Topic: Studies On Persistent Borrelia Burgdorferi Infection
METALLlC BLUE
Frequent Contributor (1K+ posts)
Member # 6628
posted
As a lot of you know, I've been reading the scientific literature regarding persistent infection -- in spite of antibiotic therapy -- and have been collecting this data for about a year.
I thought you might find some humor in this contradiction. Here is a study which was published May of 2008.
1: Tidsskr Nor Laegeforen. 2008 May 15;128(10):1175-8.Click here to read Links[Lyme borreliosis in adults][Article in Norwegian]
BACKGROUND: Lyme borreliosis is a MULTISYSTEM: tick-borne infection caused by the spirochete Borrelia burgdorferi. We present a survey of clinical stages, diagnosis, treatment and prognosis of Lyme borreliosis in adults. MATERIAL AND METHODS: The article is based on literature retrieved through database searches and own experience. RESULTS AND INTERPRETATION: In Norway, Lyme borreliosis is most prevalent in coastal areas from the south and up to Tr�ndelag. Lyme disease can be classified into three stages; localised stage, and early and late disseminated stages. A laboratory gold standard does not exist, so the diagnosis is based on a combination of clinical manifestations and indirect detection of the bacteria, most often specific antibodies. Antibody results must be interpreted with caution. No medication is needed after a tick bite, but all manifestations of Lyme borreliosis should be treated with antibiotics according to **guidelines**. The prognosis is generally good. Post Lyme disease with persistent symptoms after borreliosis is a controversial condition. No studies have demonstrated persistent infection with borrelia bacteria in patients with chronic complaints after adequate antibiotic treatment, and additional antibiotic treatment does not improve quality of life in these patients.
NEXT STUDY: The Year 1999
1: Ann Med. 1999 Jun;31(3):225-32.Links Borrelia burgdorferi detected by culture and PCR in clinical relapse of disseminated Lyme borreliosis. Oksi J, Marjam�ki M, Nikoskelainen J, Viljanen MK.
Department of Medicine, Turku University Central Hospital, Finland. [email protected]
A total of 165 patients with disseminated Lyme borreliosis (diagnosed in 1990-94, all seropositive except one culture-positive patient) were followed after antibiotic treatment, and 32 of them were regarded as having a clinically defined treatment failure. Of the 165 patients, 136 were tested by polymerase chain reaction (PCR) during the follow-up. PCR was positive from the plasma of 14 patients 0-30 months after discontinuation of the treatment, and 12 of these patients had a clinical relapse. In addition, Borrelia burgdorferi was cultured from the blood of three patients during the follow-up. All three patients belonged to the group with relapse, and two of them were also PCR positive. This report focuses on the 13 patients with clinical relapse and culture or PCR positivity. Eight of the patients had culture or PCR-proven initial diagnosis, the diagnosis of the remaining five patients was based on positive serology only. All 13 patients were primarily treated for more than 3 months with intravenous and/or oral antibiotics (11 of them received intravenous ceftriaxone, nine for 2 weeks, one for 3 weeks and one for 7 weeks, followed by oral antibiotics). The treatment caused only temporary relief in the symptoms of the patients. All but one of them had negative PCR results immediately after the first treatment. The patients were retreated usually with intravenous ceftriaxone for 4-6 weeks. None of them was PCR positive after the retreatment. The response to retreatment was considered good in nine patients. We conclude that the treatment of Lyme borreliosis with appropriate antibiotics for even more than 3 months may not always eradicate the spirochete. By using PCR, it is possible to avoid unnecessary retreatment of patients with 'post-Lyme syndrome' and those with 'serological scars' remaining detectable for months or years after infection.
And How About This Study:
3: Logigian EL, Kaplan RF, Steere AC. Department of Neurology, Tufts University School of Medicine, Boston, MA 02111.
BACKGROUND AND METHODS. Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi, is associated with a wide variety of neurologic manifestations. To define further the chronic neurologic abnormalities of Lyme disease, we studied 27 patients (age range, 25 to 72 years) with previous signs of Lyme disease, current evidence of immunity to B. burgdorferi, and chronic neurologic symptoms with no other identifiable cause.
Eight of the patients had been followed prospectively for 8 to 12 years after the onset of infection. RESULTS. Of the 27 patients, 24 (89 percent) had a mild encephalopathy that began 1 month to 14 years after the onset of the disease and was characterized by memory loss, mood changes, or sleep disturbance.
Of the 24 patients, 14 had memory impairment on neuropsychological tests,
and 18 had increased cerebrospinal fluid protein levels, evidence of intrathecal production of antibody to B. burgdorferi, or both.
Nineteen of the 27 patients (70 percent) had polyneuropathy with radicular pain or distal paresthesias; all but two of these patients also had encephalopathy.
In 16 patients electrophysiologic testing showed an axonal polyneuropathy. One patient had leukoencephalitis with asymmetric spastic diplegia, periventricular white-matter lesions, and intrathecal production of antibody to B. burgdorferi.
Among the 27 patients, associated symptoms included fatigue (74 percent),
headache (48 percent),
arthritis (37 percent),
and hearing loss (15 percent).
At the time of examination, chronic neurologic abnormalities had been present from 3 months to 14 years, usually with little progression.
Six months after a two-week course of intravenous ceftriaxone (2 g daily),
17 patients (63 percent) had improvement,
6 (22 percent) had improvement but then relapsed, and 4
(15 percent) had no change in their condition.
CONCLUSIONS. Months to years after the initial infection with B. burgdorferi, patients with Lyme disease may have chronic encephalopathy, polyneuropathy, or less commonly, leukoencephalitis. These chronic neurologic abnormalities usually improve with antibiotic therapy.
Ok, you can start laughing now. There are hundreds of studies just like these few I've posted suggesting, implying, and finally stating blatantly, that the bacteria can and does persist in spite of what is currently considered appropriate antibiotic treatment based on the IDSA guidelines.
Now take a look at the names of those people who took part in the last study. See any names that ring a bell? Let me help you. "A.C. Steere."
Now let me show you a statement made by "A.C. Steere" recently before a live audience:
"Over the past several decades, a Lyme disease counterculture has emerged that has ascribed a range of puzzling and poorly understood illnesses to this tick-borne infection. For example, debilitating fatigue or pain syndromes affect millions of people. You say, ``college students frequently feel fatigued''. But imagine the worst pain that you ever had, day after day, or that every day of your life is like your worst day. Medical tests may not reveal a cause. Patients suffer; their families suffer. As physicians, we struggle to understand and help. Such patients are sometimes now diagnosed as having ``chronic Lyme disease''.
Additionally, 5 studies of pain and fatigue syndromes following Lyme disease reported that placebo treatment with a sugar pill gave similar results as long-term antibiotics. If you ignore scientific reality, if you twist it, if you wish for a particular answer, you will miss Mars and drift in space." - Allen Steere
- Going To Mars: Ohio Wesleyan University Commencement Address
E-mail me for a list of studies if you need further proof of this fact. [email protected]
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
"No medication is needed after a tick bite, but all manifestations of Lyme borreliosis should be treated with antibiotics according to **guidelines**."
Sickening, just sickening!!!
No wonder so many people are confused!
If the Steere camp would quit creating so much ontroversy, then maybe we'd actually get somewhere!!!
What they need is to have a big roll of duct tape used on them with some superglue added for good measure!
Thanks for posting some of your research!
Love, Light, & Health, Jennie
-------------------- My Lyme dx:11/05. My Mom's Lyme dx:5/16. ISO ASAP-Lyme Literate Dr & Neurologist-Prefer IL, IN, KY, MO, OH, TN. Can travel farther. Finances limited. Prefer Drs take Medicare or Payments. Need great list to find best fit. Tyvm. Posts: 701 | From Owensboro, KY | Registered: Sep 2005
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sparkle7
Frequent Contributor (5K+ posts)
Member # 10397
posted
It's a classic case of disinformation.
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From Wikipedia-
Disinformation is the deliberate dissemination of false information. It may include the distribution of forged documents, manuscripts, and photographs, or propagation of malicious rumors and fabricated intelligence.
In the context of espionage or military intelligence, it is the deliberate spreading of false information to mislead an enemy as to one's position or course of action.
In the context of politics, it is the deliberate attempt to deflect voter support of an opponent, disseminating false statements of innuendo based on the candidates vulnerabilities as revealed by opposition research.
In both cases, it also includes the distortion of true information in such a way as to render it useless.
Disinformation should not be confused with misinformation, which is merely false information spread by mistake.
Disinformation techniques may also be found in commerce and government, used by one group to try to undermine the position of a competitor.
It in fact is the act of deception and blatant false statements to convince someone of an untruth.
Cooking-the-books might be considered a disinformation strategy that led to the Sarbanes-Oxley Act.
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One might ask, why is this disinformation going on...
I believe it's because it's a bio-engineered weapon that was either released on purpose or escaped from a lab by accident.
Posts: 7772 | From Northeast, again... | Registered: Oct 2006
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"I believe it's because it's a bio-engineered weapon that was either released on purpose or escaped from a lab by accident."
Great minds think alike!
I couldn't agree with you more!
The mere thought of that though just makes me want to !!!!!
Love, Light, & Health, Jennie
-------------------- My Lyme dx:11/05. My Mom's Lyme dx:5/16. ISO ASAP-Lyme Literate Dr & Neurologist-Prefer IL, IN, KY, MO, OH, TN. Can travel farther. Finances limited. Prefer Drs take Medicare or Payments. Need great list to find best fit. Tyvm. Posts: 701 | From Owensboro, KY | Registered: Sep 2005
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METALLlC BLUE
Frequent Contributor (1K+ posts)
Member # 6628
posted
I'm really not sure where researchers get off on saying there isn't enough, or "any" information in the scientific literature that leads one to believe borrelia burgdorferi is a persistent infection. I mean I've read the material. We're talking a very large body of data saying "Yes, persistence is a problem."
2: Rheumatol Int. 1996;16(3):125-32.Links Intracellular persistence of Borrelia burgdorferi in human synovial cells. Girschick HJ, Huppertz HI, R�ssmann H, Krenn V, Karch H.
Children's Hospital, University of W�rzburg, Germany.
To investigate if Borrelia burgdorferi can persist in resident joint cells, an infection model using cell cultures of human synovial cells was established and compared to the interaction of Borrelia burgdorferi and human macrophages. Borrelia burgdorferi were found attached to the cell surface or folded into the cell membrane of synovial cells analysed by transmission electron and confocal laser scanning microscopy. In contrast to macrophages, morphologically intact Borrelia burgdorferi were found in the cytosol of synovial cells without engulfment by cell membrane folds or phagosomes. Borrelia burgdorferi were isolated from parallel cultures. Treatment with ceftriaxone eradicated extracellular Borrelia burgdorferi, but spirochetes were reisolated after lysis of the synovial cells. Borrelia burgdorferi persisted inside synovial cells for at least 8 weeks. These data suggested that Borrelia burgdorferi might be able to persist within resident joint cells in vivo.
7: Ann Neurol. 1995 Oct;38(4):667-9. Links Comment in: Ann Neurol. 1995 Oct;38(4):560-2. Neuroborreliosis in the nonhuman primate: Borrelia burgdorferi persists in the central nervous system. Pachner AR, Delaney E, O'Neill T.
Department of Neurology, Georgetown University School of Medicine, Washington, DC 20007, USA.
Neurological involvement in Lyme disease is common, and is frequently difficult to diagnose and treat. Little is known about the fate of the causative spirochete Borrelia burgdorferi in the central nervous system (CNS). To determine the frequency of parenchymal infection and to determine localization of the organism, polymerase chain reaction/hybridization assays were performed in a newly described model of Lyme neuroborreliosis in nonhuman primates infected with B. burgdorferi. Polymerase chain reaction/hybridization of CNS tissues from 5 infected nonhuman primates was performed. Substantial amounts of B. burgdorferi DNA were detected in the CNS in all infected animals, with a predilection toward subtentorial structures. These data suggest that Lyme neuroborreliosis represents persistent infection with B. burgdorferi.
8: Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853, USA. [email protected]
In specific-pathogen-free dogs experimentally infected with Borrelia burgdorferi by tick exposure, treatment with high doses of amoxicillin or doxycycline for 30 days diminished but failed to eliminate persistent infection. Although joint disease was prevented or cured in five of five amoxicillin- and five of six doxycycline-treated dogs, skin punch biopsies and multiple tissues from necropsy samples remained PCR positive and B. burgdorferi was isolated from one amoxicillin- and two doxycycline-treated dogs following antibiotic treatment. In contrast, B. burgdorferi was isolated from six of six untreated infected control dogs and joint lesions were found in four of these six dogs. Serum antibody levels to B. burgdorferi in all dogs declined after antibiotic treatment. Negative antibody levels were reached in four of six doxycycline- and four of six amoxicillin-treated dogs. However, in dogs that were kept in isolation for 6 months after antibiotic treatment was discontinued, antibody levels began to rise again, presumably in response to [/b]proliferation of the surviving pool of spirochetes.[/b] Antibody levels in untreated infected control dogs remained high.
PMID: 8968890 [PubMed - indexed for MEDLINE]
11: Straubinger RK, Straubinger AF, Summers BA, Jacobson RH, Erb HN. James A. Baker Institute for Animal Health, Ithaca, New York, USA. [email protected]
BACKGROUND: Borrelia burgdorferi, the causative agent of Lyme disease, infects humans and animals. In humans, the disease primarily affects the skin, large joints, and the nervous system days to months after infection. Data generated with appropriate animal model help to understand the fundamental mechanisms of the disease. OBJECTIVE: 1) More clearly define the clinical manifestation and pathogenetic mechanisms of Lyme disease in dogs; 2) evaluate the effect of antibiotics in dogs infected with B. burgdorferi; 3) describe the effects of corticosteroids on dogs persistently infected with B. burgdorferi. DESIGN: Specific-pathogen-free beagles were infected with B. burgdorferi using ticks collected in an endemic Lyme disease area. Clinical signs were recorded daily. Antibody titers were measured by ELISA at two-week intervals. B. burgdorferi organisms were detected in tissues by culture and PCR. Synovial fluids were evaluated microscopically and with a chemotaxis cell migration assay. Histological sections were examined for pathological lesions. Specific cytokine up-regulation in tissues was detected by RT-PCR. INTERVENTIONS: In three separate experiments, B. burgdorferi-infected dogs received antibiotic treatment (amoxicillin; azithromycin; ceftriaxone; doxycycline) for 30 consecutive days. Two subclinical persistently infected dogs received oral prednisone for 14 consecutive days starting at day 420 post-infection. RESULTS: Dogs developed acute arthritis in the joints closest to the tick bites after a median incubation period of 68 days. Synovial membranes of lame and non-lame dogs produced the chemokine IL-8 in response to B. burgdorferi. Antibiotic treatment prevented or resolved episodes of acute arthritis, but failed to eliminate the bacterium from infected dogs. Corticosteroid treatment reactivated Lyme disease in persistently infected dogs, which had not received antibiotics previously. CONCLUSIONS: B. burgdorferi disseminates through tissue by migration following tick inoculation, produces episodes of acute arthritis, and establishes persistent infection. The spirochete survives antibiotic treatment and disease can be reactivated in immunosuppressed animals
13: 1: Infection. 1996 Jan-Feb;24(1):9-16. Links Erratum in: Infection 1996 Mar-Apr;24(2):169. Kill kinetics of Borrelia burgdorferi and bacterial findings in relation to the treatment of Lyme borreliosis. Preac Mursic V, Marget W, Busch U, Pleterski Rigler D, Hagl S. Max v. Pettenkofer Institut, Ludwig-Maximilians-Universit�t M�nchen, Germany.
For a better understanding of the persistence of Borrelia burgdorferi sensu lato (s.l.) after antibiotic therapy the kinetics of killing B. burgdorferi s.l. under amoxicillin, doxycycline, cefotaxime, ceftriaxone, azithromycin and penicillin G were determined. The killing effect was investigated in MKP medium and human serum during a 72 h exposure to antibiotics. Twenty clinical isolates were used, including ten strains of Borrelia afzelii and ten strains of Borrelia garinii. The results show that the kinetics of killing borreliae differ from antibiotic to antibiotic. The killing rate of a given antibiotic is less dependent on the concentration of the antibiotic than on the reaction time. Furthermore, the data show that the strains of B. afzelii and B. garinii have a different reaction to antibiotics used in the treatment of Lyme borreliosis and that different reactions to given antibiotics also exist within one species. The B. garinii strains appear to be more sensitive to antibiotics used in therapy. Furthermore, the persistence of B. burgdorferi s.l. and clinical recurrences in patients despite seemingly adequate antibiotic treatment is described. The patients had clinical disease with or without diagnostic antibody titers to B. burgdorferi.
14: 1: Infection. 1996 Sep-Oct;24(5):347-53. Links Borrelia burgdorferi DNA in the urine of treated patients with chronic Lyme disease symptoms. A PCR study of 97 cases. Bayer ME, Zhang L, Bayer MH. Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
The presence of Borrelia burgdorferi DNA was established by PCR from urine samples of 97 patients clinically diagnosed as presenting with symptoms of chronic Lyme disease. All patients had shown erythema chronica migrans following a deer tick bite. Most of the patients had been antibiotic-treated for extended periods of time. We used three sets of primer pairs with DNA sequences for the gene coding of outer surface protein A (OspA) and of a genomic sequence of B. burgdorferi to study samples of physician-referred patients from the mideastern USA. Controls from 62 healthy volunteers of the same geographic areas were routinely carried through the procedures in parallel with patients' samples. Of the 97 patients, 72 (74.2%) were found with positive PCR and the rest with negative PCR. The 62 healthy volunteers were PCR negative. It is proposed that a sizeable group of patients diagnosed on clinical grounds as having chronic Lyme disease may still excrete Borrelia DNA, and may do so in spite of intensive antibiotic treatment.
The urine of 74.2% of patients previously treated with antibiotics for Lyme disease was found to be positive for B. burgdorferi DNA using PCR testing. All patients (n=97) had prior documented EM rash and had received a minimum of 3 weeks to 2 months oral or intravenous antibiotics. In 4 patients, PCR results were temporarily negative after treatment, but became positive again 4-6 weeks later. All patients suffered .continuing, often gradually worsening Lyme disease-like symptoms. ...it seems to be characteristic for most of the patients in our study that, after antibiotic-free periods of a few months, they had again become increasingly ill with neurological and arthritic symptoms, so that treatment had been resumed.
21: 1: Ann Rheum Dis. 1998 Feb;57(2):118-21. Links Detection of Borrelia burgdorferi by polymerase chain reaction in synovial membrane, but not in synovial fluid from patients with persisting Lyme arthritis after antibiotic therapy. Priem S, Burmester GR, Kamradt T, Wolbart K, Rittig MG, Krause A.
Charit� University Hospital, Department of Medicine III, Rheumatology and Clinical Immunology, Berlin, Germany.
OBJECTIVES: To identify possible sites of bacterial persistence in patients with treatment resistant Lyme arthritis. It was determined whether Borrelia burgdorferi DNA may be detectable by polymerase chain reaction (PCR) in synovial membrane (SM) when PCR results from synovial fluid (SF) had become negative after antibiotic therapy. METHODS: Paired SF and SM specimens and urine samples from four patients with ongoing or recurring Lyme arthritis despite previous antibiotic therapy were investigated. A PCR for the detection of B burgdorferi DNA was carried out using primer sets specific for the ospA gene and a p66 gene of B burgdorferi. RESULTS: In all four cases, PCR with either primer set was negative in SF and urine, but was positive with at least one primer pair in the SM specimens. [b]In all patients arthritis completely resolved after additional antibiotic treatment. CONCLUSIONS: These data suggest that in patients with treatment resistant Lyme arthritis negative PCR results in SF after antibiotic therapy do not rule out the intraarticular persistence of B burgdorferi DNA. Therefore, in these patients both SF and SM should be analysed for borrelial DNA by PCR as positive results in SM are strongly suggestive of ongoing infection.
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
METALLlC BLUE
Frequent Contributor (1K+ posts)
Member # 6628
posted
23: 1: J Infect Dis. 1992 Aug;166(2):440-4. Links Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro. Georgilis K, Peacocke M, Klempner MS. Department of Medicine, New England Medical Center, Boston, Massachusetts.
The Lyme disease spirochete, Borrelia burgdorferi, can be recovered long after initial infection, even from antibiotic-treated patients, indicating that it resists eradication by host defense mechanisms and antibiotics. Since B. burgdorferi first infects skin, the possible protective effect of skin fibroblasts from an antibiotic commonly used to treat Lyme disease, ceftriaxone, was examined. Human foreskin fibroblasts protected B. burgdorferi from the lethal action of a 2-day exposure to ceftriaxone at 1 microgram/mL, 10-20 x MBC. In the absence of fibroblasts, organisms did not survive. Spirochetes were not protected from ceftriaxone by glutaraldehyde-fixed fibroblasts or fibroblast lysate, suggesting that a living cell was required. The ability of the organism to survive in the presence of fibroblasts was not related to its infectivity. Fibroblasts protected B. burgdorferi for at least 14 days of exposure to ceftriaxone. Mouse keratinocytes, HEp-2 cells, and Vero cells but not Caco-2 cells showed the same protective effect. Thus, several eukaryotic cell types provide the Lyme disease spirochete with a protective environment contributing to its long-term survival.
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
posted
Note that Mark Klempner was an author on the last study you cited. He is the one who, funded by NIH, declared that abx did not help chronic cases, not infectious anymore. For this big fat lie, which contradicted his and others previously published articles, he was richly rewarded, got a big germ lab, promotion, etc. Crime pays. Science needs policemen and jails for this kind of person. Instead they are rewarded!
Posts: 8430 | From Not available | Registered: Oct 2000
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jamescase20
Unregistered
posted
Lyme is abx resistent, thats why there stupid fake studies showed no improvment.
Thats why so many of us have turned to natural medicine.
METALLlC BLUE
Frequent Contributor (1K+ posts)
Member # 6628
posted
Reintroducing this, others may have more to say. Feel free to contribute additional studies, I'm still accumulating studies. I have 108 presently.
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
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