I wish to take the opportunity to thank Richard Gottfried and the Assembly Committee on Health for convening this hearing.

I'd like to briefly tell you of my background. I am a born and bred New Yorker and I love the beautiful state of New York. I graduated from Columbia College in New York City and from New York Medical College in Valhalla, New York where I was elected to Alpha Omega Alpha Honor Medical Society in my Junior year. I graduated second in my class and was awarded the Conrad Engerud Thuraldsen Prize in Anatomy. I am board certified in Internal Medicine and was trained and certified in Critical Care Medicine. During the course of my training I did a full year of Anatomic Pathology and performed 20-30 complete autopsies.

I went into private practice in Armonk in 1985, not realizing at the time that I had plunked myself down in the midst of what was to be a burgeoning epidemic of Lyme disease. Like many other internists, I began seeing patients with Lyme disease.

Lyme disease is a tick-transmissible infectious disease caused by the spirochete, Borrelia burgdorferi. Best known for the "bull's eye" rash, swollen knee, and Bell's palsy, it is turning out to be a very complex infectious disease with systemic effects as well as varied manifestations affecting individual organ systems such as the skin, visual and auditory systems, joints, nervous system and heart. To give you a sense of the wide scope of manifestations associated with the illness, please refer to Document 1, an outline of a talk I gave in Chicago in 1998.

The range of manifestations associated with Lyme disease has been continually expanding. It can be difficult to distinguish Lyme disease from a number of other disorders which it can greatly resemble including rheumatoid arthritis, multiple sclerosis, lupus, the chronic fatigue syndrome, fibromyalgia, Lou Gehrig's disease, Alzheimer's disease and others.

Many persons who prove to have Lyme disease have no recollection of a tick attachment and estimates varying between 20 and 80% of those with the disease having recollection of the rash associated with the illness. Testing for Lyme disease can sometimes be quite clear cut and conclusive but false positive as well as false negative test results may occur. Thus the treating physician's judgment in making a clinical diagnosis is crucial. Over-reliance on imperfect tests can result in failure to treat true Lyme disease when it is present, which can have disastrous consequences for patients.

Patients who test negative on standard tests but who really have the disease (the seronegative subset) may be most ill. There is ample precedent for variable expression of severity in infectious diseases depending on a patient's immune response. In leprosy, for example, patients having a vigorous immune response are able to contain the illness with resultant mild disease. Those with an ineffective immune response have more devastating leprosy, with deformity and loss of appendages.

For the most part, academic medical centers have restricted their studies to the seropositive subset only. At the same time assays available in certain research centers have been able to demonstrate active infection in patients who test negative on standard tests; such testing is not generally available to practicing physicians.

When I first started seeing patients with Lyme disease in the mid-1980s I found they didn't always behave the way the books said they should. Some would respond favorably to antibiotic treatment but when treatment was stopped they relapsed only to respond again to reinstitution of antibiotic therapy and relapse once again when treatment was stopped. It began to dawn on me that this might be a chronic infection that could be treated but perhaps not cured with antibiotics. Because of this I gradually lengthened the duration of treatment I offered patients.

Many reputable workers from around the world have independently proven that the Lyme disease organism is capable of surviving in both animal and human hosts despite application of antibiotic therapy, including intensive intravenous antibiotics (Documents 2,3,4,5,6,7). It seems in some cases the infection can endure for months or years and even the natural life of the host despite application of antimicrobial treatment.

Such chronic infection can induce a wide variety of pathologic manifestations both directly and mediated through the immune response. Antibiotic treatment may be viewed, then, as suppressive rather than truly curative in such cases. The outcome of the infection depends on the patients immunogenetics, the virulence of the strain of borrelia, and effects of other tick-borne co-infections. Individual response is very variable and blanket statements about what constitutes sufficient treatment can not be made. Some individuals may be cured with treatment. As in other spirochetal diseases, some may enter a latent phase of the infection which does not necessarily require continuation of treatment. However, relapse and need for re-treatment needs is a possibility which must be borne in mind and persons who have had Lyme disease need to be followed carefully over long periods of time.

Due to my background and training I began to see the more complex and more seriously ill persons with chronic and neurologic illness. I would like to share with you the case of one of the most seriously ill patients I have cared for. The case exemplifies some of the problems associated with diagnosis and treatment of Lyme disease. Also I am presenting the case succinctly in a few minutes. To have a more in depth understanding of the case please refer to my article on chronic meningoencephalomyelitis which presents the case in detail (Document 7, Case 2). The patient's wife, who will be a speaker later today, has given me consent to disclose his identity.

Case of Martin Eisenhardt:

A 61 year old outdoorsman, a resident of Cairo, NY, developed a grapefruit-sized red rash on one thigh Fall of 1985. Its significance was not appreciated and no treatment was given. The following Winter and Spring he developed a serious neurologic symptoms and spinal fluid examination showed lymphocytic meningitis. A Lyme ELISA was negative for which reason the possibility of Lyme disease was discounted. He was diagnosed with "vasculitis" (an inflammation of blood vessels) and treated with prednisone and immunosuppressive (cancer) chemotherapy agents with progressive deterioration to just above a vegetative state. In 1988 he had a positive Lyme ELISA at SUNY Stony Brook and was treated with two weeks of intramuscular Rocephin (ceftriaxone) with slight benefit. In 1992 he was transferred to Northern Westchester Hospital Center in Mount Kisco, New York in order to be re-evaluated by me. He was found to be in status epilepticus (continuous seizures). (Slide 1: CT scan of brain). Based on his history I felt it likely that he had chronic neurologic Lyme disease. I had to defend my decision to admit him to my hospital and treat him (Document 8). Initial laboratory tests were inconclusive. One of my colleagues expressed to me his opinion that the best thing that could happen to the patient was to die and have an autopsy. His wife certainly didn't feel that way. She felt he deserved a chance to be treated, and I agreed. He was treated for one month with daily intravenous Rocephin and for about one year with once weekly "pulse" Claforan (cefotaxime).

Although he was already very severely brain damaged when he was placed under my care he still improved modestly as vouched for by Greene County Public Health Nursing Service which had cared for him for years (Document 9). Treatment with intravenous antibiotics was discontinued in the late Spring of 1993 after which he was treated with oral antibiotics. He succumbed to his illness July 1993. A complete autopsy was performed by Jeff Hubbard, M.D. of Bender Laboratory, right here in Albany. Here are photographs from the autopsy showing a picture of the cut brain showing hydrocephalus (loss of brain substance)(Slide 2) and a microscopic view of brain tissue with florid chronic meningoencephalomyelitis (Slide 3). Electron microscopy of brain tissue showed structures compatible with borreliae (Slide 4); PCR of brain was positive for detection of the DNA of the Lyme organism (Slide 5) [both by Dagmar Hulinska, Ph.D. of the Borrelia Reference Laboratory of the Czech Republic], and his spinal fluid was very strongly positive for detection of OspA antigen and Lyme-specific immune complexes at neurologist Patricia Coyle's research lab at the State University of New York at Stony Brook, indicating the presence of active infection despite the treatment he had received.

This patient's illness was extremely severe, however it is not an isolated case. I have dealt over the past 15 years with many other very seriously ill patients whose nervous systems are being damaged or destroyed by the infection.

I have had a number of other fatalities due directly to Lyme disease in my practice, including in a 7 year-old child (see Document 10). This child was improving on intravenous antibiotic treatment. A successful appeal to Cigna's IntraCorp review physician resulted in extension of treatment from 3 to 6 months (Document 11). When the physician reviewer (following CIGNA's corporate policies) denied further intravenous treatment, uncontrollable status epilepticus recurred despite maximal anti-convulsant therapy. She died within one month of cessation of intravenous antibiotic treatment.

The world literature also contains numerous reports of fatal outcomes in Lyme disease (see References), but this information has not received emphasis and public health authorities (Document 12), insurance companies and their paid physician consultants insist that Lyme disease is not a fatal illness.

I should hasten to add that in contrast to these devastating cases, when Lyme disease is correctly diagnosed and treated appropriately intensively before irreversible neurologic injury has occurred, recovery to a greater or less extent is the rule. I have had innumerable cases in my practice where intensive treatment has restored very compromised individuals to normal or near normal status where they can enjoy a satisfactory and satisfying quality of life as opposed to one of utter misery and suffering.

It is vital that treating physicians be enabled to exercise their individual clinical judgment as to choice and method of administration of antimicrobial agent (e.g. oral, intramuscular or intravenous) and duration of treatment unencumbered by third party interference.

The controversies about the nature of Lyme disease and what constitutes appropriate treatment for it need to be put into perspective. At the turn of the 20th century, bitter debate raged within the medical profession about another spirochetal disease, syphilis. There was bitter controversy over what constituted appropriate treatment, duration of treatment, and criteria for cure. There was a chaos of treatment regimens and private preferences (Document 13). It has taken medical science more than 400 years to understand syphilis as a chronic multi-system infectious disease which evolves over time. We are but 25 years into understanding the spirochetal infection known as Lyme disease.

In syphilis it is a well-accepted dictum that progressing neurologic symptoms in patients with a prior diagnosis of syphilis and in the absence of a clear alternate cause for symptoms should be treated further with antibiotics, regardless of test results. There is ample precedence in the syphilis literature for seronegativity and chronic persistent infection despite prior application of antibiotic therapy (see Documents 14,15).

A major difference between the syphilis controversy of the turn of the 20th Century and the Lyme controversy at the turn of the 21th Century is the existence and influence of the insurance industry. Metropolitan Life Insurance Company had an important formative role in the creation of the National Institutes of Health (Document 16). This raises the issue of possible ongoing undue influence of the insurance industry in setting national public health priorities.

Spring of 2000, the Infectious Diseases Society of America (IDSA) published Practice Guidelines for the Treatment of Lyme Disease. It asserted that there was no significant evidence that 'chronic Lyme disease' exists as a separate diagnostic entity and that there is no role for treatment with antibiotics beyond one or at most two months for any case of Lyme disease (Document 17). Insurance companies have "glommed on" to these guidelines and routinely deny reimbursement to insureds for oral and intravenous antibiotic treatment extending beyond 60 days. Insurance company pharmacy benefit managers keep track of physician prescribing patterns. Physicians whose prescribing patterns do not conform to IDSA guidelines have been targeted and reported to State Departments of Health for investigations for medical misconduct. It is a "no lose" proposition for the insurance industry. This enmeshes such physicians in a costly, stressful and time consuming administrative process that pits them individually against the vast power and resources of the State and jeopardizes their professional reputations, practices and financial solvency. Even if they win, they lose. It sends a chilling message to rank and file physicians and undermines physicians' professional autonomy. Not surprisingly, persons with chronic Lyme disease are having increasing difficulty finding any physician anywhere willing to see them.

At the very least the IDSA guidelines are highly scientifically biased; at worst they may be frankly fraudulent. The document omits scores of articles from the worldwide peer-reviewed literature demonstrating the reality of chronic persistent infection despite prior antibiotic treatment. No clinicians who actually care for the majority of patients having chronic Lyme disease were invited to participate in drafting the guidelines. The sole academician in the IDSA known to advocate the existence of chronic Lyme disease was purged from the committee drafting the document. That some committee members involved in the creation of the guidelines had long-standing financial relationships with the insurance industry was not disclosed in the publication. Lack of disclosure of potential conflicts of interest in peer-reviewed research and publications has been the subject of a recent editorial in the Journal of the American Medical Association, decrying such practices on grounds of medical ethics (Document 18).

The single greatest obstacle to badly needed progress in development of improved methods of diagnosis and treatment for Lyme disease is the chronic persistent denial of chronic persistent infection in the illness. Such denial, in the face of so much objective evidence to the contrary, must be viewed as a type of social pathology.

The question has been raised, what is tertiary syphilis without the spirochetal bacterium Treponema pallidum? Similarly one ought to ask, what is chronic Lyme disease without the spirochete Borrelia burgdorferi?

What is being promoted as the "standard of care" for chronic Lyme disease is medical neglect, a vast de facto and unintended Tuskegee experiment, whose hapless subjects are your constituents.

Ladies and gentlemen of the committee, you can do something about it(Document 19).

Thank you for your attention.

Kenneth B. Liegner, M.D.

Summary of Documents:

Document 1

Liegner KB. Disseminated Lyme Disease: Diagnosis & Treatment(Talk Outline). Lyme Disease Foundation, Illinois Department of Health, Illinois Academy of Family Practice & Cook County Department of Health. Chicago March 23, 1998.

Document 2

Liegner KB, Shapiro JR, Ramsay D, Halperin AJ, Hogrefe W, Kong L. Recurrent Erythema Migrans Despite Extended Antibiotic Treatment with Minocycline in a Patient with Persisting B. burgdorferi Infection. J Amer Acad Derm 1993;28:312-4.

Document 3

Straubinger RK. PCR-Based Quantification of Borrelia burgdorferi Organisms in Canine Tissues over a 500-Day Postinfection Period. J Clin Microbiol 2000;38:2191-2199.

Document 4

Liegner KB, Rosenkilde CE, Campbell GL, Quan TJ, Dennis DT. Culture-confirmed Treatment Failure of Cefotaxime and Minocycline in a Case of Lyme Meningoencephalomyelitis in the United States. Program and Abstracts. V International Conference on Lyme Borreliosis. Abstr. 63 P. A11, Arlington, VA. May/June 1992.

Document 5

Liegner KB, Agricola MD, Bayer ME, Duray PH. Chronic Lyme Disease (CLD): A Costly Dilemma. Program and Abstracts, VI International Conference on Lyme Borreliosis. Abstr. P012M. Bologna, Italy, June 19-22, 1994.

Document 6

Liegner KB. Lyme Disease: The Sensible Pursuit of Answers. (Guest Commentary). J Clin Microbiol 1993;31:1961-1963.

Document 7

Liegner KB, Duray P, Agricola M, Rosenkilde C, Yannuzzi L, Ziska M, Tilton R, Hulinska D, Hubbard J, Fallon B. Lyme Disease and the Clinical Spectrum of Antibiotic-Responsive Chronic Meningoencephalomyelitides. J Spirochetal and Tick-borne Dis 1997;4:61-73.

Document 8

Liegner KB. Letter to Vice President for Medical Affairs, Northern Westchester Hospital Center defending admission and treatment of Mr. Eisenhardt, August 4, 1992.

Document 9

Letter from Greene County Public Health Nursing Service regarding Martin Eisenhardt, status in response to treatment.

Document 10

Liegner KB & Jones CR. Fatal progressive encephalitis following an untreated deer tick attachment in a 7 year-old Fairfield County, Connecticut child. [Abstract] VIII International Conference on Lyme Disease and other Emerging Tick-borne Diseases, Munich, Germany, June 1999.

Document 11

Liegner KB. Letter to CIGNA IntraCorp review physician.

Document 12

CDC, Division of Vector-borne Infectious Diseases. Lyme Disease Home Page: "Lyme disease is rarely, if ever, fatal."

Document 13

Brandt AM. No Magic Bullet. A Social History of Venereal Disease in the United States Since 1880. Oxford University Press, 1985.

Document 14

Hotson JR. Modern Neurosyphilis: A Partially Treated Chronic Meningitis(Medical Progress). West J Med 1981; 135:191-200.

Document 15

Dibbern DA & Ray SC. Recrudescence of Treated Neurosyphilis in a Patient With Human Immunodeficiency Virus. Mayo Clin Proc 1999;74:53-56.

Document 16

Harden VA. Inventing the NIH. Federal Biomedical Research Policy, 1887-1937. The Johns Hopkins University Press.Baltimore.1986.

Document 17

Wormser GP, et. al. Practice Guidelines for the Treatment of Lyme Disease. Guidelines from the Infectious Diseases Society of America. Clin Infect Dis 2000;31:1-14.

Document 18

Davidoff et. al. Sponsorship, Authorship, and Accountability.[Editorial].JAMA 2001;286:1232-1234.

Document 19

Liegner KB.(Preface) in Murray P. The Widening Circle. A Lyme Pioneer Tells Her Story. St. Martin's Press, New York 1996.

REFERENCES: CHRONIC AND NEUROLOGIC LYME DISEASE

Straubinger RK. PCR-Based Quantification of Borrelia burgdorferi Organisms in Canine Tissues over a 500-Day Postinfection Period. J Clin Microbiol 2000;38:2191-2199.

Liegner KB. Lyme Disease: The Sensible Pursuit of Answers (Guest Commentary). J Clin Microbiol 31:1961-1963, 1993.

Weder B, Wiedersheim P, Matter L, Steck A, Otto F. Chronic progressive neurological involvement in Borrelia burgdorferi infection. J Neurology 1987;234:40-43.

Ackermann R, Gollmer E, Rehse-Kupper B. Progressive Borrelien-Enzephalomyelitis. Chronische Manifestation der Erythema-migrans Krankheit am Nervensystem. Dtsh. Med. Wochenschr.110(26)(1985)1039-1042.

Preac-Mursic V, Weber K, Pfister HW, Wilske B, Gross B, Baumann A, Prokop J. Survival of Borrelia burgdorferi in Antibiotically Treated Patients with Lyme borreliosis. Infection 1989;17:355-359.

Liegner KB, Shapiro JR, Ramsay D, Halperin AJ, Hogrefe W, Kong L. Recurrent erythema migrans despite extended antibiotic treatment with minocycline in a patient with persisting Borrelia burgdorferi infection. J Amer Acad Derm 1993;28:312-4.

Lawrence C, Lipton RB, Lowy FD, Coyle PK. Seronegative Chronic Relapsing Neuroborreliosis. Eur Neurol 1995;35:113-117.

Liegner KB, Duray P, Agricola M, Rosenkilde C, Yannuzzi L, Ziska M, Tilton R, Hulinska D, Hubbard J, Fallon B. Lyme Disease and the Clinical Spectrum of Antibiotic-Responsive Chronic Meningoencephalomyelitides. J Spirochetal and Tick-borne Dis 1997;4:61-73.

Liegner KB & Jones CR. Fatal progressive encephalitis following an untreated deer tick attachment in a 7 year-old Fairfield County, Connecticut child. [Abstract] VIII International Conference on Lyme Disease and other Emerging Tick-borne Diseases, Munich, Germany, June 1999.

Fallon BA, Tager F, Fein L, Liegner K, Keilp J, Weiss N, Liebowitz MR. Repeated Antibiotic Treatment in Chronic Lyme Disease. J Spirochetal and Tick-borne Dis 1999;6:94-102.

Miklossy J, Kuntzer T, Bogousslavsky J, Regli F, Janzer RC. Meningovascular form of neuroborreliosis: Similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary Neurosyphilis. Acta Neuro Pathol 1990;80:568-572.

Oksi J, Uksila J, Marjamaki M, Nikoskelainen J, Viljanen MK. Antibodies against whole sonicated Borrelia burgdorferi spirochetes, 41-kilodalton flagellin, and P39 protein in patients with PCR- or culture-proven late Lyme borreliosis. J Clin Microbiol 1995;33:2304-15.

Bertrand E, Szpak GM, Pilkowski E, Habib N, Lipczynska-Lojkowska W, Rudnicka A, Tylewska-Wierzbanowska S, Kulczycki J. Central Nervous System Infection Caused by Borrelia burgdorferi. Clinico-Pathological Correlation of Three Post-Mortem Cases. Folia Neuropathol 1999;37:43-51.

Haass Anton. Lyme Neuroborreliosis. Current Opinion in Neurology. 1998;11:253-258.

Kohler J, Kern U, Kasper J, Rhese-Kupper B, Thoden U. Chronic central nervous system involvement in Lyme borreliosis. Neurology 1988;38:863-867.

-Kollikowski HH, Schwendemann G, Schulz M, Wilhelm H, Lehmann HJ. Chronic borrelia encephalomyeloradiculitis with severe mental disturbance: immunosuppressive versus antibiotic therapy. J Neurol 1988;235:140-142.

Petrovic M, Vogelaers D, Van Renterghem L, De Reuck J, Afschrift M. Lyme Borreliosis - A Review of the Late Stages and Treatment of Four Cases. Acta Clinica Belgica 1998;53-3:178-1+83.

Straubinger RK, Summers BA, Chang Y-F, Appel MJG. Persistence of Borrelia burdgorferi in Experimentally Infected Dogs after Antibiotic Treatment. J Clin Microbiol 1997;35:111-116.

Liegner KB, Rosenkilde CE, Campbell GL, Quan TJ, Dennis DT. Culture-confirmed Treatment Failure of Cefotaxime and Minocycline in a Case of Lyme Meningoencephalomyelitis in the United States. Program and Abstracts. V International Conference on Lyme Borreliosis. Abstr. 63 P. A11, Arlington, VA. May/June 1992.

Omasits M, Seiser A, Brainin M. Zur rezidivierenden und schubhaft verlaufenden Borreliose des Nervensystems. Wiener clinische Wochenschrift1990;102:4-12.

Liegner KB, Ziska M, Agricola MD, Hubbard JD, Klempner MS, Coyle PK, Bayer ME, Duray PH. Fatal Chronic Meningoencephalomyelitis (CMEM) With Massive Hydrocephalus, In A New York State Patient With Evidence of Borrelia Burgdorferi Exposure. Program and Abstracts, VI International Conference on Lyme Borreliosis. Abstr. P041T. Bologna, Italy, June 19-22, 1994.

Merlo A, Weder B, Ketz E, Matter L. Locked-in state in Borrelia burgdorferi meningitis. J Neurol 1989;236:305-306.

Oksi J, Kalimo H, Marttila RJ, Marjamaki M, Sonninen P, Nikoskelainen J, Viljanen MK. Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. Brain 1996;119:2143-2154.

Wokke JHJ, van Gijn J, Elderson A, Stanek G. Chronic forms of Borrelia burgdorferi infection of the nervous system. Neurology 1987;37:1031-1034.

Fallon BA, Kochevar JM, Gaito A, Nields JA. The Underdiagnosis of Neuropsychiatric Lyme Disease in Children and Adults. Psychiat Clin NA 1998;21:693-703.