Monday, March 21, 2011

18 1993 Senate Testimony On Lyme Disease, Part 2

In Part 1, 1993 Senate testimony on Lyme disease given by Dr. Joe Burrascano was posted for review. In this part, various excerpts from Steere, other researchers, and others on the Senate committee will be reviewed with comments and questions.

As much as I know the Lyme patient community disdains Steere, and as much as I consider his March 2010 slideshow disrespectful of patients, there are a few places in this testimony where I found myself actually shaking my head in agreement with what he said back in 1993.

See what you think...

Alan Steere said:

"Research is certainly needed to improve laboratory tests
for Lyme disease, particularly for the development of tests
that detect the spirochete or its genes or antigens directly. 
However, improved laboratory tests will not by themselves
solve the problem of Lyme disease diagnosis. I believe that
clinical judgment will always be necessary."

I agree with him there.

Senator Dodd. Just let me get an answer to this,
and I'd be glad to. 

Do you think we ought to spend money on it?

Dr. Steere. Yes, absolutely. I think that Lyme disease is a great 
problem, and I think studies of it, particularly basic mechanisms 
of the disease, are of great importance. And I think that's what is 
most likely to help.

Again, I agree with this. Let's look at some more testimony and exchange with the senators...

Senator Metzenbaum. Thank you, Mr. Chairman. I have a cou- 
ple questions. 

Dr. Steere, I gather that the diagnosis of Lyme disease is not 
that fully developed that the physicians around the country really 
know enough about it or know enough about how to make the diag- 
nosis. Is that the thrust of what you are saying? 

Dr. Steere. I think that there are objective clinical criteria. I 
also think that it is possible to have laboratory tests that can help 
support that diagnosis. But nationwide, there is no standardization 
of that type of testing. 

There is certainly a great need for education, including education 
of physicians, about what this disease is and what it is like. And 
certainly, further research is needed to define that even more. 

Senator Metzenbaum. I remember when one of our fellow Mem- 
bers of Congress was diagnosed as having Lyme disease, Berkeley 
Bidell, a fine member of this body, and he resigned — or stepped out 
and didn't run for re-election; I guess he didn't actually resign — be- 
cause he thought he had Lyme disease, and subsequently found he 
did not. 

I get the feeling that across this broad United States, if you go 
to see Dr. Steere or one of these other gentlemen here, that you 
probably can get an accurate answer, but that there is a reasonable 
chance that if you go to many other doctors in the country — and 
this is not a broad-brush condemnation of them — but that it is not 
easily diagnosed and not easily diagnosed even after laboratory 
tests, unless the laboratories are particularly prepared for this kind 
of diagnosis. 

Now, am I misinterpreting what you are saying? 

Dr. Steere. No. I think that is absolutely true and very well-
stated.

Senator Metzenbaum. So therefore we have the problem of how 
we get the education out and how we get the diagnosis out. 

Now with respect to the treatment, you mentioned two particular 
products that can be used— I forget what they were; I'm sure you 
know what they are — with oral 

Dr. Steere. Oral therapy with doxycycline, a tetracycline type of 
antibiotic, and amoxicillin, a penicillin type of antibiotic. 

Senator Metzenbaum. And how effective is that? 

Dr. Steere. Well, I think for nonneurologic manifestations of the 
disease, they are quite effective. Neurologic manifestations of the 
disease are harder to treat, and how best to treat them is still 
being worked out.

Italics emphasis mine.

I think everything italicized is something that is important to note... The same problems Steere mentioned back in 1993 are the same problems the Lyme patient community is facing today.

I don't agree with Steere on everything, but I do think what he said back then is still true today.

Does anyone know how standardized today's testing is?

I think more studies of the basic mechanism of the disease would help a lot - quite possibly the most, too.

How much of our tax money has gone towards basic science research on pathogenesis and study of the spirochete versus other research? This is something a lot of people are asking, and not just me.

The other points Steere mentioned - that more first-line doctors such as primary care physicians need to be better educated to diagnose and treat early Lyme disease and that how best to treat neurological Lyme disease needs to be worked out - both of those are issues which I think still haven't been adequately addressed in the 18 years since he stated them.

There is other testimony there about serological testing and exchanges with Burrascano I'm not going to get into right now, some of which I disagree with Steere based on what research I've read thus far. These particular passages have been discussed in the Lyme patient community before, so I'm going to move on to other testimony by others...

Dr. BURRASCANO. The second point I wanted to address was the 
Simplification of the treatment ot Lyme disease Many patients who 
have been diagnosed after the disease has been present for more 
than just a short period of time, those who have had the illness for 
several months to several years before diagnosis, very often are not 
returned back to normal with antibiotic therapy as we know it 
today. 

One of the problems is that we don't know why people remain 
ill. We pretty much recognize that a lot of people will remain ill 
after Short courses of antibiotic therapy when they have late 
disseminated Lyme disease. The controversy which I tried to address 
today in my testimony is that we don't know why. 

There is an establishment of physicians university based who 
claim that the 30 days of treatment cures the patients; anything 
that is leftover has to be some arthritic phenomenon or some- 
thing they don't knew what it is and they send the patients off 
to a chronic fatigue clinic or to a fibromyalgia clinic. Yet there have 
now been many, many studies showing that these people still have 
the infection. 

So apparently, the infection can persist and evade the effects of 
antibiotics, and the presence of the organism somehow drives this 
reaction to keep the people sick. 

I have here an electron micrograph, a photograph of the spiro- 
chete, done by the NIH's lab at Rocky Mountain. This was taken 
from the urine of a patient who remained ill after one and a half 
years of antibiotics. This spirochete was identified positively as B. 
burgdorferi, the causative agent for Lyme disease. So in this one 
patient — and again, there are patients that you might see in the 
audience or who have testified today who are in a similar situa- 
tion — for them, the antibiotic therapy did not work. 

So what I am saying is that we need to focus our research on 
the real world of Lyme disease. No. 1, diagnosis is not simple or 
clear; the diagnostic test is not 100 percent. We need better testing. 
No. 2, treatment strategies as you might find in New England 
Journal articles are very basic minimums and do not cover the 
more chronic patients or those who are more seriously ill, and 
these chronic patients are not now being studied systematically for 
infection, and they should be."

Is evidence of a spirochete found in urine at the NIH's lab considered a significant finding? Why or why not?

Is evidence of Bb DNA found in a sample significant - why or why not?

In the discussion of findings from various research publications, it's been stated that finding bacterial DNA is not evidence of current infection. Finding a live, whole organism can be, though.

Here's some excerpts from Dr. Joe McDade... introduction included so you know who he is:

STATEMENTS OF DR. JOSEPH McDADE, ASSOCIATE DIRECTOR 
OF LABORATORY SCIENCE, NATIONAL CENTER FOR INFEC- 
TIOUS DISEASES, CENTERS FOR DISEASE CONTROL AND 
PREVENTION, ATLANTA, GA; AND JOHN R. LAMONTAGNE, DI- 
RECTOR, DIVISION OF MICROBIOLOGY AND INFECTIOUS 
DISEASES, NATIONAL INSTITUTE OF ALLERGY AND INFEC- 
TIOUS DISEASES, NATIONAL INSTITUTES OF HEALTH, BE- 
THESDA,MD 

[...]
Dr. McDade. I certainly will do that. I think that the most im- 
portant problem that we have is a lack of recognition of Lyme dis- 
ease by the average physician. A recent CDC study in a north- 
eastern State showed that 82 percent of the cases of Lyme disease 
were reported by 7 percent of the physicians. 

Now, there are different ways of interpreting this data, but this 
was from a State in which Lyme disease is broadly endemic, and 
what that suggests is 

Senator Dodd. Which State are we talking about? 

Dr. McDade. Connecticut. 

Senator Dodd. I was afraid of that. [Laughter.] There are a lot 
of States in the Northeast, and so I was hoping 

Dr. McDade. It is not meant at all as an indictment of Connecti- 
cut. It probably reflects the situation nationwide, which is that ei- 
ther people are not reporting Lyme disease, or they aren't recogniz- 
ing it. And if they are not recognizing it, and they are not treating 
it early — and you have heard adequate testimony to this point — we 
have a serious problem. 

So to my mind, the physician awareness and education of the 
professionals is a key critical component, one that we have been 
working on and that needs a lot more attention. 

The second problem is one of diagnosis. This has been adequately 
documented and today, in testimony from a number of panelists, 
and clearly what it amounts to is a need for increased standardiza- 
tion and there is a need for increased research. CDC has been 
working in the last several months with the Association of State 
and Territorial Public Health Laboratory Directors to standardize 
some of the existing methodology, and that is currently under eval- 
uation. 

So, sounds like the same things that Burrascano and Steere said were a problem are problem in McDade's eyes, too.

To my readers in Connecticut: Do you have any research and evidence that reflects improvement in how many Connecticut doctors are accurately diagnosing and treating Lyme disease in the present and last few years?

I hope it has improved since 1993. That rate cited above - 7%? Sucks.

Dr. McDade. [...] But I think the point is that every- 
one recognizes that there are some deficiencies in the diagnostic 
criteria. The point is where do we go from here. I think there are 
in fact two different kinds of deficiencies. One is the lack of stand- 
ardization in evaluation of the existing methodologies. As I indi- 
cated, we have been working with the Association of State and Ter- 
ritorial Laboratory Directors to standardize what we have so that 
we can at least look uniformly across the States. 

Clearly, there are also many other things that are on the horizon 
that are being studied both by CDC intramurally, our extramural 
program, the NIH extramural program, which offer a lot of better 
alternatives. 

What wasn't perhaps said in some detail, without going into de- 
tails of the science, is that we are dealing with a very worthy ad- 
versary in B. burgdorferi. There are multiple strains of this orga- 
nism; it undergoes antigenic variation, and any diagnostic test that 
you have is going to be fraught with some difficulties. So this is not 
an easy problem, and everyone who is doing research on this recog- 
nizes these problems and is working toward them. But clearly, 
what we need to do is to employ our best efforts to try to find out 
which ones are there and which ones work in a real life situation. 

Here is where I wish McDade would have gone, actually - into details of the science behind B. burgdorferi. He is saying difference in strain and antigenic variation are an issue; that diagnostic tests are fraught with difficulties. I wish he would have gotten into more specifics here.

Senator Metzenbaum. Doctor, can I ask you, has CDC done any- 
thing about notifying the doctors of this country what to look for 
with respect to Lyme disease and what kind of testing is suggested 
in order to deal with it? 

I get the feeling that some doctors know about this, but there are 
a hell of a lot of doctors out there who don't know anything about 
it and just sort of push along. Am I wrong about that? Are you pro- 
viding information, or what is the fact? 

Dr. McDade. I think education is coming from a variety of 
sources, as was indicated earlier. For education of children, one of 
our cooperative agreements with the Lyme Disease Foundation — 
they have reached millions of people. Also, I can provide for the 
record if you like a list of the extramural funding; there are some 
half dozen various projects that are targeted directly or indirectly 
toward physician education. That is not to mention the general lit- 
erature, three or four articles published weekly by our Morbidity 
and Mortality Weekly Report, that address various issues, be they 
clinical, epidemiologic, prevention and control. 

There are a number of different approaches that are used. But 
as I'm sure you well can realize, any message that you might try 
to deliver, be it in the commercial sector, private sector, education- 
ally, or in medical, it is sometimes very difficult to reach 100 per- 
cent of the population, and it becomes more costly as you try to get 
100 percent awareness. 

Senator Metzenbaum. What I understand you to say is that doc- 
tors can find this information in a lot of places — in the journals and 
the medical literature — but that the Centers for Disease Control it- 
self has really — I think all of those hit a certain portion of the doc- 
tors of the country — but it seems to me that the CDC, without 
spending a fantastic amount of money, could do a much more effec- 
tive job of really getting to all the doctors in the country. 

Dr. McDade. We certainly don't at all think, Senator, that what 
we have done is enough, and we will continue to look at other ap- 
proaches and other venues in order to try to leverage resources to 
be able to reach the people maximally. I think that's about the 
most general way that I can State it. 

We are very aware not only of what we have done, but more 
aware of what we have not done. 

That sounds a lot like admitting that more could have been done when it wasn't, doesn't it?

Senator Metzenbaum. As I sit here, I get the feeling that this 
is a very challenging kind of illness or disease, but the fact is there 
is much more that can be done about it than we can do about a 
number of other illnesses, whether it is cancer or some other dis- 
ease of that kind. And what is bothering me is that I just have the 
feeling that there is a gap where the physicians in the field are 
really not up-to-speed as to diagnosis and treatment. And I think 
Dr. Steere pretty much confirmed that. And I think CDC is the 
agency to which we in Congress would look to ask, don't you have 
a greater responsibility than that which you are presently doing. 

Dr. McDade. I can say that your statement is entirely accurate, 
and CDC would love to have the opportunity to meet that chal- 
lenge.

Testimony immediately after this section goes on to discuss the recommendation that Dr. McDade request more funding from the gov't for the CDC to address this issue... Need to follow up to see exactly what happened after this, and where the funding was applied.

It seems to me that the exact same issues that concerned people in 1993 are still with us.

And now, onto Mr. LaMontagne's testimony...

[...]
Mr. LaMontagne. Lyme disease is now thought to be the most 
commonly reported arthropod-borne disease in the United States — it is 
certainly the most common tick-borne infection in the United States. 
The disease, caused by the spirochete B. burgdorferi, is transmitted 
primarily by ticks of the genus Ixodes. Lyme disease may be 
acute or self-limited or may develop into a chronic multisystem 
disease that can elicit a wide and unpredictable range of clinical 
manifestations. Current diagnostic tests, which are based on the 
detection of antibodies to B. burgdorferi, are useful, but far 
from perfect since individuals may vary widely in their immunological
response to infection, thus limiting the value of blood test 
results In the diagnostic process. 

As indicated, Lyme disease does not have a predictable clinical 
presentation or progression of symptoms. Most persons infected 
with B. burgdorferi respond to infection with strong immune 
responses, whereas others show no sign of infection in 
their blood. The organism also is very difficult and in some 
cases impossible to detect in infected individuals. Many published
descriptions indicate that the hallmark of Lyme disease is an
expanding red rash, known as erythema migrans, that may 
be accompanied by various other clinical signs and symptoms. 
Infected individuals actually present a highly variable array
of signs and symptoms, such as joint pain and nerve problems, 
that may be easily confused with those of other diseases. The 
ambiguities inherent in interpreting the results of blood tests 
for Lyme disease added to these nonspecific symptoms have led
to problems with both over- and under-diagnosis of the disease.

NIAID currently conducts and supports several projects
aimed at meeting the challenges of Lyme disease. Institute
goals for this area of research include: 

Improve our understanding of the immune response of infected 
individuals to B. burgdorferi. 

Improve our understanding of the biology and surface 
variation of B. burgdorferi. 

Develop tissue culture models of Lyme disease. 

Develop animal models of Lyme disease. 

Identify and characterize virulence factors and 
antigenic determinants of B. burgdorferi. 

Develop improved diagnostic and therapeutic strategies. 

Develop an effective human vaccine. 

Study the host range of B. burgdorferi in potential 
vector (transmitter) and reservoir (carrier) species. 

Study the biology and ecology of vector and 
reservoir species. 

Develop strategies for the control of Lyme disease 
transmission among reservoir species and to humans. 

I would like to take this opportunity to highlight for 
you recent advances made in our intramural and 
extramural programs and to briefly outline our research 
plans for the near future.

NIAID Intramural Research Program

INTRAMURAL RESEARCH ADVANCES 

Several NIAID scientists conduct Lyme disease research 
studies at the RML. Highlights of some of their recent 
efforts are summarized below. 

Scientists at RML have developed a highly sensitive 
and specific method to detect B. burgdorferi infection.
The assay works well with samples of urine, cerebrospinal fluid,
blood, and synovial fluid. Because the assay detects 
components of the infecting spirochetes rather than
immune responses to it, if it can be developed commercially,
the assay may prove useful for monitoring treatment
effectiveness as well.

A major stumbling block to developing diagnostic 
tests or a vaccine for Lyme disease is the elusive 
nature of the spirochete. The organism appears to evade the
immune system of the host by changing its surface proteins. 
NIAID scientists are studying changes in genes encoding 
two major outer membrane proteins of the spirochete. The 
studies may provide insights into the surface proteins of not only 
B.burgdorferi but also other borrelia organisms as well. 

NIAID'S researchers have genetically characterized samples
of Lyme disease bacteria taken from many patients in Europe, 
Asia, and North America. Based on genetic relatedness, the 
scientists have identified at least three distinct groups
of borreliae that can cause Lyme disease. The frequency
with which different Lyme disease symptoms occurs is 
known to vary in different geographic areas. The sci- 
entists have begun examining how the genetic distinctions 
within each group relate to clinical features of Lyme disease.

NIAID research recently showed that antibodies to 
a specific protein of the spirochete, p39, are produced 
only in response to an active B. burgdorferi infection 
and therefore can serve as reliable markers for Lyme disease. 
Using this observation, the researchers have developed 
three p39-based blood test kits that can help distinguish 
patients with Lyme disease from those with other disorders.

These kits have been approved by the Food and Drug Administration 
and are currently available to doctors, clinics, and 
hospitals nationwide. 

Scientists at the RML have demonstrated a characteristic of B. 
burgdorferi that may explain its ability to cluster in low 
numbers at the site of infection and yet cause a variety of 
reactions at other sites in the body. B. burgdorferi cells
release pouches or "blebs" from their surface that become distributed
widely throughout the body, unleashing a variety of immune system 
and tissue responses that may result in the diverse symptoms
seen in Lyme disease patients.

Coumermycin Al is an antibiotic that inhibits the enzyme
that catalyzes the coiling of DNA molecules and is required 
for bacterial replication and growth. Since the Lyme disease
spirochete has coiled molecules, NIAID investigators tested
the activity of this antibiotic on B. burgdorferi. They
found the Lyme disease spirochete to be 100 times more 
sensitive than other bacteria to this compound.

Although coumermycin Al or similar drugs are not ready
to be tested in humans, this research indicates that such
drugs should be investigated and developed further as 
potential therapies for human Lyme disease.

FUTURE PLANS 

The following future plans will be emphasized by NIAID
intramural scientists: 

Improve the sensitivity of the blood test kits and 
other available diagnostic tools. 

Continue studies of the variation and biological effect of 
Borrelial surface proteins with the goal of developing
an effective vaccine. 

Examine the attachment and penetration of spirochetes into
human cells as a possible mechanism of maintaining 
chronic infection. 

Examine the role of ticks in the maintenance and delivery
of the pathogen.

I realize that 18 years ago is a while ago, but what happened to some of this research?

Does anyone reading this know which assay they were talking about above, and if it was abandoned because of the previously stated idea that the presence of spirochetal DNA does not indicate the presence of current infection?

Is the evidence of a living spirochete the only indication of active infection? It seems there has been some argument in the literature between whether or not a small number of intact spirochetes can cause an infection and this hasn't been completely resolved. It definitely seems that serological testing isn't enough for some people.

From what is known today, there are more strains being found in different geographic locations than previously thought, with some vectors being birds - and also a greater number of disease-causing genotypes being found through Dr. Ben Lutz's studies... There's more work to be done there and it's ongoing.

How much research has the RML conducted on these pouches or bleb forms since then?

According to Tom Grier, "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."

He also wrote, "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)"

If these blebs are no longer considered significant, when did that change in opinion take place? Why don't we hear more about them today?

Why isn't Coumermycin Al being used to treat Lyme disease patients today, if Bb was considered 100 times more sensitive to this compound than any other bacteria?

Coumermycin is antibiotic derived from the bacteria, Streptomyces. Coumermycin, along with Novobiocin/Albamycin (Pharmacia And Upjohn), and Clorobiocin belong to a class of antibiotics known as aminocoumarins.

Years ago, Novobicin was removed from the market - this article from the 1970's indicates that 1 out of 5 people who used Panalba, an antibiotic made of Novobicin and Tetracycline combined, had allergic reactions to it and there were 12 fatalities recorded. So its use was discontinued.

Research on drugs that are aminocoumarins - and more specifically, DNA gyrase inhibitors - continues. So far, no treatment for patients with Lyme disease has come out of it.

In terms of that last bit - future plans of the NIAID scientists? I think they have done a lot of work on the second and fourth items, and some work on the first item, but really not much work on the third item at all.

I may be wrong, but that's my observation so far based on my own survey of the research done in, say, the past decade or so. I'd be glad to have someone point me towards more research on spirochetal attachment and penetration of human cells and chronic infection in general.

Those who are of a more conspiratorial bent may automatically point out that oversight of this item is deliberate. It may just be that with budgets not keeping pace with inflation and the fluctuating funds available, research teams decided to follow what was more profitable - vaccine and test kit development.

Or maybe researchers didn't even have a choice in what to research, and someone else decided where the funding was going for them - regardless of their own priorities and interests.

I understand the limits limited funding places on researchers - but I'd hope that if at some point one drops one of their goals, they can pick it up later.

What happened here? Why do so many physicians continue to miss diagnosis and treatment of early Lyme disease - is it lack of education, still, or is it that the clinical presentation is confounding so it's easy to miss even with education?

Have serological tests been standardized - and I don't mean in a Dearborn convention sense, which is its own separate and special issue - but for those tests which are outside of speciality labs, does there continue to be a wide range of result returns across the board?

What new antibiotic development has been undertaken? Funding has been present for more vaccine development, but requests for more new antibiotic development - even amid resistance concerns - were thwarted this past fiscal year.

There's a lot of questions I have to ask... if anyone else has followed the longer term arc of what I've mentioned above, please post your comments.

18 comments:

  1. Shit, reading all this just makes me depressed.

    If I was cognizant in 1993 (and not a one-year-old baby), I would have been totally psyched and optimistic about the future of Lyme disease treatment. Now, looking back on this, it's hard not to wonder where everything went wrong.

    ReplyDelete
  2. Anonymous,

    Sorry, it was not my intent to depress you or anyone. Many Lyme disease patients often mention Dr. Burrascano's testimony, and when I originally got infected with Lyme disease, I couldn't find a copy of his 1993 testimony online anywhere.

    I finally found at copy, and also got a hard copy. Reading the entire thing is a bit of an eye opener, so I decided to post at least some passages which caught my eye... Other passages may catch yours.

    And this is one part of why I posted it: Where did everything go wrong? What exactly happened?

    Steere was never the best physician or diagnostician when he began, according to others.

    I read Polly Murray's 'The Widening Circle', which is about her story and her part in discovering Lyme disease. When she shared her research data with Steere, Steere at that time was nice to her - polite and not dismissive of her research. Not the person he is made out to be today.

    He did seem to oddly get hooked on the idea that Lyme disease was caused by a virus, initially - and he also seemed to gloss over Ms. Murray's descriptions of the more serious symptoms of the condition even then.

    No reason known why - and others in his department and coworkers of his back then *did* acknowledge the more serious symptoms she'd reported in herself, her family, and others in Lyme and Old Lyme.

    But the thing to point out is that back when Ms. Murray worked with Steere, at the time he was actually the first person who really cared about her research and listened to her. She had seen many doctors prior to that, and they were either sympathetic but clueless and threw their hands up - or they told her to see a psychiatrist and some said she was a hypochondriac.

    This is all in Murray's book, if you find it hard to believe - get a copy and check it out yourself.

    The situation is 180 degrees in the opposite direction now. Steere's own comments and presentations - which can be found with some searching on Google - have shown much disdain for patients. It's demeaning to people who are suffering and it is unprofessional. (I know there are people who would say worse, but I've said no ad hominem attacks here and I apply this, too.)

    Something happened. I don't know if the 1993 Senate hearing was the flashpoint for more changes to come - it seems it played some role here. Prior to that, though, Burrascano points out the problems Lyme patients are all too familiar with today.

    My concern is that things haven't really changed enough for the better, and to a degree, observing what *did* happen could be key in figuring out what not to do and what *to* do next.

    ReplyDelete
  3. "My concern is that things haven't really changed enough for the better, and to a degree, observing what *did* happen could be key in figuring out what not to do and what *to* do next."

    Yes, in total accordance here.

    I really wonder what happened with Steere and why he changed his viewpoint so drastically.

    It's funny because in the parts of his testimony you posted earlier, I agree with pretty much everything he said. He was very cordial and admitted that the clinical manifestations of LD can vary greatly, and that more research was warranted.

    If someone has a Delorean and a flux capacitor laying around, maybe we can get 1993 Steere back?

    ReplyDelete
  4. This is invaluable, Camp Other! Thank you as I was not aware of this Congressional discussion and I found it just the opposite of depressing. Instead, I found it very heartening. It's really good to know that people working on our dime care about this and understand the issues at hand.

    I think the problems lie in several areas. I am not a doctor, so this is just my personal observation and my own opinion:

    A) The old model of diagnosing based on tests alone may need to die out. Perhaps the Lyme epidemic is what will shake the paradigm and change medical practice, in the future, to be more oriented to symptoms than to tests alone, or to both combined into one picture. As awful as our current situation may be, perhaps we can say thank you to the disease for promising this new medical horizon, at least in the future. Thinking optimistically, I can see this coming and hope this illness is the great teacher to medicine, world-wide.

    B) I also wondered about the coumermycin. Immediately I asked myself the question:

    Given its obvious exquisite impacts on the lyme, what are the side effects?

    If the lyme responds so beautifully to it, and given how strong herx's are with medications that don't "hit" the spirochete as brilliantly as this medication, could it be that it died out because the herx reactions were simply too strong? Could it be that the side effect profile with the drug (beyond what I am *assuming* as a *layperson* would be strong herx's) have been such that it could not be approved for marketing?

    I don't know and am just thinking out loud.

    C) I still come back to the conclusion that to enhance the body's own immune activity may be a key part of the answer, and one which can change the face of medicine if we learn from this. If the spirochete continually changes form to antigenic stimulation, then the body's own *varied* (key word) immune cells, cytokines, and other immune actions would be necessary for properly dealing with the bug.

    And if infections inhibit immunity, then to bring the immune system back into balance (not over-active, not under-active) would be key to getting rid of so tricky an infection as one that changes form.

    D) I suggest that part of what could have happened is the power of special influences. Look at how Congress is supporting the health insurance industry with bills requiring us to buy it or be penalized. Obviously the health insurance industry has power as a lobby. Therefore, it is possible that they had some influence in making sure that the inquiry from the CDC and Congress did not advance. It's just not convenient for them to foot the bill.

    Call me a conspiracy theorist but the sad truth is that the reality bears this out. The insurance co's are constantly denying people care, and I will repeat that this is a criminal matter at stake. This is deliberation and not mere neglect. There comes a point that if we say "Conspiracy theory" then we are (unwittingly, of course) protecting the wrong doers, even if that was never our intent.

    Just my thoughts.
    Thanks again, this was very heartening and valuable.

    Chiquita Incognita

    ReplyDelete
  5. Another question I have:

    What does standardizing of a test mean? What is the criterion? It would be interesting to find out more about this and see what the CDC has to say about it.

    Sometimes certification can be helpful and indicative, and sometimes it is just a piece of paper.

    Einstein flunked math in highschool, and there are many with certification who don't do their job so well, just as there are many with certification who do incredibly well. It's all as good as the people behind it and the standards that are being held.

    More information from the CDC about this would be interesting.

    CI

    ReplyDelete
  6. Anonymous,

    Steere seemed to be attentive and not dismissive to Polly Murray when he interviewed her, but from what understand it was a matter of degree. As much as he valued Ms. Murray's input, he repeatedly glossed over her reports of neurological symptoms and became fixed on rheumatological or arthritic ones.

    He seemed very intent at the time to prove his own (then incorrect) assertions were right, such as Lyme disease was caused by a virus (corrected once Burgdorfer found the spirochetes) and continued to maintain from early on that Lyme disease didn't require antibiotic treatment (when the Naval Medical Center in Groton was treating people with the EM rash with antibiotics and finding it helped them - even though they weren't sure what it was until they talked to a Danish researcher who told them about Borreliosis back in Europe).

    Was it a sense of stubbornness that drove Steere to stick to his virus idea? Was it because he was young and new to the field then, and he wanted to prove to himself he could discover something unique? Could be. But I'm not qualified to do a psychological profile on Steere, so it is all speculation.

    A lot of what I know about Steere in his younger days is through others' writings, so not knowing the man, I can't really say how much he did change. He at least didn't seem to have a negative attitude or negative characterization of patients - that came later.

    During the 1993 Senate testimony, he did indicate that he thought seronegative Lyme occurred, but very rarely, and he said a few other things that Burrascano disagreed with. So while Steere and Burrascano and the CDC staff and others may have been on the same page with some things at that time - they were not on the same page with everything.

    I don't know if we want the 1993 Steere back, but I do know there are some things I wish I could go back and change about how Lyme disease was dealt with by the government, medicine, and the media then.

    I suspect Steere would be a different man now if history unfolded another way. We'll never know.

    I think at this point, getting back on track with more research would really help, and to focus on having an independent committee free of conflict of interest from either side of the Lyme debate to sort things out would be good. How to pull that off? Good question...

    I think you can buy a fake flux capacitor online. EBay must be selling them. Don't know about the Delorean yet. Either way, we don't have the technology to get them to work for real so we'll have to use them to make 'Back to the Future IV' or something...

    ReplyDelete
  7. Hi Camp Other
    Thank you for this very helpful post! I did not find it depressing, on the contrary, I found it very hope-inspiring. It truly is good to know that there are those in Congress who are concerned and who "get it". That's comforting.

    A) What struck me about this testimony was the thought that the spirochetes may inspire medicine for the future to diagnose based on more than the test alone. As awful as our current situation is, and I don't want to understate that, I also think we can look hope-filled toward the future, realizing that this disease may shake the paradigm in medicine and transform it to something more all-inclusive, of testing and symptoms together, or even symptoms alone. GOOD! Doctors need to "hear" their patients more, not diagnose them based on formats and on paper, alone.

    B)If coumermycin hits the spirochetes so exquisitely, then my immediate thought of course was how exciting this is. The other thoughts:

    Wouldn't herx's be awfully powerful? If current meds cause herxing as strongly as they do without hitting the spirochetes as powerfully as this medication is claimed to do, then could it be that the (what I am assuming, as layperson, would be a very powerfully strong) herx profile is what had the medication laid to rest?

    And what are the other side-effects? COuld that have something to do with its demise too? I don't know of course.

    C)If the spirochetes change form, then what it seems to me is part of the solution (as I have mentioned previously) is to balance immunity. IE we don't want the immune system over-active and we don't want it under-active. If balanced, then the various forms the immune system takes----varied types of immune cells, cytokines, other immune cells and substances----can better tackle the transforming beast, I would think.

    I know at the present it is said the bug hides away from the immune system. I am not a doctor so all I can do is ask questions out loud. Could this be, in part, because of the fact that immunity is compromised in the presence of infection?

    Further, a specialist in environmental illness told me years ago, that only a weakened immune system will tolerate the presence of infections for the long-term. So even while the infection inhibits the immune system, it also wouldn't be able to remain there if immunity wasn't low to begin with. This was at least this particular specialist's opinion, and professional opinions may vary.

    This makes me wonder if immune-balancing therapy (which would fall under the category of holistic medicine) might help to tackle the evasive beast.

    And there may come a point when the whole medical paradigm has to alter somewhat. NOt to stop using antibiotics to tackle bugs, but to improve health first as a means to getting well. That time may "have to" come, I am suggesting, because of the problem of bacterial resistance to antibiotics.

    My "take" on this could be wrong, and it is possible that no matter how we help immunity, the nature of the spirochetes is such that they will continue to evade the immune system. It would be interesting to see what doctors would have to say about this question.

    continued below....

    ReplyDelete
  8. continued from above:

    D) As for the question of what else may have happened to not have progress in the area of lyme treatment, research, etc:

    Look at how currently, our Congress is forcing us to use our own pocketbooks to buy a product they demand, which happens to be healthcare. I mean, ooops! Health insurance. There is a big difference.

    Obviously the health insurance lobby has a powerful influence on Congress.

    It is not to their best interest to have to pay for treatment.

    Call me a conspiracy theorist, but I think it is all too obvious when lyme patients are routinely and massively being denied adequate care, that there is an interest in not "coughing it up".

    I want to point out that while it may never be the intention----that is fully clear, Camp Other so no misunderstandings here, please-----if we continue to point fingers at "conspiracy theorists" then we may be unwittingly supporting the wrong causes. Not intentionally of course. And as I have posted before, the concern about protecting lyme patients from being branded as "conspiracy theorists" is very well understood. I think in this situation, however, the facts bear themselves out in crystal clarity and to deal with the matter at the root cause, we have to follow the money.

    And hit them where it counts. In the pocketbook.

    Class action lawsuits may carry more weight than just getting lyme patients their treatment---as if that isn't the first concern anyway. It most certainly is. Above and beyond, it may also help to get the research movement going.

    Because as they say, follow the money.

    As regards the money, I have observed that countries which have to foot the bill for their peoples' healthcare, are often more protective of environmental purity, physician's education, and other health matters, than our country which is based on profiting in medicine. Europe requires chemical manufacturers to log onto a centralized database and do health reports, if they manufacture more than 1 ton per year. Contrast this with the USA which, according to clinical nutritionist Elizabeth Lipski, allows more than 300 new and untested chemicals per year into our environment. Canada teaches its physicians to look for root causes rather than bandaid symptoms, said an ND to me who trained in Canada. Norway has stringent environmental pollution regulations....

    You get my drift. I am not a socialist, but I do think that we may need to have single payer healthcare in order for our government to take responsibility for human health. I hate to say it, but I have seen it as I read about health, that footing the bill may make governments a bit more responsible.

    Thank you for what you are doing. Again it gives me hope and encouragement to know that there are people in Congress who "get it" and who understand our plight. That is very good to know, thank you Camp Other.

    Chiquita Incognita

    ReplyDelete
  9. Chiquita,

    My quick answers, as I need to get out the door soon:

    A) There already are more effective tests for institutions. They're not being used because they are time consuming and expensive - the aim for most labs is automated high volume tests for many patients at one go.

    B) Check out this, as I haven't yet, and report back:
    A. Maxwell, The interaction between coumarin drugs and DNA gyrase. Mol. Microbiol. 9 (1993), pp. 681–686.

    There should be something about its toxicity there. I've been looking for other references about toxicity.

    C) It is far more complicated than this, and yes, immunity can be compromised in the presence of infection - more so with coinfection.

    "And there may come a point when the whole medical paradigm has to alter somewhat. NOt to stop using antibiotics to tackle bugs, but to improve health first as a means to getting well."

    The problem is, some people were athletes who were at their peak of health and fitness when they got bit and were so sick they became dysfunctional. How do they fit into this hypothesis?

    I suggest reading up more on what Borrelia does as a whole - read about antigenic variation and let me know what you find out. Because spirochetes are in a class of their own and they are - as a friend once put it - 'crafty little buggers'.

    ReplyDelete
  10. Hi Camp Other

    A)
    Researching the link you provided on Pubmed, nothing came up about toxicity or side effects.

    I did come across this on Wikipedia, only one short statement, no further explanation:

    en.wikipedia.org/wiki/Aminocoumarin

    "clinical use of this antibiotic class has been restricted due to the low water solubility, low activity against gram-negative bacteria[5], and toxiciy in vivo of this class of antibiotics[8]."

    Perhaps this is why the drug died out? ("In Vivo" means in the body vs "in vitro", in the test tube).

    continued below

    ReplyDelete
  11. B)
    As for antigenic variation, again I am asking a question out loud and not stating anything as fact. It would be interesting to see what doctors have to say, and I bet that opinions will vary:

    Could low immunity make us more susceptible to infection?

    Could it be that the immune system is only the more easily tricked by the spirochetes because it has been compromised by them, or other factors, or both?

    If immunity was fully functional, would the spirochetes have a harder time tricking the immune system?

    Consider: If the spirochetes attach to viscous cell material (according to Buhner), then to use herbs that thicken the cell walls and render them less penetrable could surely help to block spirochete entry?

    See this study about elderberry blocking the swine flu, announced by mainstream medicine as being highly credible:

    http://www.news-medical.net/news/20090911/Elderberry-extract-prevents-H1N1-infection-in-vitro.aspx

    More info about elderberry thickening cell membranes to make them less penetrable to viruses (bearing in mind that spirochetes are bacteria, but like viruses they do embed), and stimulating cytokines (immune system cell messengers) can be seen in world-ranking phytotherapy authority David Hoffmann's book, Medical Herbalism.

    See also here, the herb can even help with syphilis, according to Hoffmann: http://www.healthy.net/Materia_Medica/Elder_Herbal_Materia_Medica/201

    I am not asserting that elder is the solution for lyme fyi. I am merely using this particular mechanism of action in thickening cell walls and stimulating immune cytokines, as an example of how other herbs might aid immunity to spirochetes.

    As before, Buhner mentions those people who do not respond to antibiotic therapy being low in certain natural killer cells, and when taking herbs to boost those exact NK cells, they respond to antibiotic therapy and they get well.

    That example certainly would indicate that immune balancing is (one) key to recovery.

    Of course there most certainly are those people who are perfectly healthy and who still get sick and run down.

    I always say: The Titanic ship couldn't be sunk. Just because we cover all the bases with immunity doesn't mean we are immortal. It only means that we are *less likely* to have problems.

    And yes, there's the problem of the changing spirochete. Sure.

    But then again there is the immune system's "Memory" for those altered antigens, and if the immune "Memory" is working well and recognizes these changed buggers, then after a while the spirochetes would surely run out of tactics? Am I wrong here?

    Are the altered spirochetes limited in variations, or are these variations truly endless?

    I don't know the answer to this question, and don't expect anybody to have to go researching this.

    I think to understand how the immune system works is part of the remedy to the antigenic alteration problem.

    A good book re. immune physiology:

    Boosting Immunity edited by Len Saputo, MD and Nancy Faas, MSW books.google.com/books?isbn=1577311272...

    I hope it is understood that we agree in many respects. I think it is entirely possible that many peoples' recovery will be aided by immune balancing, but then again many will become sick too even if in perfect health to begin with.

    Further, I want to suggest that as we find solutions, the powers that be which are impeding progress, may have to come around.

    Because the obstructionists are arguing that "there is no proof" of people getting well with antibiotic therapy beyond 2 months, no thanks to stubborn bugs and many patients who relapse or don't get well. If we have (proven) solutions to create a more hopeful get-well picture, the science and the insurance companies may be more or less forced to respond more favorably toward lyme patients. Because they will have fewer *excuses* with which to argue away the obvious: Responsibility toward patients.


    Best wishes, Chiquita Incognita

    ReplyDelete
  12. PS I am not suggesting that naturopathics are the only way to go. Not at all.

    I am merely suggesting that complimentary therapies may provide us with a lot of solutions.

    I am suggesting that the improved recovery rates using mainstream and complimentary modalities together, may pressure the powers that be to come around.

    Science: See www.pubmed.gov or Buhner's book, Healing Lyme

    I hereby yield the floor and look forward to seeing everybody's comments to your article, Camp Other!

    Thank you all, CI ps I am not a doctor, this is a layperson asking questions out loud and speculating, not stating any facts or making any assertions.

    ReplyDelete
  13. Hi Chiquita,

    Lots of questions here, and they all deserve at least a post a piece... but I'll try to give them an abbreviated response for now.

    You said,

    "Could low immunity make us more susceptible to infection? "

    Yes. Absolutely. It happens all the time with people who are under stress, who have immune deficiencies, who are on immunosuppressant drugs, and so on - low immunity exists for a variety of reasons and makes us more susceptible to infection. Some people have to take ongoing prophylactic antibiotics or be treated with IVIG because their own immune systems are incapable of fighting off infection and need a boost.

    You said,

    "Could it be that the immune system is only the more easily tricked by the spirochetes because it has been compromised by them, or other factors, or both? "

    All of the above? Borrelia have more than one survival mechanism to evade the immune system, and can 'fly under the radar' in early dissemination. A combination of factors make it a more difficult infection to fight off, as well as one that is more effective at invading.

    This is a simplistic answer at best - there's more to it.

    You said,

    "If immunity was fully functional, would the spirochetes have a harder time tricking the immune system?"

    A number of studies have shown that even with a fully functional, normal immune system, spirochetes will survive immune system attacks. Without treatment, the immune system on its own cannot clear the infection.

    I say this with qualification - there are certain genotypes that are not that virulent and less of an issue for human hosts. Some types of Borrelia do not infect humans at all - and some only have the rash as a symptom, as far as we know. Not all Borrelia infections are created equally.

    You said,

    "Consider: If the spirochetes attach to viscous cell material (according to Buhner), then to use herbs that thicken the cell walls and render them less penetrable could surely help to block spirochete entry?"

    Is there anything more Buhner said about this? What did Buhner mean by "thickening the cell walls" - and which cell walls?

    You said,

    "As before, Buhner mentions those people who do not respond to antibiotic therapy being low in certain natural killer cells, and when taking herbs to boost those exact NK cells, they respond to antibiotic therapy and they get well."

    Having more NK cells helps, as there is evidence Borrelia burgdorferi inhibits NK cell activity. Other immune cells are affected as well, and Bb inhibits the humoral branch of the immune system. (See http://en.wikipedia.org/wiki/Humoral_immunity)

    I don't think this is the entire story, though.

    (more)

    ReplyDelete
  14. (Chiquita - more, continued)

    You said,

    "But then again there is the immune system's "Memory" for those altered antigens, and if the immune "Memory" is working well and recognizes these changed buggers, then after a while the spirochetes would surely run out of tactics? Am I wrong here?"

    To quote Alan Barbour, "True antigenic variation, however, arises in a single clone or genotype in a single host and "involves the loss, gain, or change in a particular antigenic group, usually by loss, gain, or change in one of the polypeptide or polysaccharide antigens…". In most cases, this change is reversible, i.e., the information for producing the original antigen is archived in the cell and can be used in the future. The adaptive immune system of an infected vertebrate selects against the original infecting serotype, but that specific response is ineffective against new variants."

    Yes, there is an immune response to the original presentation of the bacteria. The bacteria can produce different serotypes, and one can have multiple serotypes existing simultaneously in different tissues. The immune system has to respond to each of these, and if it has to deal with them on top of a coinfection or two, it's overwhelming.

    If immunosuppression occurs, then a latent infection can also potentially be 'awakened'.

    Not all of this is well understood.

    You said,

    "Are the altered spirochetes limited in variations, or are these variations truly endless?"

    You might want to check this out:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC108403/

    It's earlier research, and I can post more recent research - this just might be an easier read than what I could post.

    Borrelia is known to go through extensive (it's even been called 'promiscuous') antigenic variation.

    More recently, Steven Norris said at the IOM workshop in 2010 that:
    "There are so many different variations produced, so many that you can’t find the same VlsE combination or sequence in the same tissue twice 28 days post-infection."

    He said that 10^32 amino acid sequence combinations are possible, and Luft's research confirms that most sequence differences are very short - 1 or 2 amino acid differences.

    In a tissue culture experiment that was conducted, the percentage undergoing variation at a given time seemed rather low. But this was a tissue culture experiment - what's the percentage of variation in an actual in vivo situation, in a human host?

    One way to learn more about antigenic variation in general is to look at Relapsing fever and learn more about it - there is a lot of research in this area.

    ReplyDelete
  15. This paper might interest you:

    Isogenic Serotypes of Borrelia turicatae Show Different Localization in the Brain and Skin of Mice:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC98298/

    Interesting to see where those variants are.

    ReplyDelete
  16. Hi Camp Other
    This is very interesting! I am indeed looking forward to reading those links, thank you!

    It's also very thoughtful of you to post the youtube about immunity, I eagerly look forward to watching it. Learning is a blast!

    Your knowledge about the immune invasion and suppression is impressive. Thank you for such motivated research and well thought out responses.

    I want to suggest that to focus on the issue of immune evasion is bound do be a depressing one,even if as a serious problem it needs to be addressed. However, if we also study healthy immune physiology we can gain hope and empowerment.

    I did not mean to imply that immune wellbeing alone would cure lyme in absence of treatment. Thank you for response and giving me the opportunity to clarify that.

    I do want to suggest that *especially!* if the buggers transform as extensively as you are saying and evade the immune system....then that's *all the more!* reason to balance and strengthen immunity. Reading Buhner's book it seems that a lot of people get well or respond very well to immune bolstering.

    You had asked me to research and post regarding the (what I was wondering could possibly be) toxicity and side effects of the drug coumermycin. I had asserted that because it hits the spirochete so exquisitely, it would also be bound to create very severe herx's, and that the herx's we have are already severe enough. Perhaps this, and perhaps some side effects, were responsible for its demise? That was the question.

    I searched the Pubmed link you offered and found nothing about this. However, I found one statement on Wiki which was not extensive or detailed, but which will tell us something:

    http://en.wikipedia.org/wiki/Aminocoumarin

    "The Clinical use of this antibiotic class has been restricted due to the low water solubility, low activity against gram-negative bacteria, and toxicity in vivo of this class of antibiotics".

    (FYI "in vivo" means in the body, vs "in vitro" which means in the test tube).

    There were no further elaborations or details given.

    Perhaps this is why the coumermycin died out?

    I also wanted to address your question above about thickening of cells and rendering them less penetrable to viruses (and perhaps, spirochetes too, I am postulating). This was in David Hoffmann's 1000+ page book, Medical Herbalism, not Buhner. He was discussing something not lyme related, just the action of the herb elder berry. I don't recall which exact cells he was referring to, and am not sure he even specified. If you are interested I will look up the information again and get back to you, let me know. (I am not stating that elder is a lyme herb fyi, I do not know that for a fact. Merely giving an example about ways that immunity can be strengthened, to offer us hope).

    This is only one way in which the herbs could possibly help, there are many other mechanisms. Buhner talks about which exact immune cells are stimulated by which herbs, as proven in clinical tests.

    These are not postulations, fyi, as you had written about on a previous post. Just wanted to mention that. It's based on testing, knowledge of herbal constituents, their actions on the body, clinical experience, plus hundreds of years of historical use.

    I think anybody who is interested to read this fabulous book which is very detailed, will learn a lot about the immune physiology involved in lyme disease and how to address it. There is a lot of hope based on the herbal studies, check out the book. It' s a very empowering read, even while it realistically addresses the immune evasion issue.

    Again I hope to make it clear that I am not "plugging" merely for naturopathics alone, I am a firm believer that everybody should go whichever medical route they each believe in. That said, to research the facts first is important, including benefits, side effects, recovery rates, and how all considered interact with our own unique physiology and our own unique needs.

    Best wishes, CI

    ReplyDelete
  17. PS Camp Other
    FYI I had posted about the Wiki/Coumermydin info prior to my post above, to which you were kind enough to respond in such a detailed way.

    It seems that there are a number of times when I have posted that it has not gone through to you. Just so you are aware of this.

    Great website and lots of good info, such good thinking and research, thank you! I am learning a lot here and will look forward to lots more. Best, CI

    ReplyDelete
  18. Short and sweet so people can get through it (grin)
    *****
    I realize that 18 years ago is a while ago, but what happened to some of this research?****

    ****Or maybe researchers didn't even have a choice in what to research, and someone else decided where the funding was going for them - regardless of their own priorities and interests.****

    BINGO!

    Always follow the money, whether it's drugs, supplements, the NIH, the AMA, insurance companies etc.

    Always.

    The supplement manufacturers---- I'll pick them out first for they have the least transparency and the least oversight. NOT that some can't be used effectively.

    Perhaps someday the supplement sellers will have some oversight. I hope so, for there's much of value there.

    ReplyDelete

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