25 Years of Experience With Lyme Borreliosis

Interview With Dr. Bela Bozsik

Dr. Bela P. Bozsik is a hungarian physician with a unique experience in diagnostics and treatment of Lyme borreliosis. After the discovery of the Borrelia spirochete early in the eighties, Dr. Bozsik was soon engaged in work in the field. With his background from laboratory medicine, he had good insight in the development of test methods, and he soon understood that both diagnostics and treatment would face greater challenges than what was initially believed. During a recent stay in Budapest, we had the opportunity to meet Dr. Bozsik.



The bacterium Borrelia burgdorferi was identified in the USA in 1982, and was connected to an epidemic of arthritis among children in the small town Lyme a few years earlier. It was known that the bacterium was transmitted by ticks. In Europe there were observations that connected tick bites to the occurrence of the characteristic dermatological conditions EM and ACA, but the fact that this newly discovered spirochete was the causative agent of illness was new, also in Europe. Several scientists took interest in this new spirochete, and Dr. Bozsik was one of the first to engage in the field. He was the first to suggest the term Lyme Borreliosis, this was accepted and immediately taken into use.


What was your background, why did you go into the work with Lyme borreliosis? The most interesting and promising aspect of this new discovery was that there is a disease that can damage the whole body, developing into a systemic disease, and the causative agent could be killed with common antibiotics. This gave an incomprehensible possibility to cure people suffering from obscure symptoms without known causes, so I decided to do research in this field. Before this I had been working with the complement system and serology in Syphilis diagnostics. The Syphilis bacterium is also a spirochete, and has many similarities to Borrelia. At this time I was head of the serology laboratory at Johan Bela National Institute of Hygiene. An infectious diseases specialist at the institute asked me to do something on the new spirochete, and we started to adapt methods for serological investigations.


We know that a bitter conflict has developed between wings, where physicians at either side have very different opinions on Lyme borreliosis. This has been very expressed in the USA. Unfortunately we have also found this conflict to be present in Europe.


How was the situation initially, when did this conflict start? During the first years there were open- hearted and good conditions for work, and there was a friendly attitude at the international congresses. The scientists wished to share experiences and develop new knowledge. In short words; we fought with Lyme borreliosis and not with our Colleagues. In 1990, at the international conference in Stockholm, the conflict came to the surface. It was during a round-table discussion that developed to a fierce debate. It almost ended in a physical fight! At the time professor Klaus Weber from Munich, the president of the round-table discussion, closed the debate by saying “We are here to help patients suffering by Lyme borreliosis, not to fight each other”. The disagreement arose from the different opinions among the experts regarding what was the most efficient antibiotic for treatment of Lyme borreliosis.


The question regarding treatment is still a matter of debate, as we all know. Health authorities in almost every country suggest treatment according to guidelines from IDSA in the USA. This happens even though it is clear that the situation is very differing in Europe and USA. In Europe we have at least three substrains, perhaps five or more, of Borrelia that cause human illness. In the USA there is one strain that is dominating. Standard treatment for borreliosis in most countries is 2-4 weeks of monotherapy with ceftriaxone, doxycyklin, or eventually Penicillin V in early stages.


Dr. Bozsik, You have been a pioneer in the development of combined antibiotic therapy for Lyme borreliosis, can you say something about the background for this work? It was obvious that monotherapy in many cases did not give a satisfactory result, and I started to think that the combination of different antibiotics could give a synergistic effect. With the help of colleagues in different Institutes I did some studies In vitro, with different strains of Borrelia in culture. We tested fluoroquinolone in combination with different other antibiotics like doxycyclin, clarithromycin etc. In all cases we saw a marked synergy, even though Dr. Wilske had presented In vitro-results at the Stockholm conference showing that ciprofloxacin was ineffective alone against Borrelia. We also saw that some patients had good effect of their treatment while others did not improve much. Professor Neubert presented results from In-vitro tests, showing that different Borrelia strains had different susceptibility to different types of antibiotics. Some time later, at the conference in Vienna in 2005, it was discussed with Brorson if tinidazole could be an efficient drug to include in the treatment regime, to target the Gemma (spheroplast, “cyst”-like stage).


The principle for the development of my treatment schedule has been to use ciprofloxacin in combination with another antibiotic to utilize the synergistic effect that was demonstrated in the laboratory studies, and in addition to include tinidazole for the Gemma. In our practice we saw that the patients had cyclic variation in their symptoms in periods of 3-4 weeks. The treatment period should last for 2-3 times the duration of the individual cycle for the patient; that is approximately 8 weeks. We experienced that clinical improvement could continue for a long time after ending the treatment, 2-4 moths even 6 monthes after. However, if the symptoms continue or flare up, the patient may need repeated treatment with a different antibiotic. It is important to know what strain of Borrelia the patient is infected with, in order to choose the best antibiotic for the treatment schedule


It was of course important to investigate the effect of the combined antibiotic treatment in a clinical practice, and not only in the laboratory. Initially I had contact with a Hungarian group of physicians who wanted to try this treatment schedule for some of their patients. Gradually we collected comprehensive data from a group of 250 patients suffering from chronic Lyme borreliosis here in Hungary. We followed these patients for 5 years, on average, and half of them were cured after one round of treatment, while others needed one or more repeated treatments. Nearly all of them were cured, not seeing the definitive pathoanatomic lesions. I have also realized that it is very important to strengthen the immune defense at the same time as giving the patient antibiotic treatment.


What the patients experience today is that it can be very difficult to get a correct diagnosis, to prove there is an ongoing Borrelia infection. The problem seems most severe for the long term ill patients. The experts accept that the immune response can be low in the early stage of the illness, but they claim that serologic testing is all reliable in the late stages of illness. In theory they can admit that seronegative borreliosis may exist, but they say it is extremely rare. In their everyday practice a negative test is used to rule out illness.


How do you think about these questions regarding interpretation and use of serologic tests, and eventual other test methods? The experts have forgotten what it means in everyday practice that serology is an indirect diagnostic method. Seronegativity means that the method (!) cannot demonstrate the presence of antibodies, -for some or other reason. It does not mean that Lyme borreliosis is not there. One should know that there is a period in the early stage of illness where production of antibodies is low, but there is also such a period of low antibody production in the late stage. That is why it is very useful to have additional methods to demonstrate active infection. I have been working a lot with classical dark-field microscopy, and I realized there was a need for methods to distinguish between the spirochete and artefacts in the preparations. I have developed a reagent (DualDur) that is added to the blood sample. This reagent makes the other objects rigid and motionless and there are no artificial products, while the Borrelia are preserved and still moving normally.


Dr Bozsik is now retired, but he is still working full time as a volunteer in Lyme Borreliosis Foundation Hungary, an organization that he founded in 1991. He has close contact with patients, physicians and scientists in several countries, and spends his time helping others. His heart is with the patients, and on every Sunday he burns a candle for the Lyme patients and their physicians.


Written by Gerd Berge, Norwegian Lyme Borreliosis Association
http://www.lyme.no/25-years-of-experience-with-lyme-borreliosis

THE COMPLEXITIES OF LYME DISEASE

Phenomenal Complexity

By Jon Sterngold

What are the symptoms of late-stage Lyme disease complex? I use the term ‘complex’ because
the spectrum of symptoms are most often caused by the Lyme germ, Borrelia burgdorferi, AND
other co-infecting pathogenic organisms that the ticks carry and transmit. With names such as
Babesia, Bartonella, Mycoplasma, and Anaplasma, these pathogens can dramatically contribute
to the degree of disease and complexity of diagnosis and treatment in infected individuals. So, as
the immune system loses control of these bugs, they spread and cause inflammation, as well as
release toxic molecules that cause symptoms and injury to cells and organs.

With so many
different possible combinations of infecting organisms and degrees of immune system
compromise, the list of potential symptoms is very long. While one person might just have
waxing and waning joint pains, another could be totally disabled with neuropathies that interfere
with the ability to walk or even to stand. Some become blind from blood clots in the eyes and
some are so fatigued that getting out of bed each day might not be possible. Many are plagued
with the dreaded ‘brain fog’ and some develop what appear to be well-known psychiatric
diseases such as bipolar disorder and severe depression. But, these patients need antibiotic
treatment as much or more than anti-depressants and other psych meds.

Many patients develop
severe pain syndromes involving the back and legs, though involvement can be anywhere in the
body. Some patients lose intellectual ability, hearing, the ability to sense heat from cold, and
coordinated movements. Most develop insomnia, and many get disabling pain in their feet.
Fevers, chills, sweats, dry cough, and body aches can make it seem that some sort of ‘chronic
flu’ is going on. Lyme disease can cause life threatening cardiac abnormalities. And the list
goes on. Some patients have only several symptoms and some have scores. It is no wonder that
non-Lyme literate physicians either roll their eyes at the prospect of taking care of a Lyme
patient or they simply refuse to believe that this constellation of symptoms is an active and
treatable infectious disease. It is so much easier to believe that these patients have psychiatric
disease (‘it’s all in your head’ type illness) or suffer the aches and pains of aging and a low pain
threshold (whiners). It makes the doctor’s life so much easier. Just say no. And believe me, as I
said before, I would not relish the notion of taking care of a patient with as complex a disease as
my own.

And it’s not even that simple! We now know that in addition to the major germ types listed
above, there are dozens to hundreds of genetic variations of these organisms. This introduces a
level of diagnostic complexity that is mind-boggling. Physicians faced with a bad disease and
complex long-term, sometimes dangerous treatment need as much diagnostic data as possible to
justify a treatment plan. But testing for these pathogens is almost a lost cause to date. There are
only a few tests for these bugs, and they miss most of the genetic variants. The tests are very
meaningful and helpful when positive, but meaningless when negative. We simply cannot ‘rule
out’ an infection with a negative test. Physicians who believe otherwise are wrong, if not
downright negligent. But wait, there’s more!

It’s not just the bugs that determine our illness. Our unique immune system genetics and
dysfunction play a large part creating the spectrum of symptoms we develop. It has been found
that some genetic types tend to develop more severe disease than others, including subtypes that
cannot get well. Some are more prone to creating antibodies that make us ill by attacking our
own tissue and some have impaired ability to break down and excrete bacterial toxins. These are
some of the reasons that one person’s Lyme disease doesn’t look another’s and why we need
Lyme experts to manage sick patients. Lyme expertise will be discussed in a subsequent article.

All Rights Reserved © 2009 Jon Sterngold
http://lifepathguide.com

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VALIDATION FOR THE CHRONIC NATURE OF LYME DISEASE

From The Johns Hopkins News-Letter

Bacterial antibiotic resistance genes discovered
By Aleena Lakhanpal
Issue date: 11/5/09

Antibacterial soap, hand sanitizer and antibiotics are all substances that we use in an attempt to kill bacteria that might make us sick.Whether we are concerned about getting strep throat, bacterial meningitis or something else, these prevention methods can offer protection. However, some bacteria, such as those that cause Staph and MRSA infections, are becoming increasingly resistant to antibiotics. Since the 1930s, researchers have been aware that bacteria may be able to resist treatment because they can morph into the L-form, or bacteria lacking cell walls.

Until the 1980s, not much else could be known about the L-form, but now, researchers at the Bloomberg School of Public Health have used a wide variety of modern molecular tools to learn more about the origin and biological functions of the L-form bacteria.Ying Zhang, a professor of molecular microbiology and immunology at Bloomberg, is the senior author of the study, which was published in PLoS ONE last month. Not all bacteria can transform into the L-form, but those that can include Bacillus anthracis (anthrax), Treponema pallidum (syphilis), Mycobacterium tuberculosis (tuberculosis), Heliobacter pylori (stomach ulcers and cancer), Borrelia burgdorferi (Lyme disease) and Escherichia coli (food poisoning).

Zhang's team used E. coli to create a culture of L-form bacteria. Although it had been difficult to culture L-form bacteria before, Zhang and his team created a new method that more closely simulated the in vivo conditions in which these bacteria form. "The presence of antibiotic stress is cell wall inhibiting, like penicillin," Zhang said. To prevent the cells from bursting because of this increased stress, Zhang's team added sucrose to the cell media.This culture represented the mechanism that occurs in the body. "L forms are formed in response to stress," Zhang said. "They have a different mode of survival and replication from classical bacteria." The cell wall-deficient bacteria cluster together in the shape of a fried egg rather than the smooth, homogeneous appearance of wild-type bacteria cultures.
Continued...

LYME DISEASE TREATMENT DENIAL

Living with Lyme: Long, often debilitating treatment flouts IDSA 'guidelines'
http://www.willitsnews.com/ci_13453460
By Jon Sterngold, MD

It is difficult enough for someone suffering debilitating symptoms due to late-stage Lyme disease to get well with the judicious, but adequate, use of long-term antibiotics. Almost no one gets better without these.

To deny patients access this care is a travesty. But this happens all the time and patients often travel hundreds to thousands of miles to see one of the small numbers of Lyme experts in this country.
How can that be?

Doctors are taught to practice medicine that conforms to "guidelines," thought to be consistent with the best approaches to disease based on what is known about the disease and effects of treatment. These guidelines are usually produced by the professional and academic organizations that represent specialty knowledge in medicine.
Guidelines for evaluation and treatment of Lyme disease are issued by the Infectious Disease Society of America, or IDSA.

The guidelines have been created by a small number of 'experts' in the IDSA, and there are a few punch lines to their conclusions. One is that the disease is hard to catch and easy to treat. Another is that anyone with Lyme disease who has persistent symptoms after a several-week course of treatment with antibiotics no longer has Lyme disease and should not be treated with more antibiotics since this just increases risk of untoward side effects and produces no clinical improvement.

They conclude many sufferers of neurologic and psychological symptoms from late-stage Lyme disease
are simply deluded or depressed and should be referred for psychiatric evaluation.

Because the IDSA guidelines have been embraced by medical boards in most states, physicians risk losing their license to practice if they do not follow the guidelines. This is the primary reason why effective care is limited. The few physicians who have braved threats to their licenses and actually taken on the challenge of getting Lyme sufferers well have found most patients can be helped, if not made well, by the careful use of long-term antibiotics. Many have found it often takes one to three years of antibiotics for these patients to turn the corner.

It is now understood why that is, but this has not yet changed the position of the IDSA guideline creators. We also know the same folks who issue these guidelines have huge conflicts of interests in this realm. One has ownership of the Lyme bacterial DNA, several have financial relationships with insurance companies that do not want to foot the bill for this expensive care, one or more have a stake in a new Lyme vaccine, and all of them have professional and economic liability if and when proven wrong.

It is the experience of scores of physicians treating many tens of thousands of Lyme sufferers over the last 25 years that they are, indeed, dead wrong. There is an increasingly massive pile of literature that supports the science and clinical management of late Lyme, flying in the face of the "guidelines." And in the past year, the IDSA has been legally challenged by the Connecticut Attorney General for creating guidelines in a manner both ethically and scientifically flawed.

This affords some hope for the future.

Another pressing reason why most doctors do not want to treat late Lyme disease is that it is a phenomenally difficult thing to do. Testing is deeply flawed and expensive.

Response to treatment is slow and peppered with setbacks. Treatment is expensive and patients often suffer horrendous debilitating symptoms. As a prior ER doctor who liked to sew up wounds and send repaired folks home, I know it would take a very special demeanor to rise to this challenge.

I don't think I'd want to manage a case as complicated as my own.

In these articles, I've shared a minuscule and space-limited fraction of what I learned during the past three and one-half years of living with late Lyme disease, as a patient and as a physician.

There is so much more.

ABOUT THE AUTHOR: John Sterngold is a Willits resident and physician.

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Lyme Disease Is Like A Stealth Bomber

http://www.willitsnews.com/ci_13453460

Living with Lyme: Bacterium can 'cloak' itself

By Dr. Jon Sterngold

Special for The Willits News

Posted: 09/30/2009 11:35:49 AM PDT

The bacterial cause of Lyme disease is called Borrelia burgdorferi, named after researcher Willy Burgdorfer, Ph.D, who first identified the germ in 1982.The spirochete, a corkscrew-shaped bacterium, is unique in the known bacterial realm because of the quantity of DNA it carries that enables it to evade detection and attack the human immune system. It can change its outer protein coat, cloaking itself from immune detection. It also can completely change form, becoming a treatment-resistant cyst, or shed its outer coat to enter our own cells to set up shop.

The success of antibiotic therapy generally depends on the activity level of a bacterium; how fast it grows and how often it reproduces. Most common bacterial diseases we encounter in medicine are from bugs that reproduce in less than 24 hours. When antibiotics "hit" the reproductive or active metabolic machinery of these germs, they die. This is why when we treat common illnesses such as pneumonia or urinary infections, people usually get better in a few days.The Lyme bacterium, however, has a reproduction cycle as short as a day but as long as about nine months. During a phase of prolonged inactivity, it is very hard to kill. This is one of the reasons an established Lyme infection can be hard to eliminate.

It also is thought, and there is real data to support this ,that the Lyme bacterium eventually takes up residence with other co-infecting bacteria, in what is called a biofilm community.On a microscopic level, the bacteria clump together in a gel-like secretion where they are insulated from our immune system and circulating antibiotics or antibodies. This is their bunker, from which they can wreak havoc by releasing the neurotoxic products of their metabolic life. It's an evolutionary match: they thrive in a body they modify to suit their needs. They can suppress our immune systems and alter other vital processes, making us ill, helping them thrive. They don't tend to kill us, though they sometimes do. It's a parasitic existence.

In addition to symptoms that stem from inflammation of the brain, nerves, heart, blood vessels, joints, and connective tissue, which the Lyme bacteria cause through multiple mechanisms, we also know the disease can induce another class of illness called autoimmune disease.Maladies such lupus, multiple sclerosis and Lou Gehrig's disease (ALS) can actually be caused by Lyme disease. These diseases are not considered to be curable, but there are many cases in which the autoimmune disease resolves completely when the Lyme disease has been treated ... always with long-term, high-dose antibiotics.

Tests to determine whether someone has Lyme disease are problematic. The common tests measure levels of antibodies we produce that are specific to the Lyme bacteria. But, if the bacteria can hide, change form, immunologically "cloak" itself, and suppress our ability to make antibodies, a person quite ill with Lyme can have totally negative tests. What commonly occurs is that after a year or so of antibiotic use,which can render some of the bacteria into fragments the immune system can recognize, the tests turn positive. The dilemma is that when someone is looking for a diagnosis, an answer to profound suffering, a physician who relies on initial test results may call it wrong, and the patient will have no answer and no effective treatment. This is part of what defines the difference between "Lyme-literate" MDs, who understand the problems with testing and treatment challenges, versus nonLyme-literate physicians who, for some very compelling reasons, can't or won't manage this disease.

The range and depth of this problem is immense, and will be discussed in the next article.

ABOUT THE AUTHOR: Jon Sterngold is a Willits resident and physician.
Copyright © 2008 - The Willits News

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LYME DISEASE ENDEMIC IN MEXICO

Clinical Microbiology and Infection,
Volume 15 Issue 5, Pages 496 - 498,
Published Online: 15 May 2009

Demonstration of Borrelia burgdorferi sensu stricto infection in ticks from the northeast of MexicoG. Gordillo-Pérez 1 , M. Vargas 2 , F. Solórzano-Santos 3 , A. Rivera 2 , O.J. Polaco 4 , L. Alvarado 1 , O. Muñóz 1 and J. Torres 1 1) Unidad de Investigación Médica en Enfermedades Infecciosas, Hospital de Pediatría, Centro Medico Nacional SXXI-IMSS , 2) Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional , 3) Servicio de Infectología, Hospital de Pediatría, Centro Médico Nacional SXXI-IMSS and 4) Instituto Nacional de Antropología e Historia, UNAM, Mexico City, Mexico Corresponding author and reprint requests: G. Gordillo-Perez, Calle Bruselas # 109-6 Col. Del Carmen, Coyoacan, México, DF 04100, Mexico E-mail: lugope2@yahoo.com.mx

Copyright Journal compilation © 2009 European Society of Clinical Microbiology and Infectious Diseases KEYWORDS Amblyomma • Borrelia burgdorferi • Dermacentor • Ixodes • Lyme disease Clin Microbiol Infect 2009; 15: 496–498 ABSTRACT Borrelia burgdorferi sensu lato infection has been confirmed in clinical cases in the northeast of Mexico; however, the bacterium has not been identified as infecting the tick vector Ixodes, Amblyomma and Dermacentor ticks were collected from mammals and plants in northeastern Mexico and examined for Borrelia. Eighteen of 214 ticks were PCR-positive for the fla and 16S rRNA genes and 15 for the ospA gene. Southern blotting with a fla probe and sequencing of ospA genes confirmed infection with B. burgdorferi sensu stricto.

These findings, together with reports of indigenous cases, fulfil the criteria that allow northeastern Mexico to be considered as a zone endemic for Lyme disease. -------------------------------------------------------------------------------- Original Submission: 18 August 2008; Revised Submission: 15 October 2008; Accepted: 19 October 2008 Editor: S. Cutler DIGITAL OBJECT IDENTIFIER (DOI) 10.1111/j.1469-0691.2009.02776.x About DOI