a preceding SARS-CoV-2 infection in our study population was higher than estimates of the contemporaneous background prevalence of SARS-CoV-2, which may be a result of recruitment bias during the pandemic, but could also indicate that GBS may rarely follow a recent SARS-CoV-2 infection. Consistent with previous studies, we found no increase in patient recruitment during the pandemic for our ongoing International GBS Outcome Study compared to previous years, making a strong relationship of GBS with SARS-CoV-2 unlikely. A case-control study is required to determine if there is a causative link or not.

Fc-gamma IIIa-V158F receptor polymorphism contributes to the severity of Guillain-Barré syndrome.

ObjectiveGuillain‐Barré syndrome (GBS) is a rare, life‐threatening disorder of the peripheral nervous system. Immunoglobulin G Fc‐gamma receptors (FcγRs) mediate and regulate diverse effector functions and are involved in the pathogenesis of GBS. We investigated whether the FcγR polymorphisms FcγRIIa H/R131 (rs1801274), FcγRIIIa V/F158 (rs396991), and FcγRIIIb NA1/NA2, and their haplotype patterns affect the affinity of IgG‐FcγR interactivity and influence GBS susceptibility and severity.MethodsWe determined FcγR polymorphisms in 303 patients with GBS and 302 ethnically matched healthy individuals from Bangladesh by allele‐specific polymerase chain reaction. Pairwise linkage disequilibrium and haplotype patterns were analyzed based on D ´statistics and the genotype package of R statistics, respectively. Logistic regression analysis and Fisher’s exact test with corrected P (Pc) values were employed for statistical comparisons.ResultsFcγRIIIa‐V158F was associated with the severe form of GBS compared to the mild form (P = 0.005, OR = 2.24, 95% CI = 1.28–3.91; Pc = 0.015); however, FcγR genotypes and haplotype patterns did not show any association with GBS susceptibility compared to healthy controls. FcγRIIIa‐V/V158 and FcγRIIIb‐NA2/2 were associated with recent Campylobacter jejuni infection (P ≤ 0.001, OR = 0.36, 95% CI = 0.23–0.56; Pc ≤ 0.003 and P = 0.004, OR = 1.70, 95% CI = 1.18–2.44; Pc ≤ 0.012, respectively). Haplotype 1 (FcγRIIa‐H131R‐ FcγRIIIa‐V158F‐ FcγRIIIb‐NA1/2) and the FcγRIIIb‐NA2/2 genotype were more prevalent among anti‐GM1 antibody‐positive patients (P = 0.031, OR = 9.61, 95% CI = 1.24–74.77, Pc = 0.279; P = 0.027, OR = 1.62, 95% CI = 1.06–2.5, Pc = 0.081, respectively).InterpretationFcγR polymorphisms and haplotypes are not associated with susceptibility to GBS, though the FcγRIIIa‐V158F genotype is associated with the severity of GBS.

Paraparetic Guillain‐Barré syndrome: Extending the axonal spectrum

AbstractThere are few reports of the paraparetic variant of Guillain‐Barré syndrome, and its pathophysiology is not well understood. We report a patient presenting with acute paraparesis following diarrhea. Serial nerve conduction studies suggested primary axonal injury, and not demyelination, predominantly in the lower limbs compared with the upper limbs. There was serological evidence of recent Campylobacter jejuni infection and strongly positive immunoglobulin G anti‐GD1a antibodies. Paraparetic Guillain‐Barré syndrome is likely to represent a regional form of Guillain‐Barré syndrome, with a nosological position within the axonal subtype.

Association of Campylobacter jejuni Infection with Childhood Guillain-Barré Syndrome: A Case-Control Study

A prospective case-control study was conducted to determine the association between Campylobacter jejuni infection and childhood Guillain-Barré syndrome in the Indian population. We found evidence of recent Campylobacter jejuni infection in 27.7% of patients with Guillain-Barré syndrome, as compared with 2.3% in neurological controls (P = .003) and 2.3% in nonneurological controls (P = .003). Of the 15 patients with Campylobacter jejuni infection, 8 (53.3%) reported having had diarrhea within 12 weeks before the onset of the neurologic illness. Our results suggest association between recent Campylobacter jejuni infection and bulbar weakness (P = .043). No statistical difference was observed between the Campylobacter jejuni positive and negative groups with respect to age, other clinical features, albuminocytological dissociation, and residual paralysis at follow-up. It is concluded that subclinical Campylobacter jejuni infection is an important antecedent illness in childhood Guillain-Barré syndrome in the Indian population.

Acute sensory ataxic neuropathy with antibodies to GD1b and GQ1b gangliosides and prompt recovery

Three patients developed acute pure sensory ataxic neuropathy. Two of the three patients had a recent Campylobacter jejuni infection. Patient 1 had monospecific IgG anti-GD1b. Patients 2 and 3 had cross-reactive IgG anti-GQ1b and anti-GD1b and patient 2 also had IgG anti-GT1a. Motor nerve conduction studies were completely normal. Sensory conductions showed reduced amplitude or absent sensory nerve action potentials with normal or slightly slowed conduction velocities. In patient 2, serial electrophysiological studies showed reappearance and improvement of sensory nerve potential amplitudes in 4 weeks. All patients recovered completely in 2 months and sensory potential amplitudes normalized in 3-5 months. Our findings: (1) confirm the existence of a pure acute sensory ataxic neuropathy with cross-reactive IgG anti-GQ1b and anti-GD1b as a variant of Guillain-Barré syndrome; (2) expand the clinical presentation of Guillain-Barré syndrome after C. jejuni infection and suggest that molecular mimicry is at the basis of acute sensory ataxic neuropathy; and (3) indicate that, in acute sensory ataxic neuropathy with prompt recovery, the site of the lesion is not in the primary sensory neurons and the pathophysiological mechanism may be functional in nature.

Does Campylobacter jejuni infection elicit “demyelinating” Guillain–Barré syndrome?

We read with interest the article by Kuwabara et al.1 Their series includes 159 consecutive patients with Guillain–Barre syndrome (GBS). There was evidence of recent Campylobacter jejuni infection in 22 patients, 16 of them being electrophysiologically classified as acute motor axonal neuropathy (AMAN), five as acute inflammatory demyelinating polyneuropathy (AIDP), and the remaining one as unclassified. Since these AIDP patients showed transient slowing of nerve conduction mimicking demyelination, the authors concluded that C. jejuni infection does not appear to elicit AIDP. We reported a patient aged 67 years with fulminant GBS who died 18 days after onset.2 One week before admission, he had an upper respiratory …

Campylobacter jejuni Infection and Guillain-Barré Syndrome: A Case-Control Study

We performed a case-control study to investigate the association between Campylobacter jejuni (CJ) infection and Guillain-Barré syndrome (GBS) or Miller-Fisher syndrome. We compared 60 cases with 109 hospital controls matched for age, gender, hospital and geographical location.To diagnose the CJ infection, we considered the association between serologic positivity for CJ and a previous diarrheal illness within 3 months of inclusion in the study. Fifteen percent of cases versus 5% of hospital controls had CJ infection (p < 0.003, OR = 3.96, 95% CI: 1.08–17.85). However, CJ infection was related to GBS only if it occurred during the previous month (p < 0.001, OR = 7.29, 95% CI: 1.43–71.28). No statistical differences were found between the cases who were positive for CJ infection and those who were negative for CJ infection when studied by stepwise multivariate logistic regression for age, gender, clinical and electrophysiological features and outcome. Recent CJ infection may be a risk factor for GBS.

Campylobacter jejuni isolates from Japanese patients with Guillain-Barré syndrome.

Serologic evidence of recent Campylobacter jejuni infection was found in 92 (45%) of 205 Japanese patients with Guillain-Barré syndrome (GBS), and 49% of those 92 patients also had antibodies to GM1. Sixteen independent clinical isolates from GBS patients were serotyped: 12 belonged to Penner's heat-stable (HS) O serotype HS-19, 3 to HS-2, and 1 to HS-4. Of the patients whose C. jejuni isolates belonged to HS-19, 80% had elevated anti-GM1 antibodies. Although the correlation was significant between C. jejuni and GM1 antibody, anti-GM1 also was detected in 25% of patients without C. jejuni infection. Polymerase chain reaction-based restriction fragment length polymorphism analysis of an flaA gene showed that all HS-19 isolates, regardless of a GBS association, had an identical and distinguishable pattern, Cj-1, suggesting that HS-19:Cj-1 isolates are distinctive among C. jejuni isolates. Lectin typing showed that all GBS-associated HS-19 isolates contained terminal beta-N-acetylglucosamine residues on their cell surface, but HS-19 isolates from patients with enteritis did not.

A longitudinal study of circulating lymphocyte subsets in the peripheral blood during the acute stage of Guillain-Barré syndrome

Activated T cells are implicated in the pathogenesis of Guillain-Barré syndrome (GBS). Blood samples from 16 patients with GBS were studied with flow cytometry during the acute stage of their disease to define circulating lymphocyte populations. During the progressive phase of GBS the T-suppressor/inducer (CD4/CD45RA) subset was decreased (10.3±4.4%, P<0.05) and the T-helper/inducer (CD4/CD29) subset was increased (34.9±9.2%, P<0.05) compared to sex and age matched patients with other neurological diseases (OND, 15.5±5.7% and 27.8±8.6%, respectively) and healthy controls (16.5±6% and 28.1±8.5%, resp.). Within the CD8 population, the activated T-cytotoxic/suppressor (CD8/CD38) subset was increased during the progressive (13±10.1%, P<0.05) and plateau phase (16.4±16.9%, p<0.01) of GBS compared to OND patients (6.2±2.3%) and healthy controls (5.8±2.5%). The proportion of activated T cells (CD3/CD25) was increased during the progressive (9.3±3.8%, P<0.05) and plateau phase (11.5±5.5%, P<0.01) compared to OND patients (6.6±2.7%) and healthy controls (5.5±2.5%). The changes of T cell subsets normalized during the early recovery phase of GBS. 2 patients with serological evidence of antecedent cytomegalovirus (CMV) infection had abnormal high proportions (mean±2 (SD) of healthy controls) of CD8 lymphocytes and correspondingly abnormal low proportions of CD4 lymphocytes during all phases of GBS. In contrast, the CD8 proportions were abnormal low in 3 patients with serological evidence of recent Campylobacter jejuni infection. There was no correlation between the proportions of lymphocyte subsets and the disability score during the maximum of the disease and after half a year. In conclusion, we found further evidence of T cell activation during the acute stage of GBS by the demonstration of an increased proportion of activated CD8+ T cells, which may be directly cytotoxic to Schwann cells. The abnormalities of the CD8 subset in some GBS patients seem to depend on the nature of the preceding infection.

Antibodies to gangliosides in Guillain-Barré syndrome: specificity and relationship to clinical features

Antibodies to ganglioside GM1 have been associated with Guillain-Barré syndrome. To clarify their role we have studied their frequency, fine specificity and relationship to clinical features in a series of patients with this disease. Antibodies to ganglioside GM1 were identified, by both enzyme-linked immunosorbent assay and binding to thin-layer chromatograms of human brain, in 12 (28.6%) of 42 patients with Guillain-Barré syndrome and in only 1 (2.4%) of 41 normal control subjects (p = 0.002). Eight sera contained IgM antibodies and six sera contained IgG antibodies, including 2 sera which contained both. The fine specificity of the sera varied. Only four of the 12 sera also showed reactivity with ganglioside GD1b and gangliotetraosyl-ceramide (asialo-GM1), consistent with reactivity with the terminal Gal beta 1-3GalNAc disaccharide. Two sera had low titre anti-asialo-GM1 antibodies of a different class to the anti-ganglioside GM1 antibodies. The antibodies in these sera therefore react with a variety of epitopes. There was a strong relationship between the presence of anti-ganglioside GM1 antibodies in the acute stage and prolonged disability, especially if IgG antibodies were present. Seven of 12 patients with anti-ganglioside GM1 antibodies had serological evidence of recent Campylobacter jejuni infection, but antigens from a strain of this bacterium not associated with Guillain-Barré syndrome did not absorb the anti-ganglioside GM1 antibodies.