Quite devastating because I had my hopes set hig, as in completely being cured one day.

He also mentioned that they (who is they?) had done a test with one mouse and one person and that the tests were sucessful and in both cases had lead to a real cure. This is interesting - has anybody heard more about this development?

Ciao,

my LLMD said a similar thing.
he said he'd finish up with 6 months of herbs to help boost my immune system, but not to expect a 100% cure.

I think they also said that to cover their own arses.

there are things I can live with (mild joint pain) and other things i can't (severe headaches)

That sounds really odd - usually with work on mice you use 20 or 200, not one.

Still, find out more if you can. If you can get a reference to any written source, I can interpret it - I've been studying bio/medicine all day every day for many months. (And I can access all journals.)

Manipulating the immune system is a fascinating idea, and sometimes I agree its the best way to a radical cure if indeed there is a way. The trouble with applying this idea to lyme is that no one can say at what point the immune system is failing - largely because no one can visually locate very significant numbers of the bacteria. This may be because of inadequate awareness of non-spirochetal forms. To the best of my knowledge, no one properly aware of the latter has searched for borrelia in human tissue.

Still, the i sys doesnt know the genome of Bb, and I do - well I havent memorized it yet but I can look it up. If only there were some way this knowledge could somehow help the i sys.

There are ~1400 distinct human pathogens, at least according to some paper I read, and most or all are probably able to dupe the i sys using some molecular machinery or other. Genomic and molecular science can probably reveal these devices in many cases. Targeting them with designed drugs might produce powerful therapies.

It could be that everyone has some level of Bb inside of them. At least with myself and my two son's, onset of major symptoms began with another major infection. I think it is the combination of things that we are exposed to including toxins, in and outside of the body and poor nutritional health along with alergies that causes the immune system to break down, and allows bacteria like Bb to take over.

It might actually be possible to rid yourself of Bb and still have your immune system out of balance. I know one doctor that thinks it is HHV-6 that is a major cause of CFIDS and Fibromyalgia.

Down the road, all of the diseases that we now consider auto-immune, including diabities and a good portion of autism will all be linked an immune deficency. So in a nutshell, a total cure will involve some modification to the immune system.

In my case, I got several long speeches about herbs, acceptance, you'll be disabled for years so don't question anything, blah blah. Then I begged for babesia and bartonella treatment. Two sets of "hopeless" symptoms are now disappearing, though they could return in the future.

There are always new abx coming out, and new combinations being tried. If you did nothing except try a new abx every month, you could probably go for a couple of years before you ran out of options.

Unfortunately, the abx that best hits my Lyme is also physically intolerable: minocycline.

Take a look at Dr. B's 2004 treatment guidelines. He is going in the direction of stronger abx and new abx combinations. You can choose whichever treatment works for you, but be aware that the one you described above is not universally embraced, and that the person who started all this, Dr. B, has a different approach.

One possibility is that we have heavy infestation of Bb inside cells, and persons with asymptomatic infection merely have some spirochetes wandering around their blood. The reason for the difference in the type of infection? Could have to do with both the host and the borrelia. We are all biochemically different - but so are strains bacteria such as Bb. A huge percentage of humans carry Heliobacter pylori in their stomachs without symptoms. In those that do have symptoms, the H. pylori usually have a big clump of genes known as a "pathogenicity island." Its the same species, but a whole different ballgame.

But all that is just a possibility. It could also be that we sickies have the same kinda infection with the same strains as asymptomatic infected humans (and asymptomatic infected white footed mice, etc) have. In this case it could be that we react much more to the organism - possibly also with cross-reaction to our own tissues (ie, autoimmunity). Personally I think this scenario is less likely.

I dont think there is necessarily any explanation for lyme such as diet, pollution, etc, tho there may be. It could also be that the time for it has just simply come. That happened with syphilis, which wasnt known til about 1500 (in Europe anyway). Every disease has to start sometime.

Recent studies from a NY Lyme conference have shown bb is a virulent and crafty pathogen able to swap DNA and trick the immune system.

The Structure of the Lyme Bacteria

The structure of the Lyme spirochete is unlike any other bacteria that has
ever been studied before. It is one of the largest of the spirochetes (0.25
microns x 50 microns) It is as long, as a fine human hair is thick. Borrelia
burgdorferi is a highly motile bacteria, it can swim extremely efficiently
through both blood and tissue because of internal propulsion. It is
propelled by an internal arrangement of flagella, bundled together, that
runs the length of the bacteria from tip to tip. Like other Borrelia
bacteria Borrelia burgdorferi has a three layer cell wall which helps
determine the spiral shape of the bacteria. What makes this bacteria
different from other species, is that it also has a clear gel-like coat of
glyco-proteins which surround the bacteria. This extra layer is sometimes
called the Slime Layer or S-layer. (See diagram 1) (45,46,59)

This means: This extra layer of glyco-proteins may act like a stealthy coat
of armor that protects and hides the bacteria from the immune system. The
human immune system uses proteins that are on the surface of the bacteria as
markers, and sends attacking antibodies and killer T-cells to those markers,
called outer surface protein antigens (OSP antigens). This nearly invisible
layer is rarely seen in washed cultures, but can be seen regularly in tissue
biopsies.(46)

The Lyme bacteria is different from other bacteria in its arrangement of
DNA. Most bacteria have distinct chromosomes that are found floating around
inside the cytoplasm. When the bacteria starts to divide and split in two,
the chromosomes divide and the new copies of the chromosomes enter the new
cell. The arrangement of DNA within Borrelia burgdorferi is radically
different. It is arranged along the inside of the inner membrane. It looks
something like a net embedded just underneath the skin of the bacteria. (46)

This means: We really don't understand the mechanisms of how Bb regulates
its genetic material during its division.

Another unique feature to Borrelia burgdorferi are Blebs. This bacteria
replicates specific genes, and inserts them into its own cell wall, and then
pinches off that part of its cell membrane, and sends the bleb into the
host. Why it does this we don't know. But we do know that these blebs can
irritate our immune system. Dr. Claude Garon of Rocky Mountain Laboratories
has shown that there is a precise mechanism that regulates the ratio of the
different types of blebs that are shed. (46) In other bacteria the
appearance of blebs often means the bacteria can share genetic information
between themselves. We don't know if this is possible with Borrelia species.
There have been reports of a granular form of Borrelia, which can grow to
full size spirochetes, and reproduce. These granules are so small that they
can be filtered and separated from live adult spirochetes by means of a
micro-pore filter. (Stealth Pathogens Lida Mattman Ph.D. 66)

The division time of Borrelia burgdorferi is very long. Most other pathogens
such as Streptococcus, or Staphylococcus, only take 20 minutes to double,
the doubling time of Borrelia burgdorferi is usually estimated to be 12-24
hours. Since most antibiotics are cell wall agent inhibitors, they can only
kill bacteria when the bacteria begins to divide and form new cell
wall.(35,59-62)

This means: Since most antibiotics can only kill bacteria when they are
dividing, a slow doubling time means less lethal exposure to antibiotics.
Most bacteria are killed in 10-14 days of antibiotic. To get the same amount
of lethal exposure during new cell wall formation of a Lyme spirochete, the
antibiotic would have to be present 24 hours a day for 1 year and six
months! Note: Antibiotics kill bacteria by binding to the bacteria's
ribosomes, and interrupting the formation of cell wall proteins.

Like other spirochetes, such as those that cause Syphilis, the Lyme
spirochete can remain in the human body for years in a non-metabolic state.
It is essentially in suspended animation, and since it does not metabolize
in this state, antibiotics are not absorbed or effective. When the
conditions are right, those bacteria that survive, can seed back into the
blood stream and initiate a relapse. (59-62,70)

This means: Just because a person is symptom free for long lengths of time
doesn't mean they aren't infected. It may be a matter of time. Whereas viral
infections often impart a lifelong immunity, Lyme, like other bacterial
infections, does not retain active immunity for long periods of time. People
are often reinfected with Lyme. (96)

How does the Lyme bacteria travel from the bloodstream to other tissues?
While we have known for a long time that the Lyme spirochete can show up in
the brain, eyes, joints, skin, spleen, liver, GI tract, bladder, and other
organs, we didn't understand the mechanism by which it could travel through
capillaries and cell membranes. (Abstract 644) Then Dr. Mark Klempner
presented at the 1996 LDF International Lyme Conference an interesting paper
that gave us part of the answer.

Many researchers have observed that the Lyme spirochete attaches to the
human cells' tip first. It then wiggles and squirms until it enters the
cell. What Dr. Klempner showed was that when the spirochete attached to the
human host cell, it caused that cell to release digestive enzymes that would
dissolve the cell, and allow the spirochete to go wherever it pleases. This
is very economical to the bacteria to use our own cell's enzymes against us,
because it does not need to carry the genes and enzymes around when it
travels. Dr. Klempner also showed that the spirochete could enter cells such
as the human fibroblast cell (The skin cell that makes scar tissue.) and
hide. Here the pathogen was protected from the immune system, and could
thrive without assault. More importantly, when these Bb-fibroblast cultures
were incubated with 10 x the MIC for IV Rocephin, two thirds of the cultures
still yielded live spirochetes after two weeks, and in later experiments for
more than 30 days. If we can't kill it in a test tube at these high
concentrations in four weeks, how can we hope to kill it in the human body?
(22,48,79,80,)

This means: The infection can enter the tissue that is optimal for its
survival, and it may evade the immune system and antibiotics by hiding
inside certain types of cells.

Another interesting observation about this bacteria is how it interacts with
our body's immune system; Dr. David Dorward of Rocky Mountain Labs made a
video tape of how Borrelia burgdorferi acts when surrounded by B-cells. (The
type of white blood cell that makes antibody.) The spirochete attached tip
first, entered the B lymphocyte, multiplied and ruptured the cell. It
repeated this process for three days until the B-cells were able to come to
an equilibrium. A matter of concern was that some of the spirochetes were
able to strip away part of the B-cell's membrane, and wear it like a cloak.
(Dorward, Hulinska 1994 LDF Conference Vancouver BC)

This means: If this spirochete is evolved enough to attack our
B-lymphocytes, then it may also be evolved in other ways that we do not yet
understand. It is for certain that its ability to kill B-lymphocytes evolved
as part of a defense mechanism to evade its own destruction. The observation
that it can use the B-cell's own membrane as camouflage indicates that it
may be able to go undetected by our immune system. The way our immune system
is supposed to work is that it recognizes foreign invaders as being
different from self, and attacks the infection.

Unfortunately, the immune system sometimes attacks our own cells. This is
called autoimmune disease. If a foreign invader has a chemical structure
similar to our own tissue antigens, our bodies sometimes make antibodies
against our own tissues. In people with Lyme disease scientists have
discovered auto-antibodies against our own tissues including nerve cells
(axons), cardiolipid, myelin (also seen in MS), myelin basic protein (also
seen in MS), and neurons (brain cells) (23,28,38-40,43,45,56,57,60,88)

When the immune system finds a foreign invader, it tags that invader in a
number of ways. A cell called the macrophage can engulf the bacteria, and
then communicate to other immune cells the exact description of the
bacteria. Another cell might mark the cell with antibody which attracts
killer T-cells. Some types of T-cells communicate to other cells what to
attack, and regulate the immune assault. But sometimes the body can produce
a type of antibody that doesn't attack or help. A blocking antibody will
attach and coat the intruder, but it won't fix compliment, and it shields
the bacteria from further immune recognition. In Lyme we have seen
quantities of IgG4 blocking antibody such as is seen in some parasitic
infections. (Tom Schwann RML 92 LDF Conference) *Note: Compliment is a term
used for a series of 18 + digestive proteins that are only activated by
signals from our immune system, such as compliment fixing antibodies.

In order for the immune system to make an attacking antibody, the immune
system must first find an antigen which it can attack. Unfortunately, as
seen by freeze fracture electron microscope, photographs of the Lyme
bacteria show that most of the antigens are on the inside of the inner
membrane, and not on the outside. (60) This makes the bacteria less visible
to the immune system and more difficult to attack. The most intriguing fact
about Borrelia spirochetes is their well documented ability to change the
shape of their surface antigens when they are attacked by the human immune
system. When this occurs, it takes several weeks for the immune system to
produce new antibodies. During this time the infection continues to divide
and hide. (1,47,63,66)

It appears that Borrelia are able to change their surface antigens many
times, and can do it quickly. In one study by Dr. Andrew Pachner MD, he
infected mice with a single strain of Borrelia burgdorferi. After several
weeks, he was able to isolate two slightly different forms of the bacteria.
The bacteria from the bloodstream was attacked and killed by the mouse's
immune sera, but the bacteria isolated from the mouse's brain was unaffected
by the immune sera. The bacteria isolated from the mouse's brain had a new
set of surface antigens. It appears that contact with the CNS caused the
bacteria to change its appearance. Since the brain is isolated from the
immune system and is an immune privileged site, the bacteria became its own
separate strain. (47,97)

This means: Infections of the bloodstream may be different from the
infections that are sequestered in the brain. While we continue to have
active immunity in the bloodstream, the brain has no immune defenses except
for circulating antibodies. So, if those circulating antibodies are
ineffective to attack the bacteria in the brain, then the brain is left
without any defenses, and the infection goes unabated.

Over 100 references, abstracts and diagrams are inserted into the text to
support the statements in this chapter.

Another peculiar observation of these bacteria is seen inside the bacteria.
When the genetic control mechanisms of this bacteria are inhibited with
antibiotics known as DNA Gyrase Inhibitors (ciprofloxin) the bacteria start
to produce bacterio-phage. A phage is a virus that specifically attacks
bacteria. In this case there are two distinct forms. This means the Lyme
bacteria at one time were attacked by viruses. It was able to suppress them,
but the DNA to make the phage is still incorporated within the DNA of the
bacteria. Perhaps activation of this phage could one day be beneficial to
treating chronic Lyme patients? (JTBD 94)

What happens when the infection gets to the brain? In the case of Lyme
disease, every animal model to date shows that the Lyme spirochete can go
from the site of the bite to the brain in just a few days. (41,60, abstract
644) While we know these bacteria can break down individual cell membranes
and capillaries, its entrance into the brain is too pronounced for such a
localized effect. When the Lyme bacteria enters the human body, we react by
producing several immune regulatory substances known as cytokines and
lymphokines. Several of these act in concert to break down the blood brain
barrier. (E.g. Il-6, Tumor Necrosis Factor-alpha, Il-1, Transforming Growth
Factor-beta etc.) In addition to affecting the blood brain barrier, these
cytokines can make us feel ill, and give us fevers. (54,60,) (JID 1996:173,
Jan)

Since the brain has no immune system, it prevents infection by limiting what
can enter the brain. The capillary bed that surrounds the brain is so tight
that not even white blood cells are allowed to enter. Many drugs can't enter
either, making treatment of the brain especially hard. For the first ten
days of a Lyme infection, the blood brain barrier is virtually nonexistent.
This not only allows the Lyme bacteria to get in, but also immune cells that
can cause inflammation of the brain. (41) *Note: The breakdown of Bb was
shown to occur by tagging WBCs, albumin, and other substances known not to
cross the BBB with radioactive Iodine. The CSF was tested, and then the
animals were infected with Bb. Then the CSF was tested everyday for several
weeks. The result: No cross over of Iodine in the control group, 100%
crossover in the infected group for 10 days. The infection had the same
result as injecting the radioactive iodine directly into the brain. (60)

When the human brain becomes inflamed, cells called macrophages respond by
releasing a neuro-toxin called quinolinic acid. This toxin is also elevated
in Parkinson's Disease, MS, ALS, and is responsible for the dementia that
occurs in AIDS patients. What quinolinic acid does is stimulate neurons to
repeatedly depolarize. This eventually causes the neurons to demyelinate and
die. People with elevated quinolinic acid have short-term memory problems.
(27,29-37,40-42,74,75, 82-84,87-90)

This means: If we think of all of our brain cells like telephone lines, we
can visualize the problem. If all of the lines coming in are busy, we can't
learn anything. If all of the lines going out are busy, we can't recall any
memories. Our thinking process becomes impaired.

A second impairment to clear thinking that Lymies experience is the
restriction of proper circulation within the blood vessels inside the brain.
Using an instrument called the Single Photon Emission Computer Tomography
scanner (SPECT scans), we are able to visualize the blood flow throughout
the human brain in 3-D detail. What was seen in the brains of chronic
neurological Lyme patients was an abnormal "swiss-cheese" pattern of blood
flow. The cortical, or thinking region of the brain, was being deprived of
good circulation; the occipital (eyesight) regions had an increase flow.
This could help explain why most Lyme patients complain of poor
concentration and overly sensitive eyes. (91)