Video's
are in WMV (can be shown with Windows Media Video player via Internet
Explorer or VLC) format made with Windows Movie Maker; some computers
may need allow activeX and/or to make *.lymerick.net and
*.ulmarweb.dk trusted websites in Internet Explorer security for the
video's to show).
Note it may take some minutes to download
part of the streaming videos, before they begin to play
automatically, but once loaded you can rewind and play them again.
While the videos are loading, you can jump down to NOTE
and read the text / explanation, later return to watch the videos
play.
If you want to watch individual videos in full screen
mode double-click on the video (ESC will return you to this webpage
after viewing video in full screen mode) or right click on video when
it is playing and use Zoom to full screen ...
Total
time to watch ALL the videos < 40 min.
#45
2006/10/29 (106 Mb, 8 min., by MK)
http://kroun.ulmarweb.dk/case/0045/0045-20061029.wmv
http://lymerick.net/0018-20121004.wmv
(coming)
----
NOTE:
These above
selected videos are presented in order to show DOCTORs with a special
interest in diagnosing and treating chronic spirochetosis / chronic
Borreliosis by doing microscopy themselves, what they need to look
out for in the microscope.
MK
only does microscopy as research on selected members of
http://daninfekt.dk
who - judged from their history, previous test results and not the
least the patients current symptomatology, visualized on symptom
scores and log curves via the Excel symptomdiary (english
& danish
version) - displays
a recurrent relapse pattern suggesting the patient could be suffering
from a currently active Borrelia infection and/or other infections
carried by ticks! -
read more about the diary and curve drawing here:
http://lymerick.net/why-diary.html
Microscopy
procedure / hints:
Bozsik's
Dualdur reagent / dobbelt centrifugation method is described in #1
video from 15-10-2008 and more
information here. Please also read more on the subject of 'why
buffycoat'.
I (MK) take a few (3-5) 5 ml EDTA full blood
samles, centrifuge one at high speed for 20 minutes, and isolate the
buffy-coat fraction (store the removed plasma in the freezer for
eventual later serology tests), and usually make 10-20 dried
bloodsmears from the buffy-coat fraction (plus make a few additional
unconcentrated bloodsmears for the differential count) and examine at
least one wet drop (around 50 microliter) of the wet buffy-coat
fraction meticulously, always
with the 100X oil objective,
too see if there are any moving microbes therein. Meanwhile the
smears are left to dry and can later be fixed, stained and examined
for microbes.
The QBC-Paralens objective, can instead of its
external UV-light source, also be used with the normal microscope
light source for doing
ordinary normal light microscopy; then a quick switch between normal
light microscopy and fluorescence microscopy is possible by just
shifting the light source; that is handy when I am using an
immunofluorescencent
stain or acridine
orange stain, it is possible to look at the same structure in
different microscopy modes without having to move the
object/viewfield; I have 2 sets of oculars, 6x and 10x, for the old
Leitz
Wetzlar Laborlux (III) anno 1957 microscope, thus I can "screen"
a buffy-coat blood sample faster at a total of 600x magnification (as
long as nothing abnormal is found), then if I encounter something
that needs a closer look at, I can quickly increase the magnification
to 1000x by shifting the 6x oculars out out with the 10x oculars and
I can exchange the right ocular with the microscope USB camera, which
I usually always do, because structures that are magnified further
digitally on the computer screen are much easier visible, than they
are by looking at them in the microscope, and besides this gives me a
more comfortable working position, I can sit leaned back looking at
the screen, while looking at the sample, which is much more
comfortable than to sit bending my neck in order to look into the
microscope oculars, where the very bright light directly in my eyes
often are quite unpleasurable and provoke headache (I am often very
light sensible); the camera also allows me to snap still pictures and
do video sequences of any moving objects in the sample and often I
have the camera running throughout the microscopy, in order not to
miss a thing, but files must be broken into several max 1 gigabyte
large video files, otherwise they can not be processed by Windows
Movie Maker; also this way the patient and I can do the microscopy
together, looking at exactly the same screen, when the patient wish
to see what is found with their own eyes, which many do; my
microscopic examination is
always done very systematically in the same meticulous way. I always
begin scanning the sample from one edge, scroll stepwise all the way
up or down to the opposite edge of the sample, then step one
viewfield sideways (in 600x), then scoll stepwise back to the
opposite edge and so forth, and continue the procedure until the
whole blood sample have been examined very thoroughly. It can take me
several hours to do microscopy of a single sample, because I
do not want to overlook anything. There
may be very few microbes, sometimes only one, in a single drop of 50
microliter buffycoat blood sample; finding > 7 (~ many) abnormal
structures per examined drop BUFFYCOAT fraction of a 5 ml EDTA blood
sample is a rare finding in the patient group I investigate, that are
chronically ill with borrelia plus eventual other tickborne
co-infections.
If
I do not find anything abnormal at all in the first sample screen,
but the patient is highly suspect of having infection that flare up
in cycles, I find it a waste of my time and effort to look more at
that set of samples, because we probably did not hit the right day of
sampling, i.e. during a microbial breakout;
instead I rather will set the patient to do detailed symptomdiary in
Excel (if not already started) and come for a new test another day,
within 12 hours after start of a new flare in the borrelia cycle, and
the day before a new anticipated flare up, for the intracellular
blood infection that we want
to look for just before the breakout of the microbes from the cells;
finding very few
microbes in circulation depends very much on if the sampling can be
timed perfectly according to the patients symptom log;
unspecific "infectious" symptoms break out within a few
hours after microbes have broken out into the blood stream from
deeper tissues (spirochetes) or from intracellular compartments
(babesia, anaplasma, ehrlichia ..) and results in a fierce immune
reaction with formation of lots of antigen-antibody immunecomplexes
(in the immunocompetent host), so when there are many enough antigens
entering the blood circulation at the same time, that bind antibodies
to them, there may actually not be any free left over antibodies in
the plasma/serum that can bind to the serology test antigen, i.e. the
patient may very well test false seronegative in the very same plasma
sample wherein antigens are detected by microscopy of the buffycoat
by meticulous microscopy!
It is probably the formation of
immune complexes that trigger innate immune system, both complement
cascade reactions (measure complement split product C4a;
C4a may be elevated in patients with Borrelia and long lasting
rheumatological complaints PDF
but was not in patients with borrelia dominated by neurological
symptoms) and a proinflammatory cytokine cascade response (TNF, IL-1,
IL-6 etc.), which should also be measured if possible, because if
there are abnormal innate immune reactions, it shows there is an
inflammatory proces going on in the patient but not the cause,
but if positive for inflammatory markers, we know for sure this
patient is feeling sick for a reason that must be sought (it is not
just in the patients head), and the patient may need antibiotic
treatment to reduce the symptoms by suppressing microbial growth,
hence abrogate the cause of the inflammatory reaction, if microbes
can be detected by tests that are sensitive enough.
The patient
may feel quite sick, despite there is not any measurable
specific antibody response,
either because all antibodies get bound into immunecomplexes, the
most of which probably precipitates inside the hosts vessels (hence
vasculitis-like reactions, petecchia, easy bruising, declive edema
indicating increased vascular permeability, are common complaint
during periods of infectious activity), or because the patient is not
able to mount a specific immune response for various reasons! -
because it is cascade reaction, that can be started by very little
amount of antigens - just like the hyperallergic patient can react
very fiercely with an anaphylactic shock reaction to minute amount of
antigens that does not bother a non-allergic person - the patient can
be very sick, despite it is so difficult to find the microbial
antigens in their blood!
Other investigators that are
less meticulous than I in their sampling as perfectly as possible
according to the patients cyclical relapse pattern and in their
methods of staining (not using both conventional light and
flourescence microscopy) and doing microscopic examination less
meticulously, like looking only at 400-600x magnification on a thin
and thick blood drop from capillary blood , taken
from either finger or ear prick i.a. doing a conventional
"malaria" screen, and who usually spend less than one hour
in front of the microscope looking at the sample and perhaps only
scan about 1/4 of a sample because they step 3-4 viewfields sideways
instead of just one - may very easily overlook the single ringformed
parasite or single moving spirochete that can actually be found in
that particular patients samples - if they would do it like I do!
In
2000-2003 I compared the usual "malaria" screen technique
with the buffycoat technique, and often found no sign of parasites in
the conventional samples, but might find sign of increased bone
marrow blood cell reproduction (normoblast i.e. immature red blood
cells and leuco-blasts (immature white blood cells), as reaction to
infection), in those patients, who turned out to show up a few
parasites / microbes in their buffycoat bloodsmear; since then I only
do examination of the buffy-coat for microbes, but might do an
unconcentrated smear examination also, just to do an oldfashioned
differential count.
I
NEED A BETTER TRINOCULAR MICROSCOPE WITH DARKFIELD, PHASECONTRAST
with SEPARATE VIDEOTUBE (c-mount), and a much better quality, very
light sensible video camera (connect to computer via USB), that can
take good pictures of even one single slim green spirochete on a very
black background, and can magnify the picture from the microscope up
to 100X!
- to get up to a total of 10.000X total magnification,
so I can take videos of spirochetes in the good quality, as dr. Bela
Bozsik and dr. Andy Wright can do (see
examples of their work on blood microscopy page from before 2006:
http://lymerick.net/Videomicroscopy.htm)
If
you can spare some bugs, please support the research by donating to
Patientforeningen DanInfekt (labelled research/forskning), see
account number on http://daninfekt.dk
at KONTINGENT subpage.
Please
beware that finding spirochetes and their alternative structures by
simple microscopy, as illustrated in videos above, is not a
"test-result" that can stand alone
-
since all spirochetes look pretty much alike in the microscope, and
since all spirochetes may undergo the same (cyclical) developmental
changes such as degranulation, formation of cysts, blebs etc., as
illustrated in this 100
years pictorial "Survival in Adverse Conditions" and
described by DeLamater
1951 and by Hindle
1912 and others, also read the historic observations on
(relapsing fever) Borrelia spirochetes; so when the human eye and/or
camera detect a few moving ("baby" or adult) spirochetes in
a blood or spinal fluid samplefrom a human patient, it is not
possible to say with absolute certainty which spirochete is in
action, though a history of tickbite(s) aquired in the temperate
climate zone followed by EM, point more likely to Borrelia
burgdorferi sensu lato / Lyme borreliosis, than to another type of
spirochete (Treponema
(syphilis)
or Leptospira
(leptospirosis
AKA Weil's syndrome, rat catchers symdrome or 7-day-fever and more
...)) .
Note that Willy Burgdorfer - the discoverer of
Borrelia burgdorferi
- in
his 1999 Keynote lecture (saved PDF printout from Medscape) was
honest enough to admit that he was wrong way back in 1951 when he did
not - as he writes / said - found evidence of "a negative phase
or complex life cycle" ...
"Although most of the above mentioned opponents of the "granulation theory" verified the formation and existence of cysts, blebs, spherules associated with spirochetes, they considered them as degeneration products." ... "Of particular interest to our discussion is the presence in freshly engorged Lyme disease ticks of spirochetes with outer membrane-associated cysts, blebs or spherules that often contain numerous granules with surrounding trilaminar membranes (Figs. 11,12). Because the internal material of these granules is similar in appearance and electron density to that of typical spirochetes and because these cysts (blebs, spherules) strongly react when treated with FITC-labeled conjugates, the questions concerning a complex life cycle of borreliae have again been raised and induced investigators to critically examine the nature and function of these formations -- a research problem referred to for the first time almost 100 years ago by Dutton and Todd. Thus, RML scientists Dave Dorward and Claude Garon using silver staining, transmission and scanning electron microscopy investigated the nature of naturally elaborated membrane blebs on the surface of cultured B burgdorferi or free in the medium, and found both linear and circular DNA (Fig. 13). The fact that his material was packaged within the membrane-derived vesicles suggested that it might play a role in the protection of genetic markers. In vivo and in vitro exposure of B burgdorferi to antibiotics (penicillin G, ceftriaxon) were shown by Preac-Mursic and associates to produce cytomorphic atypical but motile spirochetes with numerous membrane-derived vesicles (spheroblast -- L-forms) (Fig. 14).[1]. In their recent publication, Brorson and Brorson reported on the "In vitro Conversion of Borrellia burgdorferi to Cystic Forms in Spinal Fluid, and on the Transformation to Mobile Spirochetes by Incubation in BSK-H Medium."[2] Accordingly, B burgdorferi converted rapidly to cystic forms when transferred to spinal fluid. No normal spirochetes were left after 24 hours of incubation at 37° C; all were converted to cysts. When these cystic forms were transferred to a rich (BSK-H) medium, the cysts were converted back to normal, mobile spirochetes after incubation for 9 to 17 days. [young cysts]" ... "Using silver impregnations and immunochemical staining, cystic material has been demonstrated in every animal and human tissue infected by B burgdorferi. As yet, it is not known whether these forms of Borrelia represent products of degenerated spirochetes or of surviving organisms capable of transforming to typical spirochetes once the faborable environmental conditions are restored. It is tempting to speculate, however, that the survival mechanism of spirochetes is responsible for the diverse pathology of these organisms as well as for their ability to survive as cystic forms thereby producing prolonged, chronic and periodically recurrent disease." ...
Hampp
1948 did electron microscopy studies on spirochetes and wrote:
"Typical
free granules, the
end products of granule 'shedding', are shown in figure 18. They are
roughly circular in outline and sharply bounded. They consist
for the most part of what appear to be short sections of spirochetes
closely packed together. The
contents of these granules are probably responsible for the fine
lacelike appearance and the bright white, highly refractile bodies
described by Hampp (1946) under the dark-field microscope. Examples
of another type of free granule repeatedly observed are shown in
figures 19 and 20. These granules consist of tangled masses of
spirochetes or spirochetal segments. The significance of granules in
the life history of the spirochetes is unknown but certain
investigators have suggested that they may be germinative
units (Balfour,
1911; Noguchi, 1911; Noguchi, 1917; Leishman, 1918; Mudd et al.,
1943; Hampp, 1946). Others are undecided or hesitant in accepting
this hypothesis (Fantham, 1916; Akatsu, 1917; Wenyon, 1926; Warthin
and Olsen, 1930). Topley and Wilson (1936) have indicated that they
are probably particles of culture medium adhering to the sides of the
spirochetes. The electron micrographs demonstrate that this
explanation is wrong, and that free
granules are definitely a phase in the development of spirochetes.
Although it is not possible to determine from these micrographs that
the granules are germinative units their constant rhythmic
occurrence in
living cultures suggests this possibility. Further
support of this hypothesis is provided by the fact that cultures
up to 31 months old, showing only refractile granules by dark-field
examination have invariably given normal growths on transfer to fresh
medium (Hampp, 1946) ...
...
31 months ~ 2½ years! - muchlonger than the duration of the usually
for spirochetal infection recommended antibiotic treatments!
The
latter question mentioned by Burgdorfer, if cysts can convert back to
spirochetes also in vivo, have later been answered by Gruntar et al.
- APMIS 2001. PMID: 11478686
- who injected variably aged cystic form of Borrelia
garinii intraperitoneally
in mice, and found it could result in Borrelia infection, judged both
by seroconversion of the mice and by finding spirochetes in the heart
and bladder tissues of the with Borrelia cysts experimentally
inoculated mice, when they were sacrified and dissected at end of the
study!
In
order to be able to put a family name / substrain name to the
spirochete seen in the microscope, we'll need to do specific and
unfortunately expensive supplementary ANTIGEN TESTING,
depending on which spirochete we suspect it can be, judged from
patients history and previous test results, and depending on what is
availble on the marked to buy for supplementary testing, at present
it is possible to buy FITC-labelled affinity purified Borrelia
burgdorferi antibodies from KPL and ready to use solution of BSK-H
medium from Sigma-Aldrich.
While it can be quite difficult and
time consuming to get positive result with specific direct immune
stain or PCR test when there are only a few spirochetes present in
the material (usually less than 5 spirochetes are found per
buffy-coat drop) i.e. lower than the detection limit for PCR? - it
should be possible to increase chance of these methods giving a
positiv result, if
we can first get a positive culture of spirochetes, so there will be
much more spirochete material to do PCR or specific immune stain on,
thus less waste of time and expensive materials on "nothing
found" and the chance of getting a positive culture should
increase, when one can first find spirochetes by a simple microscopy
screening like above, that cost some hours of work but not much
money.
So far I've already got some positive cultures, already
in the first few tries; preliminary investigations for a future
DanInfekt Borrelia culture project, where we will attempt to culture
in BSK-H as explained by Barbour and others in my selected:
http://lymerick.net/Borrelia-culture.html;
it is probably quite important to avoid oxygen mixing since Borrelia
are microaerophilic and to keep the optimal temperature around 33-36
degree Celciis, for increasing chance of growth of Borrelia:
http://lymerick.net/Borrelia-growth-optimum.html
... in case of a positive culture, we can split a serum sample taken
from same prick / at same time as microscopy as the blood for culture
and do WB (like Mikrogen Borrelia recomBlot or Euroimmune Line blot)
abroad and DAKO/OXOID
Borrelia flagella IgM and IgG antibody analysis
on the plasma/serum, for a direct comparison, a similar study to what
Oksi et al. did in JCM 1995, se ref. below. If we can succeed in
culturing
individual patients own spirochetes in abundance in vitro, such
cultured spirochetes can then be used as antigens in a patient
specific indirect
fluorescence assay, to test if the patient has formed any
specific (IgG) antibodies that react with the spirochetes grown from
the patient. It just requires either peroxidase- or FITC
labelled anti-human-IgG antibodies,
that can be added to make eventual antibody-antigen reaction visible.
Simple.
Please note: immunoflourescence can be used both
ways to detect either antigens or antibodies.
In the primary or
direct
immunofluorescence assay
(d-IFA or DFA)
uses a single (microbespecific) antibody (achieved by vaccination of
a clean laboratory animal which serum is harvested, purified by gel
electrophoresis and absorbed for irrelevant cross-reacting antibodies
to other microbes we do not want to see reaction with) that is
chemically linked to a fluorophore
like fluorescein. The antibody recognizes the target molecule and
binds to it, and the fluorophore it carries can be detected via
microscopy.
In the indirect
immunofluorescence assay
(i-IFA, or many just write
IFA,
the missing i- or d- in front may unfortunately confuse a lot of
people) two antibodies are in the reactions; the unlabeled first
(primary) antibody (within the patients serum/plasma sample)
specifically binds to the target molecule on the test antigens; then
a secondary antibody (anti-human-IgG antibody), which carries the
fluorophore, recognises the primary antibody and binds to it, thus
visualizing that some IgG within the patients serum/plasma had bound
to the test antigens residing on the plate. Instead of fluorophore
the secondary antibody can carry an enzyme (for instance peroxidase)
that when reacting with a suitable substrate create a visible /
measurable color reaction, as in the ELISA AKA EIA.
Try doing
the ELISA and PCR procedures yourself playing a laboratory worker in
this virtual laboratory (interactive
video lectures).
Many
doctors continue to claim there is not sufficent proof of persistent
infection in "chronic Borreliosis / chronic Lyme disease" -
this can only be because the people who claim that has not read the
literature on by direct detection method proven persistent Borrelia
infection - to help find the articles and cases I long ago (first put
on Internet 2003) made a reference list Persistent
borreliosis / relapsing Borreliosis verified by direct detection
methods culture, microscopy, PCR:
http://lymerick.net/persistent-borreliosis.html
MK
noticed that some Bowen test project participants developed
neuroborreliosis / later relapsed and suffered from chronic/relapsing
Lyme borreliosis (verified by microscopy with DFA i.e. Direct
Fluorescent
Antibody
stain for Borrelia burgdorferi)
- despite they had had what is
normally considered to be "appropiate" early antibiotic
therapy for erythema migrans
-
and moreover confirmed relapses / progression of disease were seen,
both after penicillin and after doxycycline in officially recommended
doses!
Below
focus is set on some publications on European culture or PCR verified
LATE (> 3 month duration) cases / or relapses
- and DAKO
(OXOID) serology result!
-
which is of special interest to MK / danish patients, because the
DAKO test was developed in Statens Serum Institut (SSI), Copenhagen,
Denmark - by Hansen, Lebech and DAKO - and is still the ONLY test for
Borrelia in use in Denmark, however since 2006 under name OXOID
- read more about it in:
http://lymerick.net/2006-Oxoid-DAKO.html
Unfortunately danish microbiologist still refuse to to
microscopy (enhanced with acridin orange or specific direct immune
stain for Borrelia), culture nor will they do PCR for Borrelia, nor a
WB - despite new recombinant multi-antigenic, rather cheap WBs are
now available, where only the diagnostic relevant bands are selected,
i.e. the result is easy to read, creates less confusion, since most
selected bands on the test strip are Borrelia specific!
They
state they find these methods too laborious, too time consuming, too
expensive for the lab to run them - however these labs do NOT take
into consideration, what it costs the patient not to get diagnosed
and remain ill for years / lifetime from Borrelia infection, not take
into consideration what it can cost the danish health system - since
these patients go to many specialist, who must each evaluate the
chronic multi-organ-system symptomatic patients for a lot of diseases
that all come out negative/normal, because that is NOT diseases that
this patient have, nor was it very likely, judged by the history
pointing to Borrelia infection
- but doctors rather tend to do
"defensive medicine", i.e. do all the ROUTINE tests they
traditionally do on most of their patient to "outrule disease
within our field of medical speciality", and when they have done
that, the doctors feel they've done alle what they can / must do
"within their speciality", despite they have not helped the
patient to get well - none of them can't (or won't do) the test which
the tickbitten patient really need most of all, multiple tests for
tickborne infection, for immune dysfunction etc.!
- and they do
also not consider either how much it cost the danish social system,
when the long-term ill patients are way too sick to work, but can't
get a diagnosis / prognosis and must go on transfer income paid over
our taxes ...
The
laboratories that is paid by out tax money should SERVE the DOCTORS
and their patients with the BEST available tests on the marked, not
what they self developed long time ago, nor what they find is the
easiest for them to do!
WE
PATIENTS FIND IT A BIG WASTE OF OUR TAX MONEY THAT THEY ONLY WILL DO
A PROBLEMATIC ELISA SEROLOGY TEST FOR BORRELIA THAT WAS SHOWN (Oksi
1995) TO MISS NO LESS THAN 58,5% OF CULTURE OR PCR PROVEN LATE
CASES OF BORRELIA INFECTION, THAT IS BASED ON A SINGLE NON-SPECIFIC
ANTIGEN, FLAGELLIN, THAT 20 YEARS AGO (Picken
1992) WAS SHOWN TO VARY GENETICALLY ENOUGH TO BE ABLE
DIFFERENTIATE BETWEEN THREE EUROPEAN BORRELIA SUBSTRAINS ... gene
variability => antigen structure variability => antibody
structure variability! => a test based on flagella from ONE strain
of Borrelia, is probably less able to bind antibodies formed against
different strains of Borrelia? - pure logic could and should have
been applied byt the test producers already in 1992 and no later than
1995! - but instead of recognizing the problems with their test, they
chose to ignore literature speaking against their serology test!
Regarding Borrelia serology test I prefer using Line
immunoblot (either
Mikrogen og Euroimmun), because they are as highly specific as ELISAs
on the marked, but more SENSITIVE than any Borrelia ELISA on the
marked! - and is easy to do in the laboratory (run automatically
after reagent have been added to apparatus, is measured by computer -
little risk of human errors!
J
Clin Microbiol 1995 Sep; 33(9): 2260-4.
http://jcm.asm.org/cgi/reprint/33/9/2260.pdf
...
3 serology tests evaluated on 41 late (> 3 mdr.) culture or PCR
verified Borrelia cases
-
amongst them DAKO
/ OXOID
flagella ELISA came
out false serum antibody negative in 24/41 (58%) cases with symptoms
of Borreliosis for at least 3 months duration!
SSI
failed to repeat a similar study in Denmark on danish patients with
late culture confirmed Borreliosis and moreover IGNORE DISCUSSING /
REFERENCING THIS IMPORTANT STUDY IN THEIR "guidelines"
-
in DanInfekt we intend to try to examine OXOID serology in culture
verified chronic Borreliosis cases, and compare OXOID result with WB
....
Strle
et al. Clin Infect Dis. 2006 Sep 15;43(6):704-10.
http://www.journals.uchicago.edu/doi/pdf/10.1086/506936
...
in spinal fluid culture verified Borreliosis, 23 w/Borrelia garinii,
10 w/Borrelia afzelii
-
in the Borrelia afzelii neuroborreliosis group 9/10 tested negative
on DAKO/OXOID
neuroborreliosis
kit, hereof had
only two been sick for shorter than 6 months
-
i.e. 7/10 (70%) had
been sick for at least 6 months and up to seven years, with wrong or
no (?) diagnosis, and those CSF ELISA Borrelia index. neg. would not
have gotten the correct borreliosis diagnosis, if serology had been
the only test for Borrelia done (like would be the case in DK, where
microbiologist, SSI will NOT do culture nor PCR test for Borrelia on
chronic (seroneg.) patients!
Honegr
et al. Cent Eur J Public Health. 2004 Mar;12(1):6-11.
http://www1.szu.cz/svi/cejph/archiv/2004-1-02-full.pdf
...
IgG and IgM titres to the Lyme spirochete were determined by ELISA
using standard conditions as recommended by the supplier (Test-Line
Ltd, CR).
In
ELISA with sonicated antigens, a positive value was defined as 0.73
for IgG and 0.850 for IgM.
In
the IgM capture ELISA (The
98th percentile of absorbance values for the controls was used as the
cut-off level. Dako
Diagnostika GmbH),
a positive value was 0.380.
Compared IgG serology measures and which treatment failed first (from table 3 and 1), for IgM look at full text:
|
Patient’snumber |
First
treatment before |
IgG
ELISA |
IgG WB |
|
1 |
|
neg. / neg. |
pos. |
|
2 |
ROX / 4 |
neg. / neg. |
pos. |
|
3 |
DOX/ 7 |
neg. /neg. |
pos. |
|
4 |
|
pos. /pos. |
pos. |
|
5 |
DOX / 10 |
neg. /neg. |
neg. |
|
6 |
DOX / 12 |
neg. /pos. |
pos. |
|
7 |
|
pos. /neg. |
pos. |
|
8 |
|
pos. /neg. |
pos. |
|
9 |
|
neg. /neg. |
pos. |
|
10 |
|
neg. /neg. |
pos. |
|
11 |
DOX / 16 |
neg. /neg. |
pos. |
|
12 |
|
neg. /neg. |
pos. |
|
13 |
DOX / 9 |
pos. /pos. |
pos. |
|
14 |
|
pos. /pos. |
pos. |
|
15 |
|
neg. /neg. |
pos. |
|
16 |
|
neg. /neg. |
neg. |
|
17 |
DOX / 12 |
neg. /neg. |
pos. |
|
18 |
|
neg. /neg. |
pos. |
Regarding
CUT-OFF values confusion - just for comparison:
Dako
Glostrup cut-off
values, also used 98 percentile as cut-off level, but cut-off
level has changed over time, and apparently without scientific
justification, since
it seems no new validation study is searchable PubMed in between the
following article publication dates nor at a later date?!
Ann
Neurol. 1991 Aug;30(2):197-205. Cut-off for IgM:
0,300 vs. IgG:
0,160 (sent in for publ juli 25. 1990).
J
Clin Microbiol. 1992 Jul;30(7):1646-53 (PDF).
Cut-off for IgM:
0,500
vs. IgG:
0,160 (received Jan
1992) [IgM
cut-off increased with factor 1,6]
Neurology.
1993 Jan;43(1):169-75. Cut-off for IgM: 0,500 vs. IgG:
0,240 (received
Apr. 6, 1992) [IgG
cut-off increased with factor 1,5]
=>
Why / what justified the increase in cut-off values by
http://lymerick.net/2006-Oxoid-DAKO.html
in 1992?
Increased
cut-off value means the antibody level need to be ~1,5 times higher
in order for the patient get a positive Borrelia antibody test
result!
SICK
PEOPLE NEED A TEST THAT IS SENSITIVE ENOUGH (LOWER CUT-OFF) TO DETECT
THEIR LOW REACTION TO BORRELIA INFECTION, SO THEY CAN GET DIAGNOSED
AND GET ANTIBIOTIC TREATMENT!
Note that Honegr et al. - when looking at IgG - found
a discrepant / unexpected discrepant second
negative ELISA IgG results, when compared to WB!
-
a pos. WB but neg. 2nd ELISA IgG is marked with bold in table:
12/18
(2/3, 66%) were IgG ELISA neg. but were WB-IgG-positive,
and since they all had positive detection of Borreliae by either PCR
or IEM, it is the WB result that was the TRUE POSITIVE RESULT! - and
the neg. IgG ELISA was false negative result!
NOTE
that pt. #7 and #8 both developed negative IgG ELISA result, despite
they had positive IgG at first test, and despite positive WB!
-
like other cases on the persistent borreliosis reference list with by
direct method detected persistent borrelia infection post treatment,
at time of clinical and confirmed relapse!
NOTE
that 6 /18 (1/3, 33%) relapsed despite they were treated
before the first detection of Borrelia by IEM or PCR with doxycycline
...and one had roxithromycin, a drug earlier known to fail
(1992, PMID: 1357894)
- maybe this pt. was treated with roxithromycin before publication
since pts. were enrolled / detected between 1991-2000?
IMO
1/3 VERIFIABLE RELAPSES IS WAY TOO HIGH FIRST TREATMENT FAILURE RATE!
- so lets look at some probable reasons, why so many patients
relapse after doxycycline ...
Borrelia
has been detected by PCR very early - within the first 2 weeks after
the tickbite - in the central nervous system (CNS), i.e. before and
without later development of an erythema migrans:
http://lymerick.net/Bb-EarlySpread.htm
Therefore
it does not really make good common sense to treat erythema migrans
with drugs like peroral penicillin, that can not penetrate over
membranes into the CNS
- nor does it make sense to give a low
dose / shorter duration treatment for an EM, than what is recommended
for treatment of neuroborreliosis!
Thus
the Bulls-Eye rash, Erythema (chronicum) migrans (EM / ECM), is a
side-manifestation, that may sometimes occur, but it is not a
prerequisite, that EM must occur before Borrelia can spread into the
CNS and cause neuroborreliosis! - around half of patients later
diagnosed with neuroborreliosis never saw an EM rash!
Problem
is that treatment with a sub-inhibitory / sub-lethal dose / drug
concentration will not kill all Borrelia, but will select the most
resistant of the bugs, which later are those that cause the relapse,
and will need either another drug or a higher dose for the bugs to be
sensitive and be killed!
Therefore
a second antibiotic treatment with same drug and dose often does not
show as much clinical effect as the first treatment, unless using
other drugs with very good penetration to CNS, and/or if a much
higher dose is used!
Lack of a good response to
retreatment is often evaluated as if the chronic / relapsing symptoms
can not be caused by an ongoing Borrelia infection; however, when
searching for the microbes by direct method like microscopy we can
actually find the spirochetes again and again - as illustrated in
videos from different patients above - especially in patients that
has turned seronegative after the first treatment, since many or all
the antibodies they form, during a relapse with so many bacteria in
the blood stream that they can be detected by simple microscopy, are
quickly used up by binding in http://lymerick.net/Borrelia-IC.html
to all the circulating Borrelia antigens, which precipitate in
vessels, cause vascular damage and vasculitis with chronic
inflammatory cells, the micropathological Hallmark of Borreliosis
(and syphilis)! - elicit complement cascade, proinflammatory cytokine
response, like increased TNF-alfa ... it is the immune reaction that
cause the symptoms ...
Serology can detect early infection only
several weeks after aquiring the infection, when serial serology
tests confirm a positive seroconversion, and in late infection can
detect past exposure to Borrelia antigens or alike when positive
-
but since IgG serology can stay high for years in patients with
previous Lyme borreliosis (who do not have circulating antigen to
bind the antibodies) who became asymptomatic on given antibiotic
treatment, serology really has no use whatsoever in the diagnosis of
chronically ill patients of longer than 3-6 months disease
duration!
A negative serology test can not not outrule
Borrelia infection; pt. may be immune depressed or have so much
circulating antigen that all antibodies are bound in the patient so
nothing is measured by the test!
A positive serology can not
prove the patient have a currently active infection!
BUT
THE PATIENTS SYMPTOM DIARY WILL SHOW RELAPSE PATTERN CONSISTENT WITH
RECURRENT BORRELIA ACTIVITY
- and such patients should be
investigatede thoroughly, not be dismissed as if they are malingering
hypochondriacs!
CHRONICALLY
ILL PATIENTS WITH RECURRING SYMPTOMS OF BORRELIOSIS AFTER PREVIOUSLY
FAILED ANTIBIOTIC TREATMENT NEED ACCESS TO DIRECT BORRELIA DETECTION
METHODS LIKE MIKROSCOPY (w/specific immune stain if possible, but
Bb-antibodies are expensive to buy); CULTURE (cheap comparable to
serology), PCR (expensive 2-300€)!
Treatment
with (low dose) doxycyclin for Borrelia infection fails very often
(like in #45, #23, #1, #50 and
RM81 above!)
... the only patient above who did not relapse
after doxycycline was AP91, who was a child and therefore got
penicillin, not doxycycline, for her first EMs! - still she relapsed
despite penicillin in the usually recommended EM dose, not only for
the 10 days that is usually recommended here in Denmark, but for 6
weeks, as suggested by Burrascano!
- see the latest version of
his guidelines at http://www.ilads.org/lyme/treatment-guideline.php
More of 50
project participants relapsed despite early recommended treatment for
their EM !!!
- probably
because the usually recommended dosis of doxycycline 100 mg x 2 does
NOT REACH A CONCENTRATION OVER THE MINIMUM INHIBITORY CONCENTRATION
(MIC) IN CNS and other "remote areas"?!
-
since doxycycline distribute well in fatty tissues, especially fat
people 100-150 kg will have 2-3 times larger distribution volume of
the drug, hence will reach a lower tissue concentration on the same
dose that give sufficient concentration in the small 50 (-70) kg
person: http://kroun.ulmarweb.dk/doxycyclin-dosis.htm
(some text is in danish, but references and abstract is in english,
use Google translate!)
The
actually achieved steady
state concentration of doxycyclin was measured in spinal fluid
by Dotevall & Hagberg 1989
(PDF)
-
and they even used a lower MIC of only 0.6-0.7 micrograms/ml, where
others state that MIC for doxycycline for Borrelia is 1 or even 2
micrograms/ml!
Excerpt:
A
dose of 100 mg of doxycycline (Vibramycin; Pfizer Inc.) was taken
orally b.i.d. for 10 days by 10 patients, while 200 mg was taken
orally b.i.d. for 10 days by 12 patients. On days 5 through 8 of
treatment, CSF was collected 2 to 3 h after the last drug
administration. In one patient, an intraspinal catheter was inserted
for treatment of severe chronic pains, and repeated CSF samples were
taken through the catheter during the doxycycline treatment. On the
day of lumbar puncture, the patients were questioned regarding
adverse reactions to the drug. No other antibiotics were given
simultaneously. ...
Please note that NONE of the patients
on doxycycline 100 mg x 2 and even
some of the patients on 200 mg x 2, did NOT reach a concentration in
spinal fluid (CSF) over 1 microgram/ml
- which
many state is the MINIMUM INHIBITORY CONCENTRATION for doxycycline
for Borrelia!
Honegr. does not tell us dosis and
duration of the given treatments, however, if the patients - all got
the usually recommended DOXYCYCLINE dosis of 100 mg x 2 daily
-
IT CAN NOT REALLY COME AS A BIG SURPRISE TO ANYONE, THAT SO MANY OF
HONEGRs PATIENTS ON DOXYCYCLINE BEFORE THE FIRST BORRELIA ANTIGEN
DETECTION LATER DEVELOPED BY DIRECT DETECTION METHOD PROVEN
PERSISTING BORRELIA INFECTION HAD PROGRESSED TO NEUROBORRELIOSES!
WHO WAS
RESPONSIBLE FOR THE CHOICE? - AND WHY WAS A DOXYCYCLIN DOSIS OF
DOXYCYCLINE 100 mg x 2 chosen to be the recommended dose for
treatment of EM and for (early) neuroborreliosis
- when Dotevall
& Hagberg already in 1989 had showed by their experiment that 100
mg x 2 may not result in a concentration above 1 mg/ml in ANY
patient!?
-
who are NOWADAYS TO BE MADE RESPONSIBLE for continuing to maintain
the obviously bad advice of recommending too low doxycyclin dosis for
EM and neuroborreliosis?
WE
ALSO NEED TO CLEAR ANOTHER LONG TIME AGO DISPROVEN
MISUNDERSTANDING!
THERE
IS OFTEN NOT (as often stated in the media) ANY SAFE 24 HOUR PERIOD /
A DELAYED TRANSMISSION OF BORRELIA,
and TBE can be transmitted within ONE HOUR after tickbite started:
http://lymerick.net/Transmission-Bb-rate-time.htm
...
Strle
Clin Infect Dis 1996 Jul; 23(1): 61-5. PMID: 8816130
25
of 35 (71%) of patients who
remembered the duration of the infecting tickbite
got
a culture confirmed erythema migrans, despite less than 24 hour tick
attachment time!
9
of 35 (26%) even got infected with Borrelia via a tickbite of less
than 6 hours duration!
Around
1/3 of Ixodes ricinus ticks have been found to have a systemic
Borrelia infection and may thus have Borrelia in their saliva glands
all the time, and can thus transmit Borrelia immediately when they
begin spitting;
systemically infected female adult ticks may also have Borrelia in
their eggs, thus can transmit Borrelia to their larvae transovarially
/ vertically, i.e.
tick
larvae can be infective despite they have not yet had a blood meal!
Experts
who continue to inform people incorrectly / out-of -date, who does
not give a balanced review of all published literature so far on
subject tickborne infection to the public
- should be held
economically personally responsible for their actions
- by those
patients who do not remove the tick within 24 hours due to
misinformation, get infected and thereafter must suffer the
consequences, by developing debilitating disease
- because they
got bad/wrong information from the official sources, or who was
denied testing and treatment by ignorant doctors!
MY
ADVICE IS THEREFORE RATIONAL / LOGIC:
FIRST
OF ALL WE NEED TO AVOID TICK INFECTION by
informing people that SOME
TICKS CAN TRANSMIT BORRELIA IMMEDIATELY WHEN THEY BEGIN SPITTING IN
THE WOUND DIRECTLY INTO THE CAPILLARY THE TICK SUCK BLOOD FROM
- i.e. tickborne infections
are probably spread hematogenously right from start of the
tickbite!
- see the nice tick bite pictures and animation at
LDA-UK website:
http://www.lymediseaseaction.org.uk/image/tick_animation.htm
...
Animation:
http://www.lymediseaseaction.org.uk/images/kullancs/kullancs01.avi
THEREFORE
IN CASE OF TICK EXPOSURE / RISK OF TICKBITE, DO TICK CHECK VERY OFTEN
AND PULL OFF THOSE TICKS IMMIDIATELY with
fine branched tweezers or a special TICK REMOVAL EQUIPMENT / SAFECARD
- after photographing the tick in situ with date on the picture
as documentation for the bite!
- after marking the bite site,
so you can look out for development of a growing red rash / erythema
migrans.
Only
this way can all tickborne infections and disease from these agents
be totally prevented, the person will not need tests, nor treatment,
will not have sick days etc.!
IN
CASE OF A TICK BITE MEASURE
C3A & C4A COMPLEMENT SPLIT PRODUCTS ...
- since the split products from complement activation may
increase within 96 hours after a tickbite in patients that developed
signs of Borrelia infection / seroconversion ...
Borrelia
serology will NOT become positive so early in Borrelia infection,
unless the patient got reinfected with Borrelia and had memory immune
cells that can raise a very quick serology response!
The
Complement system is the first line and innate unspecific immune
defense reaction raised in infection, but
note increased split products does not tell for sure which infection
/ inflammatory proces activated the complement cascade! HOWEVER
IT MAKES GOOD SENSE TO ME TO TREAT PATIENTS WITH RECENT TICKBITE AND
INCREASED COMPLEMENT SPLIT PRODUCTS WITH ANTIBIOTICS, BECAUSE EARLY
BORRELIA INFECTION CAN BE CURED BY SUFFICIENT ANTIBIOTIC TREATMENT!
- while chronic borrelia infection > 3 months and of many
years duration is very hard to cure, meaning the patient can improve
very much while staying on antibiotic treatment and may even become
asymptomatic, but relapses are common after stopping the treatment! -
because dormant cysts can not be hit, since the microbial metabolic
processes with which antibiotics interfere are not active during
dormancy!
TREAT
EARLY LYME BORRELIOSIS / ERYTHEMA MIGRANS AS YOU WOULD TREAT EARLY
NEUROBORRELIOSIS!
-
then eventual few Borrelia that might have reached CNS / CSF already
may be killed also and those killed effectively, will not grow into
many under a sublethal antibiotic concentration, that select the most
resistant bacteria!
Undertreatment is worse than no antibiotic
treatment, because treatment removes antigens from the blood stream
(less immune stimulation) without clearing all the most "remote
areas" for bacteria, i.e. undertreatment will both switch off
the maturation of the immune response and will select the most
antibiotic resistant microbes from the surviving population
especially in "remote areas", from which new growth may
arise under favourable growth conditions, if the patients immune
system is not able to suppress growth, without help from antibiotics!
DURATION
OF TREATMENT MUST BE OPENENDED, the goal is to cure the patient!
Be aware that Borrelia
grows very slowly and may have very long dormant periods where
they can not be hit by antibiotics, until they enter growth phase
again, perhaps at long intervals (often as monthly relapses) ...
IN
CASE THE PATIENT RELAPSE AFTER ANTIBIOTIC TREATMENT AND DISPLAYS
RECURRENT RELAPSE PATTERN IN SYMPTOM DIARY
-
USE THE SYMPTOMDIARY TO DECIDE WHEN IS THE BEST TIME TO DO DIRECT
DETECTION METHODS FOR BORRELIA, FIRST
OF ALL USE THE MICROSCOPE
...
it is both fast and cheap, if you do it yourself ... you have a
probable diagnosis when you see the first spirochete swimming!
-
and if the blood looks perfectly normal in a microscopy done during a
symptomatic period, you should rather seek for another diagnostic
explanation for the patients symptoms, than an active Borrelia
infection! - and in that case you do not need to waste more energy,
time and money on doing the more difficult / more expensive test
methods for Borrelia!
Note in the old days detecting
spirochetes by microscopy in a syphilic person combined with the
clinical picture was enough for a tentative diagnosis of syphilis and
was enough justification for the doctor to treat the patient with
antibiotics! - why is that not so today also for Borrelia, when we
can detect spirochetes in the blood?
FOLLOW
THE PATIENT DURING TREATMENT WITH SYMPTOM DIARY AND REPEATED
MICROSCOPIES!
-
at least always re-examine the blood before intention to pause
antibiotic treatment!
Don't pause the treatment if the blood
look abnormal during ACTIVE PHASE (day one of a new relapse)!
If
no relapses are visible for 6 weeks in the diary and the blood also
looks very clean, pause antibiotic treatment under surveillance!
-
i.e. THE PATIENT SHOULD CONTINUE THE SYMPTOM DIARY for at least 3
months after stopping treatment; because an early relapse will show
as re-beginning flare cyclicity (usually weekly) and the symptom
score will gradually increase along as more and more spirochetes are
born, make toxins, are being killed, produce waste products, elicit
cytokines etc. ...
- then re-examine the blood and re-treat if
finding spirochetes again and related structures!
For
advice on treatment read Burrascano's guidelines at ILADS, he's got
experience since mid 1980ies from more than 10000 Borrelia patients,
and he published guidelines for 20 years, and he know this infection
better than most ... because he's had borrelia infection himself,
like myself!
Finally, getting Borrelia infected yourself
and having to find out how to diagnose and treat the tickborne
infection(s), because you get rejected by illiterate and ignorant
doctors
- is the very best teacher!
YOU are very
wellcome to get some of my blood infused (#1), if you - after seeing
the videomicroscopies and read this - continue to maintain your
stance that Borrelia is very easy to cure, since - if you are right -
you have nothing to fear by doing this experiment!
Doctors did
successful transfer experiments, including on themselves, of
the skin changes since known to be caused by Lyme Borrelia species -
erythema migrans (EM), lymphadenomatosis benigna cutis (LABC),
acrodermatitis chronic atrophicans (ACA) - after penicillin treatment
had proven very helpful since 1946; for selected historic "milestone"
references, see my Borrelia history lecture: Hull
2001; Kassel
2006.
IF YOU WON'T ACCEPT MY BLOOD OFFER, BECAUSE YOU
FIND THE SPIROCHETES IN MY BLOOD DISGUSTING, think again!
...
read, learn, look in the microscope, revise your stance and treatment
policy!
PLENTY
OF EXAMPLES ARE PRESENTED HEREIN OF PERSISTENCE OF VIABLE SPIROCHETES
INSIDE THE HOST
-
THAT RE-ENTER THE BLOOD STREAM LATER, A WHILE OR SOMETIMES YEARS
AFTER STOPPING ANTIBIOTIC TREATMENT
- WELL DOCUMENTED RELAPSING
BORRELIOSIS CASES in LONG TERM FOLLOW-UP ..
- this document
beyond any reasonable doubt that we need better DIRECT DETECTION
METHODS (culture like Advanced Labs in USA now offer) because
serology test fails in 50+% of these cases, are week and fluctuating,
often only weak positive after 2-3 months treatment has gunned the
spirochete form down, so no antigen enters serum / CSF and bind
nearly all the antibodies in immune complexes and thus remove them
from measure with antibody test (no matter which antibody test, but
depending on where cut-off is set), plus immune inhibititory factors
...
It could seem depressing, hopeless, BUT DON'T DESPAIR
- THERE IS NOW MORE HOPE OF A CURE - THAN EVER BEFORE
- because
we have learned so much about what do not work and some of what
works, but there is probably much more we need to learn :)
Research
done by Eva Sapi's Lyme research group at New Haven (in co-work with
Dr. Alan MacDonald)
has shown for certain, documented by microscopy pictures, how
Borrelia
burgdorferi,
besides the spirochete form and long known alternative cystic and
granular / round forms (100 years pictorial PDF
of spirochetes and alternative forms!), which can actually be seen
both in light and dark field microscopy (see 1951-DeLamater below),
also can form BIOFILM
communities under
adverse conditions for the spirochete form, plus antigen variation,
plus coating surface with host factors etc. etc. - all the smart
tricks the spirochetes can do!
In a very elegant culture - live
microscopy study, using BacLight
fluorescent viability stains marking
alive,
cell wall intact, bacteria green and
dead,
cell wall defect, bacteria red,
they investigated the effects on the 3 different forms of Borrelia,
of two herbal antimicrobials Samento
(TOA free cats claw) and
Banderol
- that had shown very
promising effect in Horowitz test of the Lee
Cowden protocol (presented at ILADS 2007 and later, ILADS-EU
conf. in Augsburg 2011) .. compared with Doxycycline.
The work
was published in Townsendletter (July 2010):
http://www.townsendletter.com/July2010/sapi0710.html
They found that both
Samento and Banderol, and especially when both were used together,
could hit not only the free spirochete form, the cystic / round
forms, but also the forms hiding behind biofilm,
while DOXYCYCLINE
only had effect on the spirochete form, and forced Borrelia into
producing many more cystic / round body forms,
than did both Samento and Banderol!
These findings can
readily explain, why so many patients relapse after conventional
antimicrobial treatment courses - even after long term treatment -
with for instance doxycycline alone - all examples herein except for
AP91, who never got doxycycline, because of the observed failure rate
- she had rather long fairly good periods after metronidazole plus
azithromycin for 6-12 weeks, BUT SHE RELAPSE in autumn every other
year!
We already know from previous studies by several other
researcher that other antimicrobials also only has effect on the
spirochete form, but produce more cyst / round forms, that later come
back with a vengeance, after stopping the antimicrobial treatment! -
we are awaiting further treatment study with the Cowden
protocol!
Richard Horowitz, MD in New York State has found the
Cowden Support Program to be effective in markedly improving the
condition of 70-80% of the advanced Lyme Borreliosis patients with
co-infections over 4 to 6 months time, even if the patients had
previously failed to improve on multiple courses of antibiotics. Dr.
Horowitz presented the findings of his use of the Cowden Support
Program in a fairly large group of his patients with Lyme Borreliosis
& co-infections at the ILADS conference in the fall of 2007.
One
danish patient I know and have followed for over 10 years now, was
very near to death just a few years ago, but has returned to a much
better life now on treatment by Lee Cowden :)
The best is that
the herbal remedies are relatively non-toxic and well tolerated for
long term treatment (6 months); hundreds of years of experience from
traditional treatment in South America Indians show it is safer than
the safest antibiotics, BUT THEY CREATE A HERX, and dose must be
started low and increased gradually, as all other drugs that works
for Borrelia!
Effects
of all other antimicrobial drugs for Borrelia as well as for other
microbes, should be studied in the same way!
Perhaps
combine with (some of) Klinghardts
advice, depending on which additional problems the chronic patient
has ...
The
Klinghardt Protocol (based on over 900 successful treatment
cases)
The treatment of Lyme disease requires 4
distinctive steps:
Decreasing toxic body burden/unloading the system
Improving disturbed physiology
Decreasing microbial count
Immunemodulation
Decreasing
toxic body burden/unloading the system
Sleep
Low EMF (turn off all fuses, sleep sanctuary, turquoise light/photon wave to increase melatonin and non-rem Delta sleep)
Non-toxic/allergenic bedding material (cave: flame retardants/PBDEs)
Avoid light/noise pollution at night
Klinghardt
Biological Treatment of Lyme Disease
Herbs
Used in Treating Lyme Disease
Klinghardt
Neurotoxin Elimination Protocol
I HAVE NOT PERSONALLY
TRIED ANY OF THE MENTIONED ALTERNATIVE / NATURAL TREATMENT PROTOCOLS
YET!
The patient
group I follow in DanInfekt is way too small, and not homogenous
enough, to be able to conduct true science studies on treatment
comparison!
- can only be a few more or less succesful case
reports - so I do not study treatment options, but DIRECT DETECTION
METHODS.
I have been waiting to see studies, like the one done
by dr. Eva Sapi's group, that convincingly document the effect of the
natural remedies Samento and Banderol on spirochetes and alternative
forms and biofilm - when tested in the laboratory.
I have
awaited to hear results of larger ongoing clinical treatment trials,
conducted by Dr. Horowitz and others. FIGURES, CALCULATIONS, PEER
REVIEW PUBLISHED.
I have awaited to hear personal good stories
from people I have known personally long before; it was just few
months ago, that I got the first very promising report from a danish
case on the Cowden protocol
- a movie is underways, enjoy ...
All treatment should be started as early as possible
after start of a relapse, to see if the duration of the relapse can
be abrogated compared to what the patients previous experience with
duration of relapse is, of course documented by symptomdiary; if
treatment is not started until severel months into a relapse, near to
usual spontaneous improvement, the positive effect observed may have
not resulted from the treatment, but was the natural course, a
spontaneus remission occurred ... THEREFORE patient need do the diary
and observe themselves long enough to know their patterns and can
tell the difference under treatment ...
The relapsing remitting
course of borrelia and their very slow reproduction, make it
difficult to evaluate treatment in an optimally constructed science
study.
BEFORE any trial treatment, ACTUAL INFECTION MUST FIRST
BE DOCUMENTED IN THE PATIENTS MATERIAL BY DIRECT MICROBE DETECTION
METHODS!
... if we can catch and culture the spirochetes
reliably by improving our techniques as illustrated herein (which is
not new, but copycat many other researchers descriptions! - the
findings are consistent!)
- then we can use Sapi's method to
test the actual microbe that the individual patient harbor for
antimicrobial susceptibility - and can tailor the treatment better to
what has a chance to work in that particular patient! - just like it
is routine in most other microbe infections ..
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