Parkinson’s could also be the result of an infection
Parkinson’s disease could be caused by an infection with Nocardia (a germ similar to tuberculosis). This article is extensive and has many references—equivalent to a review!
- Used Book in Good Condition
For colleagues, the book is read in 2 hours
Parkinson’s: Another Look (published in 2002 by New Century Press, based on an article of the same name in Medical Hypothesis
Broxmeyer postulates an infectious cause for Parkinson’s disease – specifically bacteria such as Nocardia asteroides or closely related mycobacteria such as Mycobacterium tuberculosis (TB) .
Broxmeyer argues that Parkinson’s disease may not be primarily caused by genetic or environmental factors, but rather by a chronic – undetected – infection that leads to neurodegenerative processes.
Why am I writing this article now
We rarely see cases of patients with a particularly rapid progression of Parkinson’s disease who, after initial improvement with neuromodulation, suffer a relapse and no longer respond adequately, in contrast to 95% of “normal Parkinson’s cases”.
In my opinion, an infectious or autoimmune neuroinflammatory component is likely here, and in the future, we will treat such patients with appropriate antibiotics (off-label/ex-juvantibus) according to Broxmeyer. The same applies to Lewis body dementia.
Case study from Vienna with convincing improvement
At the SOZO neuromodulation training in Vienna in June 2025, an excellent colleague with additional training, for example with Rolf Jansen-Rosseck (Berlin), brought her 80-year-old father with Parkinson’s disease, who had been almost symptom-free since 3 months of Broxmeyer rifampicin therapy – the concept couldn’t be demonstrated better!
Petros made an Instagram of it: https://www.instagram.com/p/DMCZ5Y7tI6u/
Table of contents and summary of Broxmeyer’s book
The book is compact (approx. 100 pages) and is aimed at physicians, researchers and those affected.
It begins with a critique of the conventional Parkinson’s etiology (e.g., dopamine deficiency due to loss of neurons in the substantia nigra) and proposes an infectious genesis instead .
Broxmeyer relies on literature reviews and case reports without conducting his own clinical studies – it is purely hypothetical but well referenced.
Structure of the book – Overview
- Introduction: Overview of current Parkinson’s research, which implicates Nocardia (a tuberculosis-like bacterium) as a possible causative agent. Broxmeyer highlights the difficulty of distinguishing Nocardia from mycobacteria (e.g., due to cross-reactions in blood tests and varying classifications even among experts, as described in Atlas’ microbiology textbook)
. - Main body: Presentation of evidence at five independent levels (see below). Discussion of historical epidemics, epidemiological patterns, pharmacological evidence, microbiological findings, and biochemical mechanisms
. - Conclusion: A call for a “different perspective” on Parkinson’s, with suggestions for antimicrobial therapies (e.g., antibiotics against Actinomycetales). Broxmeyer emphasizes that infections such as TB or Nocardia may have a chronic subclinical course and lead to Lewy bodies or neuroinflammation . He links this with modern findings, such as genetic links to TB-related diseases (such as leprosy or Crohn’s disease )
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Summary: Broxmeyer concludes that the “preponderance of convincing evidence” points to bacterial infection as the trigger for Parkinson’s disease.
Broxmeyer criticizes medicine’s ignorance of infectious causes and advocates antibiotic interventions , supplemented by historical parallels to TB.
The book is evidence-based but “officially” controversial (since Parkinson’s is classically considered idiopathic), and has been taken up in later works (e.g. Berstad & Berstad, 2017 ) that propose “dormant spores” as a mechanism
similar results when I was able to identify rheumatism as chronic toxoplasmosis
This reminds me of my toxoplasmosis article with a video interview of a “miracle cure” after 27 years of mistreatment.
The five independent pieces of evidence that Broxmeyer presents
Broxmeyer organizes his argument into five levels, each independently supporting the infection hypothesis. Each is based on literature and studies (references from the book/article). Here is a list with descriptions:
- Historical evidence
Parkinson’s and TB share historical parallels, e.g., both diseases increased with the Industrial Revolution. The substantia nigra (key region in Parkinson’s) was first identified by a tuberculous lesion in an autopsy. The last major Parkinson’s epidemic (von Economo encephalitis, 1917–1928) was clinically almost identical to TB encephalitis. In AIDS patients (often with Parkinson’s-like symptoms), mycobacteria are the most common CNS pathogens.
Key references: Blocq & Marinesco (1893): Tuberculous attack on the substantia nigra; Hall (1924): Encephalitis lethargica as TB-like; Berenguer & Moreno (1992): Mycobacteria in HIV-associated Parkinson’s
. - Epidemiological evidence
Both diseases share similar demographics (older populations, slight male predilection, chronic wasting/cachexia). Geographical clusters (e.g., high Parkinson’s rates on Guam, linked to environmental infections) and migratory risk (e.g., higher risk among the foreign-born) suggest infectious transmission. Vitamin D deficiency (common in TB and Parkinson’s) may be a common factor.
Key references: Martyn & Osmond (1995): Environmental factors in childhood; Betemps & Buncher (1993) : Place of birth as a risk factor; Mulder & Kurland (1954) : Neurological clusters on Guam; Talbot et al. (2000): TB among immigrants
. - Pharmacological evidence:
Antituberculosis drugs relieve Parkinson’s symptoms, suggesting a bacterial cause. The DATATOP study (the most important Parkinson’s therapy trial) used deprenyl, originally developed for TB. Several case reports show cure of symptomatic Parkinson’s with anti-TB drugs.
Key references: DATATOP Parkinson’s Study Group (1996): Deprenyl effects; Fuente-Aguado & Bordon (1996) , Kurasawa et al. (1997), Otaki (1994), Mital et al. (1974), Solanki & Kothari (1977) : Anti-TB therapies in Parkinson’s. (The latter studies are all from Broxmeyer articles)
. - Microbiological evidence
Serological tests show antibodies to Nocardia in 100% of Parkinson’s patients (Kohbata study), with cross-reactions to TB (same bacterial order Actinomycetales). Bacteria fluctuating between Nocardia and Mycobacteria have been isolated in blood from Parkinson’s-associated encephalitis cases. Experts classify the same strains differently.
Key references: Kohbata & Shimokawa (1993 ), Kohbata & Beaman (1991) , Beaman et al. (1994) : Nocardia in Parkinson’s; Atlas (1988) : Classification problems; Burn (1934): Gram-positive bacilli in encephalitis blood; Jackson (1954): Acid-fast forms in degenerative diseases
. - Biochemical evidence:
Both diseases disrupt similar pathways, e.g., vitamin D metabolism (TB bacteria block VDR gene, vitamin D deficiency correlates with Parkinson’s balance problems; vitamin D therapy helps in PD). Genetic links: Parkinson’s genes (e.g., LRRK2) are associated with TB, leprosy, and Crohn’s (all mycobacterial). Bacterial amyloid proteins may trigger Lewy bodies.
Key references: Gao & Raine (1994) : HSP-65 antibodies in MS/PD; Pisa et al. (2020) : Fungi/bacteria in PD brain; Chapman et al. (2002): Bacterial amyloids; studies on LRRK2 ( Michael J. Fox Foundation-funded ).
Addendum by Dr. Retzek
about chronic persistent infections
The concept of chronic persistent infection exists in conventional medicine, to my knowledge, “officially” only for
- Syphilis (3 stages)
- AIDS virus
After that, things get dark and an increased titer in the blood is interpreted as a “serum scar” after the infection has passed.
Yes, that’s right, we know about cold sores, or herpes zoster, or warts/condyloma/PAP or or or – but it doesn’t feel like it’s part of conventional medical evaluation or therapy and doesn’t give us the reflex of “chronic persistent infection” – this requires long-term anti-infective therapy
.
Examples of this cognitive neglect towards persistent infections as a causal cause of chronic “idiopathic” diseases
- Although we now know with almost 100% certainty that persistent EBV in the brain triggers multiple sclerosis (see below), this does not lead to a changed strategy:
- For MS we still only use immunosuppression instead of antiviral medication and are surprised that the long-term results with basic therapy are not really satisfactory (see Dr Richard Burr’s lecture in the Vatican in 2018 on basic therapy vs. stem cell therapy , to be honest these are horrific data!)
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- For MS we still only use immunosuppression instead of antiviral medication and are surprised that the long-term results with basic therapy are not really satisfactory (see Dr Richard Burr’s lecture in the Vatican in 2018 on basic therapy vs. stem cell therapy , to be honest these are horrific data!)
- EBV as a co-trigger of LongCovid and/or ME/CFS is deliberately ignored
. - According to neurologists , chronic Lyme disease or even “bad” neuroborreliosis does not exist
.- Due to the weakness of commercially available test kits, our laboratories are often unable to correctly identify chronic Lyme disease (see DCL)
. - Despite scientific evidence, Lyme disease is still treated with the bacteriostatic biofilm inducer doxycycline , and for far too short a time, even though the generation time of Borrelia is similar to that of tuberculosis
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- Due to the weakness of commercially available test kits, our laboratories are often unable to correctly identify chronic Lyme disease (see DCL)
- MCAS in connection with bartonellosis does not exist in our perception
. - Chronic parasitic colonization is esoteric and naturopathic nonsense, despite many studies
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