Eva Sapi's recent research calls into question everything we thought we knew about Lyme "cysts." In fact it destroys the old thinking.
We have heard
about cell wall antibiotics, intracellular antibiotics and cyst-busters. Think
She investigated the effect of various antibiotics on Lyme
spirochetes and round body forms - also know as cystic forms.
worked according to plan. Doxy inhibits protein synthesis - it kills bacteria,
including Lyme, by action within the cytoplasm, inhibiting the manufacture of
proteins required for the bacteria's survival. Doxy and others are commonly
referred to as intracellular antibiotics.
Spirochete loads decreased by
about 90% while cyst levels increased by 200% - just as expected.
amoxicillin data was presented. Amoxicillin inhibits the formation of bacterial
cell walls. Amox and similar drugs should then only be effective in killing
spirochetes with an intact cell wall. This is where the results start deviating
from the plotted course.
Amoxicillin killed 90% of spirochete forms - OK,
but -- it also killed 68% of the cystic forms! Amoxicillin and other cell wall
drugs are not cyst busters - only specific anti-parasite drugs kill cysts - or
so we thought.
Well lets think again for a second: what are cysts? Are
they balled up forms of spirochetes with a different kind of membrane - or blebs
(also described) expressed through the spirochete membrane? Maybe the former
retain much of the cell wall from the original spirochete - maybe that is why
amoxicillin works here.
This would seem to clear up a nagging question
raised by others. Are cysts and L-forms really the same thing? These results
show that cysts cannot represent a version of L-forms or spheroplasts which
result when gram negatives shed their cell walls. If this were the case a cell
wall drug would be ineffective. Cysts and L-forms are distinct and different
forms. (There may be a hole in this reasoning. I will explain later).
So we have learned something new: cell wall antibiotics can also kill some cyst
forms which are not L-forms.
Let's look at some more data. Tigecyline is
a not a cyst drug either. Wrong. Tigecycline kills 90% of spirochetes, good so
far, but it also kills 90% of cysts! Tigecycline is an intracellular antibiotic
similar to doxycycline! Another fly in the ointment.
OK. Cysts with their
lower metabolic rate, still need ribosomal proteins to survive, just not at the
levels of intact spirochetes. Tigecyline is a more powerful drug, higher levels
are delivered into the cytoplasm of the cysts. This makes sense. Cyst forms are
still essentially a pleomorphic version of Lyme bacteria with somewhat different
features. In this scenario, cysts could be L-forms. But we have already shown
that this is not true because amoxicillin can kill them. Right?
a cell wall drug. I thought so. Kersten, (antimicrobial agents and chemotherapy,
May 1995, p. 1127-1133) states that Beta-lactam antibiotics, which include amox,
penicillin and Rocephin, have been shown to cause a specific loss of total
intracellular RNA in the absence of cell wall hydrolysis. In other words, amoxil
could possibly work in part as an intracellular agent. If this is right cyst
forms of Lyme could still be L-forms. So perhaps we have not shown that L-forms
and cyst forms are different after all.
The question remains
Let's get to the Cyst-busters. It takes antiparasitic drugs,
so we thought, to kill the cysts. Cyst-busters, anti-parasite drugs, kill
parasites (and Lyme cysts) not bacteria. The so called cyst-busters were
heretofore used in combination or cycled with other antibiotics. Previous
thinking was that typical antibiotics would kill spirochetes and/or L-forms and
that cyst busters would disrupt only the cystic forms.
not kill intact spirochetes - so we are told. Very wrong this time.
cannot cover the whole Sapi study. The most exciting finding is that Tindamax
(tinidazole) - our premier Cyst-buster, is the most effective drug overall. This
"cyst-buster" kills 90% of cysts and spirochetes: by far the best drug. We don't
know it's effect on L-forms, but we can guess. Tindamax probably works by an
intracellular mechanism. If this is true it should be equally effective against
It gets even better. Tindamax is the only drug which does a
great job on biofilm colonies as well!
(not to be discussed now). More on
Tindamax passes the blood brain barrier and penetrates
well into most tissues. It has been effective in my patients with neurocognitive
deficits - neuroborreliosis.
Recently I tried it on another sort of
patient. This patient has had intractable Lyme arthritis of his knees. This
young athlete had been extensively treated with IV Rocephin followed by a year
of typical oral antibiotics. Knee effusions have persisted - until I prescribed
Tindamax. Now, after two months, the fluid in his knees has evaporated. His
knees are dry and painless for the first time in over one year.
raises the question: should Tindamax be used as mono-therapy? Well, I cannot
endorse blanket use at this time. Tindamax has a black box warning. It has been
associated with cancer in some laboratory animals. Perhaps there are more
compelling reasons to use Tindamax, but this will have to wait for another
My nagging question:
Why does penicillin kill Lyme? It
shouldn't. Lyme is a gram negative bacteria. While certain Beta-lactam
antibiotics can kill gram negative bacteria, penicillin cannot. Penicillin is
only active against gram positive bacteria.
Maybe this other mechanism
alluded to above, the alternative intracellular RNA mechanism is significant and
explains why penicillin kills Lyme spirochetes. Maybe not.
We need to
continually reevaluate things which we have assumed to be true, because many of
them are not.
Posted by Lyme report: Montgomery County, MD at 6:31 PM