1999- Annals of Medicine, 31(3):225-32
32 of 165 patients treated with 3 months of antibiotics had culture or PCR evidence of he live spirochetes in 40% of patients who relapsed. The authors concluded:
"We conclude that the treatment of Lyme Borreliosis with appropriate antibiotics for even more than 3 months may not always eradicate the sprirochetes."
1998- Annals of the Rheumatic Diseases, 57(2):118-21
Detection of Borrelia burdorferi by PCR in the synovial membrane, but not the synovial fluid from patients with persiting Lyme arthritis after antibiotic therapy.
1997- American College of Rheurmatology, Voll 40(9) Suppl, Sept,p.S270
PCR evidence for Borrelia burdorferi DNA in synovium in absence of positive serology.
1996- Infection,24(3):218-26 Formation and cultivation of Borrelia spheroblast L-forms variants. "The persistence of Bb even after therapy with antbiotics has been demonstrated in cerebral spinal fluid, in skin, iris, heart and joint biopsies." The authors suggest that atypical forms may allow Borrelia to survive antibiotic treatment.
1993- Arthritis and Rheumatism,36(11):1621-8 Persistence of Borrelia burdorferi in ligamentous tissue from a patient with chronic Lyme borreliosis.
1993- Clinical Orthopedics, 297:238-41 Chronic septic arthritis causes by Bb.
1993- Neurology, 43(12):2705-7 Stroke due to Lyme disease
1989- Survival of Borrelia burdorferi an antibiotically treated patients with Lyme Borreliosis
"...it has become questionalbe if a definite eradication of Bb with antibiotics is possible."
1993- JAMA,(270):1369. SERONEGATIVE LYME DISEASE (Steere AC.)
"THERE IS LITTLE QUESTION THAT SERONEGATIVE LYME CAN EXIST."
LymeMD- Germantown, Maryland 2008- non published. Persistent Lyme in synovial fluid.
A patient with disseminated Lyme disease including neuroborreliosis, who had received more than 2 years of antibiotics, including 2 courses of IV antibiotics, had a positive Lyme PCR of synovial fluid aspirated from knee.
Clinical Immunology- Textbook- 2008- Page 390 "Only a few intracellular bacteria, such as L. monocytogenes, are sterily eradicated once the immune response has reached its height. More often, the intracellular habitat provides a protective niche that promotes persistent infection in the face of an ongoing immune response."
10 comments:
It is amazing. Curios how the IDSA board will take this. Dr. Steven Philips at ILADS has put together some slides on it (can be hard to follow).
http://www.ilads.org/Presentation_ChronicLyme.html
Some other good ones:
“Our results suggest that pleomorphic forms, including cystic forms of Borrelia burgdorferi may persist in the brain and may explain the long latent stage and persisting infection in Lyme neuroborreliosis. . . Borrelia burgdorferi can persist in the brain in Lyme neuroborreliosis and may initiate and sustain chronic inflammation and tissue damage"
J. Miklossy, et. al., Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis, Journal of Neuroinflammation 2008, 5:40doi
"Our results show that spirochetes are viable, transmissible, and express antigen (based upon immunohistochemistry) following antibiotic treatment, particularly when commenced during the late stage of infection.”
Hodzic E., et. al., Persistence of Borrelia burgdorferi Following Antibiotic Treatment in Mice, Antimicro Agents Chemother, 52(5):1728-1736.
"it appears likely that B. burgdorferi maintains a persistent infection with live organisms"
Straubinger, R.K. et. al., Status of Borrelia burgdorferi Infection after Antibiotic Treatment and the Effects of Corticosteroids: An Experimental Study, The Journal of Infectious Diseases 2000
"Some patients with Lyme borreliosis may require more than the currently recommended two to three week course of antibiotic therapy to eradicate strains of the spirochete which grow slowly"
MacDonald A.B., B.W. Berger, and T.G. Schwan, Clinical implications of delayed growth of the Lyme borreliosis spirochete, Borrelia burgdorferi, Acta Trop 48
"The likely reason for relapse is failure to eradicate the spirochete...This is reminiscent of far advanced neurosyphilis"
Logigian E.L., R.F. Kaplan, and A.C. Steere. 1990. Chronic neurologic manifestations of Lyme disease, New England Journal of Medicine, 323(21)
"suggests that B. burgdorferi may be among the small number of bacteria that can cause chronic infection by localizing within host cells where they remain sequestered from some antimicrobial agents and the host humoral immune response"
Klempner M.S., R. Noring, and R.A. Rogers. Invasion of human skin fibroblasts by the Lyme disease spirochetes, Borrelia burgdorferi. Journal of Infectious Diseases
And more:
http://www.lymeinfo.net/medical/LDPersist.pdf, accessed February 3, 2008
Clinical implications of delayed growth of the Lyme borreliosis spirochete, Borrelia burgdorferi
MacDonald AB; Berger BW; Schwan TG.
1990
Clinical implications of delayed growth of the Lyme borreliosis spirochete, Borrelia burgdorferi.
Acta Trop, Dec;48(2):89-94
Active cases of Lyme disease may show clinical relapse following antibiotic therapy. The latency and relapse phenomena suggest that the Lyme disease
spirochete is capable of survival in the host for prolonged periods of time. We studied 63 patients with erythema migrans, the pathognomonic cutaneous
lesion of Lyme borreliosis, and examined in vitro cultures of biopsies from the active edge of the erythematous patch. Sixteen biopsies yielded spirochetes
after prolonged incubations of up to 10.5 months, suggesting that Borrelia burgdorferi may be very slow to divide in certain situations. Some patients with
Lyme borreliosis may require more than the currently recommended two to three week course of antibiotic therapy to eradicate strains of the spirochete which grow slowly..
For those who want to moan and complain (and I know they exist) that all of these studies are "old" and therefore meaningless(well, of COURSE they are old. That's the point!) here's a newer one for you...
"Persisting atypical and cystic forms of Borrelia burgdorferi and
inflammation in Lyme neuroborrelisis"
Judith Miklossy , Sandor Kasas , Anne D Zurn , Shermann McCall, Sheng Yu and Patrick L McGeer
Journal of Neuroinflammation 2008, 5:40doi:10.1186/1742-2094-5-40
Published: 25 September 2008
http://www.jneuroinflammation.com/content/5/1/40
Background
The long latent stage seen in syphilis, followed by chronic central nervous system infection and inflammation, can be explained by the persistence of atypical cystic and granular forms of Treponema pallidum.
We investigated whether a similar situation may occur in Lyme neuroborreliosis.
Method: Atypical forms of Borrelia burgdorferi spirochetes were induced exposing cultures of Borrelia burgdorferi (strains B31 and ADB1) to such unfavorable conditions as osmotic and heat shock, and exposure to the binding agents Thioflavin S and Congo red.
We also analyzed whether these forms may be induced in vitro, following infection of primary chicken and rat neurons, as well as rat and human astrocytes.
We further analyzed whether atypical forms similar to those induced in vitro may also occur in vivo, in brains of three patients with Lyme neuroborreliosis.
We used immunohistochemical methods to detect evidence of neuroinflammation in the form of reactive microglia and astrocytes.
Results: Under these conditions we observed atypical cystic, rolled and granular forms of these spirochetes. We characterized these abnormal forms by histochemical, immunohistochemical, dark field and atomic force microscopy (AFM) methods.
The atypical and cystic forms found in the brains of three patients with neuropathologically confirmed Lyme neuroborreliosis were identical to those induced in vitro.
We also observed nuclear fragmentation of the infected astrocytes using the TUNEL method. Abundant HLA-DR positive microglia and GFAP positive reactive astrocytes were present in the cerebral cortex.
Conclusion: The results indicate that atypical extra- and intracellular pleomorphic and cystic forms of Borrelia burgdorferi and local neuroinflammation occur in the brain in chronic Lyme neuroborreliosis.
The persistence of these more resistant spirochete forms, and their intracellular location in neurons and glial cells, may explain the long latent stage and persistence of Borrelia infection.
The results also suggest that Borrelia burgdorferi may induce cellular dysfunction and apoptosis. The detection and recognition of atypical, cystic and granular forms in infected tissues is essential for the diagnosis and the treatment as they can occur in the absence of the typical spiral Borrelia form.
Staris,
I am sorry that I see now that you posted that one already....my bad. The brain isn't always what it should be. Sigh.
Anyway, sorry.
Money. Power. Greed. Insanity. Arrogance.
Your struggles are not unusual -- my LLMD, Dr Joseph Jemsek, has been through medical board battles for treating Lyme. You might give him a call, perhaps for moral support? - he's now in Fort Mill, SC and listed as Jemsek Specialty Clinic.
I am a longtime patient.
The only way to change the treatment guidelines and save all good doctors like our friend here is a massive grassroots campaign. It will take strength in great numbers to make a paradigm shift.
I just came across this opportunity today. Please spread the word.
It is buried on the IDSA homepage under "Lyme Disease Guidelines Review". It was published on their site on 2/2/09.
IDSA Lyme Disease Review Panel Announces Public Input Period and Hearing Date
IDSA has convened a review panel to examine whether the Society’s Lyme Disease guidelines, published in 2006, should be revised or updated based on a rigorous review of the medical and scientific evidence on the diagnosis and treatment of Lyme Disease.
The Review Panel is initiating a 60-day input period to allow the public to submit information to ensure that all points of view are taken into consideration. There will also be an open public hearing to offer a forum for the presentation of relevant information on the diagnosis and treatment of Lyme Disease.
The 60-day public input period is now open. Interested individuals and organizations may submit information as follows:
Submissions* must be received by 5:00 PM Eastern, April 3, 2009 and must include:
1. Statement (< 5 pages) including:
a. Name and contact information of the submitter
b. Issue(s)/concern(s) and relevance to 2006 IDSA Lyme Disease guidelines; and/or
c. Issue(s) not covered in the 2006 IDSA Lyme Disease guidelines
2. Reference list of supporting data (if available) (<2 pages)
Submissions should be made to the attention of the “IDSA Lyme Disease Review Panel” at: lyme@idsociety.org.
The Review Panel is committed to considering all points of view. The Panel respectfully requests that those submitting comments not exceed the page limit in order to ensure that Panel members have ample opportunity to review all comments.
*Note that submissions may be posted Online by IDSA for public viewing.
Open Public Hearing April 27
The Review Panel will hold an open public hearing on Monday, April 27, 2009 in the Washington, DC area (location to be determined). Additional information, including how to apply to be a presenter, is forthcoming.
I have a question, this is in a way a medical question and a civil rights question. If a party sees fit to deny me medical attention through their actions towards my personal physician because of bias and or unproven accusations then do I have recourse against said parties, to include the accuser and investigating parties with a class action suit on behalf of all patients denied medical attention?
If I suffer pain and hardship as a result can I sue the accuser if she is found to be reckless and or one with ulterior motives?
Denying is a way of negligence that should be punished. Continuing with the documentation the Dr. presents here, where Lyme is not accepted even though the evidence; would like to add that also, the treatment with long course of antibiotics is denied and the symptoms are considered “post Lyme’ instead of being treated until they are gone. As a patient I can say that when treated with the appropriate antibiotic the arthritis symptom goes, when left unattended or treated with the wrong medicine it comes back; and again treated with the proper one it goes away; which demonstrates it is not a “post symptom” but a present indicator of the illness. The wrong grows with pages like this that read: “These immunological studies suggest that cell-mediated immune disruption in the Lyme patient amplifies the inflammatory process, often rendering it chronic and self-perpetuating, regardless of whether the Borrelia bacterium is still present in the host. This would be a form of pathogen-induced autoimmune disease.[162] It is therefore possible that chronic symptoms could come from an autoimmune reaction, even after the spirochetes have been eliminated from the body. This hypothesis may explain chronic arthritis that persists after antibiotic therapy, but the wider application of this hypothesis is controversial.[163][164] : http://en.wikipedia.org/wiki/Lyme_disease#Post-Lyme_disease_symptoms_and_.22chronic_Lyme_disease.22 NOT TRUE IN MY EXPERIENCE!
BAD HYPOTHESIS THAT MIGHT LEAD TO NEGLIGENCE!
MARIA J.
Wikipedia was edited. The ILADS stuff was removed.
Autoimmunity is poorly understood. It is genetically determined and effects only specific tissues in the body. This IDSA- unsubstantiated theory makes no sense based on the science as it now understood.
It is clearly known that the body cannot be sterilized of intracellular pathogens such as Lyme.
The application of this theory is not controversial. It is complete rubbish. Don't ask me; aske scientists and immunologists.
Post a Comment