your opinion?

[Guest guest]

I was doing a search on Dr. Lida Mattman and found this info on Lyme Alliance,

in one of their newsletters online. Makes perfectly good sense to me. If this is

a possibility of getting better test results, we need to find out which

researchers oppose this and make a stand. Just my opinion If this comes

across as an attachment to some, this is the URL:

http://lymealliance.org/html/december.html

And this URL has info about antibiotic treatment for Arthritis, but some info

about Lyme on the page. This also is about Dr. Mattman.

http://rheumatic.org/faq.htm

Donna

Notes and Observations on Cell Wall Deficient Forms

Written by Tom Grier

Observations concerning a lecture by Dr. Lida Mattman, Ph. D., at the Michigan

Lyme Disease Symposium in Detroit, Michigan, on October 18, 1997.

Wouldn't it be nice if, when you're on safari and you're charged by a man-eating

lion, you knew your gun was loaded with live ammo instead of blanks? I'd like to

feel that way when I think about antibiotic treatment of Lyme disease. But what

if we're just shooting blanks? At a recent Lyme disease conference in Detroit,

Michigan, that fear of shooting blanks became palpable when I listened to Dr.

Lida Mattman,

PhD. speak about cell wall deficient forms (CWD) of bacterial pathogens,

specifically B. burgdorferi, the cause of Lyme disease. Dr. Lida Mattman, a

professor emeritus from Wayne State University, has been studying spirochetes

for over fifty years. She was a protege of the great Steiner, who was

the first to establish, in a series of papers going back to 1918, that multiple

sclerosis was associated in many cases with a spirochete. Since her association

with Steiner, Lida Mattman has had a continued interest in spirochetes, but for

the last seven years she has focused the bulk of her attentions on cell wall

deficient forms.

This area of microbiology has long been neglected, and we are now paying a price

for that neglect. Dr. Mattman's work suggests that cell wall deficient forms

are prevalent, and pathogenic. Cell wall deficient forms of a mycobacterium may

be the cause of sarcoidosis. Other diseases, such as Crohn's disease, coronary

thrombosis, Kaposi's sarcoma, endocarditis, and MS may all involve cell wall

deficient bacteria. What were once thought of as anomalies and nonpathogenic are

now proving to be insidious, deadly, and nearly invisible. Hence the name of her

textbook, Stealth Pathogens. (CRC Press) What are cell wall deficient bacteria?

First, let's review some basic microbiology.

For decades, students have been taught that there are three main types of

bacteria: rods, spheres, and spirals. These shapes were maintained by a rigid

cell wall that added structural integrity to the bacteria. Since human cells

don't have cell walls, a good way to kill bacteria was to interrupt cell wall

synthesis, because this would kill the bacteria, but not harm the human host.

This is the basis of most bactericidal antibiotics, like cephalosporins

(Rocephin, Suprax, Ceftin, Claforan) and penicillins (amoxicillin,

ampicillin...). The problem is, what happens if there is no bacterial cell wall

to inhibit?

When a bacteria like a spirochete loses its cell wall, it becomes incapable of

holding it spiral shape. It becomes a sphere surrounded by a thin semi-permeable

membrane. This round sphere is like the evil counter part to the classical

spiral form. Why evil? Well, when the bacteria sheds its cell wall, it also

sheds several proteins that are markers to the human immune system. In other

words, the immune system has trouble finding and recognizing this new form of

the bacteria. It's almost like a criminal using disguises to change identities

after each crime.

Only this disguise is also bullet proof, because, without a cell wall,

antibiotics like Rocephin are useless.

What is also intriguing is the fact that these cell wall deficient forms (also

known as L-forms) can be seen from time to time as reverting back to the

classical form. This means the Lyme spirochete appears to be capable of turning

off the genes that create cell walls when it is convenient to do so, and then

the CWD form can then produce the classical spiral form when it needs to. * Does

the bacteria do this to avoid antibiotic therapy? Probably not. It might be an

evolved mechanism to dodge the mammalian immune systems, but it is doubtful it

has specifically evolved a defense mechanism against antibiotics. Survival

against antibiotics just happens to be a consequence of this particular

evolutionary morphologic development. This appears to be borne out by some work

done over sixty

years ago on syphilis patients by Warthin and Olson.

It was found that, as you sectioned a blood vessel of a syphilis patient, you

found a progression from the classical spiral form to what appears to be the

L-forms. As you entered the vessel wall and continued to enter other tissues,

the shape of the spirochete gradually changed from a spiral to a sphere. This

means that the Lyme spirochete may also favor one form over another, depending

on what tissue it is in at the time. This evolutionary strategy makes a lot of

sense. If it can survive better in the tissues in a CWD form, then the

infection can continue even if its classical spiral counterpart is wiped out and

eliminated from the blood stream. In the end, the death of one form of the

bacteria is meaningless if the infection is ultimately maintained somewhere else

in the host in its

alternative form.

Dr. Mattman said she frequently isolates L-forms from Lyme patients with

aseptic meningitis and endocarditis. How is this done? Traditional culture media

is virtually worthless, as are traditional heat - fixed blood smears. The

answer is, in many cases, a simple technique that is rarely used any more in

labs. A live wet mount is prepared using the patient's blood or buffy coat. This

is a simple procedure, where the blood sample is placed on a wet slide with

acrodine orange dye to stain the nucleic acids. Then a nonoclonal antibody

fluorescent stain that is specific for Borrelia burgdorferi is added. Then the

slide is examined under a microscope. Although this is a simple procedure that

most labs could easily do; it is not being done. Why? Simply because most labs

have no real

understanding of CWD forms.

There are some scientists who oppose the idea that CWD forms are the cause of

persistent infections. They assert that if CWD forms exist, why can't we detect

them by PCR? Even in absence of cell wall, these bacteria still have to contain

DNA. Yet no published studies exist that compare PCR-DNA amplification results

to CWD culturing techniques. Although culturing has long since been the gold

standard in proof of infection, there seems to be a standard in proof of

infection, there seems to be a double standard when accepting culturing as proof

when it comes to CWD forms. Unfortunately, both PCR and L-form culture

techniques are in their infancy, and are far from perfected or standardized.

Dr. Mattman also has a greater success with culturing the classical forms than

most other researchers that I have met. Mostly, this is due to her fifty years

of experience with spirochetes, but it also has to do with economics. Dr.

Mattman is a researcher, and as such, the priority of her lab is not to make

money, but to produce data. As a result, Dr. Mattman mixes her own culture

media, which is considerably different from the commercially available medias.

Since modern hospital labs have long since stopped mixing their own medias, the

only medias which are ever used are those which are commercially marketed to

the labs through medical suppliers. Since Dr. Mattman's media is not

commercially available, labs will never have the success rate at culturing

spirochetes that they should.

Labs are in the business of making money, and mixing up media is too hard, too

time consuming, and too costly. If it isn't on the shelf, it's being used!

More than likely Dr. Mattman's culture media will one day be commercially

available, but its success has always depended on a couple of freshly made

components, so bringing it to market isn't as easy as it sounds. Although there

are better culture medias out there to detect Lyme disease than the commercially

available preparations, it is the commercial availability of the other media

that wins the day. Thus, modified media and BSK-II are the current

standards for culturing the Lyme spirochete.

Treatment: What doe this new information on CWD Borrelia mean to chronic Lyme

patients? A medical advisor to Dr. Mattman, Dr. Philips, MD, suggested

that when a patient's therapy with a bactericidal antibiotic hits a plateau, it

might be time to switch to a different regimen of protein inhibitors, such as

the combination of doxycycline and Biaxin. These also appear to be the drugs of

choice when a patient presents with symptoms of multiple sclerosis. These drugs

do not depend on cell division and disruption of cell wall synthesis to kill the

bacteria. Instead, they affect bacterial metabolism through inhibition of

protein synthesis.

Dr. Mattman made it very clear that a second spirochete has been implicated in

causing MS. Her old mentor, Dr. Steiner, first isolated spirochetes from

MS lesions in 1918, and today the continuation of that work is being pursued by

at least three researchers. The suspected organism has been tentatively dubbed

Spirochaeta myelophthora.

Since multiple sclerosis is a collection of symptoms of an unknown cause, it is

possible that more than one cause will eventually be found. One undeniable fact

is that many Lyme patients have been previously diagnosed as having MS. Perhaps

Dr. Mattman's continued work will someday make that tragedy a rare occurrence!

Are CWD forms responsible for persistent chronic Lyme disease and negative

tests? The possibility is quite real, but the answers will not be forth coming

until more labs agree to test for CWD forms. For this to happen, the benefits of

doing tests for CWD forms as a means to save money in patient care must become

apparent. The cost effectiveness of routinely using this type of laboratory test

would most certainly benefit both patients and health insurers. Development of

a test that can be used by commercial laboratories is the next step.