# Adult Botulism of Unknown Source with Post-Toxin Anti-GQ1b Antibodies: Implications for Molecular Mimicry—A Case Report

## TL;DR

A rare case of botulism in an adult showed unexpected anti-GQ1b antibodies, suggesting possible immune system overlap with autoimmune neuropathies.

## Contribution

This case report highlights a novel immunological overlap between botulism and GQ1b-associated neuropathies, suggesting potential molecular mimicry.

## Key findings

- Anti-GQ1b antibodies were detected in a botulism patient, typically linked to Miller–Fisher syndrome.
- Botulism was confirmed through intestinal colonization of Clostridium botulinum despite no foodborne source.
- The case suggests possible immune response triggered by toxin-ganglioside interactions.

## Abstract

Background: Botulism is a rare but potentially fatal neuroparalytic illness caused by Clostridium botulinum neurotoxins (BoNTs). While adult cases usually result from foodborne exposure or wound infection, intestinal colonization is exceedingly uncommon. Diagnosis can be delayed by overlap with other neuromuscular syndromes, and confirmation requires specialized assays. Anti-GQ1b antibodies, classically associated with Miller–Fisher syndrome (MFS), have rarely been reported in confirmed botulism, raising questions about shared pathophysiology. Case Presentation: We describe an adult patient with acute dyspnea, xerostomia, and cranial neuropathies. No foodborne source was identified, but intestinal colonization of BoNT/B toxigenic Clostridium botulinum was confirmed by stool enrichment and mouse lethality bioassay. The patient improved promptly following heptavalent antitoxin. Unexpectedly, anti-GQ1b antibodies were detected during recovery, a finding typically linked to MFS rather than botulism. Discussion: This case illustrates the diagnostic challenges of sporadic cases of botulism, especially when respiratory compromise and autonomic dysfunction dominate the initial presentation. The autoantibodies finding raises the possibility of molecular mimicry, whereby toxin–ganglioside interactions expose neuronal epitopes and trigger an immune response. While causality cannot be proven, the overlap between botulism and GQ1b-positive neuropathies merits further investigation. Conclusions: Clinicians should maintain high suspicion for botulism in adults with acute dyspnea, especially when associated with cranial neuropathies, even in the absence of foodborne exposure. Anti-ganglioside antibodies in this context should be interpreted with caution, as they do not exclude botulism but may highlight immunological overlap with autoimmune neuropathies.