2016 Lyme disease conference plenary discussion/opportunity for questions

Conference to develop a federal framework on Lyme disease

May 15-17, 2016, Government of Canada Conference Centre, 111 Sussex Drive, Ottawa, ON

Conference day 2: Monday May 16, 2016, Algonquin Room

Audio Recording


Dan: [0:15]

Ladies and gentlemen, a quick announcement: for those of you who are interested in the continuing medical education, there are signup sheets at the registration that you could sign to corroborate and confirm your presence and participation at this conference.

Ladies and gentlemen, as you know, we're going to begin the question and answer session in a few moments.

We're going to have, unfortunately, a hard stop at 12:30, when we'll take our lunch period. This is how I'm going to suggest we begin. Of course, there is no way that we could accommodate everyone's question, but we'll try to accommodate as many as we can in the time that we have.

But the other point that I'd like to make is the following: We are privileged to have the speakers, and we have David who's on WebEx available for participation in this Q&A session, but we have the three presenters here in person in Ottawa. If you should not be able to pose your question to one of these three gentlemen here, they're not going anywhere today. They're captive. They're going to be here with us over lunch. They'll be here with us this afternoon, I trust. I would encourage you to connect with them if you have any specific question for any of the presentations that they would have made, or anything that you would pose of them, if we don't have the chance to do that in the room.

What I'm also going to try to do is we will start with the plenary room here. I will take the first three questions on a first-come-first-served basis, then I will go to the overflow room, accommodate them with three questions, and then we'll go on WebEx where there are a considerable number of participants and we'll give them three as well. And with the help of the operator we'll try to do that as efficiently as we can.

So that said, I'll take three questions in the conference room here, then I'll go to the extra room and I will finish the cycle with those who are - who are participating on WebEx.

So without further ado, there's a mic over here and I will ask this lady to go to the mic to pose our first question. Miss, go ahead. If you could identify yourself.

Oh, and I'll ask you to be as sharp and brief as possible for your questions. I'm asking the speakers to be as brief as possible as well so we can handle as many questions as we can. Please go.

Liz: [3:01]

Hello. It's Dr. Liz Zubek from Maple Ridge, near Vancouver, so David Patrick I welcome you from the west coast there, and I'd like to ask you a question about some of the mathematics there that didn't quite sit with me about the tests and doing 12 tests in a row. To me, the description there was more about the reproducibility of the test. For example, if somebody has a negative test and we repeat that Western Blot 12 times, is it going to still be negative? Or, if somebody's actually producing the bands, and we do that test 12 times, will all 12 tests show it up? Which would be reproducible.

It seems to me that you were using a different kind of probability model though. That you were talking about it as though you were rolling a dice and what's the chance that the dice is going to show up as a two, when you roll it 12 times. So I didn't quite understand the mathematics there.

Dan: David, would you want to respond to that please? Are you with us?

David: [4:06]

Can I be heard?

Dan: Yep. Go ahead.

Yes, thanks very much for the question, Liz. Really, if you take a look at Dr. Fallon's study, it was describing 40 discrete healthy people, and 57% of them were found to be positive. So in the study, I was talking about 12 discrete ill individuals who had been issued a positive test from the same lab and it was a lab that did use the alternate, in-house Western Blot interpretation. So in both cases, we're talking about the probability of seeing this number of people under either a false positive or a false negative hypothesis so I don't really think this is quite as you described it. The repeat test in the same individual scenario in either Dr. Fallon's study or ours.

Liz: Had you mentioned at all about how they've changed the criteria where the 31 bands, they're now going back and checking to see if there really is the OSP there or if it's a contaminant? Because that test has been changed for the past two years.

Dan: David, comment?

David: I've not tracked too much what the lab's done because like I say, I would have faith in this lab in the Canadian context if it observed Canadian criteria for recalling inadvised and inaccurate results, which it has not done. Or, and I think it would be also important to make sure that external quality control is something that's accepted by a lab if they're going to move ahead in that kind of direction. So I'm still putting my faith in the evolution of the testing in reference labs that Dr. Dattwyler is describing.

Liz: I certainly agree with the evolution, but some of the people in your alternative Lyme diagnosis study have had a culture positive from one place, they've had a lymphocyte transformation test positive from another place, and they've had a test from IGeneX with those bands, so what would be the probability of all three of those? Sure.

David: I'm sorry, I'm not going to talk about individual study patients' results. Maybe you've got some information about people that wasn't provided to the study, I don't know. But as an investigator, I can't talk about an individual case within the study. What I can say is that I was provided with Western Blot results from one US lab, none of which could be verified.

And it was interesting, really, because there were two kinds of discrepancy that could be found there. One was that tests were being called positive on the basis of bands that would not be used by a reference lab and for the reasons Dr. Dattwyler brought forward, because it would be cross-reactive with multiple other bacterial species that one would meet across a lifetime. But it was also concerning to me that they were calling positive some bands that would be used in the reference test which were not visible on a reference test, using standardized incubation. And you have to be a bit concerned because if you over-incubate Western Blots in a lab, you can see faint traces of bands and so forth.

So once again, I'm not a lab physician, but I am deeply concerned as an epidemiologist and as an infectious disease physician about the accuracy of these tests and how they're actually potentially misleading us about the cause of illness in hundreds of British Columbians.

Dan: Thank you, David. We'll go to the next question, please. Go ahead, sir.

George: [7:29]

Hi, my name's George. Question to one of the doctors or all of the doctors: I've got DVT caused by phlebitis and I've got chronic Lyme disease. According to that by Dr. Warden, McGill University, is this part and parcel of the Lyme disease infections in your opinion?

Dan: Ralph?

Ralph: [7:53]

So I can weigh in first. Chronic infection does change your likelihood to make clots, it increases the likelihood to make clots, so having a chronic infection would increase your personal risk of developing phlebitis. They might be associated in that fashion, but they would not have a direct cause and effect association.

George: It's not because of bacterial clustering in the blood vessels?

Ralph: Not in my opinion, no.

George: Okay, so you're saying, basically, it's not really related to Lyme disease.

Ralph: That's basically what I'm saying.

George: Okay, thank you.

Dan: Okay? Thank you. I'll go with the third question here. Go ahead.

Female: [8:32]

This one's for David Patrick as well. In 2011, a study by Schutser et al. titled…

Dan: Go ahead.

Female: Is it on?

Dan: It's working, yeah. You're good.

Female: Okay. In 2011, a study by Schutser et al. titled "Distinct cerebrospinal fluid proteins differentiate post-treatment Lyme disease from chronic fatigue syndrome", it utilized mass spectrometry to analyse a specific proteins in cerebrospinal fluid. They found that both groups of patients could be distinguished from each other and from healthy controls based on their specific spinal fluid proteins.

Another study in 2012 examined CSF proteins in acute Lyme and found a similar markers. Again, in cerebrospinal fluid.

My question is: why were no comparable cerebrospinal fluid analyses performed in your study which might have actually been able to distinguish between the two groups?

David: Okay, so the first thing is I think it is useful for us to be talking about the potential for proteomics and for host gene expression to aid in diagnosis in these sorts of studies. The two studies that you've just quoted are not coming top of mind to me right now. I read a lot about these sorts of things a few years ago, some of the studies were well done and others were not. But as I have mentioned, it's quite clear that in people who've really met Borrelia burgdorferi or other variants of Borrelia, that you can see a clear transcriptional signature and there's no particular reason you wouldn't expect to see a different proteomic signature.

As for CSF, inside the study that we were doing, the main focus of our study was to try and get some pilot work going originally just with medigenomics to look for pathogens within the bloodstream and so forth. We were able to build on two additional discovery platforms but we couldn't throw the entire kitchen sink at it. Certainly, in the area of chronic fatigue syndrome, CSF studies have been proving pretty useful too.

I don't know if any of you have tracked the work that was also out of Columbia University, showing some interesting patterns of cytokine expression in the CSF. So I would agree with you that CSF studies under the right circumstances are a good way to go, when we deal with large, multi-centred studies.

But also, well characterised patients. It's a lot easier to find something in somebody that really has met a bacterium unequivocally, rather than in a group of people, some of whom may have met it and others who may have not.

Female: But if you were trying to distinguish between the two, then that might have been one method of doing so and it wasn't used. So why do you think that your particular study actually proved its hypothesis?

David: I didn't say we proved a hypothesis, I was just reporting on our findings about similarities between these two different patients groups. But I will say this, we had a really small study, so you don't want to draw general conclusions from it. Dr. Fallon's study was extremely useful in terms of telling us about the predictive value of the alternate tests upon which many British Columbians are diagnosed.

But when I speak to infectious disease practitioners, rheumatologists, neurologists, in BC, there are many hundreds of people coming forward with these tests in hand, none of whom are confirming on standard testing. I think it's really important that we keep our minds open. For every complicated problem, Mencken told us there's an answer that is clear, simple, and wrong.

Dan: Dr. Fallon wants to comment on that as well.

Brian: [12:16]

I just wanted to say a little bit about that study, the spinal fluid study, which was Schutser, Dr. Schutser did. He actually took samples from our patients with Lyme encephalopathy so the spinal fluid that we collected, compared it to another group of patients with chronic fatigue syndrome, and compared it to healthy controls. And what they found was that the Lyme patients had over 600 unique proteins that weren't expressed in the spinal fluid of the chronic fatigue patients.

And similarly, the chronic fatigue patients had about 600 or so proteins that were not expressed in the Lyme patients. So what was nice about that study, using a super-it was the Pacific Northwest National Laboratory, it's one of the best proteomic facilities in the country-was that they were able to differentiate the two groups. But there's more steps that need to be taken with that study, so nobody can actually take those results at this point and create a diagnostic assay that would be usable at this point. But hopefully, I know that Dr. Schutser's continuing to work on that, and hopefully, it will come to that place.

And I also want to put in a plug for spinal fluid analyses. I know nobody likes getting spinal taps, but they can be enormously helpful because if you have a neurologic or neuropsychiatric syndrome and you're wondering or thinking that it might be related to an infection, if you have abnormal spinal fluid findings that increases the probability that it might be something specific going on in the brain. So I encourage that at least once, preferably before antibiotic treatment if you're wondering about Lyme disease.

Dan: Thank you very much. We'll now go to the overflow room. Alain Rabeau is the facilitator there, Alain, is there somebody at the mic?

Female: [14:02]

Yes. Hello everybody. Dr. Patrick has demonstrated to us a classic example of the resistance we Lyme patients face in getting an accurate diagnosis. Even when faced with indisputable clinical presentation, they still fall back on the old mantra that Canadian test are accurate when clearly to us they are not. Unaddressed is the possibility that false positives are in fact positive and are simply asymptomatic people like my husband. Or that this so-called private lab, which is so far criticized, could actually be accurate.

I had a negative Canadian test, twice. But I had a known tick bite, all the symptoms, plus I was positive for B. burgdorferi DNA and the spirochetes were seen in my vaginal secretions. Why are we not following Health Canada guidelines and supporting a clinical, strictly clinical, diagnosis?

David: [14:57]

So that's a question around clinical diagnosis. I think it's a great question, because I think it's really important to talk about the strength of observation upon which a clinical finding is made. I mean, if you've got a really good EM rash in early Lyme disease, that's a pretty good finding. Later on, if you've got hard findings in terms of actually visible arthritis, specific neurological findings, again that should be really drawing you into the diagnosis, shouldn't it?

But there are also a range of diagnostic approaches on clinical grounds that are based on more symptoms that are highly prevalent in the population and equally prevalent in areas where Lyme is circulating and not circulating. So I mean, if you go to the ILADS website, you'll see lists of symptoms which are really important symptoms and they're not asymptomatic people. We're talking about people with fatigue, with body pain, with all sorts of other things, these symptoms are equally prevalent in low prevalence Borrelia areas as in high prevalence ones.

So I think you have to stand back then and say, "Well, is Borrelia really the full on explanation for these symptoms in everybody that's got it?"

So let's look at clinical diagnosis as a high standard thing. I've taught clinical skills, many of my colleagues who are involved on either side of the debate have done the same thing. But what we don't want to do is play the 19th century physician and come up with a hocus-pocus diagnosis based on a few loose symptoms and say that's a clinical diagnosis. That needs to be challenged.

Female: 70 symptoms are not loose symptoms.

Dan: (Inaudible) that question. I will take a second question from the overflow room please.

Kamy: [16:46]

Hi, Kamy Harris. I'm a PhD student with the Atlantic Veterinary College in UPEI as well as with Mount Allison.

Dan: We'll ask the sound person to raise the sound so we can really hear your voice well. Thank you.

Kamy: I can stand up here and ask you a bunch of questions about the science and spew out journal articles but ultimately what it comes down to is we're all arguing the same thing, that the tests are flawed, whether you think there are more false positive or whether you think there are more false negatives. And so my question I guess is why are we not going based on clinical diagnosis?

And I'm going to kind of give you an example to clarify what I'm talking about. If I suffer from migraines, I can go to my clinician and he cannot feel my migraine, he cannot see my migraine, and yet we try different treatment options until I can identify that my migraines have subsided. Why are we not trying treatment for these patients? These patients don't care what's inside their body. They care that that gets out of their body. So why are we not trying treatments and reassessing after those treatments fail?

Dan: Who would like to pick up on this?

Raymond: I'll just comment. First of all, if you used serologic assays in other diseases, serologic assays are usually not diagnostic in and of themselves. A classic example would be ANA, antinuclear antibodies. ANA is a marker that's frequently found in Lupus, systemic Lupus. But it is not diagnostic of systemic Lupus and in fact, most of the time, the person with a positive ANA doesn't have Lupus.

So you have to be very, very cautious and realize the state of the art of laboratory testing. And I wrote the editorial about this lab and the positive predictive value is a very important concept because if you make a wrong diagnosis, you frequently will miss the right diagnosis. And I've seen over the years when I was at Stony brook, individuals who came in with fatigue and aches and pains treated for Lyme disease and then we found their cancer. Not good. Not usually a good outcome.

Kami: (inaudible) …ruling out another diagnosis. That's what I'm getting at.

Raymond: So I think we have to be very careful about it and realize, that I've hopefully pointed out, the tests are not perfect but we can do a lot better and we have to do a lot better. So I think I would discourage the use of these non-standardized labs because I think they do more harm than good.

Kami: …talking about the (inaudible) all agree their flawed so I don't care if they're Canadian or alternative. I'm just asking why are we not trying treatment? I can try treatment for a variety of ailments and they don't work and we rule it out, we move on, we're progressing with something.

David: It-Dave, Dave-I think it's important to-can I go ahead? I think it's important to be talking about that because the thing is there's a lot of people who have come to the end of the rope with a standardized approach and that's when the physician does need to kick in and try different things. It's interesting when you talk about whether Colleges of Physicians will be down on doctors for doing compassionate acts of alternative treatment and most of the time they won't be.

The main thing they want to make sure of is though that none of us are sitting there representing an alternative treatment that's not too well proven as the standard of care. So there should not be a limitation in which you can't try different things with your physician to try and move things forward.

Dan: Thank you. David, did you want to add on that? Or sorry, go ahead.

Raymond: I was a co-author on the Krupp study that Dr. Fallon pointed out. And what we found is that in that ceftriaxone group, fatigue did improve, but at the cost of a tremendous amount of side effects. So when we weighed the risk and the benefits, that too many people got sick from the ceftriaxone, and that you have to weigh, you always have to weigh the risks and the benefits of things.

I'm not saying don't treat but I'm just saying you have to be cautious. Antibiotics have side effects. Antibiotics also have other effects, anti-inflammatory effects, and they change proteins in other things, and you have to be-put it all in context. And I'm not saying I have the answer, I'm just saying you got to look at the whole picture.

Dan: Ralph?

Ralph: [22:04]

I just wanted to talk to the Fallon study as well and it's really odd talking about the Fallon study with the author four feet away from me. But in the Fallon paper that Dr. Patrick is continuing to allude to that discredits the in-house criteria of "laboratory B" which by common knowledge everyone understands as a laboratory that uses the identical diagnostic criteria as IGeneX lab, although it is still an unidentified "lab B".

He neglects to tell us that when the Western Blots are analyzed using the CDC defined criteria, they actually performed equally to the reference labs, and he fails to tell us that there were discordances between the labs in terms of the reference lab failing to come up with true positive diagnoses, while "laboratory B" came up with true positive diagnoses. So there are statistics…

David: Not statistically higher... (inaudible). Not at all.

Ralph: David, David, David, I am not interrupting you. And you will not interrupt me, please. So I would like to just…

Dan: Finish your point, and then David, jump in after that.

Ralph: I would just like to point out that Dr. Patrick is not telling us the whole story about the Fallon paper. Benjamin Franklin said in 1758 that half the truth is often a great lie, and I would pose to Dr. Patrick in British Columbia that if he wants to castigate the "laboratory B" that he does it with the full story and not cherry pick the truth.

Dan: David, a quick point from you, please. David, over to you.

David: Dr. Hawkins, it's abundantly clear that people have been issued tests based on the in-house interpretative criteria. That's what the patients are going to understand, that's what their providers are going to understand, they're not going to sit down there and read the fine print about whether the CDC criteria were met or not through that.

The bottom line is yeah, the reference in the specialty labs were able to pick up Lyme disease when it was there in terms of the same amount. But the false positive rate was not only unacceptably high, it was ludicrously high. I never expected it to be this bad after reading let's say, an IGeneX lab's own publication, from Europe.

Dan: Thank you. Let's go for a third question in the overflow room, please. Do you have a third question there?

Brian: Can I say one thing before you go up?

Dan: Sure. Go ahead, and if there's nobody there we will go into WebEx after that.

Alain: We do have a question Daniel.

Dan: Hold on one second, we have a comment from a panelist. Keep your question at the mic please.

Brian: [25:00]

(inaudible) this raises discussion that-hold on, can you hear me? Is this on?

Dan: Hold on, he's going to..

Brian: It got it. It got it.

So I think an important point is that diagnosis is supported by the lab tests but it's not made by the lab tests. So you can have a positive result in a healthy control that may not be a false positive, it may be that person was previously infected but never got sick from the disease, that can happen. Or you can have someone who is testing negative, using the full criteria of the two tier, but who in fact does have Lyme disease.

So the tests are helpful but they're not definitive and that's why we're here to talk about limitations of the tests, talk about limitations of our treatment strategies, so I hope that's helpful.

Dan: Thank you. Thank you, Brian. We'll go for the third question in the overflow room. And by the way, Elizabeth, you'll be the first one when we come back to this room.

Dan: Alain?

Alain: We have a question in French for our panelists.

Dan: So go ahead Ma'am, your question. French is on Channel 2, for those of you who have your phones, and English is on Channel 1. Ma'am, go ahead.

Female: Hello. I was after - four months after I was bitten, I had a - it was detected positive in Canada. So - sorry because I have illness or memory problems for the doctors' names...

Dan: One moment. I will ask you to stop for a moment to give our panelists time to put on the devices so that they can understand your question. Okay. Ma'am, go ahead, please.

Female: Okay. So four months after I was diagnosed in Canada by a Western Blot that I had Lyme disease, my infectious disease specialist prescribed me antibiotics for 28 days. It's been two years since that and, well, I have been dropped. I am cured. They gave me 28 days of antibiotics so every time I go see a doctor: "Well, you no longer have Lyme disease, you're cured; you got your 28 days of antibiotics." And it's not true. I am getting sicker but nobody wants to treat me because I had 28 days of antibiotics and I am reported to the federal Department of Health as having Lyme disease.

But what worries me is not how we can get diagnosed, it's when we are, in Quebec, I live in Quebec, what do they do to cure us? What are they doing to help us? That's my question. And anyone can answer.

Dan: Who would like to take this question? Qui voudrait prendre la question? Ralph, would you want a crack or Dr. Fallon?

Raymond: Unfortunately…

Dan: Microphone in the center please.

Raymond: [28:30]

The question is that this lady has received 28 days of therapy and her physicians are saying that's enough and but she's still symptomatic. And the question is what to do with those individuals.

And the answer right now is…

Male: (inaudible)

Raymond: She was also diagnosed in Canada. She's seropositive. So and I've seen, and other people have looked at patients who truly have had Lyme disease and yet still have ongoing symptoms, and as Dr. Fallon pointed out, the studies are not helpful very well in what to do with those individuals. They're really a problem. And if you look at the best characterized group is probably the Lyme arthritis group where 10% of individuals will continue to have arthritis post-treatment.

Now, Allen Steere's group looked at those people and tried to demonstrate whether the organism was still present in the joints. And they couldn't find it. They've also taken and retreated those individuals with antibiotics and didn't seem to make much progress in that patient population.

Now the question is: is that because of antibiotic resistance? Is that because the organism is in a protected place? The organism is gone, but an immunologic process has now developed? We don't know all the answers. And I think at this particular point in time, it's an area that unfortunately needs more research and I think most people honestly don't know what to do quite well and I have no problem saying that I don't.

Things like doxycycline may work as an anti-inflammatory. Macrolide antibiotics may work which is clarithromycin, or erythromycin. But I think that's an area of active research.

Ralph: [31:00]

So my response would be that there is clear evidence from John Aucott's work that patients who are treated for Lyme disease appropriately with the appropriate duration of appropriate antibiotic therapy that we expect to see about 60% of people have full recovery. And there's an expectation that 40% of people, 39% actually, will have either persistent symptoms or functional disabilities in spite of receiving adequate therapy.

Now this is a disease where we do not have any test, any laboratory test, to identify bacteriologic cure. We don't have a test that identifies for us that the duration of therapy has been adequate and certainly the thought that comes to my mind is that there may be inadequate treatment in that 39% of people. Perhaps the treatment duration needs to be different.

Now these different treatment durations have been tested with some of the studies that Dr. Fallon has alluded to. And the most recent one, the New England Journal paper, identified that people did pretty well if they got two weeks of ceftriaxone therapy before they got long-term oral antibiotic therapy. So I would look at the situation of the lady who posed the question and just posit that perhaps this is the type of individual where two weeks of intravenous ceftriaxone therapy might be warranted. This is a question that should be subject to proper design and research.

Dan: Thank you very much, Ralph. We'll go for the first question. Operator, please help us for the WebEx participants. We'll go for three questions from the WebEx participants at this time. Question number one.

Operator: Thank you, we have a question from Carrie Courier. Please go ahead.

Male: Carrie, go ahead, please.

Carrie: [32:59]

Hi, I'm calling from British Columbia. I'd like to get a better overview from people dealing with clinical Lyme disease in practice. Can you give the variety of symptoms that are really showing up for (inaudible) in the news, if you're seeing. Dr. Fallon, Dr. Hawkins, it's probably more directed for you two.

Dan: Can I ask you to repeat the question? We can't hear you very well. Could you repeat your question please?

Carrie: Sorry, is that better?

Dan: Oh, that's terrific. We can hear you loud and clear.

Carrie: Perfect. I would like to direct this more to Dr. Fallon and Dr. Hawkins. Can you overview the variety of clinical presentations in early, disseminated, and late-stage Lyme? It varies so much from patient to patient and it would be helpful for frontline doctors to get a real understanding of what that can look like coming in the door.

Brian: [34:01]

I think we can each contribute to that. Certainly, with early, disseminated symptoms you have common flu-like symptoms, fatigue, muscle pain, joint aches, you might have some cognitive problems that develop. The fatigue can be quite debilitating. With treatments, that typically resolves, when it's treated early enough.

Later on, perhaps, six months later, nine months later, some patients in natural history course, natural history, if they haven't been treated, might develop arthritis, with swollen joints, which tends to be a migrating arthritis or migrating arthralgia. It tends to be short-lived. Some patients might go on to develop neurologic symptoms. They can occur acutely, within the first let's say two to four weeks, such as facial nerve palsy or meningitis. Rarely, you might see meningoencephalitis where patients actually get quite confused, they might have balance problems, et cetera. But that would be rare.

And in my experience, in the psychiatric realm, certainly patients initially might have significant irritability, they might have cognitive problems in verbal fluency where they have a hard time finding the words to say what they want to say. They might have short-term memory problems where they can't recall things, particularly things that they hear as opposed to things that they see. And their speed of thinking is slow, so they have an experience of brain fog. That's the way they describe it.

Now that's not a pathognomonic cognitive profile for Lyme disease because you can see memory problems with depression, as well, but if you have a cluster of cognitive symptoms along with diffuse arthralgias and myalgias and you're from a Lyme endemic area, and you recently may have had a tick bite, you have to wonder, and perhaps that would be a good time to get testing to see if you can support the diagnosis.

Dan: Thank you.

Ralph: That is what is called a tough act to follow. The only thing I would add to that is in our clinic we usually have referrals of people with much later disease, so we are doing cognitive testing, we are doing depression testing to assess whether or not depression is out of keeping-or that cognitive impairment is out of keeping with levels of depression. We do fatigue scoring, we do digit symbol substitution test to look at the speed and accuracy of thinking, that type of an assessment is done for the neurocognitive aspects of the disease.

Many of the patients are coming with serologies and the serologies often are from the infamous lab B, which fortunately I have awareness and I do the diligence of reading the fine print and making my clinical decisions on the basis of the fine print analysis of Dr. Fallon's paper and if the lab B findings are CDC positive then I give those the same type of weight that I would give to a provincial laboratory test that is reported to me from the province of Alberta.

The only other thing that I would add about the clinical presentation is that this is a profoundly debilitating disease, and it should be allowed to be documented as a cause of disability for government forms, for insurance forms, for private forms. And to see this framework move forward we should be expecting that Lyme disease will be accepted and not questioned as a cause of disability.

Dan: Thank you, Ralph. I will go for a second question from our WebEx participants. Operator, please cue the question, please.

Operator: Thank you. We have a question from Bill Baker. Please go ahead.

Dan: Go ahead, Bill.

Bill: [38:18]

Hello, can you hear me?

Dan: Absolutely. Carry on.

Bill: Great. Thank you very much for your work. You're doing fine work. My question is the fine doctor that was speaking before, I can't remember his name, was talking about antibiotic use with Lyme disease. And the same as using it, there could be problems with the use of antibiotics with reactions and so on and so forth, that could be more detrimental than the disease itself.

My question is: with syphilis, when people start antibiotic use with syphilis, they have a terrible reaction, it's the Herxheimer reaction, which isn't attributed to a drug reaction, it's the reaction of the disease. Now with Lyme disease, when people start taking antibiotics for Lyme disease, they also have potentially, like a Herxheimer reaction, which if you're not familiar with it, it could appear that you're having an antibiotic reaction, that there's a problem with the treatment that you're taking. So therefore, we better stop this treatment.

My question is: how do you know if the treatment that you're taking is actually working on the Lyme disease, causing a Herxheimer, or is it's directly attributed to a allergic reaction to the medicine?

Dan: Raymond, did you want to take that?

Raymond: Yeah, the answer to that question is Herxheimer reactions were described with penicillin in syphilis. The number of bacteria in those individuals is high and the penicillin acutely lyses the Treponema that causes syphilis. The immune system reacts, and that's what causes a Herxheimer reaction. All of a sudden it looks like a bigger infection.

Herxheimer reactions were described rarely in acute disseminated Lyme disease when you give an effective antibiotic. The bacterial load in late Lyme disease is actually fairly low, because the body's immune system can suppress the infection. And Herxheimer reactions in late Lyme disease, I've never seen it and I ran the big ceftriaxone-you can laugh but I ran the big ceftriaxone studies and been a lot of studies. And it just didn't occur.

And what you have to realize is that any medication that works has risks and benefits. There's side effects, and what I'm saying is that you just have to weigh that in any disease. There's a whole area now that's becoming very hot in immunology and microbiology, and it's called the human biome. And the human biome is altered by antibiotics and it can have detrimental effects that no one even thought about before. Things like increased risk of diabetes, increased risk of obesity.

So we're really working with areas on the cutting edge that we have to be careful of. And the bottom line is, as I was saying, it's a risk-benefit analysis. You always have to weigh: is this worth it? And sometimes it's not.

But in answer to your question, I don't think Herxheimer reactions are at all common in Lyme disease and it's distinctly different than what happens in syphilis.

Dan: Okay. Did you want to add?

Brian: [42:15]

Just specifically to ceftriaxone, ceftriaxone has known side effect profile. It can cause biliary congestion, you can cause gall bladder problems where you might need a cholecystectomy, that's not common but it's not rare either. The main problem with the ceftriaxone is not really the medicine itself, and it's really the fact that you need an in-dwelling picc line. And it's the in-dwelling line that causes the problems, because that's an itis for skin infections, Staph infection, so you can get into a lot of trouble with that infection. It can cause clots.

So it's important to distinguish what the problems are with the side effects of the mode of delivery or the antibiotic itself versus whether or not it's effective in helping you to have reduced fatigue, improved cognition, and reduced pain.

Dan: Thank you. I will go to the third WebEx question. And who might we have online?

Operator: Thank you. We have a question from Michele Hogg. Please go ahead.

Michele: [43:29]

Hi, I was infected with Lyme disease in Newfoundland approximately 15 years ago. My health really went downhill in 2005 and then I was diagnosed with celiac, fibromyalgia, sleep apnea, chronic fatigue, and a whole host of others too. I have seen six naturopathic doctors since 2005. I have tried many, many, many treatment protocols and nothing has worked for me. I have never treated with antibiotics.

Most recently, I was told by a very well-respected Lyme-literate naturopathic doctor in Ontario that her least invasive treatment protocols were too invasive for me.

My question is: I have been told that my immune system and my digestive system has been totally destroyed by untreated Lyme disease, and I'm wondering what would be the suggestion for the next course of action for me?

Dan: Yeah? Okay, Ralph did you want to have a crack at that?

Ralph: So if I understand the question correctly, this is a question about long-standing Lyme disease with long-standing naturopathic treatments and this lady has been told that her immune system is deficient and that she has had a destruction of her digestive system and her immune system as a result of the disease and the treatment, and what would be the prospects for next treatment?

And regrettably, I don't think anyone on this panel has enough information about your clinical status to be able to answer that question with any clarity. Clearly, you are chronically and grievously ill with whatever is going on and your situation needs to be fully evaluated by someone with clinical competence.

I'm sorry I don't have a better answer than that.

David: It's David. I have to agree with Dr. Hawkins there and one thing I would suggest in Newfoundland is try and speak with the Department of General Internal Medicine at Memorial University and get a fresh referral from your doc. Because you want to be evaluated for the possibility that this is Lyme for sure, and you also want somebody who's very good at making sure that no other stone is unturned in looking after your health. So it's an important hypothesis but there are probably several other possible things that could be happening too, and you wouldn't want something else to be missed.

Dan: Good. Thank you, David. We'll go back to the main room and we have Elizabeth May.

Elizabeth: [46:34]

Thank you. First of all, I want to thank all the panelists and this is an opportunity I think, not just to ask you questions, but to ask for a bit more interaction between all of the expert panelists who are here with us this morning.

One of the things that I'm wondering is focussing on building blocks for consensus where we can find it. We are, and my bill mandates, that the federal government come up with a federal strategy, a federal framework, on Lyme disease. So I'd really love to know, particularly from Dr. Fallon, Dr. Dattwyler who will not often be in Ottawa with us, Dr. Hawkins, and Dr. Patrick, are there things that you would want to see recommended to the government of Canada that are immediate steps?

When we say we need more research that should not be communicated to patients as you have to wait and suffer. What are the interim steps we can take with what we know so that we don't leave people suffering? What are the long-term research projects? What are the most urgent ones? I took Dr. Dattwyler, it's money, we need money for research. Where do you want to see it?

And to Dr. Hawkins, thank you for your courage. And what would you want to see in a federal framework?

Dan: Who would like to go first? Dr. Dattwyler?

Raymond: I think that well-structured research projects, you're right, they do take a long time. And fortunately, there's a lot of research that's being done both in Canada, at your Canadian universities, and also at the US universities. And I think that joint collaborations can be, are in progress, and I think that can be expanded.

Certainly, my lab is very much interested in the immunology of Lyme disease and how we can use that information to make better tests. I was very happy to see that the gene, the chips, being shown. That's exactly how we do it. We continue to do that. And there's no reason why we can't share some of our data with Canadian researchers and I'm happy to do that.

I was asked if I could supply some peptides for a research effort and I said, "Sure."

We're open to it. So that would be the immediate thing that could be done.

And as far as the long-term goals, I think that scientific meetings can be put forth, we get everybody together. There's going to be a Banbury conference at Cold Spring Harbour. Banbury is a conference centre at Cold Spring Harbour where small groups of scientists can get together and actually plan. You should think about doing that with your Canadian scientists as well, and I think they could help guide you in what areas to spend your money.

Dan: David, did you want to offer a response before I go back to the panel?

David: Sure do. Thank you, Elizabeth, for the question. I agree that the research is a longer term sort of thing. So to think about the spirit of your question, I think there are quick wins in surveillance, in better being able to characterize the problem. And I think that that comes along best if we're fairly specific about what we mean. We're interested in the whole spectrum here, but we may have a case definition which is a definite case definition that nobody's going to argue with.

But there are other means to take a look at the prevalence of the symptoms that we're worried about, in so many other Canadians. And this can be accomplished through adding questions to the Canada Community Health Survey which is issued every year or so. It can be answered by working with the investigators of the Canadian Partnership for Tomorrow, the 150,000 Canadians being followed through time and space to find out how these symptoms hit people in adulthood, what their incidence is. And it can be actually neutral to the hypotheses about causation to a certain extent.

So I think we can move ahead in surveillance fairly quickly. I'd be surprised if we couldn't see something happen at the meeting.

As for research, really these new -omics technologies that have come forth just within that last few years of this decade, really give us the opportunity to look at things in a brand new way. This is like Pasteur looking under the microscope, growing things in culture for the first time. We've never been able to do it before, and I think some Canadian investment in those infrastructure platforms at major research institutions, would go a long way.

Dan: Brian, did you want to add?

Brian: Yeah, I agree. I actually agree strongly with that. I think it's very important to carefully collect samples from patients so that those samples are stored carefully and they can be probed in the future when new measures are available to teach us about what's going on in that body fluid.

So I think if that can be done on a national basis, we could learn a lot.

I think strongly, and I say this over and over again, probably in my sleep, that the clinical trials from my review of the US clinical trials support the notion that repeated antibiotic therapy can be helpful. That means repeated, that doesn't mean extended. But at least from what's been done, at least for post-treatment Lyme fatigue which is one of the more debilitating symptoms, it would be wonderful if the Canadian government adopted that as a recommendation. Because that's based on the evidence at least as I see it.

And, let's see what else was I going to say? Oh, I like something, Dr. Hawkins, something that you said earlier about definite versus probable Lyme disease. And certainly there are patients who clearly meet criteria and you know what to do with those patients and then you might give them an additional course of antibiotics to see if that helps, if they're still symptomatic. That would be a reasonable thing to do.

But what do you do with those who have probable Lyme disease? They come from a Lyme endemic area, you're highly suspicious. Do you not treat them because they don't meet the definite surveillance criteria, whatever they happen to be. From a clinician's point of view, it's common to treat with the possibility or probability of Lyme disease and see what the outcome is, even if you don't know for sure.

Now if the person doesn't respond to the antibiotics, then you have to re-evaluate your hypothesis that maybe this wasn't Lyme disease all along.

Dan: Thank you. Ralph?

Ralph: So the one thing I would add: I echo virtually every utterance that's been made on this question but the one thing I would add would be protection of prescribers. Protection of the healthcare providers so that the use of an unorthodox treatment methodology, as long as it is safe, as long as the patient is well informed and is consenting, and as long as there is some literature basis for what is being done, won't be sanctioned by the organizations that provide us licensure and regulation.

Dan: Second question from within the room? Over to you, ma'am.

Female: [54:16]

Hi there. I have a question for the infectious disease doctors.

As Mr. Patrick stated, in his comment earlier, he stated that: "we want to get to the bottom of why people are sick."

Now my question is: does that just happen in BC? Or does every infectious disease doctor have that attitude? Because I know patients in Alberta are constantly denied treatment. Infectious disease doctors refuse to see these sick people. Why is that?

Dan: Okay, thank you. Who would like to grab a hold of that? David?

David: I'll have a go at it. Clearly, when I speak to colleagues from coast to coast to coast, they're really, really keen on understanding what's going on and making sure people can be moving in the right direction. I mean, don't forget, this is the group of Canadian practitioners who have met pandemics, who have met SARS, who've dealt with Ebola, who've actually pulled ahead on things.

So to assume that the group is selectively blind to one specific spirochete, may or may not be exactly the way we go. But I think it's going to take more than ID doctors actually to sort this out.

And if we're taking a look at Dr. Fallon's interest in perhaps some repeat therapy, why do some people seem to improve with that? Well, it could be because it's addressing a bacterium. But it also could be because it's changing the gut microbiome which interacts quite a bit with the rest of the body through the proteins and other things that are secreted by bacteria. And if there's a change in what gets secreted, there's a change in what gets experienced in the central nervous system as well.

So I would say that if we are going to take a look at further therapy in some way, we have an obligation to research it, to understand why it's working. If it's working. So further trials are probably something that needs to be considered but I think we have to open our minds up to which of the many activities of antibiotics may be periodically helping people. Is it clearly antibacterial stuff? Or is it the anti-inflammatory focus? Or is it actually changing the nature of the bacteria that we have in our gut and how they communicate with our nervous system?

Dan: Thank you, David. We'll go on to the next question, please.

Female: [56:42]

This is for Dr. Dattwyler. So apart from the fact that there is faulty testing, that medical help is really difficult to find if not impossible, there's a lot of medical negation and a lot of misinformation. And I just want to address something that you wrote with other authors in the Lancet, I think it was 2011, which I think really speaks to the suffering in this room. Certainly, I can speak for myself.

So what is really causing a great deal of suffering is the mockery of those who are advocating for this disease. Unacceptable. Unacceptable.

So this piece that you wrote is called "Anti-Science and ethical concerns associated with advocacy of Lyme disease" and in it, I think it's kind of interesting that you talk about the fact that advocacy for Lyme disease has become an increasingly important part of the anti-science movement. You also speak to the fact that there is a geographically limited tick-borne infection, that's what you have said, which I just don't think is the case when actually tick-borne infections are present in 80 countries around the world. So I think that's a false statement.

And then in addition to that, you speak about the fact that we claim, we as advocates, claim that Lyme disease is insidious, ubiquitous, and difficult to diagnose and almost incurable, which I actually think is true. My experience tells me that that is true. You're negating that in this piece in the Lancet. And I'm just wondering how you would address that?

Raymond: That was in response to a series of things that were attacking us and…

Female: So then you attacked us.

Raymond: No.

Dan: Okay.

Raymond: We responded. And I think that tick-borne disease is, you're right, there's a lot of different tick-borne diseases. Lyme disease is only one of them. And I think that Lyme disease has taken on a prominence and people have forgotten all the other ones.

Female: But here you're addressing Lyme disease.

Raymond: That's true.

Female: Yes.

Raymond: So it was something that I still think that there is an anti-science bent out there. And that we were addressing that we have to do is do things in an evidence-based way based on real science and to try to help as many people as we can in that standardized fashion.

Female: And how is that working?

Raymond: Actually, I think that most people would say it's working pretty well…

Female: Really?

Raymond:…because we've made advances in, significant advances. And I think my talk pointed out that from the 1980s to the present time, we now understand things much better. It's going to allow for much better tests to come into place. The whole concept of the human biome is new. How antibiotics work and what's happening is new information. We have new tools and I think we have to use them. And that's what we were pointing out. You just can't-one side can't just attack another and-there's a lot of bad feelings on both sides. Brian Fallon and I were talking about an incident that happened in the United States where really we-a politician actually sued everybody including scientific organizations.

And it really didn't help any-it cost a lot of money, didn't resolve things. And I think we have to really calm down, ratchet it down and do the science. And that's what we were trying to do. And we're trying to point that out.

Male: Brian, did you want to add to that?

Brian: Yeah, I just want to say that it really is the science that's moving things forward. I agree with that, because there's been so much progress and the patients who are chronically sick at this point may not fully appreciate it because they are still sick and still suffering, and obviously we need to devise better treatments for them.

But the accelerated advance of what we're learning about, what's going on immunologically in patients who have early Lyme versus patients who have later symptoms that continue despite antibiotic treatments will lead to better treatments and certainly are leading to better tests.

And Dr. Dattwyler has some really interesting tests. So one of the tests he talked about earlier was based on the QuantiFERON tuberculosis approach which actually allows you to distinguish active infection from past infection. Now that would be a fantastic test for us all to have because that would get rid of the debate whether or not one has active infection or not.

And one of the problems with the antibody test is all they do is they tell you whether or not you've had previous infection. So you could still be infected and test positive or you could not be infected anymore and still test positive. In fact, one of the first positive IgG Western Blots I ever saw was in my research assistant. I was drawing his blood as a healthy control, and he came out fully positive on this IgG Western Blot.

And I said to him, "You've had Lyme disease at some point in the past."

He said, "No, I never had Lyme disease."

And so, we need, obviously, tests that tell you whether or not there's active infection.

Dan: Thank you. I'll go to the overflow room and given the time that we have left, I'm going to go for one question there, one question WebEx, and back to this room. Question from the overflow room, please.

Linda: [1:02:46]

Hi, I'm Linda. And I've heard a lot of answers be referred to as "we need more research, more money". Well, I'm here at this conference and if I wasn't in a Lyme group, I wouldn't know this conference was going on. I watch the news twice a day. I've seen nothing. I've seen no advertising on it. I've done marketing, I've done promotions. In order to get money, in order to get funding, you need to get the word out there. So what are you doing to raise this money and then when you get it, where is it going to go?

Male: Who are you posing the question to?

Linda: To whoever would like to answer. The two people that keep answering "we need money, we need research", those would probably be the ideal people to speak up to this question.

Brian: I'm happy to say something because another talk I give sometimes is based on the tremendous advances that private donors have made to supporting researchers who might start to study this area, that who might not be initially supported by the National Institute of Health, because they haven't done the background work in Lyme disease. They don't have the history. But they have expertise in related areas. And as a result of that, a whole slew of new super outstanding researchers including Dr. Zhang here and others have started their work which is leading to really important findings.

So I think that the advocacy at least in the United States has led to the decision that the best way to make differences is by supporting really excellent researchers to probe and try to work on the toughest questions. And I see that happening. So I'm very optimistic and enthusiastic about what the patient community has been able to do. As a result, they're channeling their anger into effective action.

Dan: Okay. Thank you. We'll go on to…

Linda: You're leaving it up to us. You said you're leaving it up to us, the suffering, the sick, who can barely manage to stand up and shout and get money so you can do the research. When is it going to come from somewhere else? Why? I repeat the question. Why was this not on the news? When we hear conferences, when we hear fundraising about Lyme, MLS, any other diseases. It's on the news for months. Where was the talk about this? Where is the things going out saying, "We need money, people are suffering"? It shouldn't be the advocates of the ill trying to raise this money. We are already poor and our advocates are using everything they have to keep us alive.

Dan: Thank you for your question. I would like to point out that there are several officials from the Public Health Agency of Canada who are here, who are going to be listening to the types of suggestions and ideas and contributions that you will have over the next couple of days, and whose job it is to contribute to the shaping of a framework including the engagement that all of this conference will have between now and the end of the day tomorrow and beyond this conference and we'll hear more about it tomorrow.

Let me go to a WebEx question, please, before I return to the main room. Operator, is there a question from the WebEx participants? Going once. Operator, any questions from the WebEx participants?

Operator: Thank you. We have a question from Rozeanne Ravensbergen. Please go ahead.

Rozeanne: [1:06:34]

Hi, can you hear me?

Dan: We can hear you. Speak as close as you can to your phone or whatever device you're using.

Rozeanne: Okay, is that better?

Dan: Yes. Please go ahead.

Rozeanne: Okay. I have late stage Lyme disease. I was undiagnosed for three years here in Canada. Since then, two of my siblings have come up with late stage Lyme as well. I was negative on my testing according to CDC standards, positive IGeneX, and since then, I have been treated with IV antibiotics for a year. I did it all myself at home three times a day and I took seven oral antibiotics as well. In the opinions that I've heard so far, this is a very extreme way to treat Lyme. But it has worked for me, I was severely disabled and now I'm functioning again. At this point, I'm able to heal my system and carry on with life.

So my question is: what are we doing about the late stage people with Lyme disease? I mean, we're not getting caught on the testing either, and like I said, my siblings have come up with Lyme as well. They've tested positive as well, and they came straight bang into the late stage. There were no early symptoms. We don't remember being infected in any way with a tick bite. So technically, according to standards here, there's no reason why we should have Lyme disease. But I've responded to the treatment and I'm a lot better now. How come these people are getting missed and what can we do about the late stage Lyme disease?

Dan: Who'd like to take this one?

David: Rozeanne, it's Dave Patrick. What part of the country are you from?

Rozeanne: I'm Ontario.

David: Right. So I'm delighted to hear that you're better by any course. Even when there are disagreements about what treatments may be optimal, it's really good to hear people's stories when they're improved like this.

The big question, though, is when you take your experience, and you say, "Could that be generalized into experience for other people like me?"

That's where the clinical trials come in and that's where there'll be a lot more talk later today about what those clinical trials meant. Dr. Fallon is saying and I'm listening to him that he's thinking that there may be yet some really good benefits.

Others interpret the trails as saying, "Well, yeah, there's benefit, but there's also benefit in the placebo group". And so, could that mean that some people heal themselves or that there's a benefit to thinking that a therapy's coming through? I don't know. But the controversy really is that to take your excellent experience and generalise it to other people does take the right kind of studies. And we need to be able to predict that it's going to do good for other people.

Rozeanne: See this is the problem. I am not recognized as having Lyme disease in Canada at all. Not at all. So nobody is coming to me and asking me questions.

Dan: David, did you want to respond to that?

David: Just to this point, and really, I think you've identified a real identification with the diagnosis. And I don't know how it was made so I don't want to comment on your particular case. But it really is important to say that there's a lot of people suffering the sort of symptoms that you have, some may call it Lyme disease, some may call it chronic fatigue syndrome, and it's really important to take a look at the strength of evidence for whether the bacterium is there, causing something. We really have a common interest in making sure that we understand the full array of therapies for debilitating fatigue, body pains, and so forth.

And I think back to the research question that was posed earlier on, NIH and CIHR are getting less uncomfortable with the idea of funding for chronic fatigue syndrome, maybe because people are saying, "Oh look, we're intellectually being honest. We're not dead sure exactly what's going on."

And that's beginning to cause funding to come through. I think what we have to do is continue those conversations in the Lyme realm as well, to see if we can open up the coffers of the major funding research institutes to sort of help answer these questions in the long run.

Rozeanne: But there's just one more thing I wanted to briefly address. People are coming to me with tick bites, obviously they know I have Lyme, so in my local area, they're at the schools, they're in everybody's backyards.

People are coming and saying, "What do we do? The tick's been stuck in me for a while, but it's the wrong type of tick to get tested. It's not a black legged, it's a brown tick or some other type of tick. Can we still get infected?"

Well, there's controversy even in that field, as to whether or not another type of tick can infect people with Lyme. So the only type of ticks that are getting tested are the black legged. I'm wondering why that is and why they won't expand that out to other types of ticks? Why would only one type of tick be able to carry Lyme and co-infections?

Dan: David, quick response, please?

David: Okay. Well, I mean, first of all, there are with all vector-borne diseases, there are unique species combinations where a given insects is much better at carrying a pathogen than others and we're certainly seeing this unfold in South America with the Zika virus, for example.

But that said, and it's worth our furthering this conversation with Nick Ogden and others, when there are deliberate efforts to collect ticks from people or from the environment, it is worth our while taking a look with, in a very open-minded way, at different species of ticks just to make sure they're not carrying things that we would be worried about.

And not just testing for Borrelia. I think we're in an era now where there's a number of studies going on. I think Janet Sperling's doing it at UofA, and we're involved in doing this at UBC, where you're taking a look at new molecular methods to look for a full array of bacteria or other pathogens that could be in a tick so that we fully understand what the ecology is. So I think that's part of the surveillance discussion and I hope it gets brought forward to the next session.

Dan: Thank you, David. I'll take one last question.

Holly: [1:13:14]

Thank you, moderator and scientific panel. I'm a Canadian. I'm a very proud Canadian and I'm very proud today to be able to share this moment with all of you, because it's, in my opinion, a landmark moment, and I think we're setting a precedent for the rest of the world.

My name is Dr. Holly Donohoe, I'm from Ottawa. It's here where I was infected. It's here where I was misdiagnosed. I am fighting through a flare of Lyme-related carditis to stand here and share my story. But I did that last night. And what I want to do today is speak to the fact that there is a war. I have this unique perspective because I work at the University of Florida. I specialize in Social Science related to outdoor recreation, as well as workplace risk related to tick-borne infection.

My research is inspired by my own experience with Lyme disease. Yep. So I want to commend the panel for their bravery in coming forward because in the United States, science has been interrupted if not entirely shut down by patient groups who attack scientists. Scientists have received death threats and I want to reiterate what the moderator said last night which is very important as we go through the next couple of days.

And that is: "We need to be hard on the issues, and we need to be soft on the people."

My question to the panel is, knowing that a vaccine, a cure, treatment modalities, and more, are long-term strategies, what is the role of science as well as public health agencies and other officials in developing prevention programs? Because my research shows people don't know about it and they're taking absolutely no precautions. And those who do know are still not taking precautions.

Dan: Thank you. Who would like to respond? Who'd like to start?

Raymond: Since I run a research group, I'll respond...

David: That they're…

Raymond: …Oh. Go ahead.

Dan: David, hold on. We're having Raymond respond and you can jump in right after.

Raymond: No, I think that the amount of support could be better. And I think that there needs to be better communication between the scientific community and people. That being said, in certain regions of the United States now, the public health agencies are trying to educate people about tick-borne diseases much better than in the past. I think in less endemic areas that they need to catch up and I know New York State, and Connecticut, Massachusetts, New Jersey, have strong public health educational things, where they do mailings and things like that.

But I agree with you that more needs to be done. There are things in the works that deal-there's a Bate vaccine that they're looking at where they can immunize the rodent population which is the major reservoir of Lyme disease and take Lyme disease out of areas that's-There are people working on new vaccine constructs that may be better. But again, all of this stuff is longer term.

Holly: The immediate need in my opinion is that we need to work on increasing public awareness. You know, developing a vaccine is going to take years. In Canada, awareness is key. It can happen now and it can protect our children, our family, our neighbours, and it's really important. And it's the only method we have to fighting this disease right now.

Dan: And I'll encourage you to bring those points back to the awareness group and education…

Holly: I will. Thank you very much.

Dan: Any other comments? Oh, David, yes. David, would you add to that?

David: I think it's been well said already. Prevention is an area that I don't think there's going to be too much controversy on its importance. It's really a matter of how to get the word out. Even in areas of lower endemicity, nobody wants a tick bite and ticks, even if they're not carrying Lyme can carry other things. So we really need to make sure that everybody's aware of how to avoid tick bites.

Dan: Thank you. Ladies and gentlemen, my apologies to those of you who have not been able to pose a question. Two possible approaches that you might take: one is over the lunch period, the panelists who are here present are accessible, available, and they'll entertain your questions; the other option that you have is in the smaller breakout sessions that we're going to have after lunch. Feel free to pose those questions there, and hopefully you'll get an answer.

One quick point for lunch: lunch is available and I'm going to ask you to leave the room as much as possible to give the maintenance staff the opportunity of cleaning the tables so that you go and obtain the lunch and come back here in 15, 20 minutes. But there's also availability in the Confederation Room, in the corridor, and in the cafeteria that's just down the hall.

We will start again at 1:15. Please join me in thanking the panelists.

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