Key Questions About Fluconazole for NeuroLyme

[Guest guest]

Here are the questions I would like to see answered about

Fluconazole for neuroLyme:

1) Questions About " Herxing " on Fluconazole

a) If Schardt is correct about the mechanism, Fluconazole would

weaken Borrelia burgdorferi, not kill it outright like a

bacteriocidal drug. I would expect any 'herx' to be quite a bit more

mild, and to occur only when the Fluconazole has been given long

enough for Bb to succumb. Why are some patients 'herxing' on the

first dose?

As I recall, Schardt's orginal sample favored those who had

already undergone the standard regimen for neuroLyme, IV Rocephin.

They likely have lightened spirochete loads. Do these

patients 'herx' early on, or is it mostly those who have less prior

antibiotic treatment?

c) We saw with the Unnameable Protocol that any adverse response was

often referred to as 'herx' - how do we know that isn't true here,

as well?

d) Assuming " Herx " does come into play, is it possible that this

Fluconazole treatment should be AVOIDED by those who have not

undergone extensive antibiotic therapy in the fairly recent past? Do

we really 'know' that this is a safe and appropriate treatment for

those whose CNS spirochete loads may be substantially higher than

Schardt's initial sample?

e) Assuming that some who embark on Fluconazole for neuroLyme do

experience 'herx', how does that manifest, in what types of

symptoms, and how is it distinguished from yeast-die off. Which

leads to:

f) Most patients who have been on long antibiotic regimens are more

at risk for yeast overgrowth than an average person. Yeast die off

can be unpleasant. How do we know these 'herxes' aren't really

triggered by that?

2) As I recall, Schardt's patients got feeling a lot better very

quickly, by Lyme standards, within a few weeks of commencing

treatment. Why exactly do we assume this is because of action

against a slow-cycle spirochete like Lyme?

3) Is the logic of combining antibiotics that Schardt's mechanism

may allow Fluconazole to weaken or soften up the bugs rather than

kill them, so that a more overtly bacterocidal drug is needed to

polish them off?

4) As I recall, the initial course of treatment Schardt contemplated

was fairly brief, a month or two. Are we seeing people now adopting

longer term (someone mentioned 9 months) Fluconazole treatment for

the purpose of putting neuroLyme into remission?

5) Does Schart's mechanism really permit there to be non-responders?

If Fluconazole impacts Bb as Schardt envisions, shouldn't we see an

across the board response? If not, what are the variables that might

conceivably distinguish responders from non-responders over the same

course of treatment?

6) When will we see before-and-after neuropsych assessments like

those used by Fallon, to show measurable gain in function through

neuroLyme treatment?

7) Has Schardt produced such studies of his original patients? Are

the doctors administering Fluconazole for neuroLyme using measures

like these to guage the effectiveness of treatment? Or is there a

general reliance on self-reported improvement?