|
| |
|
SCIENTIFIC PROOF OF CHRONIC LYME |
NONE
of the work on this page is mine. I have provided direct links to the
original work. If this work is from your site and you do not want it displayed
here please email me and I will remove it immediately. b10g7@verizon.net
FROM:
Cheryl's Lyme Info .Net Website Lyme Files
SPECIAL COMPILATIONS OF SCIENTIFIC ABSTRACTS:
The following files were developed by a Lyme patient, and are provided here
with permission. They require Adobe Acrobat which, if not already on your
computer, can be downloaded for free at:
adobe.com If you have acrobat reader, but still experience difficulty
viewing the files, see "Enabling
the Browser"
http://www.lymeinfo.net/LDPersist.pdf
and
http://www.lymeinfo.net/lymefiles.html#sci
From: http://www.lymealliance.org/research/grier/grier_5.php
Chronic Lyme Post-Mortem Study
Needed
Editorial by Tom Grier:
SNIPPED to references:
- Schmidli J, Hunzicker T, Moesli P, et al, Cultivation of Bb from joint
fluid three months after treatment of facial palsy due to Lyme Borreliosis.
J Infect Dis 1988;158:905-906
- Liegner KB, Shapiro JR, Ramsey D, Halperin AJ, Hogrefe W, and Kong L.
Recurrent erythema migrans despite extended antibiotic treatment with
minocycline in a patient with persisting Borrelia burgdorferi infection. J.
American Acad Dermatol. 1993;28:312-314
- Waniek C, Prohovnik I, Kaufman MA. Rapid progressive frontal type dementia
and death with subcortical degeneration associated with Lyme disease. A
biopsy confirmed presence of Borrelia burgdorferi post-mortem. A case
report/abstract/poster presentation. LDF state of the art conference with
emphasis on neurological Lyme. April 1994, Stamford, CT*
- Lawrence C, Lipton RB, Lowy FD, and Coyle PK. Seronegative Chronic
Relapsing Neuroborreliosis. European Neurology. 1995;35(2):113-117
- Cleveland CP, Dennler PS, Durray PH. Recurrence of Lyme disease presenting
as a chest wall mass: Borrelia burgdorferi was present despite five months
of IV ceftriaxone 2g, and three months of oral cefixime 400 mg BID. The
presence of Borrelia burgdorferi confirmed by biopsy and culture. Poster
presentation LDF International Conference on Lyme Disease research,
Stamford, CT, April 1992 *
- Haupl T, Hahn G, Rittig M, Krause A, Schoerner C, Schonnherr U, Kalden JR
and Burmester GR: Persistence of Borrelia burgdorferi in ligamentous tissue
from a patient with chronic Lyme Borreliosis. Arthritis and Rheum
1993;36:1621-1626
- Lavoie Paul E MD. Protocol from Rakel's: Explains persistence of infection
despite "standard" courses of antibiotics. Lyme Times-Lyme Disease
Resource Center 1992;2(2): 25-27 Reprinted from Conn's Current Therapy 1991
- Masters EJ, Lynxwiler P, Rawlings J. Spirochetemia after continuous high
dose oral amoxicillin therapy. Infect Dis Clin Practice 1994;3:207-208
- Pal GS, Baker JT, Wright DJM. Penicillin resistant Borrelia encephalitis
responding to cefotaxime. Lancet I (1988) 50-51
- Preac-Mursic V, Wilske B, Schierz G, et al. Repeated isolation of
spirochetes from the cerebrospinal fluid of a patient with
meningoradiculitis Bannwarth' Syndrome. Eur J Clin Microbiol 1984;3:564-565
- Preac-Mursic V, Weber K, Pfister HW, Wilske B, Gross B, Baumann A, and
Prokop J. Survival of Borrelia burgdorferi in antibiotically treated
patients with Lyme Borreliosis Infection 1989;17:335-339
- Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the Lyme
Disease spirochete, Borrelia burgdorferi from ceftriaxone in vitro. J.
Infect Dis 1992;166:440-444
- Haupl TH, Krause A, Bittig M. Persistence of Borrelia burgdorferi in
chronic Lyme Disease: altered immune regulation or evasion into
immunologically privileged sites? Abstract 149 Fifth International
Conference on Lyme Borreliosis, Arlington, VA, 1992 *
- Lavoie Paul E. Failure of published antibiotic regimens in Lyme
borreliosis: Observations on prolonged oral therapy. Abstract presented at
the 1990 Lyme Borreliosis International Conference in Sweden.*
- Fried Martin D, Durray P. Gastrointestinal Disease in Children with
Persistent Lyme Disease: Spirochetes isolated from the G.I. tract . 1996 LDF
Lyme Conference Boston, MA, Abstract*
- Neuroboreliosis: In the journal Annals of Neurology Vol. 38, No 4, 1995,
there was a brief article by Dr. Andrew Pachner MD, Elizabeth Delaney BS,
and Tim O'Neill DVM, Ph.D. The conclusion of the article was simple and
concise: " These data suggest that Lyme neuroboreliosis represents
persistent infection with B. burgdorferi." The study used nonhuman
primates as a model for human neuroborreliosis, and used a special PCR
technique to detect the presence of Borrelia DNA within specific structures
of the brains of five rhesus monkeys. The monkeys were injected with strain
N40Br of Borrelia burgdorferi, and later autopsied for analysis.
From: http://www.centurytel.net/tjs11/bug/blot1.htm#n6
"These data suggest that LYME NEUROBORELIOSIS REPRESENTS PERSISTENT
INFECTION WITH b. BURGDORFERI."
The study used nonhuman primates as a model for human neuroborreliosis, and
used a special PCR technique to detect the presence of Borrelia DNA within
specific structures of the brains of five rhesus monkeys. The monkeys were
injected with strain N40Br of Borrelia burgdorferi, and later autopsied for
analysis.
ABSTRACT SUMMARIES:
- Abstract # D654 - J. Nowakowski, et al. Culture-Confirmed Treatment
Failures of Cephalexin Therapy for Erythema Migrans. Two of six patients
biopsied had culture confirmed Borrelia burgdorferi infections despite up to
21 days of cephalexin (500 mg TID) antibiotic treatment.
- Abstract # D655 - Nowakowski, et al, Culture-confirmed infection and
reinfection with Borrelia burgdorferi. A patient, despite antibiotic
therapy, had a recurring Erythema Migrans rash on three separate occasions.
On each occasion it was biopsied, which revealed the active presence of
Borrelia burgdorferi on two separate occasions, indicating reinfection had
occurred.
- Abstract # D657 - J. Cimperman, F. Strle, et al, Repeated Isolation of
Borrelia burgdorferi from the cerebrospinal fluid (CSF) of two patients
treated for Lyme neuroborreliosis.
Patient One was a twenty year old woman who presented with meningitis but
was seronegative for Borrelia burgdorferi. Subsequently, six weeks later
Bb was cultured from her CSF and she was treated with IV Rocephin 2 grams
a day for 14 days. Three months later, the symptoms returned and Bb was once
again isolated from the CSF.
Patient 2 was a 51 year old female who developed an EM rash after tick
bite. Within two months she had severe neurological symptoms. Her serology
was negative. She was denied treatment until her CSF was culture positive
nine months post-tick bite.
She was treated with 2 grams of Rocephin for 14 days. Two months
post-antibiotic treatment, Bb was once again cultured from her CSF.
In both of these cases, the patients had negative antibodies but were
culture positive, suggesting that the antibody tests are not reliable
predictors of neurological Lyme Disease. Also, standard treatment regimens
are insufficient when infection of the CNS is established and Bb can survive
in the brain despite intravenous antibiotic treatment.
- Patients with ACA shed Bb DNA post treatment: Aberer E, et al. Success and
Failure in the treatment of Acrodermatitis Chronica Atrophicans (ACA) skin
rash. Infection 24(1):85-87 1996.
ACA is a late stage skin rash usually attributed to Borrelia afzelii, it
is sometimes mistaken for scleroderma.
Forty-six patients with ACA were treated with either 14 days of IV
Rocephin or thirty days of oral penicillin or doxycycline and followed up
for one year. Of those treated with IV, 28% had no improvement, and 40%
still shed Bb antigen in their urine. Of the oral group, 70% required
retreatment. Conclusion: Proper length of treatment for ACA has yet to be
determined.
- Logigian EL, McHugh GL, Antibiotics for Early Lyme Disease May Prevent
Full Seroconversion but not CNS Infection. 1997 ABSTRACT # S66.006 Neuloogy
Symposia, NEUROLOGY 1997; A388:48.
In this study, 22 late-stage neurological patients who met the Centers
for Disease Control (CDC) criteria for Lyme disease were studied over a
three year period.
Eighty-five percent of seronegative patients who still had active
disseminated infection had been treated within one month of tick bite. This
means that early antibiotic treatment may make you test negative, but you
still progress to develop encephalitis.
Without antibodies your brain has no natural immunity or local immune
system to fight the infection, so WITHDRAWING ANTIBIOTICS CAUSES THE
INFECTION IN THE CENTRAL NERVOUS SYSTEM (CNS) TO GO UNABATED. Patients who
go on to develop brain infections despite antibiotics, may have suppressed
antibody production thus worsening any remaing active infection in the
Central Nervous System.
- Arthritis: A three year follow-up: Valesova H, Mailer J, et al. Long-term
results in patients with Lyme disease followed for three years after two
weeks of IV Rocephin. Infection 24(1):98-102, 1996.
This study represents another of the problems with author's bias
interpretation of data. Thirty-five Lyme arthritis patients were treated
with a two week course of IV Rocephin. They were then followed for three
years.
At the end of the study, six patients had complete relapses, nineteen had
marked improvement, four had new Lyme symptoms, and the rest were lost to
follow up. The authors conclusion: " The treatment results for this
group of 35 Lyme arthritis patients are considered successful."
Let's look at the figures more closely; Out of a total of 29 patients out
of 35 that were contacted post treatment: 19 improved = 65% 6 relapsed = 20
% 4 worsened = 15 % Does a total of 35% of patients still suffering sound
like successful treatment to you?
This is a treatable disease, but you have to treat it! What if a doctor's
child was one of the 35%? Do you think they would continue go untreated as
suggested by the ACP? How many patients have to relapse before treatment is
considered unsuccessful? Six patients or 20% had complete relapses yet the
conclusion of the study was that in general treatment was considered
successful!
We get better cure rates for Tuberculosis!
Animal vs. Human Studies: Support for the theory that BORRELIA
BURGDORFERI CAN FIND SAFE HAVENS IN SEQUESTERED SITES despite antibiotic
therapy comes from several animal model studies.
However, only a few human cases have yet been published. This is because
the tissue studies that are required almost demand that they be done in a
post-mortem exam. (See Stanek and Appel's work on skin biopsies versus
post-mortem exam of deep tissues in Lyme infected and antibiotic treated
beagles)
- Abstract # D607 - M.J.G. Appel, The persistence of Bb in Dogs after
antibiotic treatment. Seventeen Beagle puppies were infected with Bb from
infected ticks, eleven were treated for four weeks with either Doxycycline
or amoxicillin in doses according to weight. Six were control dogs. 1/11 had
Bb isolated from skin, but 7/11 dogs had Bb isolated from other tissues
during post-mortem.
All of the persistent infected pups had persistent arthritis. Conclusion:
Skin biopsies are not predictive of persistence of infection. Also the
standard excepted four week course of antibiotic treatment in dogs is not
sufficient.
To date, no major multi-center post-mortem Lyme disease study has ever
been done on humans. Without this type of post-mortem study, the debate
between the two disagreeing camps will almost certainly continue.
Results from the European Alzheimers study done by Dr. Judit Miklossy
suggests that post-mortem exams should not only look for persisting
spirochetes in deceased Lyme patients, but should also look for spirochetes
in the brains of deceased dementia patients as well.
- Miklossy Judit. Alzheimer's disease a spirochetosis? Neuro Report
1993;4:841-848o
Thirteen out of thirteen Alzheimer patients had spirochetes in the brain.
None of the age-matched control subjects had evidence of spirochetes in
their brains.
This study suggests that there is a correlation between an Alzheimer's
dementia and CNS spirochetosis in Swiss patients. In other words spirochetes
might contribute to a CNS dementia similar to Alzheimer's disease.
This is not to suggest that all Alzheimer's is caused by spirochetes, but
even if a small percentage of dementia can be prevented by antibiotics then
further studies are justified. None are currently being done!
- Miklossy J, Kuntzer T, Bogousslavsky J, et al. Meningovascular form of
neuroborreliosis: Similarities between neuropathological findings in a case
of Lyme disease and those occurring in tertiary Neurosyphilis. Acta Neuro
Pathol 1990;80:568-572
- [AUTHORS: Jobe DA; Rawal N; Schell RF; Callister SM
TITLE: Detection of borreliacidal antibodies in Lyme borreliosis patient
sera containing antimicrobial agents.
AUTHOR AFFILIATION: Microbiology Research Laboratory, Gundersen Lutheran
Medical Center, La Crosse, Wisconsin 54601, USA.
SOURCE: Clin Diagn Lab Immunol 1999 Nov;6(6):930-3
CITATION IDS: PMID: 10548588 UI: 20018406
ABSTRACT: The borreliacidal-antibody test has been used for the
serological detection and confirmation of Lyme borreliosis. However, the
presence of antimicrobial agents in serum can confound the accurate
detection of borreliacidal antibodies.
In this study, we developed a Bacillus subtilis agar diffusion bioassay
to detect small concentrations of antimicrobial agents in serum.
We also used XAD-16, a nonionic polymeric resin, to adsorb and remove
high concentrations of amoxicillin, cefotaxime, ceftriaxone, cefuroxime,
doxycycline, and erythromycin without significantly affecting even small
concentrations of immunoglobulin M (IgM) or IgG borreliacidal antibodies.
High concentrations of penicillin could also be removed by adding 1 U of
penicillinase without significantly influencing the levels of borreliacidal
antibodies. These simple procedures greatly enhance the clinical utility of
the borreliacidal-antibody test.]
To do these kind of tissue studies of sequestered spirochetal infections takes
nearly heroic efforts in time, costs, and diligence. Yet the few times that
these types of studies have been applied to humans have suggested that Borrelia
burgdorferi can indeed survive and thrive within the human body despite a
complete course - or even several courses - of antibiotic therapy.
Camp A maintains that Lyme disease is relatively easy to diagnose by means of
serology and is easily cured with antibiotics. So it follows that any study
proving active infection post-antibiotics would disprove their position.
Yet despite several such studies and case histories, Camp A still maintains
that persistence of symptoms post-antibiotic treatment of Lyme disease is not
due to persistence of infection.
Why? How can they maintain this position if it has been repeatedly disproved?
|