Bottom line, a piece of Borrelia is similar to a human one, antibodies are developed, they attack neuronal tissue=> you get MS/ME even when the bacteria is gone. This was always the theory against autoimmunity but they never found an autoantibody. Well, at least in two patients, they now have and it's called anti-enolase.
Before you jump to say this is CDC research, the researchers are from Italy...
I think it is good for all of us to keep an
open mind and examine everything that is researched about
chronic lyme. There is a flood of antimicrobial research showing persistence, but this one is a different study, tackling autoimmunity in a novel way.
I do not necessarily want to go hunting borrelia, i want to get better. If this turns out to be an autoimmune disease in the end, and if i can get better, i do not necessarily want to brag i kill spirochetes during my free time ...
Comments welcome...
Autoimmunity against a glycolytic enzyme as a possible cause for persistent symptoms in Lyme diseaseAbstract
Some patients with a history of Borrelia burgdorferi infection develop a chronic symptomatology characterized by cognitive deficits, fatigue, and pain, despite antibiotic treatment. The pathogenic mechanism that underlines this condition, referred to as post-treatment Lyme disease syndrome (PTLDS), is currently unknown. A debate exists about
whether PTLDS is due to persistent infection or to post-infectious damages in the immune system and the nervous system. We present the case of a patient with evidence of exposure to Borrelia burgdorferi sl and a long history of debilitating fatigue, cognitive abnormalities and autonomic nervous system issues. The patient had a positive Western blot for anti-basal ganglia antibodies,
and the autoantigen has been identified as γ enolase, the neuron-specific isoenzyme of the glycolytic enzyme enolase. Assuming Borrelia own surface exposed enolase as the source of this autoantibody, through a mechanism of molecular mimicry, and given the absence of sera reactivity to α enolase, a bioinformatical analysis was carried out to identify a possible cross-reactive conformational B cell epitope, shared by Borrelia enolase and γ enolase, but not by α enolase. Taken that evidence, we hypothesize that this autoantibody interferes with glycolysis in neuronal cells, as the physiological basis for chronic symptoms in at least some cases of PTLDS. Studies investigating on the anti-γ enolase and anti-Borrelia enolase antibodies in PTLDS are needed to confirm our hypotheses.
/doi.org/10.1016/j.mehy.2017.10.024Patient
The patient is a 37-year-old man. Since 1999 he has been afflicted by
severe fatigue, memory impairment and lack of concentration. At that time, he was 19 and he had never had any neurological symptom before.
In the early years, the abovementioned symptoms presented with a cyclic trend of relapses and recoveries. In 2002, a flu-like illness precipitated his condition which has since become chronic. During the last 15 years, he has been experiencing other symptoms, such as muscular and joint pain, acral hypoesthesia, post-exertional malaise, and orthostatic intolerance, resulting in him being house-bound. He fulfils the 2015 diagnostic criteria published by IOM [23] for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In August 2014, the patient presented at Trieste University Hospital, where he resulted positive to Borrelia both by PCR and Western Blot, as shown in Table 1. The patient was also positive to HHV6 (past infection). Current infection by Helicobacter pylori was detected and treated (Table 1). In 2000, the patient presented with a nodule of one centimeter in diameter, located on one nipple. It was investigated with echography and mammography and cancer was ruled out. Its etiology was not further investigated at that time and the lesion resolved spontaneously within months. That lesion was compatible with a nodular form (Spiegler-Fendt type) of lymphadenosis benigna cutis (LABC) of areola mammae, which is a typical second stage manifestation of LD in Europe [24]. Patient was submitted to antibiotics, with complete and rapid resolution of acral hypoesthesia and only partial and temporary improvements in the other symptoms.
In 2015, an extensive panel of anti-neuronal antibodies was performed (Table 2). Positive anti-Basal Ganglia Antibodies and anti-γ enolase antibody were detected.