P-591. Infection with Campylobacter and Risk of Guillain-Barré Syndrome: a Meta-Analysis

TL;DR

This study finds a strong link between Campylobacter infection and Guillain-Barré Syndrome, showing infected individuals have over 68 times higher risk.

Contribution

A meta-analysis quantifying the association between Campylobacter infection and GBS using updated data from 1990-2024.

Findings

Campylobacter-infected patients have a 68.21 times higher odds of developing GBS compared to controls.

No heterogeneity or publication bias was observed across the 29 included case-control studies.

The pooled analysis confirms a strong and statistically significant association between Campylobacter and GBS.

Abstract

Campylobacter is one of the common bacterial agents for gastroenteritis worldwide. Guillain-Barré Syndrome (GBS), an autoimmune disorder of the peripheral nervous system, can be triggered by Campylobacter infection. Though 20-31% of GBS cases are estimated to be attributed to Campylobacter, the updated quantification of Campylobacter infections and their association with GBS is crucial for informing risk prevention strategies.The flow diagram illustrates the study selection process for inclusion in the analysis conducted in the COVIDENCE software.Figure 2.Forest plot illustrating the odds ratio of Campylobacter positivity in Guillain–Barré syndrome (GBS) cases compared to controls.

The flow diagram illustrates the study selection process for inclusion in the analysis conducted in the COVIDENCE software.

Forest plot illustrating the odds ratio of Campylobacter positivity in Guillain–Barré syndrome (GBS) cases compared to controls.

A peer-reviewed paper published from 1990-2024 was obtained from various databases. MeSH terms created using inclusion: patients of any age, gender, and ethnicity with confirmed Campylobacter infection through stool culture, serology, or PCR, and developed GBS from Campylobacter infection; and exclusion: recent Influenza vaccine within 2 weeks, studies with insufficient data to calculate risk, and any other disease associated GBS (e.g. COVID-19) criteria. Manuscripts were systematically reviewed in the COVIDENCE software. Data (Figure 1) were extracted on characteristics, number of events, exposure status, participants' age, country, and study designs. Pooled odds ratios (ORs) were calculated from a random-effects model using R packages and R Studio. Heterogeneity, publication bias, and analysis sensitivity were evaluated.

Case-control studies (n=29) comprising 2621 GBS cases, 2688 controls, and 1046 GBS with Campylobacter infections were included. The pooled mean age of the participants was 34.33 years [95% CI: 22.65-46.02]. The pooled OR was 68.21[43.90-105.99] (Figure 2). No heterogeneity was observed (I2 = 0.0% [0.0%; 41.9%]; tau2 = 0 [0.00; 0.31]). The Egger’s test and funnel plot symmetry indicated the absence of publication bias (p = 0.31). A leave-one-out sensitivity analysis showed no single study substantially influenced the pooled effect size.

Patients with prior Campylobacter infection have 68.21 times higher risk of GBS compared to uninfected individuals. This demonstrates a strong and statistically significant association between Campylobacter infection and the subsequent development of GBS. Further analysis for incidence, relative risk, and subgroup analysis (to be shared in the final presentation with additional review) will preserve the strength of association we found.

Sharjeel Ahmad, MD, MPH, FACP, FIDSA, Karius, Inc: Advisor/Consultant

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