Discussion in 'Infections: Lyme, Candida, EBV ...' started by Andy, May 20, 2019.
Open access, https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-019-3495-7
Early Lyme investigators threw antibiotics at their young patients, and when those often failed, concluded that Lyme was of a viral etiology. They were wrong.
It would take a few years to realize the causative agent behind the single strain of microbe infecting neighborhoods around Lyme CT was bacterial. They immediately started different abx regimens. (Although some patients were selected to not get any treatment at all so that researchers could see how the disease might play out, but that's a different story)
When antibiotics continued to fail in too many patients, early researchers unilaterally - some patients might have argued arbitrarily - bifurcated symptoms into Major vs Minor. Major symptoms included mostly things a doctor could see or measure, eg, gross encephalitis, swollen knees, palsy, etc. Minor symptoms were things like nausea and pain and cognitive decline and balance and many other subjective measures. These doctors said they could cure Lyme in a majority of cases except for a few lingering minor symptoms that didn't amount to much more than a transient inconvenience.
So even as they began to downplay symptom severity in patients whose symptom cluster did not resolve with treatment, they were willing to admit that anywhere from 10% to 40% or more of treated patients didn't recover. As we got closer to diagnostic standardization, and the associated windfall from a bourgeoning diagnostics market (thank you Bayh-Dole Act), and the looming opportunities associated with vaccines, that number shrank until it was pretty much accepted at 10% to 20%. But 10-20% of just a few thousand each year of a hard to get easy to cure infection was no big deal.
We now know that currently over 400,000 cases of Lyme occur each year in the US alone. That number climbs annually. The 10% to 20% number now appears alarmingly large. So an Old Guard study found back in 2015 or there abouts that really less than 5% of treated patients reported persistent symptoms after several years. Lyme advocates quickly pointed out that this study concentrated on early stage Lyme. It seemed to ignore patients who were failed by the diagnostic protocol and never got treatment until after Borrelia had coursed through their bodies and entered privileged sites, where abx had a hard time reaching and when it could, was met by biofilms etc.
If those victims were included, that 5% number would likely balloon. Even if it only ballooned up to 10% - the low end of the once widely acknowledged spectrum of patients who did not recover - that would mean 40,000 very sick patients, many disabled, were being added to the failed-treatment roles year after year after year.
The realization that abx believed to be effective against most strains of Bb sl - like doxy and Rocephin and amoxicillan - were actually ineffective against persister cells in vitro was a watershed moment. But the IDSA and its proxies were quick to counter that persister cells were not all that uncommon afterall, and the normal way of things would be for a patient's immune system to mop up what the abx failed to eradicate.
The problem with that logic was the bacteria at question had evolved a unique capability for fooling human immune systems. This it was truly gifted at. Bb is a little bug with a genius for eluding our immune systems' defenses, not the least of which - beyond changing shapes and building biofilms - was antigenic variation.
Between persister cells immune to most abx, and the bacteria's innate savant-type strategies to thwart the most able immune attacks, the ability to claim medical authority over a substantive portion of Lyme sufferers' infection(s) is fast fading.
I wrote this off-the-cuff, so I apologize for vagueness or any inadvertent mistakes. I think the gist is right, though.
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