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

A solution not currently being pursued is better drug delivery systems. In 1991 I proposed to the company I worked for at the time, Wyeth labs, that research be done on better CNS delivery systems for amoxicillin.  

With the advent of diseases like AIDS and Lyme it seemed that we needed a better way to get drugs safely into the brain in higher concentrations where they were needed. While old drugs like amoxicillin can no longer be patented, the drug delivery systems can be patented for more than a decade. This could give new life to many old drugs. Better delivery systems make dozens of drugs available rather than just concentrating on a singly new drug option.  

Devises that optimize direct infusion of antibiotics into joint and brain is one method of accomplishing this, and the use of fat soluble carrier molecules conjugated to or surrounding the drugs is another method (lipo-spheres, DMSO etc). The response to a 28 page proposal that I drafted in 1991 to my employer, was a single sentence in a short letter. “ Dear Mr. Grier: At this time there is no interest or economic feasibility in developing new treatments for Lyme disease ...there are not enough new cases of Lyme annually to warrant development of clinical treatments. ”  

Since economic interests seem to be the main concern in researchers developing better tests for diagnosis and better drugs for the treatment of Lyme disease, it appears that Lyme disease research may be left in the hands of foundations still willing to fund research directed by need and not economics. The bonus is that almost any new treatments will be economically viable because of use in Lyme and other emerging infectious diseases.  

Here is a list of areas of research that have not been aggressively pursued and that I believe have potential in producing useful breakthroughs in diagnosis and treatment.

First we need to devote less monies to tick studies and urban exposure studies and more monies to basic pathology and microbiology studies. In a world filled with people traveling via SUVs and airplanes, Lyme disease can occur to anyone who travels through Lyme endemic areas. We need to put research money into science and not into the politics of boundaries. 

I care less about which counties have Lyme, and more about what long term untreated Lyme is doing to our medical system? If Lyme patients have been misdiagnosed as having M.S. how many Lyme patients have in the last 50 years been draining insurance companies out of money for long term care of patients with MS-like disorders caused by Lyme. We don’t know the answer and we will only find out by doing autopsies on enough dementia patients to establish an accurate percentage. Even if just a few percent of dementia patients are found to have spirochetes in the brain at the time of death, this translates to billions of health care dollars wasted on caring for sick patients when it would take just a fraction of that money to treat patients caught earlier.  

A very simple study that has never been done but would be quite revealing about tick-borne illnesses is a quality of retirement-life study that looks at the differences between the quality of health of retirees in professions that are at high risk for tick-borne illness compared to lifestyles with professions at a low risk of contracting tick-borne illnesses. Previous studies have shown a higher incidence of M.S. among agricultural workers, owners of large dogs, and in Europe M.S. is highest in areas of high rodent infestations. Perhaps a large-scale quality of life study would tell us if outdoor living is really a healthy lifestyle? Is there a greater risk for forestry workers to get M.S. than say a secretary? A survey of this type would be simple and cheap to do.  

Pathology: I am sorry to say it but the only way to get a definitive answer to the question of whether Lyme can still be an active infection post treatment, is to do autopsies and recover and test biopsies done on chronic Lyme patients that die of any other cause (cancer, heart attack etc) and do labor intensive searches for the bacteria using immuno-fluorescent tissue stains and silver stains of selected tissues. If we find it in the brain after treatment then all the arguments for not treating patients who respond to antibiotics becomes moot! Borrelia burgdorferi has been found in so many tissues that it makes sense that any autopsy study that is undertaken should investigate many tissues to determine what tissues are target tissues and are most resilient to successful antibiotic therapy.  

Receptor site research : It appears that the Lyme spirochete has an affinity for certain tissues. It seeks out connective tissue and may use N-Acetyl Glucasamine as a food source. Borrelia burgdorferi also attaches to specific cells in animal models of Lyme disease including endothelial cells, B-cells, fibroblasts, peripheral nerves, and specific brain cells. It may be that the bacteria has receptor sites that can be blocked by new and specialized therapies? If so this may be both an effective treatment and a preventative.  

To do this we need more and better animal models including mammalian brain models that investigate the pathologic mechanisms of Borrelia.  

In Switzerland a Neuropathologist Judith Miklossy showed that when she looked for spirochetes in the brains of Alzheimer patients that she found them in an alarming percentage of Alzheimer’s patient’s brains. Since this is a bacteria that is invisible in human tissue unless you look for it and stain for it post-mortem, we need to do more dementia based autopsies to determine the role and frequency of spirochetes in debilitating neurological, and neuromuscular diseases. Part of Miklossy’s work showed an association of the location of the spirochetes in the patient’s brain with amyloid plaques. What role can this bacteria or other bacterial pathogens play in producing amyloid in mammalian brains? Better animal models of brain cell metabolism and infection are needed to find out.  

In summary we are still essentially diagnosing and treating patients in the same manner as we did in the 1980s and the bulk of Lyme disease research seems to be oriented around everything except pathology, and treatment. I believe to make significant strides in patient treatment we need to devote more time and money to pathology, better drug treatments and better drug delivery systems. I also believe privately funded foundations are the best hope of directing and funding these kinds of projects.  

Tom Grier  

References:
Steere AC, Gibofsky A, Patarroyo ME, Winchester RJ, Hardin JA, Malawista SE. Chronic Lyme Arthritis: clinical and immunogenetic differences between Lyme Arthritis and Rheumatoid Arthritis. Ann Intern Med. 1979;90:896-901  

Murray, Polly. The Widening Circle: The Woman Who First Suspected JRA Was Somehow a Contagious Entity- A Lyme Disease Pioneer Tells Her Story. St. Martin’s Press, 321 pages 

Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme Disease: Meningitis, cranial neuritis, and radiculoneuritis. Neurology 1985;35:47-53

Coyle PK, Schutzer SE, Deng Z, Krupp LB, Belman AL, Benach JL, Luft BJ. Detection of Borrelia burgdorferi antigens in antibody negative cerebrospinal fluid in neurologic Lyme disease. Neurology 1995;45(11):2010-2015  

References continued next page

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