CDC writes a "bogus article" on Mycoplasma in the blood and Chronic Fatigue.
 

Lyme/LYMErix Cryme Reveals  New Paradigm in Health/Disease:
"Bacterial/Viral Coinfections";
TLR2 (fungi)Signaling Depletes IRAK1 and Inhibits Induction of Type 1 by TLR7/9  (viruses)--  -CV Harding, 2012  (More in the chart at the bottom of this homepage)

CFIDS = Seronegative Chronic Active EBV

"Multiple Mechanisms of Immune Suppression by B Lymphocytes" (New and Trashes Yale and IDSA)

NIH's Treatment Recommendations for Chronic Active Epstein-Borreliosis, the chronic illness also induced by OspA vaccination or exposure to molds.

The Antics of the Crazy Stalker Durland Fish and the New Genre in "Education."
 

--Watch Pat Coyle and Ray Dattwyler.

 

They *TOTALLY* knew what was going on, and how LAME the trial was.

 

--And Vijay Sikand did not report his adverse events.  They reported to the

FDA only 2 adverse events.  [There were TV cameras dashing in, as soon

as Parenty's turn came to speak, at the LDF conference.  Some people

literally got up and left in the Lyme Foundation Conference, when Parenti said that-- Only 2 adverse events.    As soon as his talk was done, he buzzed out into the lobby, and said to someone, something to the effect: "Wphew, I got through it," and acted like he'd just had been driving the get-away car.]

 

 

This is a riot, this testimony:

 

==============================

 

 

"Inclusion criteria were individuals who were 18 years of age or older

and in good health at the time of enrollment, and individuals who were

considered to be at high risk of acquiring Lyme disease.  That is, they

lived in an area known to be endemic for Lyme disease, and they also had

reasons for being outside either through their job or through hobbies so

that they would be expected to be exposed.   ***The case definition was

essentially that that was agreed to by the Advisory Committee Meeting in

1994 and finalized by agreement with the FDA.  In essence, this meant

that a person to be considered a definite case of Lyme disease had to

have clinical symptoms at the time they were seen by a physician.

Usually these were manifestations of early Lyme disease, primarily

erythema migrans.  Also, it required laboratory confirmation of the

infection, either through a positive skin biopsy culture or through

Western blot serology using the Dearborn criteria of sero

conversion.***"

 

----

WRONG:

The Connaught trial started in March 1994, with the Dressler/Steere

(Dearborn) Criteria, the 1994 FDA vaccine meeting minutes were in June, 1994, and Dearborn took place in October, 1994.

 

And they could not read their blots.

----

 

VIJAY SIKAND, EAST LYME CT (regarding the disease that does not actually

exist any more, according to the ALDF and Mark Klempner):

 

"In one study, over 80 percent of the patients who presented with

definite Lyme disease did not remember a tick bite.  It is therefore

very hard to correlate the incidence of definite Lyme disease cases with

preceding tick bites, and this is well known.

Furthermore, as has been eluded to earlier, the recurrence of disease

in individuals is also well known.  Unfortunately, in the majority of

patients, the vast majority of patients, natural infection with Borrelia

burgdorferi does not confer protective immunity.  Difficulties in

clinical diagnosis of this disease are also well known, and it is not my

place today to give you an overview or detailed presentation of the

clinical aspects of Lyme disease.  However, a couple of issues that do

spring up and which I would like to address are as follows.  In

particular, the specter of asymptomatic infection is something that

troubles me a great deal and troubles a great number of my colleagues

who need to treat Lyme disease.  The obvious analogy with syphilis

infection with Treponema pallidus is there to consider.  ***It is well

known that Borrelia burgdorferi indeed after asymptomatic infection can

lurk or secrete itself in certain areas of the body, perhaps the central

nervous system or perhaps the joint spaces, only to reappear months or

maybe years later in the form of late stages of illness which are harder

to diagnosis and treat.***

In terms of the variability of Lyme disease, it is indeed a very

variable infection, if not a very complex infection.  In its very

simplest form, it is erythema migrans, well localized, which we can all

recognize and which we can all easily treat and from which most patients

can get better.  However, erythema migrans is not a single beast.

Certainly this is the one which we easily recognize and which I just

referred to.  Before I continue with further slides, let me point out

that the erythema migrans lesions you are about to see are all biopsy

lesions which were laboratory proven to be caused by Borrelia

burgdorferi.  Sometimes erythema migrans can present as a pustular

lesion as is this one in the popliteal fossa inviting the scalpel of a

surgeon.  Sometimes the lesions are vesicular in nature, inviting a

diagnosis perhaps of herpes simplex infection.  Sometimes our round

lesion is actually triangular.  Sometimes it doesn't even look round or

red at all and invites a diagnosis of an intertriginous fungal infection

in the groin of this patient who was biopsied and proven to have Lyme

disease.  Sometimes the lesion is more plaque-like, inviting diagnosis

of nummular eczema, psoriasis, or other similar lesions.  Sometimes it

is in unusual locations.  Sometimes it is large like this one.

Sometimes it is small with satellite areas.  Sometimes it is multiple,

appearing almost like urticaria or erythema multiform.  Sometimes, as in

this individual who was a placebo recipient in the Lyme 008 SmithKline

Beecham trial, it presents with other manifestations of early

dissemination.  This individual came in mainly because he was concerned

about his face and it felt kind of funny and it was weak on one side.

When I asked him whether he had had any unusual rashes, he said oh do

you mean this one, and he showed me his arm with that EM.  This is

simply to illustrate the infranuclar 7th nerve palsy with which he

presented.  This patient, by the way, had no history of a tick bite or

any unusual antecedent illness which he could remember.

The next slide is the electrocardiographic tracing of a 37-year-old

mom from Lyme, Connecticut, mother of three.  Generally healthy and no

medical problems.  Early on the day that this electrocardiogram was

taken, she went to her local health club and did her usual work-out,

which went fine.  However, when she came home that day, she noticed that

she had some palpitations, a little shortness of breath, malaise, and

things just didn't seem quite right, but she wasn't sure what.  When her

husband came home, she told him that maybe she had worked out a little

bit too hard at the club.  A few minutes later, he was reading the

newspaper in an armchair and he heard a thump on the floor above.  He

ran up the stairs to find his wife unconscious briefly on the floor and

called 911.  On arrival at the emergency department, the patient

presented with this tracing, which in retrospect was a superventricular

tachycardia representing an escape rhythm.  There was fortunately a very

vigilant emergency physician who didn't understand quite why a

37-year-old healthy woman had completely passed out, and she had what

was a relatively benign rhythm at that point.  But he was wise and

admitted her to the coronary care unit for further monitoring.  Late

that night and the early hours of the following morning, the CCU nurse

noted that the patient had gone through progressive degrees of AV block

culminating in complete atrial ventricular dissociation.  A cardiologist

was summoned.  He inserted a temporary transvenous pacemaker.  The

patient was started on intravenous antibiotics for about a week in the

hospital followed by a few more weeks as an outpatient.  This patient

also had no history of a tick bite.  

Besides the difficulties in clinical diagnosis, we are all aware that

quandaries in laboratory diagnosis are rife.  We rely pretty much on

serologic testing in the United States today to assist us in diagnosing

Lyme disease.  Unfortunately, serologic testing, as with other

infectious diseases, provides only indirect evidence of infection.  When

we order a serologic test, it just tells us that the patient has been

exposed to Borrelia burgdorferi and doesn't tell us whether the

infection is active or whether it is a past infection.  It is probably

worth noting, since I have learned a lot, that we don't have the

clinical luxury in private practice that we had in the SmithKline

Beecham trial in which we had baseline sera on all the patients who

enrolled so that when they presented with symptoms, we could draw acute

and convalescent serologies so as to compare them with each other and

with baseline to better understand what symptoms they are presenting

with.  But your average physician in the office just can't do this.  A

patient comes in with symptoms or signs of Lyme disease and you have to

make a clinical diagnosis and it is not always easy and serology doesn't

help.  ***The fact that in particular the ELISA creates a great deal of

false positive results is also problematic.***  In particular and

commonly in infectious mononucleosis and other spirochetal disorders,

even healthy people, juvenile rheumatoid arthritis and other autoimmune

disease all can produce false positive results.  ***Indeed, even with

Western blotting recent reports have shown that infection with the agent

of human granulocytic Ehrlichiosis can cause false positive Western

immuno- blots.  The false negatives that we deal with are generally

caused by use of serology testing in patients who have early Lyme

disease and in whom the serologic response with immunoglobulin M has not

occurred to the extent to which it can be measured.***

What do we have in the way of direct testing to try to see if the

organism itself is actually there or evidence of it?  Well, culture and

PCR are what are out there right now.  However, these are unreliable and

impractical.  Culture and PCR are certainly not warranted for the

diagnosis of erythema migrans.  The polymerase chain reaction is indeed

sensitive in joint fluid.  ***However, the diagnosis of Lyme arthritis

does not require PCR testing since serology is almost invariably

positive at that stage.***  

 

Clinical conditions such as complex neurological conditions when a test

like sensitive PCR would be useful, unfortunately cannot be diagnosed

that way because PCR and indeed culture are not sensitive for

cerebrospinal fluid, nor are they sensitive for urine, blood, and other

body tissues when later in the disease one might care to employ these

techniques.

 

***Finally, there are indeed many dilemmas in therapy.  In particular,

untreated or inadequately treated Lyme disease may lead to the chronic

morbidity with which we are very familiar.  Most commonly arthritis and

the not common but complex neurological syndromes are what often result

and which confront the primary care physician in the office

diagnostically and therapeutically.  These particular outcomes result in

much more intensive, long-term expensive therapy, often in the form of

long-term intravenous antibiotics.  These are the patients who often are

refractory to treatment.  Indeed, these are the patients in whom

symptoms seem to persist despite what we have given in terms of adequate

antibiotic therapy by any known measure.***

In conclusion, we need a vaccine for Lyme disease because it is

increasing in incidence and geographic spread.  We need a vaccine for

Lyme disease because there are problems in clinical diagnosis, its

laboratory evaluation, and its treatment.  We need a vaccine for Lyme

disease because preventive measures are unfortunately ineffective.  Lyme

disease is indeed vaccine preventable.  ***Availability of this vaccine

would lead to a significant reduction in chronic sequelae and

substantive morbidity.***  Lyme vaccine is thus a critical new public

health approach to the primary prevention of Lyme disease in the United

States.  Thank you very much."

===========

 

I call it Lyme Paranoia-- Robert Schoen

It brings to mind Munchausens' and Munchausen's by Proxy-- Lenny Sigal

Lyme is easily cured and there are no adverse outcomes in Pregnancy--

Eugene Shapiro

etc...

 

----

DR. DATTWYLER:  "I agree with what Dr. Schoen has said.  One point

though is that chronic arthritis under any circumstances has become a

rare event.  The most comment -- the scenario of Lyme arthritis is what

Dr. Steere's described, arthralgias followed by usually knee effusion,

spontaneous remission, and the sequence is repeated.  And gradually the

interval between episodes lengthens and the disease goes away.  ***So

real chronic arthritis is not the rule, it is the exception.***  And I

think that that is an important point that everybody should realize.

But otherwise, I agree with what was said."

 

 

So, it is exceptional, and not the rule, to test positive to Dressler/Steere or Dearborn CDC criteria, and Lyme Arthritis is a Relapsing Arthritis..

 

---

VERY IMPORTANT-- The vaccine did not prevent infection in animals:

 

DR. COYLE:  I think the possibility that vaccination might change the

clinical picture of infection is of some concern.  Really, the vaccine

is not 100 percent effect.  It is not just of theoretic interest.  There

are two distinct animal models that suggest that when this single

protein vaccine is used, some of the hosts do get infected but it is a

smoldering infection that becomes more difficult to detect.  Now

vaccination is going to mess up serologic detection.  I think in the

monkey model, you had antigen and PCR and pathologic data of infection

in some of the animals vaccinated.  And in the rabbit model, you lost

EM, which was a very good marker of infection.  And this brings us back

to the possible Lyme disease group, which is somewhat problematic.  We

hear that at least some of 2.2 perhaps may be explained by co-infection

with HGE.  You would like the same rigorous application to the

asymptomatic sero positives to document that they are not co-infected as

well.  But it doesn't explain 2.1.  Even with the laboratory data being

negative, that doesn't exclude that they had a valid EM.  So my question

is for those possible Lyme disease patients, were they treated or were

they not treated?  And if they were not treated, have they been followed

and have any further specific testing been done in that group?

 

 

[Lame answer, of course-- Basically, "Oh, I assume so."]

 

 

 

COYLE:  I just have three quick questions.  In the proliferation

interferon gamma assays, lipidated OspA was not used because the lipid

acts as a mitogen.  If you use lipidated OspA, what do the placebo and

vaccine patients look like?

***DR. STEERE:  I don't know.  I haven't done it.***

DR. COYLE:  It wasn't done.  Okay.  Secondly, knowing how this vaccine

would have to be used if it was approved in endemic areas, is there any,

any, any animal or human data on repetitive vaccinations -- multiple

times?

DR. PIETRUSKO:  Dr. Lobet, is there anything in animal repeat?

DR. LOBET:  Your question relates to multiple --

DR. COYLE:  Multiple vaccinations.

DR. LOBET:  No, but there are -- there is no animal model that has

been used for that, but we have some human data on this.

DR. COYLE:  Some human data on like how many times?

CHAIRPERSON FERRIERI:  How many boosters or challenges?

DR. PIETRUSKO:  Dr. Parenti?

DR. PARENTI:  We have one study where approximately 500 subjects have

received 4 doses in a year -- 0, 1, 2, and 12.  We have ongoing studies

where people have received 0, 1, and 12 and have gotten a booster at

month 24, and another cohort of about 150 or 200 who have gone 0, 1, 12,

24, and 36.  And from the safety data we have right now, we are not

aware of any unusual events happening in these people who have received

four or five doses.

 

[4/13 miscarriages, Later --> 15/173 new breast neoplasms

in females, etc... 4th injection.]

 

DR. COYLE:  And my final question, this exclusion in the Phase III

study of patients with joint problems was a little bit vague.  So I am

trying to get a feel of who was excluded.  Would anybody in general

complaining of any history of joint pains have been excluded or current

joint pains?  Obviously rheumatoid arthritis and osteoarthritis, fine.

But was it extrapolated, and just give me a sense of who was excluded

based on joint problems.

 

---

[And this is where the VAERS failed, and the Twilight Zone, Luft talked

about

in the subsequent 2001 meeting.]

---

DR. PARENTI:  Yes, that is a good question.  The gist that we tried to

give the investigators was that we did not want people in this study in

whom it would be difficult to assess for Lyme disease later.  I mean one

of the endpoints is looking for arthritis.   So if you started out with

arthritis -- we didn't want to make it -- we didn't want to have

subjects who already had unexplained knee effusions, for example.  So

with those guidelines, we asked the investigators to use their

judgment.  ***So some investigators felt that back pain obviously wasn't

an issue.***  They could clearly differentiate back pain from Lyme

disease.  There were investigators who had had some of these subjects in

their private practice for years and years, they knew their

osteoarthritis -- they knew their patterns of osteoarthritis and felt

very comfortable that they could discern in a given patient whether

there was a new event, for example.  So we knew that this was an issue

and we went back and looked at all the subjects who had musculoskeletal

complaints at baseline to see if, again, vaccinees who had a previous

history of musculoskeletal complaints or had something on physical exam

at the beginning of this study were at increased risk of developing

subsequent musculoskeletal events.  And from the table I have up here --

I apologize that the numbers are not really very clear -- you will see

that as you go from dose 1 to 2 to 3 and look at musculoskeletal

disorders, there is no difference between the two groups.   So if you

had a baseline history of a musculoskeletal event and got vaccinated,

you did not appear to be at increased risk.  ***And it looks as if there

was over 2,000 such subjects***.  So 20 percent of the population

already has some baseline musculoskeletal event, which is pretty much

what you expect when you are looking at 40, 50, 60 et cetera year

subjects.

 

DR. COYLE:  Thank you.

---

DR. COYLE:  I'll just mention that it is also going to make potentially

diagnosis of vaccine failures more difficult.

 

 

CHAIRPERSON FERRIERI:  Dr. Coyle?

DR. COYLE:  ***Yes, as definite Lyme was defined for the time

period.***

 

[LMAO]

 

CHAIRPERSON FERRIERI:  And Dr. Dattwyler?

DR. DATTWYLER:  Yes, with the suggestion that there be a warning in

the first year that it is only 50 percent efficacy.

 

 

DR. DATTWYLER:  Just one comment.  I think that 2.1 probably does

contain some people with real Borrelia burgdorferi infection.  I think

the sponsors data would support that even in culture-proven cases that

not everybody sero converts.  So that the serologic data cannot be used

as a gold standard.  And the fact that someone has erythema migrans and

doesn't sero convert doesn't mean that that is not a Borrelia

burgdorferi infection.  

 

 

DR. PARENTI:  Again, there were only about six positive people at

baseline at study entry.  I honestly don't recall their ages.  Their

titers were extremely low and again they didn't boost on getting

vaccine.

 

 

DR. COYLE:  Don't you think it is an important point that if this winds

up being approved by the FDA that it be clear that people be actively

discouraged to use experimental protocols until you have something

documented?  I mean, I don't know if you can say mandated, but you might

really be in trouble if you switched the schedule.  And granted, it is

far from optimal.  That one year of not being protected 50 percent is

poor frankly.  But how could you have people experimenting with well let

me do it once a month for three months.  We can't extrapolate.  

 

----

 

DR. LOBET:  Yes, we have already sequenced the OspA gene from 80

different strains that were collected during the efficacy trial. ***20

of these strains were coming from the vaccinees or the breakthrough

cases.***  So those are basically all the strains that are available.

And we see basically no difference between those strains and any of the

other known strains that were known previously -- those that I

mentioned, N4297 and so on.  You have basically variations in three

positions.  For each of these three positions in most cases there are

just two possible amino acids.  You have actually five different

categories and those correspond to different combinations of those

variations.  

 

DR. DAUM:  ***That is wonderfully reassuring.***  And now that you

have proposed to give the vaccine to millions of people, you may see

something different.  So all I am asking for is that it be monitored and

thought about.