Lyme Disease and Lewy Body Dementia: Spirochetes Found at Autopsy.

Lyme disease and dementia can share cognitive symptoms
Borrelia was detected in the brain and spinal cord at autopsy
The case does not prove that Lyme disease caused the dementia

Can Lyme disease cause dementia? A woman treated for Lyme disease at age 54 later developed progressive cognitive, behavioral, and movement symptoms consistent with Lewy body dementia. After her death, researchers detected Borrelia DNA in her amygdala and spinal cord and identified an intact spirochete-like structure in spinal cord tissue.¹

The findings raise important questions about the persistence of Borrelia burgdorferi in the central nervous system after antibiotic treatment. However, this was a single case, and the researchers could not determine whether the infection contributed to the woman’s neurodegenerative disease.

Lyme disease diagnosed at age 54

The woman was diagnosed with Lyme disease at age 54 after developing a well-documented erythema migrans rash accompanied by severe headaches, joint pain, and a fever of 104°F. Her Lyme disease testing was positive by ELISA and both IgM and IgG Western blots.

She was treated with doxycycline for 10 days, and her initial symptoms resolved.

Two years later, she developed a REM sleep behavior disorder. Four years after her Lyme disease diagnosis, cognitive problems emerged and gradually worsened. These included slower processing speed, difficulty with mental tracking, and word-finding problems.

Additional symptoms included sensitivity to light, paresthesias, muscle twitching, and myoclonic jerks. Neurocognitive testing revealed impaired visuospatial and executive functioning with relative preservation of verbal skills, suggesting a neurodegenerative process.

Brain imaging and laboratory findings

A brain MRI showed mild atrophy and scattered nonspecific white matter hyperintensities without enhancement. A SPECT scan demonstrated decreased perfusion in the right posterior parietal and temporal lobes.

Blood PCR testing for Borrelia burgdorferi, Babesia microti, and Bartonella henselae was negative. Her C6 ELISA was also negative, but her Lyme IgG Western blot remained strongly positive, with 9 of 10 bands present.

At age 62, cerebrospinal fluid testing detected four Lyme IgG Western blot bands. However, paired serum and cerebrospinal fluid ELISA testing was not performed, so the researchers could not determine whether she had produced Lyme-specific antibodies within the central nervous system.

Her cerebrospinal fluid did not show an elevated white blood cell count or protein level. The authors therefore noted that she did not meet full diagnostic criteria for Lyme neuroborreliosis.

Cognition temporarily improves after antibiotic treatment

At age 60, the woman received eight weeks of intravenous ceftriaxone followed by six months of oral amoxicillin.

According to the case report, treatment produced an estimated 60% improvement in cognition and interpersonal engagement. Unfortunately, the improvement was not sustained. Later treatment with minocycline provided no clear benefit.

Her visuospatial and executive functioning continued to deteriorate, and her anxiety worsened. The authors cautioned that an anti-inflammatory effect of antibiotic treatment could not be excluded as an explanation for the temporary improvement.

Progressive symptoms suggest Lewy body dementia

Additional brain imaging demonstrated diffuse cortical hypometabolism, particularly in the posterior parietal and temporal lobes. The woman developed expressive aphasia, visual agnosia, difficulty naming objects, impaired executive functioning, calculation problems, and mild memory impairment.

She eventually developed paranoia, personality changes, severe movement abnormalities, and oral dystonia that made feeding increasingly difficult. Her early movement symptoms and REM sleep behavior disorder favored a clinical diagnosis of dementia with Lewy bodies.

She died at age 69, approximately 15 years after her initial Lyme disease infection.

Autopsy confirms Lewy body pathology

Autopsy examination identified Lewy bodies in the substantia nigra and cerebral cortex. Additional testing demonstrated numerous alpha-synuclein-positive Lewy bodies and fibers in the substantia nigra, hippocampal formation, and neocortex.

The researchers concluded that the pathology was characteristic of dementia with Lewy bodies accompanied by features of Alzheimer’s disease, a combination that is commonly observed.

Borrelia detected in the amygdala and spinal cord

The researchers examined tissue from the woman’s amygdala, pons, and spinal cord using several laboratory methods.

Nested PCR testing detected Borrelia DNA in the amygdala and spinal cord. The pons was negative. Immunofluorescence testing identified an intact structure with the expected appearance of a Borrelia spirochete in the spinal cord near a blood vessel.

Researchers also attempted to detect Borrelia RNA, which might have provided information about whether the organism was metabolically active. However, degradation of RNA in the autopsy tissue prevented a reliable assessment of viability.

One of seven control specimens from individuals without a known history of Lyme disease was also positive by PCR. Those control tissues came from a Lyme-endemic region, so the authors noted that unrecognized prior infection was possible. No obvious spirochetes were identified in the control specimen by immunofluorescence.

Did Lyme disease cause the Lewy body dementia?

The autopsy findings demonstrated that Borrelia could be detected in this patient’s central nervous system years after antibiotic treatment. They did not establish that Lyme disease caused her Lewy body dementia.

The infection and dementia may have been unrelated. Alternatively, persistent infection or the immune response associated with infection could have contributed to neurological injury. A single case cannot distinguish among these possibilities.

The patient also did not meet full diagnostic criteria for Lyme neuroborreliosis during life. Furthermore, the study could not determine whether the detected organism was viable or capable of causing ongoing disease.

In a later review, Wormser and colleagues concluded that there is no convincing evidence that Borrelia burgdorferi causes Alzheimer’s disease or Lewy body dementia.² Their assessment reinforces the distinction between detecting Borrelia in one patient’s central nervous system and demonstrating that the infection caused her neurodegenerative disease.

The findings are therefore important but should be interpreted cautiously. They support additional research into the possible relationship between persistent infection, inflammation, and neurodegenerative illness without proving a causal connection.

Frequently Asked Questions

Can Lyme disease cause dementia?

Lyme neuroborreliosis can sometimes produce cognitive symptoms that resemble dementia. However, this case does not prove that Lyme disease causes Lewy body dementia or other common neurodegenerative disorders.

Can Lyme disease mimic dementia?

Yes. Lyme disease can be associated with memory problems, slowed processing, impaired concentration, word-finding difficulty, and other cognitive symptoms that may resemble a dementia syndrome. Progressive symptoms still require an evaluation for neurodegenerative and other medical conditions.

Can dementia associated with Lyme disease be reversible?

Some cognitive problems associated with an active infection may improve with appropriate treatment. Established neurodegenerative diseases may continue to progress. The woman in this case experienced temporary improvement after antibiotics, but her cognitive decline later resumed.

What did the autopsy prove?

The autopsy confirmed Lewy body pathology and detected Borrelia DNA in the amygdala and spinal cord. An intact spirochete-like structure was also identified in the spinal cord. The findings did not prove that the organism was viable or that it caused the dementia.

Did the patient have confirmed Lyme neuroborreliosis?

No. Although Lyme IgG bands were detected in her cerebrospinal fluid, the necessary paired testing was not performed to demonstrate intrathecal antibody production. Her cerebrospinal fluid also did not show lymphocytosis or elevated protein.

Would longer initial treatment have prevented the dementia?

That cannot be determined from this case. The report does not establish whether a different initial treatment duration or earlier retreatment would have changed the patient’s neurological outcome.

Clinical Takeaway

Physicians evaluating progressive cognitive decline may need to consider potentially treatable infectious, metabolic, medication-related, and structural conditions while also evaluating patients for neurodegenerative disease.

This case demonstrates that detecting Borrelia in central nervous system tissue does not by itself establish that the organism caused the patient’s neurological illness.

The study raises an important question about persistence after treatment, but it does not prove that Lyme disease caused this woman’s Lewy body dementia.

This article discusses a published case report and is not medical advice. Individual patients with cognitive or neurological symptoms should be evaluated by qualified medical professionals.

Related Articles

Can Lyme disease cause dementia?
An 80-year-old with Lyme encephalopathy instead of dementia
Reversible causes of dementia and normal pressure hydrocephalus

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. doi:10.3389/fneur.2021.628045.
2. Wormser GP, Marques A, Pavia CS, Schwartz I, Feder HM Jr, Pachner AR. Lack of convincing evidence that Borrelia burgdorferi infection causes either Alzheimer disease or Lewy body dementia. Clin Infect Dis. 2022;75(2):342–346. doi:10.1093/cid/ciab993.

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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