Archive for the ‘Testing’ Category

LDo’s Top 10 Lyme Research Questions


Press release: releases “Top 10 Lyme Disease Research Questions,” as federal government weighs options in fight against growing epidemic.



Suppression of Microscopy for Lyme Diagnostics – Professor Laane

Interview With Professor Laane About the Suppression of Microscopy for Lyme Diagnostics

Written by Huib Kraaijeveld


Around 2003 the WHO encouraged research into microscopy as a direct test for the Borrelia spirochete, the pathogen causing Lyme disease. When a promising new and simple technique was discovered in 2013, it was however violently attacked. Not on the science itself, which is the normal procedure in science, but personally. Now retired professor microbiology Morten Laane was fired after he gave a lecture at a scientific conference in 2014. Moreover, his laboratory was closed down, the website of the scientific journal was hacked and the article disappeared. An exclusive interview.

“If experts treated airplane accidents in the same manner as an average medical scientist studies disease, I would book my next travel to the USA by ship.”

Professor Laane

Courtesy of Under Our Skin

Who is professor Laane?

Born in July 1940, in the small city of Toensberg, Morton Laane grew up during the second World War. “My mother visited her sister in the city of Bergen the ninth of april 1940 the day war broke out in Norway. They survived the severe attacks by the German warships. My mother travelled along the coast by a Norwegian local ship to the small city of Toensberg where the family lived close to the Oslo fjord. This was not a very smart idea, as several ships were attacked and destroyed by German submarines.

My father was in Finmark, the arctic part of Norway, together with a substantial number of Norwegian soldiers as a medical officer. When I was born, my mother, who had professional training in handling weapons, sat alone with a hidden gun in a small flat close to the German headquarter across the street. When the free artic part capitulated a couple of months after the start of the German invasion, he was first arrested by the Germans, later released and went back to Toensberg.

In 1947 my father showed me how to detect the Syphilis spirochete by very simple microscopy. Numerous sailors lived in this city known for its substantial commercial fleet. Back then, Syphilis infection was not uncommon in sailors.

My father had a small, old Leitz brass microscope of high quality. A tiny sample from the patient was mixed with an equal part of drawing ink on the glass slide made for microscopy. Drawing ink consists of extremely tiny black particles (coal). They do not penetrate into the bacteria. Normally they are almost invisible. Light pass through the unstained bacteria against a total black background.

This started my interest for microscopy. Later my father specialised in psychiatry. He had no use of his microscope and I got it as a gift. Looking back, almost everything in my life started as a hobby.

I became scientific assistent in general experimental genetics. My boss, Dr. Øistein Stromnaes worked with the fungus Penicillium. Nobody had seen its chromosomes before, but I discovered a simple method to count them in the light microscope.

So I was offered a research fellowship a the University of Bergen, I continued my research there and my PhD dissertation took place in 1971. The committee evaluated my theses as very good and suggested that I might have the qualifications of a personal professor position for life time and further develop new methods in genetics.

One of my discoveries regarding Penicillium brought me in contact with Lynn Margulis, then Lynn Sagan, wife of the famous Carl Sagan. Her research on cellular evolution and endosymbiosis led to the understanding that the energy-converting organelles, the mitochondria and chloroplasts, are actually bacterial symbionts living inside eukaryotic cells. This discovery earned her the reputation of being the most famous scientist in evolutionary biology after Charles Darwin.

My discovery was connected with her spirochete research, which focused on the symbiotic nature of the relationship between spirochetes and their hosts, in particular the noted ability of these bacteria to form dormant “round bodies” that are capable of reactivation. Nobody in the world knew more about spirochetes than Lynn.*

Later I discovered a somewhat similar structure in the slime mould (Physarum) which was much used for experimental research. I got in touch with Professor Ivar Giaever, a Nobel laureate in Physics and we cooperated for many years supervising Master and Ph.D. Students.”

Microscopic Lyme diagnostics

Microscopy is considered the Golden Standard in diagnostics for Syphilis. Given his background and expertise in microscopy, it made sense to Laane to try and find a method to detect the Borrelia in infected blood.

Laane: “My coworkers and I had published a series of papers in the Norwegian journal ‘Biolog’ regarding a problematic sheep disease called “alveld”. The papers contained unusual and spectacular images of possible toxic blue green algae (bacteria) that were suspected to be connected with this disease.

The Biological Institute then asked for cooperation regarding Lyme infections in order to compare microscopy and molecular tests. The Institute was responsible for administration regarding formal permissions to do medical research. It turned out that no reliable data were obtained from the molecular studies. The institute was responsible for this part. Microscopy showed, however, characteristic spirochetes in a number of patients together with other organisms such as Babesia.

The syphilis and Borrelia spirochetes share many properties. They cause permanent infections in humans which cause long-lasting, multi-stage diseases. They exist in more than one form – sometimes in the long spirochete form, but also in a round “cyst-like” form. The spirochete form can be made visible by simple methods and observed with a microscope.

Borrelia spirochetes in dry smears and in isotonic solutions appear as very thin cells, only 0.2 micrometers wide, and as very long – in the range of 50 to 100 micrometers. These are visible above the resolution limit for light microscopy – due to what we call light interference – by slight defocusing. In dry preparations, a focus error of more than 1/1000 mm renders them invisible under the microscope. In wet preparations, the cells swell substantially.

My colleague and I published the results of our part of the project due to our firm belief that microscopy is useful for detecting these infections. Beforehand we were assured by the Institute that formal permissions were granted by the health authorities. It turned out that the Institute, somehow had forgot to point out in a formal enough manner that a substantial part of the project included microscopy by us!

Our project leader was educated as a medical doctor, and had later became a biologist. He was also Head of the Institute to which the project was connected. We, my colleague and I, got a copy of the first page of the application accepted and signed by the Health authorities. We did not, unfortunately, see the entire application before it was too late, as the project description was incomplete in that it did not express without any doubts that about half of the project involved extensive use of microscopy to analyze samples.

The project leader knew of my cooperation with Oeystein Brorson, the extremely clever technician who was able to grow Borrelia from infected blood samples. We had agreed that the application should be written to state that extensive microscopy was needed for the project as a way to confirm the results of molecular tests.

The Institute received around 2 million euro (NOK 20 mln) and bought two DNA machines. The test project was thus an official Institute project, not an application by a group of three scientists. In hindsight, we should have asked to see the complete application, but we did not and went on the trust for our project leader. This turned out to be a mistake, as we were later blamed for not reading the regulations for medical research and additional legal papers.

The trust that caused us to not read the full application was labelled as “intention,” to mean we intended to subvert the regulations when we embarked on this project. This is simply not true.

Silenced for speaking

After publishing the 2013 article ‘A simple method for the detection of live Borrelia spirochetes in human blood using classical microscopy techniques’, professor Laane was invited to give a lecture at the 2014 Norvect conference in Oslo. An English patient saved the pdf, so you can still read it, via the link provided.

I was present at that conference and still remember how nervous he was. The reason was that several medical professors complained to his university. He was threatened with losing his job, if he would speak at the conference.

In fact, he did not literally speak – as you can see in the movie below – but used performing arts to show the slides of the spirochetes. Professor Laane was fired anyway and his laboratory was closed down.

Laane: “As for being forbidden to speak, Waldemar Broegger, a Geology professor in the late half of the nineteenth century was forbidden to speak about Charles Darwin’s evolution theory. Lynn Margulis was originally ridiculed for her theories on the evolutionary origins of mitochondria and chloroplasts and later received numerous awards for this discovery. As both of these scientists were found to be right and later became famous, I feel I am in good company.

The 2013 publication of ‘A simple method for the detection of live Borrelia spirochaetes in human blood using classical microscopy techniques’ in the journal Biological and Biomedical Reports resulted in much opposition by conservative medical doctors and some scientists, most of whom had little or no microbiology experience working with spirochetes in a laboratory environment.

The article and research was criticized because the cellular objects we were observing were presumed to be “artifacts,” meaning objects of some other origin that just magically appeared in our samples. It’s extremely important to point out that all of our principal research was performed under highly controlled conditions, and our results were confirmed using more than one microscopy method. The critics of our work have yet to explain how these supposed “artifacts” we observed were able to reproduce and even move like spirochetes, which we observed them doing, and even more importantly, the critics have failed to explain how an “artifact” could possibly contain nucleic acids from Borrelia.

Yet, in that same year Dr. Alan MacDonald found out independently the same as me regarding how to detect chronic Lyme infections in human blood. Before this the assumed borrelia bacteria had been found by a Norwegian microscopist, who had an extremely ill son from Lyme.

MacDonalds arguments in these two videos (part one and part two) are brief, but very much to the point. He has later developed methods to detect single Borrelia bacteria direct in a microscope slide by exact molecular methods.

Oeystein Brorson is also mentioned by MacDonald. He was the researcher who grew all known strains of Borrelia in Norway, sent me samples and cooperated with Lynn Margulis and me, until he got disabled due to disease and had to leave his job.

After my lab was closed down, also the website of the scientific journal that published our article was so severely hacked that it stayed offline for three years. Once it came back up, our article had dissapeared.

The hacking of the Journal ‘Biological and Biomedical Reports’ seems to be done with a person knowing more than my closest enemies. And was someone with access to a quite advanced compilator system. Why this was done might well have been political or personal prestige.

I have never seen this happening on any topic in science before.”

Proof or propaganda?

In 2016 the Norwegian Health Department (FHI) published the study ‘Validate or falsify: Lessons learned from a microscopy method claimed to be useful for detecting Borrelia and Babesia organisms in human blood’. It stated,

“microscopy by the LM-method identified structures claimed to be Borrelia- and/or Babesia in 66% of the blood samples of the patient group and in 85% in the healthy control group”.

The TV2 reporter in the infamous documentary ‘Deceit or Borrelia’ misquoted this sentence by claiming that “it was proven that Dark Field microscopy produces 85% false positives”.

There are however suspicions that the Norwegian study was set up to discredit professor Laane’s work, using contaminated blood.


“Officially, on their website The National Institute of Public Health claimed that the only known case of Babesia in Norway was a veterinarian that have had his spleen removed, and else that Babesia was unknown in the Norwegian population.

But I found a faked sample of Babesia. It was blood from a cow (or ox). It was mixed with human blood from a socalled control person and sent to me by mail.

Of course, this sample clotted impossible to see anything in the sample by microscopy except lumps of erytrocytes and fibrine fibers. If I had got the original sample unmixed, I would have found them at once. The FHI showed me a few images from a preparation they had made themselves, BEFORE it was mixed with human blood. The Babesia images there were the same as I found in several so-called control samples.

When I showed them, they looked a little worried – like school children not telling the truth to their teacher – but they would not admit that control samples contained Babesia merozoites.”


Borrelia stained with the Mysterud-Laane method, blue color.


Live biofilm of Borrelias developing in a mixture of blood and sodium citrate (this patient was tested positive also by molecular methods by American laboratory).


In the introduction to their 2016 article, the FHI authors also state that Lyme serology has a 70-90% sensitivity in the earliest stages and a sensitivity of almost 100% in later stages, which suddenly seems to become the new mantra in several countries. This seems to have been taken from a 2016 article written by IDSA and CDC authors, which was criticised for using circular logic.


“A recent report presented in Norwegian newspapers claim that inaccurate science, especially in medical topics, is common. Norwegian Professor Oeyvind Oesterud has written several short articles in Aftenposten, Norway’s largest newspaper about science and popular science papers.”

He points out that false conclusions are favoured by both journals and media on the criteria that discoveries should be spectacular. Unless they are not, they are not accepted. Also the official evaluation system for research grants favours this. Many of these discoveries can not be repeated. But it generates much money for the universities.

Such scientists believe in accepted science. Any deviation shown by experiment may be interpreted as incorrect or false. One may wonder why they publish at all. Regarding deviating disease data they are often neglected – according to what the medical scientist was taught as a student by his professor. The deviating results are never studier further and ignored as “errors”. Up to about half of recent medical papers may contain this.

The result is delayed progress, sometimes with big consequences for severely ill patients. Patients that could be saved. Disease problems are very complicated and there is need for research listening to what both the patients tell and meticulous analysis of unexpected data.

As a final thought:

“Travel by modern airplanes is now very safe. If experts treated airplane accidents in the same manner as an average medical scientist studies disease, I would book my next travel to the USA by ship.”  Professor Laane

Exception or a pattern?

The European Union has recently provided a 2 million euro grant to a cooperation of three parties to develop a better Lyme test, as the current one is considered imperfect. At best.

So why are there several indication of the active repression and sabotage of new, better and direct ways to diagnose Lyme? Is professor Laane’s story unique or showing a doisturbing pattern?

“This never happened before on any topic in the history of science in Norway”, Laane said in his interview with the makers of ‘Under Our Skin Emergence’. Yet also in other countries scientists have been attacked for working on promising new and direct Lyme tests.

In 2014, French lab director Schaller was fined was fined with paying 280,000 euro to the government and was sentenced to nine months in jail. Also in 2014 the American Centers for Disease Control and Prevention (CDC) publicly attacked the credibility of Advanced Laboratory Services, which had developed a culture-based test for Lyme disease diagnosis. The basis for the CDC’s attack has since been proven wrong, yet the CDC has never retracted the article in which the errant criticism was made.

A direct and ‘no false-positive’ DNA test for Lyme was no longer made available to the general public, after its inventor was fired from a Connecticut hospital in 2010. And recently media attacked the tests of specialised labs in Germany, using undercover reporters and twisted patients’ stories, claiming they were either not ‘FDA approved’. As professor Ahern explained in her recent interview, none of the tests promoted by the CDC or your national Health agencies are ‘FDA approved’.

The next interview with Dr. Lee will look into what happened around the development and public accessibility of the DNA diagnostics mentioned above. It will be published very soon.

* Professor Laane and I will work together on a future article about the work of Lynn Margulis, as too few people seem to have heard of her important work.

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Ahern – Flawed Lyme Policies, Diagnostics, and Treatment

The flawed science behind the current global Lyme policies, diagnostics and treatment

Written by

The flawed science behind the current global Lyme policies, diagnostics and treatment

Holly Ahern is a professor of microbiology as well as the mother of a child that was severely affected by Lyme Disease. Because of this personal experience and her professional background and training, she was able to dissect the flaws in scientific reasoning that underlie decades of wrong policies, invalid diagnostics and treatment that fail too many. An interview with a mother who went deep into the (anti)scientific Rabbit Hole of the Lyme science.


Can you introduce yourself and share how did you got personally involved with Lyme disease? 

I am a professor of microbiology at SUNY Adirondack, which is a small State University of New York college located at the southern end of a 6.1 million acre state forest preserve known as the Adirondack Park. Prior to 2009, my program of undergraduate research focused mostly on environmental microbiology with an emphasis on small lake ecosystems, of which we have many here in the Adirondack region.

In 2009, my youngest daughter was a freshman in college and excelling both academically and athletically. In her first year, she had broken college records in her sport (swimming) and had just qualified as All-American in her first NCAA Nationals. Within a month of those achievements, she called to say she wasn’t feeling well and wanted to come home for the weekend. She went to bed that night, and didn’t get up again to fully return to her life for almost a year.

It was early spring when she got sick. There were no ticks to be seen, she did not have any kind of rash anywhere, and her physician never considered that her illness could be a tick-borne disease. She was referred to a rheumatologist (because she had profound joint and muscle pain), a cardiologist (because she had tachycardia and pain in her chest), and a neurologist (because she was having debilitating headaches, was constantly dizzy and had pain, tingling and on several occasions complete numbness and paralysis of her right arm and leg). After several rounds of blood tests, a CT scan, and a couple of MRI’s, there was still no diagnosis.

Then, in May, my husband attended a presentation at the school where he works given by one of his colleagues. The topic was Lyme disease, and after listening to the presentation and talking further with the presenter, he felt that our daughter’s condition could be related to Lyme disease.

We requested a blood test for Lyme disease, to which her physician reluctantly acquiesced. We were all surprised when it came back positive, and I remember at the time how relieved we all felt because at last, there was a diagnosis. Little did we know…

When the prescribed oral antibiotic was completed and she immediately relapsed, I realized that what I — as a microbiologist — thought I knew about this disease from textbooks and the CDC was wrong. So I started reading the scientific literature, and quickly realized that the dominant medical view of Lyme disease being a bacterial infection that was “hard to catch and easy to cure” was profoundly wrong, that the bacteria and the disease symptoms it caused were not like other bacterial illnesses, and that the CDC-recommended approach to diagnosis and treatment of this disease lagged well behind the science.

My struggles to pull my daughter out from under the weight of the chronic disease that had consumed her, made me realize that her experience mirrored that of hundreds of thousands of other people who were also being gaslighted by their physicians and marginalized by public health agencies. As my daughter’s condition improved, my attention turned first to educating the public about the dangers of ticks and the diseases they carry, followed by governmental advocacy to change the outdated and harmful health care policies of the CDC.

Along the way, I co-founded a 501-c-3 organization called Lyme Action Network, and now also serve as scientific advisor for two other organizations; Project Lyme which focuses on educating the public about ticks and tick-borne disease, and for the Focus On Lyme Foundation, which is raising funds for research toward better diagnostic tests and treatment for tick-borne diseases.

Focus On Lyme is also working to address one of the most significant roadblocks to scientific research on tick-borne diseases in humans, which is the lack of a readily accessible, no strings attached, biorepository of well-characterized human blood samples.

I (and many others) have come to realize that the path forward to accurate diagnostic tests and effective treatments will have to come from those who are most affected by the disease, through patient-centered (and often funded) projects such as this, because there is little to no leadership coming from governmental agencies on this issue.

You recently gave a testimony at the senate commission hearing of the State of New York and you gave a lecture at the Focus On Lyme 2017 conference about the science backing up Lyme and co-infections. What have you discovered?  Can you summarize your strong criticism of the mainstream assumptions surrounding Lyme in a way that everybody can understand?

Over the past 5 years, I believe it is safe to say I have read most if not all of the published science on borreliosis (the broad name for diseases caused by bacteria in the Borrelia genus).

It is very important for people to realize that when they hear medical or public health professionals proclaim that the medical guidelines dictating the practice of medicine and insurance reimbursement for Lyme disease are based on the best available science, such assertions are rhetorical hyperbole and little else.

The mainstream approach to medical practice for Lyme disease is currently guided by a relatively small number of clinical studies which are overly focused on one feature of this very protean disease – the appearance of a “bulls-eye” rash after a tick bite.

From 1977-1980, a team at Yale University headed by Alan Steere “discovered” and then defined a new disease, which he initially called Lyme arthritis. Steere noted in his early publications that approximately 25% of the people in his study cohorts had a very unique clinical feature – a rash called an erythema migrans or EM which resembles a bulls-eye – that sometimes accompanied other non-specific but debilitating symptoms (joint/muscle pain, headaches, peripheral nerve pain and sensations, fatigue).

As a newly minted “Epidemiology Fellow” of the CDC, he had been trained to look for clinical signs associated with disease symptoms, which could be “objectively” observed by a physician without relying on “subjective” reports by patients about what aches and pains they might be having. The unusual skin rash was just such a perfect, pathognomonic, feature.

Having noted and associated this unique rash with patients showing a similar cluster of subjective symptoms, his next studies set out to investigate the association of the rash with the disease. Steere’s subsequent studies were DESIGNED to CONFIRM what he wanted to be true – that the EM was a clinical sign of this new disease – as opposed to designing studies to impartially study the occurrence of the rash in people with the cluster of symptoms typical of people with Lyme disease. This is an example of a notable type of research bias, referred to as confirmation bias.

Steere also overemphasized the significance of joint swelling as a clinical sign of “Lyme arthritis,” because he was, after all, a rheumatologist, and therefore pain in a joint that was swollen could be taken as a “sign” of a disease process. Joint pain without obvious swelling was considered a nonspecific symptom that did not point to anything in particular.

The 1980s came along and New York decided that maybe they should look into this “new” disease since Long Island shares a body of water with Connecticut. SUNY Stony Brook on Long Island had a research team looking at ticks and diseases, so in 1982, the NYS Department of Health launched a study to find out just how many cases of this new disease there were in New York, to decide if the State should consider whether a public health response was needed.

The design of this study was for the Department of Health to alert New York State health care providers, through newsletter publications and also by sending letters to 300 primary care physicians, about the new disease and provide them with specific and detailed information and pictures about what to look for FIRST — a unique rash shaped like a perfect bulls-eye.

The letters directed health care providers to fill out a form for each patient seeking medical care for (in order of emphasis): a rash with a bulls-eye appearance; aseptic meningitis; facial paralysis (Bell’s Palsy); or large joint arthritis with swelling.

The inherent bias in the design of this research is obvious. The study directed a naïve population to be on the lookout for a new disease hallmarked by a specific type of rash shaped like a bulls-eye.

So what do you think got noticed by the physicians who participated in this study – the patients walking in the door with a bulls-eye rash, or the ones complaining about fatigue or headaches or pain in their non-swollen joints?

Before this investigation of the “Epidemiological Features of Lyme Disease in New York, the rate of association between an EM rash and Lyme disease symptoms ranged from 25-40%, as gleaned from a review of the published research from this period. In the New York study, 77% of the case reports were about people who exhibited an EM rash.

The perceived authority of this one study, published 33 years ago in 1984, serves as the ANCHOR for the misconception currently advanced by the CDC and other public health agencies, that 70-80% of the people who get Lyme disease will show a bulls-eye rash as a clear clinical sign.

Even though this assertion has been REPEATEDLY and REPRODUCIBLY shown to be false (with the true rate of association between and a bulls-eye shaped rash and a diagnosis of Lyme disease being only 10-40%), anchor bias perpetuates the myth that most people get an EM rash as a sign of “early” Lyme disease.

The bad news for patients is that since at least the late 1990s, the medical guidelines for diagnosing and treating Lyme disease patients have been based on clinical trials heavily influenced by this strong and pervasive anchor bias. Every research study that investigated the clinical course of Lyme disease in humans since the late 1970, used the appearance of a bull’s-eye rash as the main criteria for either inclusion in the study, or as an end point of the study.

Which means that all of the clinical research done to date has EXCLUDED from study 60-90% of people who actually have Lyme disease.

And even worse – a search of the NIH-funded clinical trials currently in the pipeline for Lyme disease returns with 20 studies currently enrolling or inviting participants. The “Inclusion Criteria” (to be eligible as a participant in the study) for these studies requires that a person must either meet the CDC case definition for Lyme disease, or meet the criteria set forth in the clinical practice guidelines developed by the Infectious Diseases Society of America, which are in practice one and the same. Briefly, those criteria are 1) the bulls-eye rash; and/or 2) “laboratory evidence” of infection.

“Laboratory evidence” is another way of saying “diagnostic test.” Diagnostic tests that would serve as laboratory evidence of an infectious disease like Lyme disease, either show direct evidence of infection with the bacteria causing the disease (such as growing the bacteria in culture or detecting their DNA or proteins in a blood sample), or indirectly demonstrate a past or present infection by measuring antibodies specific for the disease-causing agent in a person’s blood.

This latter method, called serology, is currently the ONLY type of laboratory testing recommended by the CDC for diagnosing a case of Lyme disease – even though serology has been REPEATEDLY and REPRODUCIBLY shown to be very inaccurate with a high rate of false negative tests (serology is falsely negative in 1 out of every 2 tests). A research paper just published takes it one step further and shows that serology is next to useless in persons who received antibiotic treatment before the test was done.

Ironically, a quote from the CDC website states: “Before CDC will recommend new tests, their performance must be demonstrated to be equal to or better than the results of the existing procedure, and they must be FDA approved.”

The explicit use of the term “FDA approved” by the CDC is interesting, because currently there are NO FDA APPROVED tests for Lyme disease, and that INCLUDES the serological tests the CDC recommends. Serology has been CLEARED by the FDA for marketing as a medical device, based on it being “substantially equivalent” to something already being marketed, which is, in essence serology itself, since serology was and is the only test in routine use across the globe.

FDA APPROVAL requires more than just a comparison to the existing standard, it requires additional evidence of the test’s safety and effectiveness. Serology, compared only to itself, has never actually gone through the FDA approval process.

This and other rhetorical twists of the existing science by the CDC has severely limited the use of any other test that could serve as “laboratory evidence” of Lyme disease, particularly ones which rely on the direct observation (such as culture or microscopic examination) or detection of biomolecules (such as DNA or RNA). Which is illogical, because direct detection of the microbe or molecules from it should yield no false positives, and therefore a person showing this type of laboratory evidence could be correctly diagnosed and treated.

What all this means is that we actually know next to nothing about the true nature of disease in persons infected with Borrelia or tick-borne coinfections, in the majority of persons who actually have Lyme disease. And if the status quo is maintained, we won’t be learning anything new from NIH-funded research on Lyme disease for the next 20 years.

If it was up to you to create an action plan for Lyme disease, what would you do? 

My action plan would start by making Lyme disease a national (and international) research priority, to the same extent that AIDS was prioritized in the 1980s. Given that there are annually more than 6 times the number of cases of Lyme disease as there are HIV/AIDS, with Lyme disease patients often experiencing a higher level of disability, this elevation in status is clearly warranted.

There are three areas related to tick-borne diseases that desperately need more research: diagnostics, treatment, and prevention. I would argue that diagnostics should be the first priority, because at this moment we are overly reliant on 40+ year old tests that are supposed to detect antibodies against a bacterium that can successfully “hide” from and even alter how and what types of antibodies are produced during an immune response to infection. There is currently no real way to differentiate between past or recent exposure to Borrelia in these tests, and no way to track the efficacy of treatments.

Once we have a way to directly detect infection – and I believe we are close to achieving that goal with several methods, including professor Laane’s work on a simple, direct method to detect the Borrelia with microscopy, direct detection of antigensDNA sequencing, or nucleic acids from all tick-borne microbes – then it would be possible to reassess the existing dogma about the human course of this disease through well-designed, unbiased, hypothesis-driven research. Eva Sapi as another scientist using advanced microscopic methods for detection. This is the article describing her work on skin tissues.

The foundational research already exists – on bacteria grown in culture, and in animal models ranging from mice to dogs to non-human primates. Some of that research (new antibiotic dosing strategies, existing drugs with superior efficacy over the antibiotics currently medical guidelines recommend) is ready to advance to human clinical trials and only awaits funding.

Historically, research on preventing Lyme disease in humans has focused on vaccines and most recently, on a pre-exposure prophylactic (PrEP) that would render Borrelia burgdorferi incapable of causing an infection. The problem with this singular approach is that someone who is vaccinated or receives PrEP would NOT be protected against infection by other tick-borne microbes (such as other species of Borrelia, or Babesia, Bartonella, or Anaplasma) that also cause human diseases.

Existing research shows potential for a vaccine to prevent ticks from staying attached or transmitting microbes, and that type of vaccine deserves significantly more research attention, because it would reduce the human risk of acquiring any tick-borne disease, not just Lyme disease.

I would also argue that additional research is warranted to investigate other potential routes of transmission for the microbes labelled “tick-borne.” In the United States, CDC disease surveillance data reveals that Lyme disease is not just the “fastest growing vector borne disease,” it is the SECOND MOST COMMON infectious disease period, with only sexually-transmitted chlamydia causing more cases of disease per year. Gonorrhea comes in third.

Since there is scientific evidence of congenital transmission of Borrelia and research suggesting that sexual transmission occurs as well, it seems likely that Lyme disease is not all that “hard to catch” after all.

Professor Holly Ahern

Interviewer: Huib Kraaijeveld

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Scottish Doctor Gives Insight on Lyme/MSIDS

We don’t have perfect tests for diagnosis of Lyme

Written by Huib Kraaijeveld (On Lyme Foundation)

Dr. Jack Lambert is a Scottish doctor who is currently working as an Infectious Diseases consultant in a public hospital in Dublin, Ireland. He has started treating Lyme Borreliosis patients 20 years ago in the USA and during the last 5 years in Ireland. He has also successfully treated a number of young women who fell ill after their HPV vaccination, which seems to have stimulated a latent Lyme infection to reactivate. In this exclusive interview in two parts, Dr. Lambert shares his experience with different emerging serious conditions caused by complex infections and looks at similarities and differences as to how they present clinically and are treated.

Dr. Lambert: I am a Infectious Diseases (ID) specialist that is managing a wide range of different infectious diseases, in parallel with being an academic doctor, research and teaching at the Medical School. In my 25 years career I have seen many different infections in immuno-compromised hosts, like HIV Hepatitis C and those immunocompromised by cancer treatment and transplant recipients. Many of the textbooks describing these infections were written by my former mentors and bosses; some of whom were nominees for the Nobel prize in Medicine.

In the last couple of years, it has become very clear to me that there are many similarities between HIV, Hepatitis C, transplant medicine and the many complications that patients with Lyme and co-infections live with.

Billions are invested annually into HIV research, billions are put into transplant medicine, but for some reason little money is spent on researching Lyme and co-infections for example Anaplasma, Babesia and Bartonella. Yet these infections can be just as damaging and debilitating as HIV and Hepatitis used to be, before we found medicines to treat these conditions.

Seronegative infections

My early experience with difficult diagnoses with imperfect techniques was when I was training in Rochester, New York, in adult and paediatric medicine training programme. By default I ended up taking care of the HIV infected pregnant women as well, as few were willing to take care of them in this time period. So I also took care of a lot of seropositive mothers, who had delivered their babies prematurely.

My first presentation on this subject was about seronegative babies who were born to HIV seropositive Afro-American mothers, which were initially put in the premature nursery but died at home after being released from the hospital. They were dying from what was believed to be SIDS or cot death. When I saw the pathology reports on these children and cultivated the HIV virus from their blood in my laboratory from post mortem blood samples, I discovered that they had died of HIV and their blood cultivated positive for the HIV virus. Yet in none of these children had the ‘standard’ HIV antibody tests showed up positive. If one looked at the clinical signs however, they were all the same as of the ones of children who were HIV seropositive.

The main question of my paper was that HIV and AIDS was masquerading as SIDS. We thought it was SIDS, because it looked like it and nobody had another diagnosis. But looking back, these children were premature, they had had blood and exchange transfusions, they were severely so immuno-compromised that they had no antibodies, and we did not have the technology that we have now to culture the HIV virus.

So I learned the lesson very quickly: a positive test is helpful, but if you have a child coming from a high-risk group, who has all the signs and clinical manifestations of HIV and AIDS, while the antibody test is negative, the conclusion is not ‘oh, they don’t have HIV and AIDS”. The proper conclusion is “we don’t have the optimal test”.

With Lyme and co-infections I see the same thing. If you have a positive test and you have consistent clinical manifestations of the disease, that combination gives you an answer – but basically it is just using common sense. It is the work of a clinician to put the pieces of the puzzle together.

Did somebody have a tick-bite, who is sick with a Lyme-like illness – either acutely or chronically – and the test is negative? Then you should pursue the clinical manifestations and look for alternative testing. Or treat them; even if the testing is negative. We do this for most other infectious diseases, use clinical diagnosis, when testing is ‘imperfect’ or when not available. And when patients get better with our treatment, we say we have had a ‘therapeutic success’.

Current situation

I work fulltime in a public hospital clinic in Dublin, but I also have the opportunity to see patients privately, often those who don’t want to go into public care for privacy reasons, or for convenience and flexibility. I treat many highly functioning people, both from Ireland and abroad, who want confidential treatment or who want an alternative opinion as they are unhappy with the current opinion give by other doctors.

These patients come in for different reasons, travel medicine, HIV, other STI infections, but over the last several years I have seen a sharp rise of the number of Lyme patients, especially those with ‘chronic Lyme’. Because of my experience in America, I have been identified as probably the only Infectious Disease doctor in Ireland who was willing to see patients with symptoms that were suspicious for Lyme – despite the fact that many of the antibody tests were negative. These patients had not been willing to accept the ‘atypical’ and unknown diagnoses being given to them by other specialists.


So I went through the same awakening with these patients as I did early on with these children who were dying of HIV AIDS. If you see all these patients who have a negative test, who had an obvious tick bite, who were previously well, or went off travelling, developed a fever, came back sick and were still sick 12 months later with disseminated clinical manifestations in the joints, neurology, etc, etc – then you need to take their history seriously, and investigate and treat them properly.

Many of my patients had looked for other Lyme tests, which they had to pay for themselves. Often when their standard (serological) Lyme test was read as ‘false positive’, still the pieces of the puzzle were easily put together, when I took their history. They were previously healthy, went traveling to Lyme endemic areas, came back and fell ill with consistent clinical manifestations of Lyme. Many had short term treatment and had gotten temporarily better and then their symptoms had returned.

They may have had neurological or rheumatoid symptoms, and often had been seen by neurology or rheumatology specialists and were given what I call ‘garbage bag’ diagnoses: Fibromyalgia, chronic fatigue (ME), chronic pain syndrome (CRPS) or atypical neurological diagnoses such as “a-typical MS”, “a-typical Parkinson”, “a-typical ALS”. So it was very clear that these neurologists and rheumatologists didn’t know what caused their symptoms, and indeed most of the treatments given to them had not helped them, and in many cases made them worse.

Immunologists and hematologists saw many of these patients who also had low white cell counts and were working them up for cancers, lymphomas or similar disorders. But it simply took a look at the history: these patients were previously well, had a sudden onset of illness, were coming from a Lyme endemic area, they had low white cell counts and they had fevers and sweats. It wasn’t only low white cell counts; they had manifestations of multisystem disease. Some of the more forward thinking hematology specialists then referred these patients onwards, as up until then no one had entertained an infectious etiology.

Lyme and co-infections are not on the ‘radar screen’ of most specialists in Ireland, and they are not aware of the complexities of the diagnostic issues. They follow the IDSA mantra that a negative test means you don’t have it. So on top of my standard clinical public hospital practice, this is what I have started doing over the last five years with some 500 patients who have been treated. Unfortunately I have become too busy to keep accurate statistics on these patients, but in about 70 percent of the people, who follow my treatment regime, there is recovery. Either fully or they improve so much that they can get their lives back.

The Irish governments only reports a few dozen cases over the last years. On their surveillance website, they only keep track of ‘neuroborreliosis’, so you have to end up in the hospital with a lumbar puncture to be counted. So what about all those with a bite or a non specific manifestation, who does not end up in the hospital? They don’t count? I would say that many additional cases are been missed. We have imperfect surveillance of the incidence of Lyme in Ireland. We don’t keep records of patients with these conditions, so it is easy to say there is no Lyme in Ireland. And its not all about Lyme; there are other infections you can get from a tick, the co-infections; not on anyone’s radar screen it seems.

This may be a reason why my colleagues don’t know about Lyme, but it’s quite surprising to me. I don’t really know why my colleagues quote the national government statistics, when they know they are not accurate. In contrast there are the Sexually Transmitted Infections (STI’s). Everybody is aware that the statistics about STI’s are also not well documented and recorded in Ireland, but we all know there is sex in Ireland and people get STI’s. And we know there are a lot more cases of herpes and genital warts, as the under reporting of these conditions is well accepted. My colleagues accept these statistics, those of STI’s , but do not use the same thought process when it comes to Lyme.

We have Lyme endemic areas in Ireland, where ticks are found in large numbers and people pick the ticks off their bodies and their pets bodies in the summertime. But still, the government and our doctors don’t believe these conditions exists in any significant fashion. Vets seem more aware and keyed into this issue in Ireland than the medical doctors. There seems to be a “Lyme denial” in this country, as there is in many other countries, including those within the EU.


After my qualification as an Infectious Diseases specialist in America in 1991, I became a member of the IDSA. Although I’ve never been active politically, I personally know many of the doctors in IDSA leadership positions. Many of my old bosses are past presidents and committee members of the IDSA.

Before moving to Ireland I never paid much attention to ILADS, because I never found the need to look for more information on this disease. There is a huge body of knowledge on these other infectious diseases that is coming out of the IDSA and I found it very helpful. The IDSA had provided me with the accurate and up-to-date knowledge on other severe infectious diseases, such as HIV, Hepatitis and Tuberculosis, so I assumed they would also provide that same quality of information about Lyme and co-infections. However, further inspection of their documents on Lyme and co-infections find a very selective choice of studies, and not a comprehensive view of the subject.

I would even say that when it comes to Lyme and co-infections, there is just a very limited – I would say “censored” – kind of opinion. I don’t even think there is a broad understanding of Infectious Diseases doctors on the literature about Lyme and co-infections. So I found out I actually had to also become member of ILADS, because they have made an effort to really study these tick borne diseases more intensively and look at the scientific literature on the subject to support their claims that a. antibody testing is imperfect (which we all know is the case) and that b. the current recommended treatments by the IDSA are too limited and fail many patients.

Very few IDSA members have the experience of treating Lyme patients in the same numbers and often with the same complexity when compared to ILADS members. So I’ve found it very helpful to learn from the ILADS doctors and to bring my knowledge up to speed and also learn about chronic Lyme. As a regular ID specialist in a public hospital you might see a few chronic Lyme patients a year. But if you are specialised in chronic Lyme, you may see hundreds or thousands of patients. You do learn from your patients, and the more you see of a certain patient group, the more you can understanding the commonalities that these patients present with.

Officially almost everybody follows the IDSA Guidelines, but increasingly many of my ID colleagues have started referring their patients, often at the insistence of the patients, when they see the treatment fails them or when they want a second opinion or another type of test. They are starting to understand that they may be missing a lot of infected patients, because of the rigidity in testing policies; and sometimes they reconsider their opinion when they see that patients are getting better because of longer antibiotic treatments and combination antibiotic treatments.

With an infection such as Lyme that one cannot culture in most clinical settings, meaning there is no ‘before and after’ measurement, clinical treatment results are the best indication of the infection being cured. If the symptoms return when you stop treatment, you probably need to treat a bit longer. However doctors are afraid to treat for longer for Lyme. If it is a prostatitis, there is no issue with treating longer, but if it is a life affecting condition. Doctors are afraid to treat longer, as the IDSA guidelines say 2 to 3 weeks.

And after that, it must be post infectious, even if the patient is not better. And does not get better until antibiotics are restarted and continued for a longer period of time. So who made this law that forbids doctors to treat for longer, especially when patients are getting better with the recommended treatment? Guidelines are suggestions for protocols to follow, and patients must be individually treated, as patient centred medicine is critical to all infectious diseases.


This paradox with Lyme is puzzling to me. Back in the days when we had HIV AIDS, in 1981 before we knew it was HIV AIDS as we didn’t have an antibody test until 1984 and we couldn’t culture the virus until 1987, when we saw that something was wrong with a patient, we stood up for them. We performed evaluations of gay men in New York and we knew they were immuno-compromised and that they were infected with all these opportunistic infections. We knew there had to be something we missed and we kept looking until we found it. It took a lot of hard work, science, resources and thinking ‘outside of the box’ to come up with the right diagnostics tests and later with medication which has changed the course of history with regards to HIV and AIDS.

We have done the same, put energy and initiative into the evaluation, understanding and ultimately optimal treatment for Syphilis, Tuberculosis, HIV AIDS and Hepatitis, among other diseases. Why we don’t do it for Lyme and co-infections, which are affecting an awful lot of people in a tragic way, is a mystery to me. The notion that many governments (e.g. Australia, Norway, France and many other European countries including the Netherlands) are suddenly repeating the 2016 publications by some IDSA doctors and CDC authors, is ridiculous. These guidelines are outdated and not evidence based in my opinion. We are sticking to the old traditional view even when the data and the patients in front of us do not fit into the ‘guidelines’.

Following the analogy of other spirochetal infections such as Syphilis, everybody knows that in the acute stage the blood tests are relatively reliable, but may be negative during the ‘window period. But in later stages the syphilis antibody titres go down and may often go negative. Why we don’t use such same wisdom with Lyme – another spirochete – puzzles me.

So how are these antibody tests supposed to perform optimally, when used in chronic patients who are immuno-compromised? We all know these infections go into the immune cells of the human body. They cause inflammatory and auto-immune responses, so there should be no surprise that these patients don’t have an optimal antibody response. We have imperfect technology, and to use a test that is not 100% sensitive in early infection, when the bacteria is circulating in the blood stream and in highest quantities. And then to say for chronic Lyme the same test must be used makes no sense. Just like with Syphilis and other infections, antibody titres decrease with treatment and also just decrease without treatment, so chronic Lyme sufferers suffer even further when standard antibody tests, never really validated in this population, are used.

Chronic Lyme?

If you look at major medical microbiology and infectious disease textbooks, they state that after 4 weeks you can’t find the Lyme bacteria anymore. Therefore Lyme is then categorised as ‘post infectious’. But I get back to the point I’ve made before: if you can’t culture it, you cannot know anything about its viability. You do not have a organism specific test (culture or PCR), that guides your ‘test of cure’. How do you say that a bacteria is killed, when you couldn’t grow and measure it in the first place?

All you have as a doctor managing the patient in the treatment partnership, is your patient’s response to treatment. If they say they are better on the treatment, you believe them. And make decisions accordingly. If they are not better, you have an option as a doctor: you can say to your patient, that their symptoms are post-infectious, to just ‘bite the bullet’ and give it time………

Or you can treat them for longer and see if they then improve.Many of such patients get better and get cured. To withhold treatment is this clinical scenario is fraught with significant problems, breaching a doctor’s responsibility to his patient and also basic human rights legislation.

We operate, as clinicians, in such a manner in all of our clinical career for other clinical conditions. I treat people with diabetic foot infections of the bone and I keep them on treatment for months – until their clinical symptoms are gone and their inflammatory markers go down. The textbooks don’t say how long to treat, or say treat for six weeks, at which time the infection should be eradicated. Then you wouldn’t say it’s ‘post-infectious’ after a few weeks, when the patient is still not better.

So why cant we manage with the same algorithm of ‘cure of infection’ with Lyme in parallel to the way we operate with other infectious diseases, is beyond me. Especially when we see patients getting better after treating longer than the guidelines say’ and that they relapse when the treatment is stopped too soon. Relapse with a diabetic foot infection is a treatment failure, not a post-infection or a “Post Treatment Syndrome”.

The guideline for Infectious Disease specialist is “continue treatment and make clinical assessment”. Of course we don’t want to treat people unnecessary, following antimicrobial stewardship guidelines. Yet we can treat acne with six months of antibiotics, but we cannot treat a severe infection like Lyme? Acne is just a cosmetic issue, while Lyme is a debilitating, life-changing disease.

In the absence of ideal diagnostic tools, when you think your patients may have the disease, treat them for a reasonable duration of time and assess and reassess the treatment response. One of the rules of infectious diseases medicine is that once you stop treatment and the patient stays better, they are cured. When they get worse, the infection has returned and they have relapse of infection and need repeat treatment. My ID colleagues live by that rule with most other infections, but not with Lyme.

Most of the Lyme patients I see have chronic Lyme, but I also try to see people with acute infections, which are often misdiagnosed as ringworm, a non-specific rash or as cellulitis.. I find that in cases of acute infection mostly a short course of antibiotics works well. For people who have been sick for 5, 10 or 20 years this short course treatment is not enough.

If their “a-typical” MS, Parkinson or ALS would have really been MS, Parkinson or ALS, they would not improve after treatment for a bacterial infection. Often these are young people, who are given diagnoses that rarely occur at a young age and who also responded negatively to their neurological medication. That is a red flag to me that someone is ‘missing the boat’.

Not every case of these diseases will be Lyme, but I am sure it is being missed a lot of the time. That is wrong to miss a treatable disease: MS is a life-long disease, ALS is a death sentence, while Lyme disease is a potentially curable disease that will never relapse again, when it’s appropriately treated. And patients can go back to a normal life with full function.


After we discovered the right test for HIV and proper treatment was developed, many scientists and doctors jumped on that bandwagon to move forward with the successes of the new treatments. But my interest started waning, as my interest is really in the early discovery and understanding of infectious diseases. So the first part of my career I focused on HIV as it was poorly understood and very few people were working in this arena. Around 2000 I moved into the field of Hepatitis C, because there was a huge portion in the world population suffering from it, while we did not have good drugs at that time and it affected a very vulnerable population. The severity and impact on a large population of the world was similar to HIV.

That is why, when I realised there was a very small burden of HIV in Ireland and a large burden of HCV disease, I focused on doing studies on Hepatitis C, and between 2008, where we conducted the first clinical trials with the new drugs for HCV, we now have easy cures, and the job is done. There are lots of people who want to jump on the bandwagon when the work is done, to get involved in the implementation science, and that is also very important.

But I think it was time for me to jump ‘off this bandwagon’ and look for a new poorly understood and challenging infectious disease area. What more challenging than Lyme? I initially became involved in HIV when nobody seemed to care about it, especially HIV in pregnant women. I was involved in Hepatitis C when there wasn’t a huge interest in it. So I saw Lyme as an opportunity or as a challenge. Because there are lots of unknowns, many people are severely disabled by it and I am in the position to contribute.

I work at a university, I publish, I teach at a medical school. In five years from now, when we have much better diagnostics tests for Lyme, better knowledge and treatments, there will be hundreds of doctors and scientists willing to take over the work, I hope. To me this is a really exciting time to get involved in this field, as so much good can occur if we just come together and quit the Lyme Wars. The side effect of such war is the patient suffering and being denied recognition of their disease and their symptoms.

The most exciting part is to see your patients get better! And to see them being validated that there is really something wrong with them, as they have so many rejections from the medical community. It’s just amazing; you have these patients who have seen multiple specialists with their very complex conditions. They have previously run marathons, and now can barely walk because of chronic pain and they are told that they are “seeking pain killers”. But actually they are in pain because they have an inflammation in their brain and inflammation in their joints, which is not being picked up on ‘standard testing’.

So all of a sudden these high performing people are considered to be crazy. Most are frustrated because their previously successful life in society is over and it’s hard for them to lie down and just give up, because nobody can figure out their problem. I say that if all the tests are negative and the patient is sick, the answer is not “there is nothing wrong with them”. The problem is we are not doing the right test or we have not yet developed the right test.

They get labeled wrongly, because the specialists and GP’s get tired of them. I love to see these patients, who weren’t willing to lay down and roll over. And to accept the opinion of their consultations. They are the ones who are thinking out of the box; and not the doctors that are supposed to take care of them. These patients come up with ideas and answers, seeking out people that would help them and many of them get better. As a result of this persistence and refusal to ‘throw in the towel’.

For me as a physician, most of these patients are very satisfying to work with. I have never seen such pro-activeness by such patients in any other disease area and it amazes me. They are stubbornly pursuing wellness against the negative opinions of the medical profession, who should really be accepting their condition and not writing them off.

That is the current paradox: we, the medical profession, often treat patients with suspected Lyme and Co-infections without dignity and respect, and discount their symptoms when they do not fit into our traditional ‘medical tick box’.




Please notice Lambert’s acknowledgement that the HPV vaccination has served to activate latent Lyme/MSIDS infections.  This is why I keep pounding the vaccine issue.

Please know that vaccines are filled with ingredients that your body considers toxic.

Vaccines are contaminated with other pathogens:

Vaccines have adjuvants which your body considers neurotoxic:

Mercury (thimerosol) is another neurotoxin proving to cause severe side-effects:

Mechanisms of vaccine injury:

The Lyme vaccine is deadly:

There are moral & ethical issues to consider with vaccines:

For a review of numerous vaccines, go here and read my highlighted notes on Dr. Gentempo’s 9-part vaccine series:

The HPV vaccine is also deadly:  (Other links at end of article on the deadly HPV vaccine)  Dr. Lapenta weighs in on the HPV vaccine:  they protect against less than 50% of the cancerous types of HPV, they are made by mixing antigens of each type of HPV in a single solution, i.e., a biological bomb provoking death and irreparable health conditions, contains aluminum (a neurotoxin) is an adjuvant, and has caused severe side-effects such as CFS, POTS, and sudden death.

A link has also been connected between the HPV vaccine and Bartonella:

The first peer-reviewed study using vaccinated vs unvaccinated kids  The study suggests that fully vaccinated children may be trading the prevention of certain acute illnesses (chicken pox, pertussis) for more chronic illnesses and neurodevelopmental disorders like ADHD and Autism. The scientists also found that children born prematurely, who were vaccinated, were 6.6 times more likely to have a neurodevelopmental disorder.

A short quiz to determine if you know facts about vaccines:


First Report of Bartonella quintana Immune Reconstitution Inflammatory Syndrome Complicated by Jarisch-Herxheimer Reaction

The First Report of Bartonella quintana Immune Reconstitution Inflammatory Syndrome Complicated by Jarisch-Herxheimer Reaction.

DallaPiazza M, et al. J Int Assoc Provid AIDS Care. 2017 Jul/Aug.


Bacillary angiomatosis (BA) is a rare complication of human immune deficiency virus (HIV) infection in the post-antiretroviral therapy (ART) era, and few cases of BA-associated immune reconstitution inflammatory syndrome (IRIS) have been described. We report the case of a 50-year-old man who presented with mass lesions involving the skin, subcutaneous tissues, muscle, and bone. The diagnosis of Bartonella quintana BA was confirmed by serum polymerase chain reaction. The patient’s treatment course was complicated by both IRIS and Jarisch-Herxheimer reaction. The case had a favorable outcome with supportive care and continuation of ART and doxycycline.


28393665 [PubMed – in process]



Patients infected with tick borne infections (TBI’s) are also immunocompromised and get bacillary angiomatosis (BA).  Recently, Dr. Phillips stated that the research on Bartonella is about where Lyme disease was 30 years ago, and frankly, no one is keeping track of this in relation to TBI infections.  Bartonella is a persistent infection where antibiotics mainly slow down reproduction.  The immune system is extremely important in fighting off Bart.

More on Bartonella:

Lyme/MSIDS patients will identify with numerous symptoms presented below:  Bacillary angiomatosis is a vascular, proliferative form of Bartonella infection that occurs primarily in immunocompromised persons. While the disorder is treatable and curable, it may be life threatening if untreated…Lesions can also occur in the oral mucosa, tongue, oropharynx, nose, penis, and anus. Bone pain, frequently in the forearms or legs, can also occur.

Diagnosis is most often based on clinical features coupled with biopsies of lesions. Histology reveals vascular proliferation with the presence of neutrophils adjacent to the blood vessels and masses of bacteria, which can be demonstrated by modified silver staining (Warthin-Starry silver stain). Detection of Bartonella DNA in tissue specimens by polymerase chain reaction (PCR) assay or of Bartonella antigens by immunohistochemical methods is diagnostic. [4]

Radiography can be used to find bone lesions; chest radiography can reveal pulmonary parenchymal nodules.  Computed tomography (CT) scanning of the brain can detect intracerebral bacillary angiomatosis. CT scanning and magnetic resonance imaging (MRI) can be used in the diagnosis of peliosis hepatis, while chest and abdominal CT scans may reveal mediastinal, retroperitoneal, or mesenteric lymph node enlargement.

Bacillary angiomatosis can be cured in most patients with antibiotics. Clinical experience strongly favors the use of erythromycin or a tetracycline derivative in this disorder.


Amy Hilfiger & Lyme

Published on Oct 31, 2017

Ally Hilfiger shares her experiences at Focus on Lyme 2017

Ally Hilfiger, daughter of famous fashion designer Tommy Hilfiger, has struggled with Lyme disease since childhood. We included an excerpt of her book “Bite Me: How Lyme Disease Stole My Childhood, Made Me Crazy, and Almost Killed Me” in our Fall 2016 Lyme Times issue. To take a look, click here:…


Lyme Wars – Part 3  (Click on link for news video)

Erica Byfield reports on a Johns Hopkins University research center dedicated to curing the tick-borne illness. This is the third in our five-part series on Lyme disease and the debate over the controversial diagnosis of chronic Lyme.



Christine Heidt of the University of Alberta has written a clear treatise on the issue of the persistence of Lyme (borrelia) TheCaseforthePersistenceofLymeDiseaseAfterAntibioticTherapy

In a study published over 20 years ago, it was reported that “Antibiotic therapy with penicillin, doxycycline, and ceftriaxone has proven to be effective for the treatment of Lyme borreliosis. In some patients, however, it was noticed that borreliae can survive in the tissues in spite of seemingly adequate therapy.”(14) Interestingly, recent studies support this same conclusion. Additionally, researchers have observed that either of the two antibiotics that were administered in the IDSA studies were found to initiate the transformation of the LD spirochete into treatment resistant persister cells and other bacterial forms.(5,6,9,10,11,12,13,14,15,16) Ironically, the four clinical trials meant to support the IDSA’s PTLDS model actually serve to support this recent research, which in turn supports ILADS assertion of reversion to persistent bacteremia causing ongoing symptoms, rather than the IDSA’s expert opinion that the infection has been eradicated and residual symptoms remain indefinitely….

A recent research article co-authored by, Dr Paul Auwaerter (President-elect of the IDSA), entitled “Drug Combinations against Borrelia burgdorferi Persisters In Vitro: Eradication Achieved by Using Daptomycin, Cefoperazone and Doxycycline” suggests that perhaps even the IDSA’s own members are not fully convinced of the IDSA’s version of chronic Lyme disease.(10) While Auwaerter asserts that the cause of PTLDS is unknown, he admits that “findings that suggest the continued presence of B. burgdorferi in some form indicate that current Lyme disease treatment may not sufficiently eliminate B. burgdorferi persisters or that the immune system fails to clear persisting organisms or bacterial debris, which may be the underlying cause for those who suffer from unresolved Lyme disease symptoms.”

Prior to this publication, Dr Auwaerter co-authored a publication with IDSA LD Guidelines members entitled “ Antiscience and ethical concerns associated with advocacy of Lyme disease” where he and the other authors attempt to discredit any research that does not support the IDSA’s PTLDS theories, with statements such as “Some activists portray Lyme disease, a geographically limited tick-borne infection, as a disease that is insidious, ubiquitous, difficult to diagnose, and almost incurable; they also propose that the disease causes mainly non-specific symptoms that can be treated only with long-term antibiotics and other unorthodox and unvalidated treatments. Similar to other antiscience groups, these advocates have created a pseudoscientific and alternative selection of practitioners, research, and publications and have coordinated public protests, accused opponents of both corruption and conspiracy, and spurred legislative efforts to subvert evidence-based medicine and peer-reviewed science.”(21)  

The truth is that over 50% of the IDSA’s guidelines are based on “expert opinion” rather than “evidence-based medicine” as their publication suggests. A further 31% of the IDSA guidelines are based on observational studies. Only a meagre 29% of the IDSA Guidelines fit into “evidence-based medicine”.(22,23,24,25,27) Importantly, the IDSA’s own research supports these very findings.(22) Furthermore, various IDSA members that co-authored the “Antiscience and ethical concerns” publication(21) were also involved with the creation of the Lyme Guidelines although they, themselves hold competing interests. Some members hold patents for LD products, some own shares in companies that have vested interests with the diagnosis and treatment of LD and some act as “expert witnesses in malpractice litigation” against any Dr that dares to question their “expert opinion”.(22,26) Rather than sharing information and learning from others, the IDSA continues to belittle, publicly attack and/or attempt to jail any Dr or researcher that does not endorse their Lyme disease Guidelines and policies.(22) 

Animal studies have also shown detectable borrelia DNA:  Straubinger’s dog study (persist & reactivate).pages

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.  by Stephen W. Barthold, DVM, PhD

It’s been demonstrated in dogs, mice, and monkeys that non cultivable spirochetes persist following antibiotic treatment.  So, researchers have been able to detect borrelia DNA but they have not been able to culture it from tissues.  This has led many researchers to conclude that after treatment with antibiotics, spirochetes are viable but not infectious.

Stricker and Johnson state that the Embers et al. monkey study provides animal evidence for persistent infection when three quarters failed antibiotic treatment and had persistent infection showing up in tissues at necropsy using PCR.  It’s also important to note that “small numbers of intact spirochetes were recovered by xenodiagnosis from treated monkeys.”

What this means is researchers put ticks void of infection upon the monkeys after treatment.  After a blood meal they removed the ticks and found spirochetes in them proving there were still spirochetes in the treated monkeys.

This has been done in humans too:

Dr. Betty Maloney states that the positive xenodiagnostic test in a persistently ill post-treatment subject is highly significant evidence of persistence infection; however, she feels the authors went to great lengths to discount the significance and only questioned whether the recovered DNA was just dead remnants that happened to be in the tick bite site, or due to patient noncompliance with previous therapy, inadequate blood levels of antibiotics, or re-infection.  The authors concluded there was insufficient evidence.

To read Dr. Horowitz’s comment about episode 3 on his FB page: He too lists studies as well as the fact treating physicians have found antibiotics to significantly help improve the quality of life of patients and that recent peer-reviewed studies have shown borrelia can persist like TB and leprosy due to biofilms and dormant forms.

And so the circle goes round and round without end.  The IDSA states none of this proves infection.  We ALL want to know why folks are still sick.

And the IDSA wants to have us believe Lyme disease is simple.  Really?