SUNY's Volkman slams UConn;s Henry Feder
Beach
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Subject: SUNY's Volkman slams UConn's Henry Feder
Date: Jan 25, 2008 1:40 AM
(Others mention all the persistence studies, including the CDC report
where they
acknowledge that Lyme spirochetes are intracellular, agreeing with
CDC's top
weaponeer, Mark Klempner, that spirochetes are intracellular and
therefore hide
from antimicrobials:
http://www.actionlyme.org/Mark_Klempner_Fibroblasts.htm
CDC on intracellularity in nerve and brain cells:
http://www.actionlyme.org/LYME_PERPS_INDICTMENTWEAR.htm
========================
To the Editor: The article by Feder et al. on the proper therapy of
chronic Lyme
disease addresses a very timely concern. Unfortunately, the authors'
statement
that there are no "scientific data" that support persistent B.
burgdorferi
infection in the face of negative serologic test results is erroneous.
In 1988,
we reported on 17 patients who had all had erythema migrans, received
inadequate
antibiotic therapy, had vigorous T-cell blastogenesis to borrelia
antigens, and
were seronegative on the basis of enzyme-linked immunoassay.1,2 The
majority of
these patients had improvement after definitive antibiotic therapy.
Seronegative
infection was confirmed by other laboratories using polymerase-chain-
reaction (PCR)
assays to document the presence of microbes in seronegative patients.
3,4 Abrogation
of a humoral response by removal of the bulk of microbial antigens has
been seen
in other settings, including infection with Treponema pallidum.
Although the use
of repeated courses of antibiotics for a putative borrelia infection
is unsupported
and may cause serious morbidity,5 persons with evidence of previously
inadequately
treated Lyme disease may be seronegative and may benefit from adequate
antibiotic
therapy. Fortunately, erythema migrans is now more readily recognized,
and occult
Lyme disease is rarer. In the absence of antibiotic treatment, most
persons become
seropositive.
David J. Volkman, M.D., Ph.D.
State University of New York at Stony Brook
Stony Brook, NY 11794
volk...@optonline.net
References
1. Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ, Thomas J,
Golightly MG. Seronegative
late Lyme borreliosis: dissociation of specific T- and B-lymphocyte
responses to
Borrelia burgdorferi. N Engl J Med 1988;319:1441-1446. [Abstract]
2. Volkman D. Prophylaxis after tick bites. Lancet Infect Dis
2007;7:370-371.
[CrossRef][ISI][Medline]
3. Keller TL, Halperin JJ, Whitman M. PCR detection of Borrelia
burgdorferi DNA
in cerebrospinal fluid of Lyme neuroborreliosis patients. Neurology
1992;42:32-42.
[Free Full Text]
4. Oksi J, Uksila J, Marjamäki M, Nikoskelainen J, Viljanen MK.
Antibodies against
whole sonicated Borrelia burgdorferi spirochetes, 41-kilodalton
flagellin, and P39
protein in patients with PCR- or culture-proven late Lyme borreliosis.
J Clin Microbiol
1995;33:2260-2264. [Abstract]
5. Klempner MS, Hu LT, Evans J, et al. Two controlled trials of
antibiotic treatment
in patients with persistent symptoms and a history of Lyme disease. N
Engl J Med
2001;345:85-92. [Free Full Text]
========
http://content.nejm.org/cgi/content/full/358/4/428
An Appraisal of "Chronic Lyme Disease"
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by Feder, H. M.
- PubMed Citation
To the Editor: Feder et al. (Oct. 4 issue)1 review the great
controversy surrounding
"chronic Lyme disease." For most patients with this diagnosis, the
authors
advocate against the use of antibiotics.
But before the decision is made not to use antibiotics for patients
with post-tick-bite
symptoms, anaplasma, babesia, bartonella,2 and ehrlichia must be ruled
out. These
tick-borne2 intracellular pathogens are difficult to diagnose and can
establish
long-term, persistent infection.3,4,5 Anaplasma, babesia, and
bartonella are underdiagnosed:
the nonspecific symptoms of infections with these organisms tend to be
ascribed
to the more easily identifiable Lyme disease, which often accompanies
them.2,3,4,5,6
Indeed, when studied prospectively, 65 of 161 patients with Lyme
disease (40%) were
coinfected with babesia, and 11 of 161 (7%) with anaplasma.6 Accurate
diagnosis
of these infections helps steer successful treatment: babesia3 and
bartonella5 are
especially difficult to eradicate. Accurate diagnosis is also
important, since babesia3
and anaplasma4 can spread through blood transfusion.
As Feder et al. note, "chronic Lyme disease" is often unrelated to
borrelia.
If symptoms occur after a tick bite in the absence of evidence of
active borrelia
infection or if they persist despite anti-borrelia treatment, another
tick-borne
infection should be suspected. If such an infection is found, the
patient may indeed
benefit from appropriate antibiotics.
Lawrence Mayer, M.D.
16 Hudson St.
Lexington, MA 02421
lma...@axigenmail.com
Susanne Merz, B.S.
Jungfrudansen 34
S-17156 Solna, Sweden
References
1. Feder HM Jr, Johnson BJB, O'Connell S, et al. A critical
appraisal of
"chronic Lyme disease." N Engl J Med 2007;357:1422-1431. [Free Full
Text]
2. Adelson ME, Rao RV, Tilton RC, et al. Prevalence of Borrelia
burgdorferi,
Bartonella spp., Babesia microti, and Anaplasma phagocytophila in
Ixodes scapularis
ticks collected in northern New Jersey. J Clin Microbiol
2004;42:2799-2801. [Free
Full Text]
3. Krause PJ, Spielman A, Telford SR III, et al. Persistent
parasitemia after
acute babesiosis. N Engl J Med 1998;339:160-165. [Free Full Text]
4. Dumler JS. Is human granulocytic ehrlichiosis a new Lyme
disease? Review and
comparison of clinical, laboratory, epidemiological, and some
biological features.
Clin Infect Dis 1997;25:Suppl 1:S43-S47. [CrossRef][ISI][Medline]
5. Rolain JM, Brouqui P, Koehler JE, Maguina C, Dolan MJ, Raoult D.
Recommendations
for treatment of human infections caused by Bartonella species.
Antimicrob Agents
Chemother 2004;48:1921-1933. [Free Full Text]
6. Krause PJ, McKay K, Thompson CA, et al. Disease-specific
diagnosis of coinfecting
tickborne zoonoses: babesiosis, human granulocytic ehrlichiosis, and
Lyme disease.
Clin Infect Dis 2002;34:1184-1191. [CrossRef][ISI][Medline]
To the Editor: Feder et al. fail to adequately inform readers about
the science
underlying the "chronicity" debate. Multiple researchers have
documented
Borrelia burgdorferi's ability to penetrate human cells. In
demonstrating the
presence of the organism inside neurons and glial cells, Livengood and
Gilmore established
that it can exist in an intracellular state within a protected site,1
characteristics
favoring persistence and necessitating longer courses of antibiotics.
B. burgdorferi's
pleomorphic abilities also favor persistence. One study suggested that
penicillin,
ceftriaxone, and doxycycline are ineffective against the bacteria in
its cystic
form.2 The study by Yrjänäinen et al. revealed that B. burgdorferi can
survive standard
therapy, lending further credence to the theory of bacterial
persistence.3 Krupp
et al. found that retreatment was beneficial; 69% of the treatment
group, as compared
with 23% of the placebo group, had significant improvement in fatigue.
4
"Clinical assessment remains the most important method for determining
the
efficacy of treatment."5 Persistent symptoms in patients with late
Lyme disease
suggest treatment failure and the need for a new approach.
Elizabeth L. Maloney, M.D.
25611 West Comfort Dr.
Wyoming, MN 55092
References
1. Livengood JA, Gilmore RD Jr. Invasion of human neuronal and
glial cells by
an infectious strain of Borrelia burgdorferi. Microbes Infect
2006;8:2832-2840.
[CrossRef][ISI][Medline]
2. Kersten A, Poitschek C, Rauch S, Aberer E. Effects of
penicillin, ceftriaxone,
and doxycycline on morphology of Borrelia burgdorferi. Antimicrob
Agents Chemother
1995;39:1127-1133. [Abstract]
3. Yrjänäinen H, Hytönen J, Song XY, Oski J, Hartiala K, Viljanen
MK. Anti-tumor
necrosis factor-alpha treatment activates Borrelia burgdorferi
spirochetes 4 weeks
after ceftriaxone treatment in C3H/HE mice. J Infect Dis
2007;195:1489-1496. [CrossRef][ISI][Medline]
4. Krupp LB, Hyman LG, Grimson R, et al. Study and treatment of
post Lyme disease
(STOP-LD): a randomized double masked clinical trial. Neurology
2003;60:1923-1930.
[Free Full Text]
5. Moellering R Jr, Eliopoulos G. Monitoring the response of the
patient to antimicrobial
therapy. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas,
and Bennett's
principles and practice of infectious diseases. 6th ed. Vol. 1.
Philadelphia: Elsevier,
2005.
To the Editor: The patient community discussed in the article by Feder
et al. does
not suffer from "mild and self-limiting subjective symptoms." These
symptoms
are disabling, precluding employment and school attendance. Patients
have severe
pain and cognitive dysfunction. Antibiotics have helped many such
patients reclaim
their lives.
A careful reading of the article shows that a diagnosis of Lyme
disease is all but
impossible without certain objective symptoms. These symptoms
determine which patients
receive the diagnosis, are treated, and are enrolled in research
studies. Table
1 of the article shows objective symptoms present in a minority of
patients. Erythema
migrans rash may be undetected or misdiagnosed in persons infected
with B. burgdorferi.
Thus, many infected persons do not receive the diagnosis.
Patients who are seronegative for B. burgdorferi often do not lack an
antibody response.
A patient may have a strong positive response (IgG or IgM) to two
genus-species-specific
immunoblot bands for B. burgdorferi and have negative serologic test
results because
of the existing test criteria. For these reasons, some doctors may
treat patients
without qualifying clinical or serologic evidence of Lyme disease. In
my view, many
of these patients are helped greatly by treatment.
Karen D. Holmes, B.S.E.E.
1381 Peggy Ave.
Campbell, CA 95008
holm...@sbcglobal.net
To the Editor: The article by Feder et al. on the proper therapy of
chronic Lyme
disease addresses a very timely concern. Unfortunately, the authors'
statement
that there are no "scientific data" that support persistent B.
burgdorferi
infection in the face of negative serologic test results is erroneous.
In 1988,
we reported on 17 patients who had all had erythema migrans, received
inadequate
antibiotic therapy, had vigorous T-cell blastogenesis to borrelia
antigens, and
were seronegative on the basis of enzyme-linked immunoassay.1,2 The
majority of
these patients had improvement after definitive antibiotic therapy.
Seronegative
infection was confirmed by other laboratories using polymerase-chain-
reaction (PCR)
assays to document the presence of microbes in seronegative patients.
3,4 Abrogation
of a humoral response by removal of the bulk of microbial antigens has
been seen
in other settings, including infection with Treponema pallidum.
Although the use
of repeated courses of antibiotics for a putative borrelia infection
is unsupported
and may cause serious morbidity,5 persons with evidence of previously
inadequately
treated Lyme disease may be seronegative and may benefit from adequate
antibiotic
therapy. Fortunately, erythema migrans is now more readily recognized,
and occult
Lyme disease is rarer. In the absence of antibiotic treatment, most
persons become
seropositive.
David J. Volkman, M.D., Ph.D.
State University of New York at Stony Brook
Stony Brook, NY 11794
volk...@optonline.net
References
1. Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ, Thomas J,
Golightly MG. Seronegative
late Lyme borreliosis: dissociation of specific T- and B-lymphocyte
responses to
Borrelia burgdorferi. N Engl J Med 1988;319:1441-1446. [Abstract]
2. Volkman D. Prophylaxis after tick bites. Lancet Infect Dis
2007;7:370-371.
[CrossRef][ISI][Medline]
3. Keller TL, Halperin JJ, Whitman M. PCR detection of Borrelia
burgdorferi DNA
in cerebrospinal fluid of Lyme neuroborreliosis patients. Neurology
1992;42:32-42.
[Free Full Text]
4. Oksi J, Uksila J, Marjamäki M, Nikoskelainen J, Viljanen MK.
Antibodies against
whole sonicated Borrelia burgdorferi spirochetes, 41-kilodalton
flagellin, and P39
protein in patients with PCR- or culture-proven late Lyme borreliosis.
J Clin Microbiol
1995;33:2260-2264. [Abstract]
5. Klempner MS, Hu LT, Evans J, et al. Two controlled trials of
antibiotic treatment
in patients with persistent symptoms and a history of Lyme disease. N
Engl J Med
2001;345:85-92. [Free Full Text]
To the Editor: The appraisal of chronic Lyme disease by Feder et al.
requires reevaluation.
The strong recommendations made by the authors are based on a
relatively small number
of subjects, do not reflect clinical evidence, and do not take into
account the
International Lyme and Associated Diseases Society (ILADS) clinical
practice guidelines.
It is time the medical community acknowledged Lyme disease as another
example of
"clinical equipoise" -- an absence of consensus within the clinical
community
-- and established publishing standards accordingly.
When clinical equipoise exists, it is even more critical for the
medical community
to be able to evaluate conflicting positions, the basis for the
medical evidence
cited, study criteria, and professional agendas and conflicts of
interest that may
exist. Only by airing these different points of view will the medical
and scientific
communities reach a better understanding of controversial topics such
as chronic
Lyme disease.
Currently, medical experts in support of the ILADS clinical practice
guidelines
are rarely, if ever, included in the process of scientific reviews. In
the spirit
of good science, I would suggest that this be changed.
Daniel J. Cameron, M.D., M.P.H.
First Medical Associates
Mt. Kisco, NY 10549
cam...@lymeproject.com
To the Editor: As an infectious-diseases consultant practicing in a
highly Lyme-endemic
area for more than 30 years, I have often seen patients who, convinced
that they
have chronic Lyme infection, leave my office disappointed or even
angry at my refusal
to prescribe prolonged antibiotic treatment. The article by Feder et
al. is a valuable
resource that I have already installed on my desktop. I salute the
authors'
efforts to refute those who would offer potentially hazardous
treatment that is
not evidence based, bolstered by reams of meaningless data from
"special"
laboratories and from Web sites rife with testimonials but bereft of
scientific
evidence. The balance between compassion for patients in distress and
adherence
to the evidence is exemplary and should be a help to patients and to
their physicians.
Good intentions do not justify improper treatment.
Mark S. Drapkin, M.D.
Newton-Wellesley Hospital
Newton, MA 02462
The author replies: My colleagues and I agree with Mayer and Merz that
Ixodes scapularis
ticks can transmit Anaplasma phagocytophilum, Babesia microti, or
rarely, both of
these pathogens, and that in the right clinical setting, appropriate
diagnostic
testing for these agents is warranted.1 There is no evidence that
these or any other
ticks transmit bartonella.1 There is also no evidence for the
existence of chronic
anaplasma infection in humans, nor is there any published clinical
evidence that
an active tick-borne coinfection is the explanation for symptoms in
the vast majority
of patients with post-Lyme disease syndrome.2
Maloney raises several issues that we fully address in our article. B.
burgdorferi,
like other spirochetes, predominantly resides in the extracellular
matrix. Moreover,
patients with post-Lyme disease syndrome who received a 2-month course
of doxycycline,
an antibiotic that enters cells, had no greater improvement than those
who received
placebo.2
Holmes attaches undue significance to serologic reactivity that fails
to meet conventional
guidelines for seropositivity. It is important to recognize that
reactivity to one
or more antigens of B. burgdorferi on immunoblot occurs in more than
50% of the
general population because of the production of cross-reactive
antibodies directed
at either other bacteria or nonbacterial antigens. Indeed, the
principal reason
that the U.S. Public Health Service recommended both two-tier testing
and the use
of evidence-based criteria for interpreting immunoblots in 1995 was to
reduce the
number of false positive results. Use of immunoblot criteria with poor
specificity
contributes to substantial numbers of misdiagnosed cases and furthers
public misperceptions
of Lyme disease.
We disagree with Volkman. Seronegativity is unexpected in patients
with any manifestation
of late Lyme disease (e.g., Lyme arthritis).1 Cell-proliferation
assays do not provide
adequate evidence for the existence of seronegative Lyme disease
because this method
has an unacceptably high rate of false positive results (in one study
the specificity
was only 33%3). Similarly, certain studies using PCR assays in
patients with possible
Lyme disease also failed to meet high-level standards for scientific
evidence. False
positive results for the detection of DNA of B. burgdorferi by PCR
testing are well
recognized.4 Approaches to improving the reliability of PCR tests
include avoiding
nested-primer protocols, sequencing amplicons to confirm their
identity, and using
positive controls with distinctive sequences. Positive results may be
confirmed
by amplification of multiple gene targets and testing in separate
laboratories in
different locations.
The term "clinical equipoise," used by Cameron, is difficult to
justify
in view of the published reports of five double-blind, randomized,
placebo-controlled
clinical trials that have convincingly demonstrated that antibiotic
treatment of
post-Lyme disease symptoms is not in the best interests of patients.5
Our article
summarizes the consensus among clinicians who practice evidence-based
medicine,
such as Drapkin, whom we thank for his comments.
Henry M. Feder, Jr., M.D.
University of Connecticut Health Center
Farmington, CT 06030
hfe...@nso2.uchc.edu
for the Ad Hoc International Lyme Disease Group
References
1. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical
assessment, treatment,
and prevention of Lyme disease, human granulocytic anaplasmosis, and
babesiosis:
clinical practice guidelines by the Infectious Diseases Society of
America. Clin
Infect Dis 2006;43:1089-1134. [Erratum, Clin Infect Dis 2007;45:941.]
[CrossRef][ISI][Medline]
2. Klempner MS, Hu LT, Evans J, et al. Two controlled trials of
antibiotic treatment
in patients with persistent symptoms and a history of Lyme disease. N
Engl J Med
2001;345:85-92. [Free Full Text]
3. Zoschke DC, Skemp AA, Defosse DL. Lymphoproliferative responses
to Borrelia
burgdorferi in Lyme disease. Ann Intern Med 1991;114:285-289. [ISI]
[Medline]
4. Aguero-Rosenfeld ME, Wang G, Schwartz I, Wormser GP. Diagnosis
of Lyme borreliosis.
Clin Microbiol Rev 2005;18:484-509. [Free Full Text]
5. Halperin J. Prolonged Lyme disease treatment: enough is enough.
Neurology
(in press).
cowabu...@yahoo.com
> �To: SpinL...@yahoogroups.com, kshep...@calea.org, fitz...@gmail.com,
> patrick.fitzger...@usdoj.gov, modelt1...@sbcglobal.net,
> jdra...@nejm.org, lett...@courant.com, Jgerberd...@cdc.gov,
> len...@courant.com, michael.c...@po.state.ct.us,
> conn...@po.state.ct.us, executive-edi...@nytimes.com, managing-
> edi...@nytimes.com, news-t...@nytimes.com, the-a...@nytimes.com,
> biz...@nytimes.com, fore...@nytimes.com, me...@nytimes.com,
> natio...@nytimes.com, dv...@cdc.gov, brigidcalla...@optonline.net,
> t...@hotmail.com, ubi...@courant.com, m...@concentric.net,
> campb...@courant.com, jhornber...@fff.org, thomas.car...@usdoj.gov,
> thomas.r...@po.state.ct.us, kur...@washpost.com,
> georgew...@washpost.com, hor...@courant.com,
> commissioner....@po.state.ct.us, cohencol...@aol.com,
> FalNie...@aol.com, bransfi...@comcast.net, vtsh...@comcast.net,
> o...@po.state.ct.us, d...@davila-dilzer.com,
> scott.mur...@po.state.ct.us, governor.r...@po.state.ct.us,
> attorney.gene...@po.state.ct.us, randall.samb...@usdoj.gov
> Cc: fran...@ucia.gov, dr-ahmadine...@president.ir,
> eugenerobin...@washpost.com, hor...@courant.com,
> bmil...@newstimes.com, t...@hotmail.com, rastr...@aol.com,
> billcurr...@gmail.com, thomas.car...@usdoj.gov, amcgui...@rms-law.com,
> rjmur...@aol.com, paulcraigrobe...@yahoo.com,
> sidney_blument...@yahoo.com, criminal.divis...@usdoj.gov,
> karla.dobin...@usdoj.gov, christopher.chris...@usdoj.gov
>
> References
>
> � �1. Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ, Thomas J,
> Golightly MG. Seronegative
> late Lyme borreliosis: dissociation of specific T- and B-lymphocyte
> responses to
> Borrelia burgdorferi. N Engl J Med 1988;319:1441-1446. [Abstract]
> � �2. Volkman D. Prophylaxis after tick bites. Lancet Infect Dis
> 2007;7:370-371.
> [CrossRef][ISI][Medline]
> � �3. Keller TL, Halperin JJ, Whitman M. PCR detection of Borrelia
> burgdorferi DNA
> in cerebrospinal fluid of Lyme neuroborreliosis patients. Neurology
> 1992;42:32-42.
> [Free Full Text]
>
> References
>
> � �1. Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ, Thomas J,
> Golightly MG. Seronegative
> late Lyme borreliosis: dissociation of specific T- and B-lymphocyte
> responses to
> Borrelia burgdorferi. N Engl J Med 1988;319:1441-1446. [Abstract]
> � �2. Volkman D. Prophylaxis after tick bites. Lancet Infect Dis
> 2007;7:370-371.
> [CrossRef][ISI][Medline]
> � �3. Keller TL, Halperin JJ, Whitman M. PCR detection of Borrelia
> burgdorferi DNA
> in cerebrospinal fluid of Lyme neuroborreliosis patients. Neurology
> 1992;42:32-42.
> [Free Full Text]
Wow! This is so rare, an actual on topic post from you and for the
most part without any of your insane babbling preceding it (only a
little bit).
What you should note is that no one is "slamming" anyone else here.
What is going on is a civil discussion pointing out differences.
In fact, the difference between volkman (a man of the people) and
Feder are minor and probably more minor than you would like to think.
When Volkman says that the seronegative patients might benefit from
"adequate" antibiotic therapy he probably means a few weeks or months
at most, not forever as the llmds prescribe.
But no one is calling one another names or accusing one another of
crimes.
In other words this is how actual real scientists conduct discussions.
They don't rant rave babble or scream.
If you weren't lying about being a scientist you would realize that.
Maybe your method of discussion is common among neo nazi lunatic
pieces of shit though.
cowabu...@yahoo.com
most part without any of your insane babbling preceding it (only a
little bit).
What you should note is that no one is "slamming" anyone else here.
What is going on is a civil discussion pointing out differences.
In fact, the difference between volkman (a man of the people) and
Feder are minor and probably more minor than you would like to think.
When Volkman says that the seronegative patients might benefit from
"adequate" antibiotic therapy he probably means a few weeks or months
at most, not forever as the llmds prescribe.
But no one is calling one another names or accusing one another of
crimes.
In other words this is how actual real scientists conduct
discussions.
They don't rant rave babble or scream.
If you weren't lying about being a scientist you would realize that.
Maybe your method of discussion is common among neo nazi lunatic
pieces of shit though.
>
> References
>
> � �1. Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ, Thomas J,
> Golightly MG. Seronegative
> late Lyme borreliosis: dissociation of specific T- and B-lymphocyte
> responses to
> Borrelia burgdorferi. N Engl J Med 1988;319:1441-1446. [Abstract]
> � �2. Volkman D. Prophylaxis after tick bites. Lancet Infect Dis
> 2007;7:370-371.
> [CrossRef][ISI][Medline]
> � �3. Keller TL, Halperin JJ, Whitman M. PCR detection of Borrelia
> burgdorferi DNA
> in cerebrospinal fluid of Lyme neuroborreliosis patients. Neurology
> 1992;42:32-42.
> [Free Full Text]
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