Can antibiotics cause Guillain-Barré syndrome?: Separating fact from speculation

October 12, 2025 •

3 min read

A large population-based study in Denmark showed a strong temporal association between community antibiotic prescriptions and a subsequent increased risk of Guillain-Barré syndrome (GBS). However, this is largely attributed to the underlying infection being treated, with the syndrome potentially arising from an autoimmune response, not the medication itself. Certain antibiotics, such as fluoroquinolones, have been implicated in rare instances, but direct causality is complex.

Quick Summary

The link between antibiotics and Guillain-Barré syndrome is largely temporal, with the underlying infection often acting as the true trigger. A rare association exists for specific drugs, primarily fluoroquinolones, based on case reports and pharmacovigilance data, but the infection is the principal driver.

Key Points

Infection is the Main Trigger: GBS most commonly follows an infection, such as those of the respiratory or gastrointestinal tracts, which precedes antibiotic treatment.
Autoimmune Response: The mechanism for GBS involves the immune system mistakingly attacking peripheral nerves after fighting an infection, a process known as molecular mimicry.
Temporal Association: A large Danish study found a strong time-based correlation between both serious infections and antibiotic prescriptions and the onset of GBS, with the infection itself likely being the driving factor.
Specific Antibiotic Class Risk: Fluoroquinolone antibiotics (e.g., ciprofloxacin, levofloxacin) have been linked to GBS in rare cases reported to the FDA Adverse Event Reporting System (FAERS).
Risk-Benefit Assessment: The risk of GBS from an untreated infection is much higher than the extremely low, potential risk associated with specific antibiotics.
Report Any Concerns: Patients should complete their prescribed course of antibiotics but report any new or worsening neurological symptoms to their healthcare provider immediately.

Guillain-Barré syndrome (GBS) is a rare neurological disorder where the body's immune system attacks its peripheral nerves. GBS commonly follows an infection, often respiratory or gastrointestinal. Given antibiotics treat bacterial infections, a link to GBS might seem plausible. However, understanding this relationship requires considering the sequence of events.

The Temporal Association: Infection as the Primary Trigger

Evidence strongly suggests the infectious illness preceding antibiotic use is the primary driver of GBS. A Danish study found a temporal association between hospital-diagnosed infections and antibiotic prescriptions and a later GBS diagnosis. The risk peaked in the first month and remained elevated for up to five months. The study indicated that infection severity is a key risk factor.

The Role of Molecular Mimicry

The main theory for infection-triggered GBS is molecular mimicry. During infection, the body produces antibodies. Sometimes, these antibodies mistakenly attack components of the body's nerve cells. This damages the peripheral nerves, leading to GBS symptoms like muscle weakness and tingling. Campylobacter jejuni, a common cause of gastroenteritis, is frequently linked to GBS because its surface proteins resemble nerve cell molecules, causing this autoimmune cross-reaction.

Documented Link with Specific Antibiotics

While infection is the main cause, case reports and data suggest a rare, direct link between certain antibiotics and GBS. Fluoroquinolones are the most noted example.

Fluoroquinolones: A Notable Exception

Peripheral Neuropathy: Fluoroquinolones like ciprofloxacin and levofloxacin are known to cause peripheral neuropathy.
GBS Reports: Reports to the FDA (FAERS) have identified GBS as a potential, rare, and severe form of peripheral nerve damage associated with fluoroquinolones. A 2014 study found a significant disproportionality of GBS reports for fluoroquinolones, specifically ciprofloxacin.
Direct Mechanism: The exact cause of fluoroquinolone-induced GBS is unclear, but theories involve immune system changes and effects on neurotransmitters.

Comparison of GBS Triggers: Infection vs. Antibiotics


Feature	Infection-Triggered GBS	Drug-Associated GBS (e.g., Fluoroquinolones)
Primary Trigger	A bacterial or viral illness (e.g., Campylobacter jejuni, influenza)	A specific medication, with antibiotics being a very rare trigger
Immune Mechanism	Molecular mimicry, where immune antibodies target both pathogen and nerve tissue	Less understood; involves adverse drug reactions and possible immune dysregulation
Incidence	Accounts for the vast majority of GBS cases; a common risk factor	Extremely rare; represents a small fraction of GBS cases
Strength of Evidence	Strong, with extensive epidemiological and clinical data demonstrating a clear temporal and mechanistic link	Weak by comparison, primarily based on case reports and pharmacovigilance data
Relative Risk	The risk of GBS from an infection, such as the flu, is far greater than from receiving the vaccine for it	The risk is very low, but the potential for severe adverse effects warrants caution for certain individuals

The Critical Context: Weighing Risk and Benefit

It's important to differentiate risks. Someone taking antibiotics has an underlying infection, a much more probable GBS trigger. The antibiotic treats this infection, which itself carries a higher risk of complications, including GBS. The extremely rare risk of GBS from specific antibiotics must be weighed against the significant danger of an untreated infection. For example, septicemia has a high odds ratio for GBS.

What This Means for Patients

If prescribed an antibiotic and concerned about GBS, complete the full course. The risk of complications from an untreated infection is far greater. Understanding rare associations, especially with fluoroquinolones, aids informed discussions with your doctor, particularly with existing nerve issues. Report any new or unusual symptoms like nerve pain, tingling, or weakness to your doctor promptly.

Conclusion: Separating the Infection from the Cure

While there's a temporal link between antibiotic use and GBS, evidence overwhelmingly points to the underlying infection as the primary trigger. This distinction is crucial when considering medication side effects. Specific antibiotics, notably fluoroquinolones, show a rare but more direct link in case reports and monitoring. These instances seem to be due to complex adverse drug reactions rather than the infection-related mechanism. For most patients, the benefit of treating a bacterial infection outweighs the minimal associated risk. Judicious antibiotic use and informing your doctor of any pre-existing neurological concerns are key.

For more detailed information, consult the study in Neurology.

Frequently Asked Questions

No, antibiotics are not a common cause of Guillain-Barré syndrome (GBS). The vast majority of GBS cases are triggered by an underlying infection, such as Campylobacter jejuni or influenza, not the antibiotic used to treat it.

An infection-triggered GBS occurs due to the immune system's response to the pathogen, causing an autoimmune attack on the nerves. In contrast, antibiotic-associated GBS is extremely rare and likely involves a different, drug-specific immune-modulating mechanism, independent of the original infection.

Yes, some antibiotics have been reported in rare cases. The most notable are fluoroquinolones like ciprofloxacin and ofloxacin, which have been associated with both peripheral neuropathy and, in a small number of instances, GBS.

Drug-induced GBS is considered a very infrequent adverse event. Most reports of GBS occurring around the time of antibiotic use are ultimately attributed to the infection that prompted the prescription.

The most common bacterial trigger for GBS is Campylobacter jejuni, which causes gastroenteritis. Other infections include influenza, cytomegalovirus, Epstein-Barr virus, and Zika virus.

No, you should not avoid taking prescribed antibiotics out of fear of GBS. The risk from an untreated bacterial infection is far more significant than the very small, potential risk associated with the medication itself.

If you experience new or worsening neurological symptoms such as tingling, numbness, spreading muscle weakness, or difficulty walking after starting antibiotics, you should contact your doctor immediately. This is especially important for individuals taking fluoroquinolone antibiotics.