Chronic Lyme Post-Mortem Study Needed


Editorial by Tom Grier

Key Words:

  • Antibody: A protein produced by a white-blood-cell to attack bacteria and viruses.
  • Titer: Another word for level, as in level or amount of antibody measured in the blood.
  • Seronegative: Despite an infection there is an absence of antibodies in the blood or serum of the patient.
  • Spirochete: A spiral bacteria in the same family of bacteria as Syphilis.
  • Borrelia burgdorferi: The spirochete bacteria that causes Lyme disease.
  • Erythema Migrans: A red expanding rash on the skin caused by an infected tick bite. An EM rash is diagnostic for Lyme disease even in absence of a positive test.
  • Antigen: Refers to a foreign substance in our blood that is capable of causing an immune response.

There isn’t a disease in the past 100 years that has polarized the medical community more than Lyme disease. From the very beginning, it was misunderstood. In the early 1970’s, two concerned mothers, Polly Murray and Judith Mensch, were convinced that the epidemic of juvenile rheumatoid arthritis (JRA) cases they were seeing in their neighborhoods in Old Lyme, Connecticut, were being contracted as a result of some kind of environmental exposure rather than a genetic disorder. After the state health department admitted that the JRA incidence rate in that area was at least eight times the national average, they somewhat reluctantly decided to investigate the observations of these two woman. Murray and Mensch had to present actual patient case histories they had collected before an investigation was started.

In 1975, a rheumatologist named Dr. Alan Steere first described in medical literature these abnormal cases of JRA as a new type of arthritic disorder. He coined the term “Lyme Arthritis”. This led to an immediate misunderstanding of Lyme disease, which was incorrectly thought of as strictly an arthritic disease for many years.

Six years later, in 1981, the actual cause of Lyme disease was discovered to be a new species of spirochetal bacteria transmitted to humans from the bite of infected deer ticks. Almost ten years after Steere’s description of Lyme disease as an arthritic disorder, it was now becoming recognized that Lyme disease was in fact much more than just a new type of arthritis. Lyme disease was now recognized as being equally capable of causing severe and devastating neurological disorders. [Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme Disease: Meningitis, cranial neuritis, and radiculoneuritis. Neurology 1985;35:47-53]

Dr. Willy Burgdorfer was the first to isolate the spirochetal bacteria from the midgut of Ixodes Scapularis (deer ticks) gathered from the Shelter Island area, located near the coast of New York and New Jersey.

Shortly after the cause of “Lyme Arthritis” was discovered to be a bacteria, articles appearing in medical literature quickly assumed that the Lyme spirochete was similar to other bacterial infections. Many treatment studies based their protocols of antibiotic treatment on other bacterial infections, such as strep throat. The conclusions from most early studies having short patient follow-up concluded that you could expect Lyme disease to respond to 10-14 days of antibiotics. The antibiotics tested in the test tube and deemed to be effective at that time included erythromycin, tetracycline, and penicillin.

From the very beginning, treatment failures were seen in virtually every antibiotic study done. The longer the patient follow up, the higher the incidence of treatment failure. The medical community blamed early treatment failures on the older antibiotics erythromycin, tetracycline, and penicillin, and determined that these antibiotics were not very effective at curing Lyme disease. Ignored was the fact that the newer antibiotics were also consistently failing to prevent relapses of active infection. Since these early treatment studies, the concept that two weeks of antibiotic therapy is adequate treatment for Lyme disease has remained ingrained in the medical community’s collective consciousness. [The Long-Term Follow-up of Lyme Disease: A Population-Based Retrospective Cohort Study. Authors: Shadick NA; Phillips CB; Sangha O et al. Ann Intern Med 1999 Dec 21;131(12):919-26]

*Data presented by Dr. Nancy Shadick at an International Lyme Symposia showed that patients in the Nantucket Island study followed for up to 5.2 years after initial antibiotic treatment had ever-climbing relapse rates. Relapse rates in patients receiving two weeks of IV Rocephin (ceftriaxone) could expect a relapse rate to exceed 50% after five years.

Other factors that contribute to relapse post-treatment seem to include length of infection before diagnosis, choice of antibiotic, and severity of symptoms at time of evaluation.

While from the very beginning there have been thousands of patients who have complained of still being sick and symptomatic despite supposed adequate antibiotic treatments, most of the medical community has ignored the patient’s observations and labeled them as being cured – despite the fact that they still have most of the same symptoms that brought them to their doctors in the first place. So, what determines a cure if the patient still has the symptoms of the disease? In many cases, it is not the patient’s disability that determines the disease state, but rather the presence or absence of natural immune factors or antibodies. The problem is that antibodies are not a direct measurement of active infection.

How could this have happened? Part of the problem was the newly emerging science and technology of antibody serology testing known as ELISA tests (Enzyme-Linked Immunosorbent Assay).

[ELISA tests look for an enzymatic color change that indicates the presence or absence of Lyme antibodies in a patient’s serum. If you still see a color change when a patient’s serum is diluted with 512 parts water, then it is said a patient has a dilution titer of 1:512. Note: Higher titer numbers do not have any correlation to how sick a patient is feeling. In fact, a high number indicates the presence of lots of immunity. A patient with a high titer is better able to fight the infection than someone who is producing low numbers of antibody or has a borderline or even negative titer.]

Not only was it clear that ELISA tests were quick and easy to develop, but they were cheap and easy to administer. The convenience of ELISA tests was a powerful enticement to both doctors and patients. Let’s face it, taking a 10 cc vial of blood is more convenient and inexpensive than having several brain, skin, bladder, or heart biopsies costing thousands of dollars done. The problem from the very beginning was that it was assumed and generally accepted these tests were a better diagnostic tool than patient evaluations based on symptoms and a response to treatment.

It was erroneously accepted that absence of antibodies in the blood meant no infection was present anywhere in the patient’s body. Even more disturbing was the incorrect assumption that the drop in antibody levels during treatment indicated a microbiological cure. Thus, many studies concluded that patients were cured if they eventually tested negative for Lyme antibodies. Both assumptions were and continue to be incorrect.

On paper, it certainly looks good for a doctor if he can tell a patient that, based on the test, they are negative for Lyme disease. However, in reality a more accurate statement would be that the patient is simply negative for the presence of those antibodies for which that particular test is sensitive for. Absence of antibodies does not mean the patient cannot have active infection.

ELISA tests can vary greatly from lab to lab. Since each lab holds a patent on their particular test, they are all competing to say they have the best test. It is a competitive business and certain buzz words, such as specificity, sensitivity, efficacy, and accuracy, are used to try to outsell one’s competitors lab tests.

This gives rise to many methods of testing efficacy implemented by competing labs in order to say that their test is better than the competition’s. This is usually based on predetermined laboratory standards. Unfortunately, laboratory methods of determining an ELISA test’s efficacy and accuracy does not directly correlate to accuracy in determining infection in a human being.

If a laboratory tests its’ ELISA on 100 test tubes of an identical known sample and, simultaneously, on 100 test tubes of distilled water (the control group), and picks up 99 of the 100 samples and only one of the control samples, they can claim their test is 99% accurate. It had a 1% rate of false negatives and a 1% rate of false positives. (The lab chooses what dilution titer it accepts as positive. For one lab it maybe 1:256, while for another it may be as high as 1:1024)

A 99% sensitivity sounds great, and most doctors and lay people would determine that this ELISA test is 99% effective and accurate. But these tests cannot tell you if a patient who is infected but makes no antibodies (seronegative patients) has active Lyme disease. Also, there is evidence that in humans with high titers, the tests can still be as high as 55% inaccurate.

What if I told you that some manufacturer’s tests are sensitive to only one of the antibodies we produce to the Lyme bacteria, and it is an antibody that is rarely elevated in late Lyme? What if I told you this test only had moderate sensitivity and requires highly positive serum to have a reagent color change? What if I told you that out of over 100 different Lyme ELISA tests by different labs, each was slightly different? What would you think if I told you that each lab holding a patent on an ELISA test presents data in such a way to make their test appear to look better than the competition in order to increase their profit? And, what would you say if I told you that many medical institutions are actually corporations that own patents on these Lyme tests, and that the reputations of these institutions and the researchers who developed them are all on the line if their test is found to be fallible?

What are the consequences to the reputations of these institutions if patients who say they are still sick after treatment are denied treatment because of these fallible tests? What if a patient becomes disabled or dies? The admission that the Lyme bacteria is alive and sequestered in some seronegative patients is not welcome news to the developers of these tests. But, rather than do the type of autopsy and tissue studies that would truly compare these tests, the manufacturers have chosen to manufacture patient studies that compare their tests to other equally bad serum tests. If a carpenter has a yard stick 29 inches long and he tests its precision with another yardstick 29 inches long, it will always appear that his yardstick is accurate.

How do laboratory claims to the efficacy of these tests actually stand up in the real world for the diagnosis of Lyme disease? Hundreds of labs and ELISA tests were evaluated by independent sources and were found several times to be less that 65% accurate. (This was based on triple-paired identical positive serum samples that were sent to 516 labs across the United States.) In some cases, some labs were far below this average. Without even arguing that some Lyme patient’s blood can be antibody negative despite an active infection, the patient whose blood is highly positive runs as much as a 45% chance or higher of still testing negative with an ELISA test. So they can have loads of antibody and still test negative simply by virtue of the lab’s inability to deliver consistently accurate results.

Now consider this. By today’s diagnostic criteria, if you test negative by ELISA, you don’t have Lyme disease. But, if you do test positive, you still do not have Lyme disease until you also test positive by Western Blot. A recent study shows that the Western Blot can be less than 50% accurate. So, statistically, if the ELISA test is 65% accurate and a Western Blot is 50% accurate, multiplying these probabilities gives less than a 33% chance of testing positive using the two tiered testing approach.

The biggest problem for Lyme patients today is that the medical community still by and large makes the same two incorrect assumptions about blood-based testing. This includes the more recent PCR DNA blood tests, which have the same pitfalls as antibody serologies in that the absence of infection of the bloodstream does not mean absence of infection in the body. Two important points to remember about antibody and PCR testing are:

  1. The absence of antibody (or bacterial DNA) does not prove absence of infection and
  2. the drop in antibodies (or the absence of Bb DNA) does not guarantee that a patient is cured or that the patient won’t relapse from active infection.

Example: Let’s consider that antibodies or bacterial DNA in the patient’s serum are like hailstones you see during a hailstorm. Standing in your yard with a five-gallon pail for several seconds, you don’t collect a single hailstone. What can you conclude? The absence of hail stones in your small bucket doesn’t exclude the fact that it could have been hailing in your yard. You can use a larger bucket and increase your odds, but what if the hailstorm is just in one corner of your yard? Likewise, a small 10 cc vial of blood may be inadequate to find an infection that isn’t even in the blood.

A very important observation is that there is a history in medical literature of symptomatic seronegative Lyme patients who have received aggressive long-term antibiotic therapy and still have been culture positive for active infection post-therapy. Tests can be and are fallible, and infection can persist despite lengthy and aggressive antibiotic therapy.

Other persistent infection studies have shown the presence of Borrelia burgdorferi antigens, bacterial particles, bacterial DNA/RNA, and the presence of the bacteria in tissue biopsies of patients despite antibiotic therapy. Using staining techniques that are sensitive for spirochetes, researchers have found the bacteria in tissue biopsies from living patients as well as sequestered in patient’s tissues at autopsy. All of these methods are a much more direct measurement of the presence of Lyme bacteria than antibody blood tests. But they are impractical tests for the average doctor to perform on a daily basis.

Why can infection be present in the body without the immune system making measurable antibodies? Once an infection has left the bloodstream, a patient may not make enough antibodies to test positive. Once the infection has found a safer place in the body to hide, it can avoid the immune system and also avoid any antibiotics that are mainly circulating in the blood. Here is a list of mechanisms of immune escape:

  • Bb can be coated by human blocking antibody and become invisible to killer immune cells.
  • Bb can coat it self with B-cell membrane and cloak itself in human proteins.
  • Bb can find places like inside joints and tendons where it is sequestered from the immune system and even antibiotics.
  • Bb can go metabolically inactive.
  • Bb can hide in the brain, heart, bladder, and possibly skin cells. It is motile so it seeks out survivable places.
  • Bb may have another form that lacks cell wall and therefore lacks many of the antigens the human immune system would use to attack.
  • Bb may hide inside some human cells.

Without infection being in constant contact with the blood-borne immune system, the body shuts off antibody production. Antibody levels will fall despite the fact that the infection is still sequestered deep in the body, such as the brain, tendons, heart, nerves, bladder, eyes, and joints. How do we know this? Patients who have been repeatedly seronegative for antibodies have been culture positive for the Lyme bacteria. Patients who have been aggressively treated with antibiotics have been culture positive for the Lyme bacteria. Despite repeated negative Lyme antibody tests, these patients still had symptoms – symptoms that, in most cases, responded to extended antibiotic therapies. [See references]

Because the medical community has by and large refused to accept a patient’s symptoms as proof of infection and have continually based their diagnosis of Lyme disease on Lyme serologies, there has been an ever growing schism between so called “chronic Lyme patients” and a medical community that refuses to accept their claims of still having active infection post-treatment. In many cases, not only are serologies used to determine the diagnosis, but the drop in antibodies is often used to indicate a biological cure.

It has been the variable nature of the disease and its’ wide range of symptoms, and the reliance on unreliable tests that has given rise to two different camps concerning the diagnosis and treatment of Lyme disease. Let’s discuss the evolution of these two opposed paradigms of diagnosis and treatment in the next section.

The Need For A Post-Mortem Lyme Study

The medical community is unevenly divided into two opposing camps on three major issues concerning Lyme Disease:

  • What constitutes a proper diagnosis of Lyme disease?
  • What constitutes proper treatment for patients with Lyme disease who have symptoms that persist beyond four weeks of antibiotic therapy?
  • What role should Lyme tests play in both diagnosis and treatment?

The first camp on the diagnosis and treatment of Lyme disease:

The first camp, which I will call Camp A, represents the majority of the medical community and is spearheaded by researchers from Yale Medical, the American College of Physicians (ACP), and several other major medical institutions. In general terms, this camp believes that Lyme disease is best diagnosed through the use of two consecutive serology tests; the ELISA test followed by a confirming Western Blot. This is known as two-tiered testing. With very little opposition from the medical community, two-tiered testing has now become the diagnostic standard of most major medical centers.

Camp A also maintains that Lyme disease, despite the stage or severity, is usually cured with just a few weeks of oral antibiotics. This is by far the most popular position within the medical community and the health insurance industry at this time.

How does Camp A make a diagnosis of Lyme Disease?

In the past, a history of a tick bite followed by a bull’s-eye skin rash or erythema migrans rash was diagnostic of the disease, but a diagnosis based on the rash and symptoms alone has come under increasing attack by several advocates of two-tiered testing, including Yale Medical [See Yale Medical Report] and the ACP.

A video training tape by the ACP is quite explicit that, in the absence of an erythema migrans (EM) rash, the diagnosis must be made by dual serologies and more than two weeks of antibiotics is almost always unnecessary. In one of the video scenarios, the tape suggests to treating physicians that patients who insist that they have persistent symptoms post-treatment should be referred to psychiatrists. The logic of this psychiatric referral stems from the premise that, since antibiotics are accepted as curative, any persistence of symptoms has to be purely psychological. So if a patient doesn’t feel better post-treatment, send them to a shrink!

The second camp on the diagnosis and treatment of Lyme disease:

The second camp, often referred to as “Lyme advocates,” which I will call Camp B, believes that most of the persistent symptoms post-antibiotic treatment are caused by persistent infection. This camp maintains that antibody serologies are poor at detecting a spirochetal bacterial infection that has sequestered in deep tissues and is no longer found within the bloodstream. They believe spirochetes that have found sequestered, or privileged, sites tend to hide in the body and are poorly detected by any means. As proof of their position, this camp offers numerous studies which have shown persistence of Borrelia infection post-antibiotic treatment. Listed below are several of these published cases of persistent infection in humans and animals post-treatment as confirmed by either culture or tissue biopsy and stain:

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.

(For further information, please refer to the compendium of references to the persistence or relapse of Lyme disease at

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 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.

Valesova H, Mailer J, et al. Arthritis: A three year follow-up: 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 above figures mathematically, based on the 29 patients out of 35 who were contacted and assessed:

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 to 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 verses 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 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

Miklossy Judit. Alzheimer’s disease a spirochetosis? Neuro Report 1993;4:841-848 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! ?

To do this type of tissue study 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.


More on Grier:

Lyme on the Brain, part 1:
Lyme on the Brain, part 2:
Lyme on the Brain, part 3:
Lyme on the Brain, part 4:

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