1 DR. STEVEN SCHUTZER, ASSOCIATE

2 PROFESSOR OF MEDICINE, UNIVERSITY OF MEDICINE AND

3 DENTISTRY OF NEW JERSEY: And I thank you for having

4 me here. And I'm really speaking mostly from my

5 scientific work, rather than as a physician, but I

6 will add that I do have board certification in

7 internal medicine, allergy, immunology and diagnostic

8 laboratory immunology. And I'll try to avoid terms,

9 so we don't get mixed up in semantics.

10 Just sort of by way of background, the

11 reason I even got involved in Lyme disease, I was

12 wondering -- somewhat perplexed why a number of

13 people who clearly had erythema migrans, which was

14 the best clinical marker about -- certainly over ten

15 years ago that they had Lyme disease, why they seemed

16 to test negative on these conventional antibody

17 tests. And so it's a biological problem. And

18 eventually -- I waited for someone to look into this,

19 and then that didn't happen and so I went about it

20 myself. And the hypothesis was that they were making

21 antibodies, because someone 30 years old is not

22 really immune deficient -- you know, that's rare. So

23 that these antibodies might be binding to part of the

24 organism, either circulating in the body or fixed to

25 tissue. And a number of the previous speakers had

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1 cited my research. I don't really have to go into

2 it.

3 But the bottom line was in a blinded

4 study we were able to discern which patients had had

5 erythema migrans by looking at their blood samples

6 and isolating these bound antigen-antibody complexes,

7 splitting them apart chemically, and then releasing

8 the antibody and seeing if it reacted on the regular

9 test, which they did in the cases of the erythema

10 migrans cases. So, this -- without calling the

11 seronegative cases, that's what people had referred

12 to. And this is absolutely common in every

13 infection. That in the beginning of day one you

14 certainly aren't making antibodies. It takes several

15 days before your lymphocytes can make antibodies.

16 So, of course, the window period of seronegativity

17 will vary in each disease. Lyme disease, it may be

18 longer than others.

19 But, in essence, it opened the door to

20 the fact that this may be occurring and it may be a

21 possible explanation of some of the cases of

22 seronegativity. So, that kind of kicked off the

23 research. And then leaping ahead through the years

24 that we continued to focus on this and started

25 looking at antigens that seemed to be unique to the

177

1 Lyme agent, so that they wouldn't be confused with

2 another infection. And not only not confused with

3 another infection, but they were specific during an

4 infection. So, there's a difference. There is a

5 great difference when you grow an organism in a test

6 tube and look at everything it expresses than what it

7 expresses when it's in the body. So, if you don't

8 discern between that you may get into murky waters.

9 So much of the work is focused on some

10 of the Osp proteins, like OspA that had been

11 described by the other speakers. There are other

12 proteins, which you haven't heard of, and I won't,

13 you know, beleaguer anyone with, but these are the

14 kinds when we focused in on early Lyme disease that

15 seemed to be expressed in infections during the early

16 period. And that's where more of the solid ground is

17 on, you know, before extrapolating to other periods.

18 So, that's what we're continually focusing on.

19 You know, again, avoiding semantics, we

20 have to say, well, what is the difference between

21 detection and identification? I mean, you could be

22 suspicious that someone has something, you could have

23 indirect evidence that they may have it, but in

24 essence what we like to have, and being very

25 rigorous, is evidence that the organism was there by

178

1 culture -- and not just the culture, but showing that

2 that organism that you've isolated is actually

3 Borrellia burgdorferi. And that would take things

4 like DNA studies or microsequencing. And, in a way,

5 one could start with the CDC definition and even make

6 it tighter, for research purposes -- again, for

7 research purposes, not for clinical diagnostic

8 purposes. Because when you do do a study, you want

9 it to be very rigorous so that there will be little

10 doubt that those patients had the disease that you're

11 looking for, and that way your data is more credible.

12 So, just to sort of sum this up, I

13 think part of the problems that seem to be apparent

14 are related to the fact that the driving factor,

15 which is research, has not fully been operative. I

16 mean, but that's the way things are in any disease.

17 But that will be the driving force, and with that

18 will come the answers of scientific evidence, and

19 then that will mold the clinical opinions.

20 So, it's okay to have a clinical

21 opinion that you see from a patient, and it may be

22 anecdotal and you get your ideas, but then you have

23 to design studies that will substantiate that. And I

24 think I'll end there, if there are any questions.

25 MR. GOTTFRIED: What does a clinician

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1 do, or what should a clinician do, to determine

2 whether -- to determine reliably whether a patient

3 has Lyme disease, particularly persistent Lyme

4 disease, so as to -- well, for example, if the

5 physician is concerned that either -- that the

6 symptoms may either be of something other than Lyme,

7 or maybe psychosomatic or what have you, what should

8 a clinician do?

9 DR. SCHUTZER: Well, you know, I

10 certainly can't give the answer that's going to work

11 for everyone. I could say that what one should try

12 to do -- you know, you have to really keep an open

13 mind. No one has yet discussed the issue of

14 co-infections. And these ticks carry more than one

15 organism, and some of them I understand Dr. Barkley

16 will be talking on, so -- she'll be talking on the

17 ones that we know about. But if there are ones we

18 know about, there may be ones we don't know.

19 The good news is that we're developing

20 the methodology to go after that question. You know,

21 that's the need for the research, and then the

22 answers will come from that. It's quite conceivable

23 that, you know, you can get bogged down in words

24 that -- there's Lyme disease which I would ascribed

25 to Borrellia burgdorferi and -- in fact, when you

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1 look at the neurological symptoms, you have to

2 distinguish between the European literature and the

3 North American literature, because there may be

4 different manifestations of the disease. So, you

5 can't really mesh them together.

6 So, to be more specific, if someone has

7 an infection, it could develop into Lyme disease.

8 It's possible that they may have another phenomenon

9 going on, either another infection or an autoimmune

10 reaction or an inflammatory reaction at a low

11 level -- not, you know, massive, that one might see

12 in lupus, but that can account for some of the

13 persistent symptoms. And I think we have to keep in

14 mind the numerator and denominator question. You

15 know, it's not so much a question of did one person

16 have persistent infection, it's how many do. That's

17 where the debate seems to center.

18 And I think I would even contend

19 that -- you know, I've heard it described they're two

20 camps, but I don't really believe there's a third

21 camp which is -- you don't hear about because it's a

22 little more mundane. But that's just being -- taking

23 a good history, taking a good physical, doing

24 appropriate tests, excluding other diseases. And if

25 it doesn't work, go back and -- re-examining the

181

1 situation. So, the best I could say is, if you're

2 not sure, then you go back or use the ability to get

3 consults, to get other opinions on. But there's no

4 magic test at the moment that will, in every case,

5 give you 100 percent sure answer.

6 MR. GOTTFRIED: But, I mean, other

7 witnesses have talked about, where you have a

8 seronegative ELISA test, doing a Western blot anyway,

9 doing a PCR test. Are those steps significantly more

10 valuable?

11 DR. SCHUTZER: Well, you know, it

12 depends where they're done. And that's the one thing

13 that has not been emphasized. You know, it's one

14 thing to take DNA tests for forensic evidence, that's

15 done, you know, in a major laboratory, and then take

16 someone who is just fooling around with it or just

17 beginning with it. And so we have to keep in mind,

18 like, where was it done? What were the controls?

19 Often the controls are more important than the actual

20 specimens you're analyzing. But it's appropriate to

21 go for those. And I think that we should push to

22 further the science, because the more definitive it

23 is, a lot of these questions will just dissipate.

24 MR. GOTTFRIED: Thank you.

25 MS. O'CONNELL: Thank you, Dr.

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1 Schutzer, and welcome.

2 You're a professor of medicine in New

3 Jersey. We've heard this morning -- and in your

4 capacity as a professor, I wanted you to comment on

5 some of the things that we've been hearing all day -

6 I wasn't sure if you were here earlier today - where

7 my sense was there is an institutional resistance on

8 the part of medical community to learning more about

9 this, recognizing this, push for research -- you

10 know, and many aspects of what's going on right now

11 in this controversy regarding Lyme disease.

12 Where do you see the role -- you know,

13 your role as a professor, or maybe, perhaps, in a

14 public policy capacity as we're in, in terms of

15 educational needs, to move this process forward, to

16 better educate physicians about this, to stimulate

17 some interest in finding the answers to some of these

18 questions, stimulate research, and sort of breaking

19 down that -- what I'm hearing is an institutional

20 resistance. Would you make just, perhaps, comment on

21 that from your perspective as a professor?

22 DR. SCHUTZER: Sure. I would say that,

23 you know, some of this is a lot of myth. And I think

24 you're focusing on those who reach a certain level -

25 you know, in the limelight, so to speak - and missing

183

1 the large body of people who just know how to do

2 scientific experiments. You know, it doesn't matter

3 what they're working on, they'll have the same

4 controls, the same rigorous standards. And the best

5 way to, I think, eliminate this is dialogue. And

6 that's the purpose I came up here for. I'm not

7 saying I agree with things that were said before.

8 And I'm sure if you stood in a room with academic

9 physicians and scientists, you would be quite

10 surprised that there's the diversity of opinions.

11 You know, it's not all one unified opinion. I

12 imagine it's the same in, you know, private practice

13 situations.

14 So, the thing I think that you could do

15 would be -- frankly, is to keep the dialogue going,

16 keep it unbiased, you know, take -- it's okay to have

17 the passion, but, you know, remove it from the

18 structure of it. And if there are ways that you

19 could drum up research funds and make people -- you

20 know, in other words, integrate them to work

21 together, I think then, hopefully, there will be

22 other answers. I know it's difficult times now, with

23 other situations going on, but effectively when you

24 set the goals or something where people can work

25 together, then I think they will.

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1 MS. O'CONNELL: Thank you, Dr.

2 Schutzer.

3 MR. GOTTFRIED: Any questions?

4 Okay. Thank you very much.

5 DR. MILLER: The question is, what time

6 is the train?

7 MS. O'CONNELL: We know you're in a

8 hurry.

9 DR. SCHUTZER: I was hoping there

10 wouldn't be any dental questions.

11 MS. O'CONNELL: He's known to pull

12 teeth here and there.

13 MR. GOTTFRIED: Thank you.

14 Okay. Our next witness is Dr. Brian

15 Fallon of Columbia, in the Department of Psychiatry,

16 and Director of Lyme Disease Research -- of the Lyme

17 Disease Research Program at the New York State

18 Psychiatric Institute.

19 Was he on video?

20 MS. O'CONNELL: Yeah, but he was --

21 somebody was supposed to --.

22 MR. GOTTFRIED: Okay. Dr. Fallon will

23 be -- just keeping with our ever-developing world of

24 innovation, will be testifying by a video -- which, I

25 guess, means we're not going to get to swear him in.

185

1 (Off-the-record discussion)

2 MR. GOTTFRIED: I'm advised that Dr.

3 Fallon is at Columbia today, meeting with people from

4 the National Institutes of Health. Okay. I guess

5 we're going to need the lights lowered again.

6 DR. BRIAN FALLON, COLUMBIA UNIVERSITY,

7 DEPARTMENT OF PSYCHIATRY, DIRECTOR, LYME DISEASE

8 RESEARCH PROGRAM OF THE NEW YORK STATE PSYCHIATRIC

9 INSTITUTE: My name is Dr. Brian Fallon. I'm an

10 Associate Professor at Columbia University in the

11 College of Physicians and Surgeons.

12 I'm Director of the Lyme Disease

13 Research Program, and we're conducting a study of

14 chronic Lyme disease that is funded by the National

15 Institute of Health, with two main goals, really:

16 One is to see what is the benefit and effectiveness

17 of a repeated course and a longer course of IV

18 antibiotic therapy for patients with chronic Lyme

19 disease; and the second is to try to understand what

20 is going on with these patients who have persistent

21 memory problems, persistent cognitive problems. Is

22 it due to active infection? What is actually going

23 on with the brain?

24 And I bring this up because this is

25 actually the reason that I can't come in person to

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1 speak to you at this hearing. The National Institute

2 of Health -- many members are coming to visit me at

3 Columbia to discuss the progress of the study and the

4 science of the study. So, I apologize if this has to

5 be done on a video as opposed to in person.

6 I'm not going to belabor this. I just

7 wanted to the make a few points. One is that

8 neurologic Lyme disease is very different than Lyme

9 arthritis, and one way it's different is that it's

10 somewhat harder to diagnose. The most common

11 presentation of late neurologic Lyme disease is

12 something called Lyme encephalopathy. And

13 encephalopathy refers to confusion, cognitive

14 problems. Sometimes these people have sleep

15 disturbances, sometimes they have mood problems. So,

16 sometimes they actually look like they have

17 depression rather than a cognitive encephalopathy.

18 So, that's one of the difficulties with the

19 recognition of neurologic Lyme disease -- is that it

20 causes encephalopathy, that can cause considerable

21 disability, and yet be hard for standard internists

22 or practitioners to recognize.

23 So, oftentimes it does take a

24 specialist who has seen a large number of patients

25 with similar symptoms to recognize the profile of the

187

1 patient with neurologic Lyme disease. For example,

2 one thing that's not commonly appreciated is that

3 patients with Lyme encephalopathy do not often have

4 joint problems or joint complaints. They will not

5 have big, swollen joints. So, if you make the

6 diagnosis only on the basis of swollen joints, you

7 will not recognize Lyme encephalopathy.

8 The CDC, unfortunately, doesn't even

9 have a category for patients with Lyme

10 encephalopathy, even though it's recognized as the

11 most common late neurologic feature of Lyme disease.

12 So, anybody who adheres only strictly to the CDC

13 clinical guidelines is going to really maltreat their

14 patients. Because the CDC clinical guidelines are

15 there for epidemiologic surveillance of large

16 populations and changes over time in those

17 populations, but they're definitely not meant for the

18 purposes of solely making a clinical diagnosis. And

19 to rely on them and -- those criteria alone would be

20 a big mistake. And that's widely recognized and the

21 CDC would acknowledge that.

22 So, another point I wish to make is

23 that Lyme disease, and chronic Lyme disease in

24 particular, is a real entity. It's well-recognized.

25 There was a well-publicized study that was published

188

1 this past spring in the New_England_Journal_of_

___ _______ _______ __

2 Medicine about chronic Lyme disease and the treatment

________

3 of chronic Lyme disease, and they had two main goals:

4 One was to describe the patients, and the other was

5 to see if the treatment protocol they were using

6 worked. And when they described the patients, what

7 they found was that a quarter of the patients had

8 abnormal spinal fluids -- mildly abnormal, but a

9 quarter of them had abnormal spinal fluids, and they

10 had a level of disability that was comparable to

11 patients with congestive heart failure. So, clearly

12 patients with chronic Lyme disease exist. They have

13 quite a significant disability, so it's a real

14 serious problem. And, thirdly, there are objective

15 markers of abnormalities in the spinal fluid. And

16 that was shown both in elevated protein levels in the

17 spinal fluid, as well as in elevated levels of an

18 enzyme called matrix metalloproteinase (phonetic

19 spelling).

20 So, a third point I would like to make

21 is that the treatment of chronic Lyme disease has not

22 been well-studied. There's really been only one

23 double-blind, placebo-controlled study in the

24 literature, and that was the one that came out last

25 spring. That particular protocol for that

189

1 heterogenous group of patients was not shown to be

2 effective. However, the study that's being funded by

3 the National Institute of Health, with us at

4 Columbia, is a $4.7 million study to really address

5 the question: What if you give patients a longer

6 course of IV antibiotic therapy, and we're giving ten

7 weeks of IV antibiotic therapy in a

8 placebo-controlled design? The reason that was

9 funded is because it's an open-ended question. We

10 don't know the answer. So, any group or person who

11 claims to know the optimal treatment for chronic Lyme

12 disease is telling a falsehood, because we do not

13 know, and I do not know, and that's the reason these

14 scientific studies are being done.

15 I do know that a study that will soon

16 be published or -- coming from Stony Brook, indicates

17 that a repeated course of antibiotic therapy was

18 effective for a group of patients with significant

19 fatigue after being treated for Lyme disease. So, it

20 may be that select sub-samples of patients with

21 chronic Lyme disease do, in fact, benefit, such as

22 patients with a cognitive problem, who I will be --

23 or I am studying, or patients with post-Lyme fatigue,

24 or other subgroups who haven't yet been adequately

25 studied.

190

1 In the process of doing our study, we

2 are screening a huge number of patients. And we took

3 a look at the first 500 patients, who we evaluated,

4 who had been treated with IV antibiotics in the past.

5 And what we found was the mean amount of prior

6 treatment with intravenous antibiotics was four

7 months among those patients with chronic Lyme

8 symptoms. So, clearly the common practice in the

9 community throughout the northeast - because most of

10 our patients come from throughout the northeast - is

11 to give repeated courses or longer courses of IV

12 therapy, and certainly longer than what's indicated

13 in the published literature.

14 So, I'm making these points, and I'm

15 going to close here, really, to state that there are

16 so many things that are unknown about Lyme disease;

17 number two, we should not be making statements about

18 what the optimal treatment is for a condition that

19 hasn't been adequately studied yet; three, patients

20 with chronic Lyme disease are quite disabled.

21 They're in considerable pain. Oftentimes, a quarter

22 of those patients with chronic Lyme symptoms are

23 unable to functions in the jobs that they used to

24 function in. So, economically, as well as

25 physically, they're suffering.

191

1 The physicians who treat these patients

2 are in many ways a brave group of physicians, because

3 they are trying to help these patients in a way that

4 they know -- and they're trying to help these

5 patients despite the absence of adequate guidelines.

6 So, they're trying different things, some of which

7 may be the perfect treatment, some of which may not

8 be. But the point is that we don't have the optimal

9 answers at this point. And so I request that good

10 judgment be applied and that we allow physicians to

11 treat each patient individually in the way he or she

12 feels is best, based on his or her reading of the

13 literature and based on his or her clinical

14 experience with patients who have had this illness.

15 And I think that patients will be given the best

16 opportunity for recovery if you allow them the choice

17 of which doctors they see, as well as allow doctors

18 the freedom and the flexibility to treat the patients

19 as best they can.

20 MR. GOTTFRIED: Okay. Well, that was

21 good. We don't get to ask him any questions, but --.

22 FROM THE FLOOR: Excuse me, Mr.

23 Chairman. We do have Dr. Robert Bransfield, who is a

24 psychiatrist, that could fill the neuropsychiatric

25 questions, if you have any, when he testifies later.

192

1 He'll be glad to answer anything on the

2 neuropsychiatric aspects.

3 MR. GOTTFRIED: Okay. I think maybe

4 we'll hold till later, if he's going to be testifying

5 later. But thank you.

6 Okay. We will next hear from Carolyn

7 Britton, Dr. Carolyn Britton, a neurologist at

8 Columbia Presbyterian. Excuse me?

9 FROM THE FLOOR: That is a video

10 presentation.

11 MR. GOTTFRIED: Oh, okay.

12 FROM THE FLOOR: They're both at the

13 study today.

14 MR. GOTTFRIED: Okay. Take the lights

15 down again.

16 DR. CAROLYN BRITTON, NEUROLOGIST,

17 COLUMBIA PRESBYTERIAN HOSPITAL: Good morning, I'm

18 Dr. Carolyn Britton. I'm an Associate Professor of

19 Clinical Neurology at New York Presbyterian Hospital.

20 I am indeed sorry that I could not join you today for

21 the hearings regarding treatment of Lyme disease and

22 the harassment that is currently being experienced by

23 many practitioners who are involved in the care of

24 patients with Lyme disease. I am making this

25 videotape so that I can voice some of the concerns

193

1 that have occurred to me, as I have participated in

2 the Lyme study at New York Presbyterian Hospital over

3 the last year and have had the opportunity to see

4 many of these patients.

5 First, however, I would like to

6 congratulate the Health Committee on convening these

7 hearings. I think this takes a great deal of

8 courage. With Lyme disease, there are a number of

9 problems that have occurred and other infections:

10 One, people may not have serologic reactivity that --

11 to the agent that is diagnostic of infection. Our

12 diagnostic criteria in general for medicine are done

13 such that they include all of the positives and

14 exclude negatives absolutely, but they don't include

15 all of the positives absolutely. That's part of how

16 we set criteria so that we know that we have

17 everybody that has the disease, for the most part,

18 but it should never be taken as an absolute standard.

19 Part of what has happened in the

20 dynamic of dealing with Lyme disease is we're held to

21 a standard of absolutes by the insurance industry

22 that are applicable to a dynamic situation like

23 medicine. If you take an infectious disease and you

24 say, how can I decide that a patient has an

25 infectious disease -- we have the core principles

194

1 that we mentioned, in terms of having antibodies or

2 being able to isolate the organism and having the

3 clinical criteria, but sometimes you only have one or

4 more of those. In some cases, you make a diagnosis

5 by inference; that is, if there is an epidemiological

6 risk for the infection.

7 For example, if you take patients who

8 have cancer, who come into a hospital with fever,

9 those patients will be suspected to have an infection

10 until proven otherwise. So, you treat the infection

11 with antibiotics, and you treat it by principles that

12 we call empirical treatment; that is, the patient

13 comes in with a clinical syndrome. You order your

14 diagnostic tests like blood cultures and other

15 cultures. Suppose all tests come back negative? And

16 the physician may decide, okay, the fever has gone on

17 these antibiotics, I'm going to stop the antibiotics.

18 If they stop the antibiotics and the fever recurs,

19 everyone would agree that, since the fever appeared

20 to respond to the antibiotics in the first place, you

21 would resume the antibiotics until the incident had

22 cleared. This is known as empirical treatment.

23 Perhaps one of the greatest disservices

24 that has been done in the treatment of Lyme patients

25 is the confusion of empirical treatment and

195

1 experimental treatment. The treatment for any

2 infection is antibiotics or antiviral agent. The

3 appropriate antimicrobial agent is the treatment for

4 an infectious disease. The duration of treatment is

5 one that sometimes is best worked out empirically.

6 What has happened in the treatment of Lyme patients

7 is there has been a pronouncement that no one with

8 Lyme needs more than two days, two weeks, one month

9 of antibiotics, and that all patients with Lyme are

10 cured by one month of antibiotics. This may be true

11 for the substantial number of patients. However,

12 their experience in the care of these patients, who

13 have opted to treat patients for longer periods of

14 time, because they have obtained a clinical response.

15 This is not experimental treatment,

16 because antibiotics for a presumed infectious disease

17 is not experimental. It is the standard treatment.

18 It is an empirical treatment decision. It is one

19 based on the existence of a clinical syndrome that

20 could be explained by an infection. In many cases,

21 although there may not be a history of a tick bite,

22 there is an epidemiologic risk for a tick bite if the

23 person lives in an endemic area or has been around

24 people who are exposed and who have known

25 fully-diagnosed Lyme disease, thus adding to

196

1 epidemiologic risk. So, the patient is symptomatic,

2 that's one; and second, the person has an

3 epidemiologic risk.

4 Thirdly, the physician decides, after

5 doing extensive evaluation, that this could possibly

6 be an infectious illness and to give an empirical

7 treatment trial of antibiotics, following which the

8 person improves. Thereafter, when relapse occurs,

9 some clinicians diverge as to what the management is.

10 Some say it's impossible that it's infection. But

11 others have said, "Let me see if antibiotics will

12 again benefit the person," and they find that they

13 do. In those cases, patients have been given

14 protracted antibiotics with clinical response in

15 terms of their report to the physicians managing

16 them, and often in response also to -- as measured by

17 clinical data, such as spec. scans or other things

18 that might be done to follow a patient. This is

19 empirical treatment.

20 Medical science is not sufficiently

21 definite to state with certainty that all patients

22 who have Lyme disease are cured within a month.

23 There has to be room for empirical treatment made by

24 physicians who are skilled in managing patients, who

25 do a thorough and comprehensive evaluation of

197

1 patients for all potential causes of their symptoms,

2 and who then embark on empirical treatment based on

3 epidemiologic risk or a known history of prior Lyme

4 disease. The ability of a person to clear an

5 infection even with the appropriate antimicrobial is

6 affected by many factors, some which we understand

7 and some which we don't. But one of the areas that

8 is a giant Pandora's box is the influence of the

9 person's own immunologic makeup; that is, how they

10 respond to an infection. We know from the HIV

11 epidemic that you fail to clear infections with

12 standard antimicrobial treatment if you are

13 permanently immunosuppressed. So, full-scale

14 immunosuppression may not be the only reason that you

15 fail to clear infection. Some persons may even have

16 selective immunosuppression for certain ages that we

17 don't currently measure by our techniques.

18 The other issue is stating that it's

19 absurd that patients need such protracted treatment

20 for this organism. Plus, in the face of our

21 experience in treatment of microorganisms -- for

22 instance, the statement that no bacterial infection

23 requires more than a few weeks of treatment for

24 eradication is patently false: First, in the example

25 that I gave you of patients who have

198

1 immunosuppression due to HIV infection; and secondly,

2 in patients who have tuberculosis. Tuberculosis is a

3 well-known bacteria, and yet treatment of it in its

4 primary stages requires a year and, if you have

5 secondary disseminated tuberculous, may require up to

6 three years to eradicate the organism and to treat

7 relapse.

8 Thus, I think that a lot of the debate

9 that has gone on has centered around many financial

10 considerations, rather than looking at how physicians

11 make decisions, how physicians make decisions that

12 are, hopefully - and I think in this case,

13 certainly - based in the best interests of the

14 patients and those things that appear to benefit the

15 patient.

16 Thus, I think that the Legislature,

17 after hearing from patients, from clinicians expert

18 in their management, and infectious diseases experts,

19 should look at trying to come up with a way to

20 have -- return to physicians and their patients some

21 autonomy in decision-making that is medically

22 reasonable. I don't think what is being requested is

23 medically unreasonable. I think that if you look in

24 what we currently know about the behavior of

25 microorganisms, you will find that there is

199

1 substantial reason to believe that there are

2 organisms that behave in this way.

3 Thank you very much for your

4 consideration, and I hope that this is clear and that

5 I didn't wander too much. Thank you very much for

6 your courage and for taking the testimony that you're

7 doing.

8 MR. GOTTFRIED: Well, that was good. I

9 also went to Columbia. Okay. Actually, Dr. Britton

10 didn't go to Columbia; she works at Columbia. Okay.

11 Dr. Miller went to Columbia. Well, we went to

12 different schools at Columbia.

13 Okay. Dr. Marilynn Barkley. Is she

14 here?