Autopsy Finds Lyme Disease Spirochetes in Patient With Lewy Body Dementia

A woman diagnosed with Lyme disease at 54 later developed Lewy body dementia.
An autopsy confirmed Borrelia burgdorferi spirochetes in her brain and spinal cord.
Whether the infection caused or contributed to her dementia remains an open question — but one clinicians should consider.

Can Lyme disease cause dementia? This case does not answer that question definitively — but it raises it in a way that cannot be ignored.

Researchers describing this case found Borrelia burgdorferi spirochetes in the brain and central nervous system of a woman who had been diagnosed with Lyme disease years earlier and later developed Lewy body dementia. The authors could not determine whether the infection caused her dementia — but they could not rule it out either.

For a broader clinical overview of the Lyme disease and dementia overlap, see Lyme disease and dementia: when cognitive decline has another cause.

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Lyme Disease Diagnosed at Age 54

At age 54, the woman was diagnosed with Lyme disease based on a well-documented erythema migrans rash, along with severe headaches, joint pain, and a fever of 104 degrees. Lyme testing was positive by ELISA and both IgM and IgG Western blots.

Her initial symptoms resolved with 10 days of doxycycline treatment.

Over time, however, she developed a sleep behavior disorder and cognitive problems including slower processing speed, difficulty with mental tracking, and word-finding difficulty. Additional symptoms included light sensitivity, paresthesias, fasciculations, and myoclonic jerks.

Neurocognitive testing revealed deficits in visuospatial skills and executive functions with preservation of verbal skills — a pattern suggesting a neurodegenerative process.

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Symptoms Progress — Brain Imaging Abnormal

Brain MRI showed mild atrophy and non-specific scattered white matter changes without enhancement. Brain SPECT scans showed decreased perfusion in the right posterior parietal and temporal lobes.

At age 60 — six years after her initial Lyme diagnosis — she was treated with an eight-week course of intravenous ceftriaxone followed by six months of oral amoxicillin.

Treatment resulted in approximately 60% improvement in cognition and interpersonal engagement. However, the initial improvement was not sustained. Subsequent antibiotic therapy with minocycline provided no clear benefit, and her visuospatial skills and executive functions continued to deteriorate while anxiety worsened.

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Lewy Body Dementia Diagnosed at Age 62

At age 62, the woman was diagnosed clinically with Lewy body dementia. Early and severe movement disorders, REM behavioral disorder, paranoia, and personality changes all supported this diagnosis.

She died at age 69 — 15 years after her initial Borrelia burgdorferi infection.

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Autopsy Reveals Spirochetes in the Brain

The authors performed an autopsy to evaluate whether antibiotic treatment had failed to eradicate the infection or whether there had been a reinfection.

The autopsy confirmed that Borrelia burgdorferi spirochetes were present in the brain and spinal cord tissue — despite years of antibiotic treatment.

The authors acknowledged they could not directly attribute Lyme disease as causing the Lewy body dementia. The finding may represent an unrelated incidental discovery — or it may reflect a relationship between persistent CNS infection with Borrelia burgdorferi and the development of a neurodegenerative dementing disorder. The authors concluded the question remains open.

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What This Case Means Clinically

Researchers have long investigated reversible and potentially modifiable causes of dementia. This case illustrates that Lyme disease deserves consideration as a possible contributor — even when initial antibiotic treatment produces improvement.

It is not clear whether longer initial treatment at the time of the erythema migrans rash, or earlier retreatment, would have changed the outcome for this patient. These are the kinds of questions that only long-term follow-up and further research can begin to answer.

What the case does confirm is that Borrelia burgdorferi can persist in the central nervous system despite treatment — and that this persistence may have clinical consequences that extend beyond the initial infection.

For documented cases where Lyme-related cognitive decline improved with treatment, see Lyme disease mistaken for dementia: when confusion is reversible and reversible causes of dementia.

For a broader overview of how Lyme encephalopathy is documented in the medical literature, see Lyme encephalopathy symptoms and complications.

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Frequently Asked Questions

Can Lyme disease cause Lewy body dementia?

This case documents Borrelia burgdorferi spirochetes in the brain and spinal cord of a patient who developed Lewy body dementia after a documented Lyme disease infection. The authors could not determine whether the infection caused the dementia — but they could not rule out a relationship either.

Can Borrelia burgdorferi persist in the brain after antibiotic treatment?

Yes. This autopsy case confirms that Borrelia burgdorferi can persist in central nervous system tissue despite multiple courses of antibiotic therapy — including intravenous ceftriaxone and oral amoxicillin.

Did antibiotic treatment help this patient?

Yes — initially. An eight-week course of intravenous ceftriaxone produced approximately 60% improvement in cognition and interpersonal engagement. However, the improvement was not sustained and subsequent antibiotic therapy did not provide additional benefit.

Should Lyme disease be considered in patients with Lewy body dementia?

When a patient with Lewy body dementia or another neurodegenerative diagnosis has a history of Lyme disease — particularly with ongoing or worsening cognitive symptoms — an infectious contributor deserves consideration. This case supports that clinical instinct.

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Clinical Takeaway

This case does not prove that Lyme disease causes Lewy body dementia — but it demonstrates that Borrelia burgdorferi can persist in the central nervous system for years after treatment and may contribute to a progressive neurodegenerative course. The 60% cognitive improvement following IV ceftriaxone suggests the infection was clinically active years after the initial diagnosis.

When a patient with neurodegenerative disease has a history of Lyme disease — particularly when cognitive symptoms fluctuate or partially respond to antibiotic treatment — persistent infection deserves consideration alongside the primary diagnosis.

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Related Articles

• Lyme Disease and Dementia: When Cognitive Decline Has Another Cause
• Lyme Encephalopathy Symptoms and Complications
• Lyme Disease Mistaken for Dementia: When Confusion Is Reversible
• Reversible Causes of Dementia: Three Clinical Cases
• Lyme Disease or Dementia? A Case of Reversible Cognitive Decline
• Neurologic Lyme Disease

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References

1. Gadila SKG, Rosoklija G, Dwork AJ, Fallon BA, Embers ME. Detecting Borrelia spirochetes: a case study with validation among autopsy specimens. Front Neurol. 2021;12:628045.
2. Karrasch M, Fingerle V, Boden K, et al. Neuroborreliosis and acute encephalopathy: The use of CXCL13 as a biomarker in CNS manifestations of Lyme borreliosis. Ticks Tick Borne Dis. 2018;9(2):415-417.

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Dr. Daniel Cameron, MD, MPH
Lyme disease clinician with over 30 years of experience and past president of ILADS.

Symptoms • Testing • Coinfections • Recovery • Pediatric • Prevention