PubMed · 4029451
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1985. Lyme disease.. https://pubmed.ncbi.nlm.nih.gov/4029451/
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Here is proposed a hypothesis that a completely unsuspected biology exists for pathogenic spirochetes, namely that the cystic spirochetal forms (long thought to be static and resting or just a dormant cohort) actually are capable of killing mammalian host cells. At least two "lethal" scenarios are proposed; first, the host cell destruction from the "inside out" by small caliber cystic forms invading the host cell cytoplasm, and second host cell destruction by engulfment of entire host cells by large caliber cystic spirochetal forms. Conventional thinking about spirochetal cyst forms is divided between two polar spheres of influence; one a majority community that completely denies the existence of spirochetal cyst forms, and a second group of academically persecuted individuals who accepts the precepts of such antebellum scientists as Schaudinn, Hoffman, Dutton, Levaditi, Balfour, Fantham, Noguchi, McDonough, Hindle, Steiner, Ingraham, Coutts, Hampp, Warthin, Ovcinnikov, and Delamater. Microscopic images of cystic spirochetes are difficult to ignore, but as has been the case in this century, academic "endowments" have nearly expunged all cystic spirochetal image data from the current textbook versions of what is the truth about the spirochetaceae. If the image database from the last century is obliterated; many opportunities to diagnose will be lost. Variously sized cystic spirochetal profiles within diseased nerve cells explain the following structures: Lewy body of Parkinson's disease, Pick body, ALS spherical body, Alzheimer plaque. Borrelia infection is therefore a unifying concept to explain diverse neurodegenerative diseases, based not entirely on a corkscrew shaped profile in diseased tissue, but based on small, medium and large caliber rounded cystic profiles derived from pathogenic spirochetes which are..."hiding in plain sight".
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In a 63-year-old, 165-cm-tall woman with a history of repeated tick bites, dilative cardiomyopathy, osteoporosis, progressive head ptosis with neck stiffness and cervical pain developed. The family history was positive for thyroid dysfunction and neuromuscular disorders. Neurological examination revealed prominent forward head drop, weak anteflexion and retroflexion, nuchal rigidity, weakness of the shoulder girdle, cogwheel rigidity, and tetraspasticity. The lactate stress test was abnormal. Electromyograms of various muscles were myogenic. Muscle biopsy showed non-specific myogenic abnormalities and generally weak staining for cytochrome oxydase. Mitochondriopathy with multi-organ involvement was suspected. The response to anti-Parkinson medication was poor. In conclusion, dropped head syndrome (DHS) may be due to multi-organ mitochondriopathy, manifesting as Parkinsonism, tetraspasticity, dilative cardiomyopathy, osteoporosis, short stature, and myopathy. Anti-Parkinson medication is of limited effect.