The annual incidence of Lyme disease, caused by tick-transmitted Borreliella burgdorferi, is estimated to be at least 476,000 cases in the United States and many more worldwide. Ten to 20% of antimicrobial-treated Lyme disease patients display posttreatment Lyme disease syndrome (PTLDS), a clinical complication whose etiology and pathogenesis remain uncertain. Autoimmunity, cross-reactivity, molecular mimicry, coinfections, and borrelial tolerance to antimicrobials/persistence have been hypothesized and studied as potential causes of PTLDS. Studies of borrelial tolerance/persistence in vitro in response to antimicrobials and experimental studies in mice and nonhuman primates, taken together with clinical reports, have revealed that B. burgdorferi becomes tolerant to antimicrobials and may sometimes persist in animals and humans after the currently recommended antimicrobial treatment. Moreover, B. burgdorferi is pleomorphic and can generate viable-but-nonculturable bacteria, states also involved in antimicrobial tolerance. The multiple regulatory pathways and structural genes involved in mediating this tolerance to antimicrobials and environmental stressors by persistence might include the stringent (rel and dksA) and host adaptation (rpoS) responses, sugar metabolism (glpD), and polypeptide transporters (opp). Application of this recently reported knowledge to clinical studies can be expected to clarify the potential role of bacterial antibacterial tolerance/persistence in Lyme disease and PTLDS.
What’s truly sad is none of this is new.  This 2017 study talks about the stringent response, and this 2016 presentation by Dr. Zhang discusses the importance of persisters, or the dormant form borrelia takes when it feels threatened.  And this 2017 study also points out that Bb mutates (changes form) as previously described by Barbour and Hays way back in 1986.  I’m sure there are many more older studies presenting all of this.
Why is this simple fact still not believed and accepted?

What is not discussed in this article is the fact most Lyme/MSIDS patients are infected with multiple infections simultaneously, further complicating their cases, and requiring different medications.  This article shows that higher doses of antibiotics are required to eliminate a bacterial infection when other microbes are present, yet corrupt public health ‘authorities’ continue to push a faulty one pathogen, one drug paradigm based on faulty testing that misses 70-86% of cases!

What is also not discussed in this article is the larger subset of patients (30-40%) that are diagnosed and treated late – thereby not even making the PTLDS group, and therefore never studied in research.  This is a huge chunk of people are often seronegative in testing and don’t have the EM rash.  This is me, and everyone I work with.  There is ZERO data on us.  ZERO.

The PTLDS moniker is confusing at best and misleading at worse.  The whole ball of wax is based on faulty premises and faulty researchTime for a do-over.

For more:

Similarly to polarization on COVID treatment, it’s not a scientific debate. It’s a political one.
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