“What Lyme Disease Research Needs To Be Done And Why”  
By  Tom Grier  

In 1981 when the culprit of the illness was isolated both from the suspect tick and from human Lyme rashes, it was all but decided by the medical community that while Lyme disease was a real concern, it was easily treated. This assumption was based on the fact that “Lyme Arthritis” was caused by a bacterium: and with few exceptions bacterial pathogens are all successfully treated with just a few weeks of antibiotics.  

While in the test tube the Lyme bacteria Borrelia burgdorferi responded to many common antibiotics including erythromycin, tetracycline, doxycycline, penicillin and amoxicillin, the truth was that in the early days of treatment, in every human trial of antibiotic drug treatment, some patients either did not respond at all, or their symptoms quickly relapsed.  

The unfortunate fact of Lyme disease is that more than twenty years later medical science has not developed any significant breakthroughs in either diagnosis of or the treatment of this disease. Despite all of what we have learned about Borrelia burgdorferi , our diagnostic tests are still poor, and our treatment regimens are for the most part unchanged for the last two decades.  

The early Lyme tests that were developed made heavy assumptions that a patient’s level of antibody was a consistent marker of exposure and active infection. More distressing is that most early treatment studies considered a drop in antibody levels during antibiotic treatment as a quantitative marker for indicating a cure. Researchers inappropriately accepted a negative antibody titer as an absence of active infection. It was not considered that the bacteria was surviving beyond the reaches of the bloodstream’s immune system.  

Despite the overwhelming evidence that seronegative Lyme is common and that infection can persist despite treatment, today’s researchers and manufacturers of these tests still squabble over patents and royalties and spend more time thinking up clever ways of making their indirect tests more competitive in the drug market rather than creating better direct tests.  

An example of this was when a new PCR test by the U of MN was compared not to other PCR tests but to culturing Lyme rashes. Assuming only a 4 % success rate of culturing rashes the press release for the new test was complete with cost for the test and boldly stated that this test was 4 times more accurate than culturing. To the lay person this sounds good but it really meant the new PCR test was accurate only in 1 out of every 5 patients with a bull’s eye rash. This kind of research is not in the best interest of the patient.  

So what research needs to be done that isn’t being done?  

In the last twenty years the goal of medical research has become so economically competitive that so much of the work being done is secretive and proprietary, many institutions won’t even pursue research that doesn’t look economically rewarding. In today’s bottom line medical system, most institutions will not do work in an area that might duplicate the work of a competitor who may already own patents on the end product. Yet work on endless “me-too” versions of existing tests continues simply because manufacturers see more money in patient testing and vaccines than in treatment.  

I have said it many times before and still believe that Lyme patients would be better off if no test had ever been developed, and Lyme treatments were based entirely on symptom response to therapy. I don’t have a quick solution to the problem of the current patent-or-parish mentality of universities, but I do think more time needs to be spent on some old technologies such as blood smears and tissue stains before we listen to any more press releases from universities and drug companies telling us how their new test is better than that of their competitors.

In truth I have little hope in ever developing a quick easy reliable blood test for Lyme and feel we are better off without the ones currently being demanded by insurance companies and HMOs.  

My first suggestion for research is to spend less money developing tests for the living, and spend more money investigating the disease process in the dying. Understanding the pathology of this disease is paramount to making any significant advances in the treatment of this illness.  

We have seen in animal models going back to the 1980s that the blood brain barrier of mammals is quickly breached by this bacterium. (4) What role does early invasion of the Lyme spirochete into the human brain mean to patients? Is there long-term sequela to CNS invasion? These are questions are left wholly unanswered and require a deeper commitment to research than what has been allocated to Lyme disease!  

In the 1990s we learned that the Lyme spirochete has a predilection for and attaches to the lining of blood vassals. When this occurs the endothelial cells break down and creates blood vessel holes. No one has suggested or pursued any receptor site research. Perhaps one form of treatment might be finding a way to block these attachment sites?  

Drug Therapy: While we have in the past twenty years explored the use of dozens of antibiotics and combinations of antibiotics, we have not made any real advancement in antibiotic therapy. The quick and easy answer is to say we should develop newer and better antibiotics. While this is obviously true it still falls far short of what else can be done.  

One of the problems of treating Lyme disease is that the bacteria is known to penetrate difficult to reach and difficult to treat areas of the body. While the argument still persists on whether Lyme disease is an intracellular disease, there is no argument that the bacteria can get inside the joint, connective tissue and the brain which are tissues difficult to treat. In most cases you must overdose the rest of the body in order to penetrate these tissues.  

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