The Lyme disease epidemic continues to rage world-wide in addition to the frightening explosion of confirmed cases in the US, and yet the CDC (Center for Disease Control) and the IDSA continue to publish the clearly untrue statement that Lyme disease is hard to contract and easy to treat.

What many people do not understand is that the western blot was never meant to be a diagnostic authority but a tool to support clinical diagnosis.  The test measures antibodies, not the actual bacteria so if you have any positive bands on the western blot it means you have been exposed to Lyme disease.  It is the controversial (although why there is controversy is confusing in the extreme) amongst any intelligent mind, perhaps even more so with trained medical minds, why a western blot with any positive bands be considered a “false positive” or worse yet “negative” when the patient exhibits all of the symptoms of Lyme.

Add to that puzzle the requirement of a bulls-eye rash when researchers know that some viral strains of borrelia do not cause bulls-eye rashes (and even when they do, the rash is easily hidden in hair where tiny ticks could easily hide as they take their meal) and we must wonder if the CDC is purposefully dropping the ball.

Now, as science around Lyme and other tick-related diseases become more precise, the question begs to be asked: “Why isn’t the western blot more accurate?”

Furthermore, the proteins evaluated within the test are purposefully limited – in fact originally the test evaluated more proteins, some of which were much more indicative of the presence and activity of Borreliosis burgdorferi.  The extra bands were later removed along while at the same time the criteria for positive results was raised to demand more positive bands (five), even though one positive band should be enough to confirm a clinical diagnosis keeping in mind the CDC’s own instructions to use the western blot as a confirmation tool NOT a diagnostic tool.

Currently, Lyme disease tests in the United States are geared to detect a strain or two of a single species: Borrelia burgdorferi sensu stricto (SOURCE:GALDA – Georgia Lyme Disease Association.)  Even though we know there are many more strains capable of causing illness. (Some strains do not cause illness in humans, and some do not cause a rash.)

Another reason for negative results with Lyme infected specimens is due to differing proteins found among numerous strains of various B. burgdorferi species which provide further explanation for the reason some suspected Lyme patients may only show a positive band or two instead of the CDC’s required five.

A Chinese study found that changing western blot criteria to detect the prevalent strain of Lyme bacteria in their region increased the accuracy of the tests. Another study in the United States proved that mixing two infectious Borrelia strains in a western blot assay increased the test’s sensitivity. If simply adding other strains of the same Lyme species increases the western blot’s sensitivity, the changes needed in order to detect various Lyme species may be incredible.

“Up to now, the only species in the complex Borrelia burgdorferi sensu lato known to cause Lyme borreliosis in the United States has been B. burgdorferi sensu stricto. However, some atypical strains closely related to the previously designated genomic group DN127 have been isolated in the United States, mostly in California. [...] we analyzed the nucleotide sequences of the rrf-rrl intergenic spacer regions from 19 atypical strains (18 from California and one from New York) and 13 North American B. burgdorferi sensu stricto  strains (6 from California). [...] A heterogeneous group comprising strains belonging to the previously designated group DN127 clustered separately from B. burgdorferi sensu stricto. Within this cluster, the deep branches expressing the distances between the rrf-rrl sequences reflect a high level of divergence. This unexpected diversity contrasts with the monomorphism exhibited by B. burgdorferi sensu stricto. [...] We conclude that the taxonomy and phylogeny of North American B. burgdorferi sensu lato should be reevaluated. For now, we propose that the genomic group DN127 should be referred to as a new species, B. bissettii sp. nov., and that other related but distinct strains, which require further characterization, be referred to as Borrelia spp. ” (SOURCE: Journal for Clinical Microbiology: “Expanded Diversity among Californian Borrelia Isolates and Description of Borrelia bissettii sp. nov. (Formerly Borrelia Group DN127)” December 1998

For excellent information to better understand the current process for diagnosing Lyme and specifically the western blot, please read http://www.lymenet.de/labtests/brenner.htm

Following are recently published medical abstracts courtesy of Journal of Clinical Microbiology:

“Genetic Heterogeneity of Borrelia burgdorferi Sensu Lato in the Southern United States Based on Restriction Fragment Length Polymorphism and Sequence Analysis”

T. Lin, J. H. Oliver Jr.,L. Gao,.T. M. Kollars Jr., and K. L. Clark

Finally, a test to ask for (unless you live in Europe)! This revolutionary new test determines the existence of acute and chronic Borrelia burgdorferi (Lyme) by evaluating the specific immune response in patients. The NEI (Neuro-Endo-Immune) Connection published the following information by Sirid Kellermann, Ph.D. in November 2010.

People who are sick with Lyme disease and treating the disease for years with antibiotics and/or alternative treatments – sometimes with a single protocol and sometimes using several protocols at once – are beginning to wonder, “…maybe I don’t have Lyme, maybe it is something else.”

The  problem continues to rest with inadequate testing for a clear diagnosis. Researchers in Italy and subsequently in the UK have recently (October and November 2011) published findings that demonstrate Bartonella heslslae transferring DNA to human endothelial cells. Endothelial cells are the thin layer of cells that line the interior of blood vessels.  It doesn’t take a lot of imagination to consider the impact of this information with respect to the neurological aspect of our disease(s).

According to Dr. James Schaller (who actively researches and collaborates with doctors from around the world), Bartonella is far more common than Lyme and is spread not only by ticks but by just about every other biting insect you can think of.  He writes in his soon-to-be-published textbook on human infections spread by flea and ticks:

Bartonella is no footnote and is more common than Lyme.  Many years ago when I first got involved in the super specialtyof tick and flea infection medicine, no one took Bartonella seriously.  It was presented as an easy to kill infection, and of no real concern.  It was rarely discussed at infection medicine meetings, in guidelines or infection textbooks.  (I noticed the same thing after publishing four books on Babesia–the parasite books I purchased only had two pages on this serious infection).

When I published the most recent book on Bartonella, it showed that Bartonella did not have two or three skin patterns, but vast numbers.  This was a fully new and massively expanded diagnostic tool based on reading the world literature and examining heavily infected patients.  I was also surprised that no one was looking for the chemicals altered by the presence of Bartonella and the dynamic of these chemicals when both Babesia and Bartonella are present.  You can read this in the latter sections of my textbook, Babesia 2009 Update.

This year a new human Bartonella species was added to the over thirty five Bartonella species publically published in Genetic Data banks.  It was discovered and highlighted by the talented veterinarian researcher Edward Breitschwerdt.  He has said things more clearly than the ideas I was pondering in 2005, while doing most of my Bartonella book reading. 

Dr. Breitscwerdt has said simply, but with devastating and highly useful clarity that Bartonella testing is terrible, the treatments are poor, it is typically found on the outside of red blood cells, and the current research on Bartonella is pathetic (referencing one study at NIH.)

 If this was not enough, he said in 2011 “Bartonella is carried by more vectors than any infection on the earth.”  So it is hardly a backdoor “co-infection.”  Indeed, this month Bartonella was literally shown to alter human DNA.  The implications of this possibility are staggering, and may support what I reported six years ago—Bartonella is not killed simply or easily.  My appeal is simple: treating it like a footnote infection is outdated and harmful.

The symptoms of Bartonella are very similar to Lyme but may include other more specific symptoms such as swollen lymph glands, sore throat, painful soles of feet especially in the morning and hyperacusis (sharp pain from sound).  See more on Bartonella.

Medical researchers and Lyme-literate doctors have known for some time that co-infections complicate the recovery from Lyme borreliosis and in some cases prevent it but the reason for such difficult complications was unclear.

After the discovery of the role of biofilms in Lyme disease by Dr. MacDonald, subsequent research has uncovered evidence of communication within the biofilm between different pathogens that may illuminate the key factors of the problem and hopefully lead to reliable solutions. See 2008 slide show re Borrelia in Biofilm.

Biofilm Overview

The National Institutes of Health estimates that 60% of all human infections and 80% of refractory infections (def. unresponsive to medical treatment) are attributable to biofilm colonies.

• The protection conferred upon microorganisms by biofilm allows them to achieve a high level of antibiotic resistance, stealth and invisibility.

• Biofilm not only provide a physical barrier to antimicrobial agents (pharmaceutical antibiotics) and host antibodies, but facilitate the exchange of antibiotic-resistant genetic material between organisms and may contain antibiotic-degrading enzymes.

• In fact, biofilm communities can be 1000 times more resistant to antibiotics than free-floating bacteria.

• The decreased growth rate of sessile microorganisms (def. Permanently attached to a substrate; not free to move about; “an attached oyster”) also reduces their antibiotic susceptibility as most antimicrobial agents require rapid cell growth in order to effectively kill or inhibit the microbes.  Biofilm thus render pathogenic microorganisms enormously difficult to eradicate, and can almost single-handedly contribute to localized or systemic inflammatory reactions and delayed wound healing.

• Depending on the type of biofilm, one or more species of pathogens may be found embedded in the extracellular polymeric substance (EPS).  Bacterial EPS maybe a carrier of, or may have heavy metals embedded in them which may require chelation.

Pathogenic bacterial known to reside in biofilms include, but are not limited to: Borrelia burgdorferi (Lyme bacteria), Escherichia coli, Candida albicans (yeast and fungal mutation), Clostridium difficile, Clostridium perfringens, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Listeria monocytogenes, Pseudomonas aeruginosa, Salmonella typhimurium, Staphylococcus aureus, Staphylococcus epidermidis, and Vibrio cholerae.

The number of human diseases shown to be associated with biofilms is ever expanding and includes: chronic bacterial prostatitis, chronic rhinosinusitis (chronic sinus infections), cystic fibrosis pneumonia, infective endocarditis, periodontitis, recurrent otitis media, and virtually all device and implant related infections.  Strong evidence is also beginning to emerge for an etiologic (causative) role of pathogenic mucosal biofilm in gastrointestinal diseases, such as Irritable Bowel Disorders (IBS): Crohn’s disease and ulcerative colitis.

Biofilms can be composed of multiple species of pathogens.

Lyme biofilms are composed of the covering of the biofilm which forms a matrix rich in sugars, called extracellular polymeric substance (EPS).  In addition to polymers, it is composed of extracellular DNA, proteins that are expressed by the pathogens, polysaccharides, metals, and minerals such as calcium, magnesium and iron. 

Lyme bacteria exhibit a double cell membrane envelope structure (with an outer and inner membrane ). However, the structure of the spirochete envelope is significantly different from the typical double membranes of gram-negative bacteria . At this time (2011) the outer membrane of Borrelia is determined to be fluid-like, and it is composed of 45-62% proteins (high in lipoproteins), 23-50% lipids (high in glycolipids), and 3-4% carbohydrates.

Lipoproteins (made of proteins and lipids) in Borrelia play a major role in the inflammatory response within the infection sites in the body. One of the functions of the lipoprotein is that it acts as an adhesion in order that the organism can stick to surfaces. Unfortunately the organism itself appears to have a pump system, whereby substances that are internally toxic to it may be removed – these substances include detergents, bile salts, antibiotics , dyes, and heavy metals.

Biofilm pathogens talk to each other

According to the massive textbook “Borrelia: Molecular Biology, Host Interaction and Pathogenesis” recently published by Caister Academic Press, biofilms act like an intelligent community of pathogens, and embedded pathogens appear to have a signaling communication system. Bacteria can produce chemical signals (“talk”) and other bacteria can respond to them (“listen”) in a process commonly known as cell-cell communication or cell-cell signaling. This communication can result in coordinated behavior of microbial populations.The pathogens aggregate together, then signal one another to secrete the sticky, protective covering and express proteins.  As biofilms stick to the tissue, inflammation and tissue damage occur.

Biofilm communication was first discovered in the 1970s, when scientists at Harvard University and Scripps Institute of Oceanography began to report on a unique and fascinating phenomenon.  The system they were investigating was the production of bioluminescence by the marine bacterium Vibrio fischeri (then called Photobacterium).  As a result of extensive studies, scientists Nealson, Platt and Hastings published their findings which indicated that the bacteria was “estimating” their population density, which of course implied that they were in communication with one another.  In 1970 the idea was absurd to mainstream science but today it is commonly accepted phenomena known as “quorum sensing”.

Montana State University (blog picture courtesy of Montana State University) has a National Science Foundation Engineering Research Center that focuses exclusively on biofilms.  They have found that each of the quorum sensing mechanisms they have examined is highly individualized to the specific bacterium possessing it.

Bonnie Bassler at Princeton University explains that this “census-taking” enables the group to express specific genes only at particular population densities. Quorum sensing is widespread; it occurs in numerous Gram-negative and Gram-positive bacteria. In general, processes controlled by quorum sensing are ones that are unproductive when undertaken by an individual bacterium but become effective when undertaken by the group.

She has also discovered that in addition to their “private languages”, many bacteria have developed generalized chemical messages that can be interpreted by members of other species. In lectures she postulates that in the future, we can hope to develop microbes that can “turn-on” good behavior and “turn-off” bad behavior.

For scientists in the biofilm community this information is like a lightning bolt that has sparked numerous implications in medicine.  For those of us with chronic Lyme, some believe that this may explain why and how co-infections stall or prevent recovery from our unique “Lyme soup.”

SOURCES: University of Montana, Borrelia: Molecular Biology, “Host Interaction and Pathogenesis” by Caister Academic Press, Princeton Department of Molecular Biology, Klaire Labs

According to “Private MD News” , a team of researchers recently reported that there may be a simpler way to treat early Lyme disease rather than six weeks of Doxycycline.

Researchers from Ludwig Maximilian University in Germany found that the application of a local antibacterial gel to the site of a bug bite that transmitted the infection may quickly kill the entire virus responsible for the disease. Of course it is important to recognize that some forms of Lyme disease create a rash but do not invade the blood stream to attack any other part of the body.  This makes it difficult for doctors to know just what kind of Lyme they are treating.

This new therapeutic approach would be easier for patients to complete, but oral antibiotics would still be necessary due to the possibility of a virulent form that enters the blood stream immediately and can enter the central nervous system within 24 hours of infection.

The therapy still needs to be tested in humans, as the currently trial involved testing on animals. However, the researchers said they believe that if it turns out to be as effective in people as it has proven to be animals it could represent a significant advancement in the treatment of Lyme disease.

The treatment is currently being tested in humans as part of a phase III clinical trial, which means that if it is proven effective, it could be approved relatively soon.

As Amy speaks to groups and continues to write about Lyme and her experience, the biggest question always pops up – is this really a cure? 

Of course trying a homeopathic treatment that is$20 – $50/month seems possible financially, especially if you don’t know how long it will work and even IF it will work. Even a treatments such as Rife which can range from $75 – $5,000, is tempting but beyond most people’s resources. So when you consider spending $40,000, you want to be completely certain it works 100% of the time, because we know that insurance companies are unlikely to help cover costs.

This blog post was originally posted back in 2008, and due to the number of questions I still get about Amy’s health, I thought I would re-publish this and publish Amy’s last update on her physical condition,

Here are some more excerpts from Amy’s blog www.HealthcareHacks.com:

It seems I have to answer this, totally emotionless, once and for all. I may paste it on my forehead and the signature tag line in my e-mail. I get asked it so many times that my answer seems canned.

And despite absolutely loving that I can inspire hope in so many via the phone and e-mail, prospective patients need a place to go and read this for themselves. Over and over if they wish…..
Question: “Are embryonic stem cells a cure for Chronic Lyme Disease?”

Short answer: I believe (disclaimer: Although I am not in any way a medical professional qualified to advise, so please consult your own…) that in conjunction with antibiotics, embryonic stem cells can be a cure for debilitating symptoms associated with Chronic Lyme Disease. I feel that this can happen in two ways. One, by pumping up the immune system to better cope with the infection and other issues and diminishing chances of a relapse (with the help of adequate antibiotic treatment and possibly supplements and alternatives); and two, by helping to repair the body’s degeneration which can be causing many symptoms because of damage to the body systems (such as nerve damage, heart damage, etc.).

Long answer: In my opinion, nothing kills the Lyme bacteria and other co-infections except antibiotics (and anti-parasitic medication, etc.). However, the bacterial load is not the only problem with Lyme Disease. And often after one has gone through rigorous treatment protocols, it may not be any part of the problem. The degeneration of the body due to having an untreated or undiagnosed infectious disease for so long is a huge challenge (arthritis, brain lesions, a damaged nervous system, heart problems and the list goes on).

Western medicine is there to help treat the actual infection (even if it’s near impossible sometimes thanks to this nightmarishly “smart” bacteria). But, what can we do to repair our tormented bodies once doctors have helped us erradicate the bacteria?

As well as all of those lovely issues of degeneration, a severely compromised immune system makes things worse by allowing the body to become a sponge, soaking up every little germ, chemical and whatever else might be floating around an environment. To take it a depressing step further, a patient’s system can’t detoxify properly so they becomes stuck with all of that inside of them. Even the simplest of ways most people detoxify such as urine and sweat, are not reliable.

Many Chronic Lyme patients over time, will become unable to sweat since it is a function of the nervous system, causing a further problem with detox. If the kidneys don’t work right, then toxins may not be excreted through urine. An immune system that doesn’t work though, goes far beyond that, keeping the body in a state of inability to control the Lyme infection, as well as often becoming misdirected, turning on your body instead of the infection (autoimmune diseases).

Yes, we can all agree how important it is to strengthen and support our immune system, but will this new treatment actually finish off any remaining bacteria that antibiotics and other protocols have destroyed?

The title of the following excerpts from: http://healthcarehacks.com/the-embryonic-stem-cell-proof-is-in-my-brain-scan

I am still marveling at the color copies of my SPECT brain scan, although somewhat in disbelief. My passion for photography does not come close to producing pictures like the ones that manifested from last week’s scan, just days before I left India.

In fact, I could not intentionally capture colors so vivid, or an image so real and telling of an illness that has now officially lost its battle, little by little and day by day since my first stem cell injection December 11, 2007. I hold in my hands not only pretty pictures; but proof so substantial that I dare to invite even the most mainstream, by-the-book, anti-embryonic-stem-cells-because-it-just-can’t-be-if-I-didn’t-invent-it-doctor, to contest.

When I got to Delhi in December of last year, my brain scan revealed three lesions in the frontal lobe of my brain (both sides). That was two more than I had after the torturously aggressive treatment in the U.S. to try to stop the progression of Chronic Lyme Disease, and subsequently, the degeneration of almost every body system in my 28-year-old being (including my brain tissue).

The embryonic stem cell treatment has now completely demolished two lesions, and near but eradicated the last one. I study the images of my brain trying to locate the last part of the one remaining lesion. It’s improved beyond recognition, so much so that I’m having a hard time deciphering where its exact location is.

The part that stuns me the most I suppose, is that I left Delhi with two lesions in February of this year. One disappeared during my two-month treatment there. But consistent with the research that embryonic stem cells continue to work for months and years, they were repairing my body long after I left India and stopped receiving daily stem cells shots.

Dr. Geeta Shroff’s embryonic stem cells are the future of treating incurable and terminal illness. Like it or not Western world, here they come. You can try to slow down this remarkable technology, but you can’t stop it. And if you ever met the two doctors behind this, you’d silently laugh at anyone who thought otherwise.

After failing the mini-round of IV antibiotics due to boycotting veins in India, we decided a month of oral antibiotics would suffice. This is just to make sure the infection stays under control, if there is any still left at all. I hate the pills and the pills I have to take to make sure those pills don’t hurt me (my liver, kidneys, etc.). And I despise worrying that my stomach will just one day decide it hates me, enough to fall completely apart.

But, I have this healthy, vibrant, functioning body and the inconvenience of the medication is a small price to pay for big “insurance.” I feel like sometimes I’m holding on so tight that I’ll crush the mere possibility out of a far-fetched theory that this disease could ever do again to me, what it once did.

This might just be the shortest blog post in the world for a girl as wordy as me. But, what can I say? My overcomplicated life has become so simple that it takes less and less words to describe.

And in all fairness, compared to the indisputable proof that embryonic stem cells regenerated an otherwise progressively degenerating 20-something-year-old brain — does anything else really even matter?

Thanks to Amy Scher for generously sharing her amazing and wonderful story.  I hope we will find more and more stories of people who are willing to step out of the box and forge new trails for the diseased families and individuals whose lives are falling apart.

This story gives us all something solid to hold on to when we are herxing and feel like giving up.

NEVER give up!

Now jump forward to http://www.lymediseaseresource.com/wordpress/where-is-amy-scher-did-her-stem-cell-treatment-cure-her-chronic-lyme-disease/!

CALDA printed the following information in their blog recently.  The article, “HARDSCIENCEONLYME: Lyme Culture Made Easy, Antibiotic Effectiveness, and Mechanisms of Persistence ” written by CALDA’s President Lorraine Johnson can also be found on CALDA’s website http://www.lymedisease.org/:

Dr. Eva Sapi and colleagues have published an important study today, “Evaluation of in-vitro antibiotic susceptibility of different morphological forms of Borrelia burgdorferi”. I have included the link to the article, which is available free of charge at Dove Press, at the end of this post and encourage you to read it.

The study is broad ranging, but makes a significant contribution to Lyme research in a number of areas: culturing techniques, cyst and spirochete antibiotic susceptibility, and the role of biofilms in persistence.

The most important result of the research was the development of a new culture technique that dramatically increases the growth of Borrelia burgdorferi (Bb), the corkscrew-shaped bacteria (spirochete) that causes Lyme disease, making it easier to detect persistence of the bacteria. The new culture technique is also better able to grow the cyst form of the bacteria that is thought to be metabolically dormant. 

One mechanism of persistence of Bb is believed to be its ability to convert from the spirochete form to the cyst form in vitro when presented with an unfavorable environment.  This conversion would allow the bacteria to evade the immune system and resist destruction by antibiotics that rely on cell division for effectiveness.  When the environmental conditions become more favorable, the organism can then revert back to the spirochete form.

The ability to easily culture the cyst form as well as the spirochete form of the bacteria permitted the researchers to determine the effect of various antibiotics on each form of the bacteria.  Some antibiotics decreased the number of spirochetes but increased the number of cysts, while other antibiotics reduced both spirochetes and cysts, but at different rates.

Finally, the researchers were able to develop biofilm colonies of the Lyme bacteria.  These colonies are made up of bacterial clusters coated in slime, and they have been shown to promote persistent infection in other diseases. The effectiveness of antibiotics for Bb in biofilm colonies was greatly reduced, with viable organisms detected in 70-85% of the biofilm colonies.

In summary, the study achieved an important new advance in culture techniques for Bb, demonstrated varying sensitivity of the cyst and spirochete form of Bb to different antibiotics, and confirmed mechanisms of persistence of Bb by converting from spirochete to cyst form and by forming biofilm colonies that protect the organism from antibiotics.

The research was supported by grants from the California Lyme Disease Association, Turn the Corner Foundation and the University of New Haven. The full text of the article is available without charge at Infections and Drug Resistance.

Back in 1985, Dr. Alan MacDonald stunned the medical world with a special slide show on neo-natal tissue that he had amassed over years of autopsying stillborn babies as the pathologist at South Hampton Hospital.

Using a darkfield microscope technique to capture the images on film, Dr. MacDonald presented his shocking hypothesis to the world in Vienna at the Second International Symposium on Lyme Disease and Related Disorders.

Instead of pictures of swollen knees, Dr. MacDonald showed slide after slide of spirochete infected tissue from these babies who were never able to survive outside the womb.

The hostility from the other scientists was at that time more of direct censure than verbal assault, but few doctors could believe what their own eyes were showing them. Lyme disease cannot be contracted in the womb, or passed from the mother in vitro – so the old guard insisted.

His pictures of cyst forms and other bizarre shapes and truncated strings did not look like the clear spiral shape of Borrelia, but when Dr. MacDonald added special chemicals to the tissue, these shapes showed up in the same way that spirochetes do – emitting a soft fluorescent glow.

This convinced Dr. MacDonald that the Lyme spirochetes were behaving exactly like syphilis spirochetes by carefully researching literature from the world’s top experts on syphilis. The queer shapes – hooks, rings balls and truncated strings mixed in with a few clear spirals. This was evidence of the morphic nature of the bacteria, and further proof for his hypothesis.

It wasn’t surprising that Dr. MacDonald the researcher began working with Dr. Burrascano the practicing physician. Together they became more and more convinced that Lyme disease was the mystery infection behind significant illnesses, chief amongst them, Alzheimer’s.

Unfortunately, the hounds were unleashed and a host of doctors were run out of town by medical professionals who followed the tenets of Dr. Steer in Boston, MA. Dr. MacDonald eventually found the adversity too much to bear and moved to Texas where he was haunted by the unanswered questions of his research. Specifically, was Lyme disease causing Alzheimer’s?

Fast-forward to 2006, Dr. MacDonald has returned to New York, this time to St. Catherine of Siena Medical Center in Smithtown, on the Long Island Sound where he immediately revived his research. He began by ordering ten Alzheimer’s brains from a brain bank to slice and study under the darkfield microscope.

What he found, is beyond alarming. To read the full text of his actual reports click here.

He found that seven of the ten brains “…lit up like a Christmas tree.” They were loaded with a genetic Frankenstein – DNA of the spirochetes combined with human chromosomes.

The medical term, “transfection” is not so frightening, but the reality is devastating. It basically means that your own body begins producing the infection. As Dr. MacDonald said, “Once it is in your DNA and you’re churning it out yourself, you’re cooked!”

For the people who are churning it out, it will certainly mean a constant struggle, but for those who are just beginning to get sick, Dr. MacDonald’s work may bring a miracle.

To see Dr. MacDonald’s website click here.

To read PubMed’s abstract on Dr. MacDonald’s research on “Transfection”, click here.

To read Dr. MacDonald’s compiled medical hypothesis click here.

NOTE: This was originally published in 2008 before Dr. MacDonald retired – ironically due to Alzheimer’s.  Thankfully, different aspects of his work is being continued by many researchers across the country.

The bacteria that cause Lyme disease, one of the most important emerging diseases in the United States, appear to hide out in the lymph nodes, triggering a significant immune response, but one that is not strong enough to rout the infection, according to a new report by researchers at the University of California, Davis

Results from this groundbreaking study involving mice may explain why some people experience repeated infections of Lyme disease. The study appears online in the journal Public Library of Science Pathogens.

“Our findings suggest for the first time that Borrelia burgdorferi, the bacteria that cause Lyme disease in people, dogs and wildlife, have developed a novel strategy for subverting the immune response of the animals they infect,” said Professor Nicole Baumgarth, an authority on immune responses at the UC Davis Center for Comparative Medicine.

“At first it seems counter intuitive that an infectious organism would choose to migrate to the lymph nodes where it would automatically trigger an immune response in the host animal,” Baumgarth said. “But B. burgdorferi have apparently struck an intricate balance that allows the bacteria to both provoke and elude the animal’s immune response.”

“Science Daily” recently reported these findings, and yet so many medical experts still maintain that there is no such thing as chronic Lyme disease.  As each year passes and studies continue to pile up proving the personal testimonies of hundreds of thousands of suffering victims. Thanks to U.C.Davis we have more concrete proof.

Swollen lymph nodes, or lymphadenopathy, is one of the hallmarks of Lyme disease, although it has been unclear why this occurs or how it affects the course of the disease. The UC Davis research team set out to explore in mice the mechanisms that cause the enlarged lymph nodes and to determine the nature of the resulting immune response.

They found that when mice were infected with B. burgdorferi, these live spirochetes accumulated in the animals’ lymph nodes. The lymph nodes responded with a strong, rapid accumulation of B cells, white blood cells that produce antibodies to fight infections. Also, the presence of B. burgdorferi caused the destruction of the distinct architecture of the lymph node that usually helps it to function normally.

While B cells accumulated in large numbers and made some specific antibodies against B. burgdorferi, they did not form “germinal centers,” structures that are needed for the generation of highly functional and long-lived antibody responses.

“Overall, these findings suggest that B. burgdorferi hinder the immune system from generating a response that is fully functional and that can persist and protect after repeat infections,” Baumgarth said. “Thus, the study might explain why people living in endemic areas can be repeatedly infected with these disease-causing spirochetes.”

In addition to Baumgarth, members of the UC Davis research team include Stephen Barthold, director of the Center for Comparative Medicine; Emir Hodzic, director of the Real-Time PCR Research and Diagnostics Core Facility; staff scientist Sunlian Feng; graduate student Christine Hastey; and Stefan Tunev, formerly of the Center for Comparative Medicine and now at Medtronic Inc.

Sources:

University of California – Davis (2011, June 17). Lyme disease bacteria take cover in lymph nodes. ScienceDaily. Retrieved June 21, 2011, from http://www.sciencedaily.com­ /releases/2011/06/110616193911.htm

Stefan S. Tunev, Christine J. Hastey, Emir Hodzic, Sunlian Feng, Stephen W. Barthold, Nicole Baumgarth. Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation. PLoS Pathogens, 2011; 7 (5): e1002066 DOI: 10.1371/journal.ppat.1002066

On June 20, 2011, The New York Times published an article, “Once Rare, Infection by Tick Bites Spreads” by Laurie Tarkan; bravely presenting  evidence that shows the alarming spread of Babesiosis  (Babesia – a malaria-like parasite that attacks the red blood cells, and has been considered by many of us to be a common co-infection of Lyme disease.)

Finally the extraordinary mystery surrounding the wide range of differing symptoms and intensity of various symptoms have been set under the umbrella of Babesia microti (although there could be many different and as of yet unlabeled variations of the parasite) while only months ago, and today in some hospitals, Babesiosis was only considered if the symptoms were life threatening.  My own primary care doctor told me five years ago – in spite of my symptoms – that I wasn’t sick enough to have Babesiosis.

Not surprisingly, the fatalities were always in the spotlight, and it has not been until recently with the release of some new studies that more is being understood about Babesiosis, and more in depth questions being brought to the fore.

The CDC recently announced that there has been a twenty-fold increase in Babesiosis  between 2001 and 2008 – in only seven years!  Another study on Block Island showed that Babesiosis is only 25% less common than Lyme disease in the 70% of islanders tested.  Even more alarming is that one quarter of the adults, and one half of the children that tested positive for Babesiosis showed no symptoms at all!

These frightening results affect our society on so many levels, many of which are immediately obvious.  Thankfully government officials are not closing their eyes like they have with Lyme disease but have immediately considered the ramifications concerning the nation’s blood supply.  As you may or may not know, blood banks do not screen blood for Lyme and/or the many co-infections including Babesiosis.

Additionally, it appears that contracting Babesiosis from blood transfusions is more likely to end in fatality according to a study by the American Red Cross – 30% of those infected through infusions died.

The good news is that more effort is being made to find a reliable screening tool to discover these pathogens as soon as possible. The Rhode Island Blood Center has become the first in the country to use an experimental new test to screen blood for the parasite which will hopefully develop into a blood test for those of us trying to find a diagnosis for our mysterious disease symptoms.  The pressure is definitely on.

For more information: http://www.nytimes.com/2011/06/21/health/21ticks.html?_r=3

and http://www.ncbi.nlm.nih.gov/pubmed/19624607