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In this episode, you will learn about unraveling Bartonella.
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About My Guest
My guest for this episode is Dr. B. Robert Mozayeni. B. Robert Mozayeni, MD is an expert in Translational Medicine, the science and art of advancing medical science safely and efficiently. He is the Chief Medical Officer of Galaxy Diagnostics, LLC. He is a co-founder of the Foundation for the Study of Inflammatory Diseases. He serves as an advisor to pharmaceutical and nutraceutical companies and serves on an Institutional Review Board specializing in nutraceutical products for pain management. He is the immediate past President of ILADS, the International Lyme and Associated Diseases Society where his goal was to advance the science of translational medicine. In late 2019, Dr. Mozayeni launched T Lab Inc., a research and clinical laboratory engaged in research using advanced microscopy to understand better the pathogenesis of disease in inflammatory conditions associated with persistent infections. He has research and clinical expertise with regard to autoimmune diseases and the effects of chronic infection and inflammation on vascular physiology and neurovascular conditions seen commonly with autoimmune and neurovascular diseases. With a strong foundation in the basic sciences and evidence-based medicine, he analyzes complex medical cases using a combination of basic scientific principles and clinical experience along with the balance of the evidence base. Dr. Mozayeni has published numerous papers on immunology and cerebrovascular blood flow hemodynamics. He has been actively researching and publishing his work on chronic rheumatic diseases and their relationship to persistent human Bartonella spp. infection. Of note, chronic persistent Bartonella spp. infections are strongly associated with neurovascular diseases. Thus, Dr. Mozayeni is uniquely qualified in the combined areas of chronic persistent endovascular infections and related rheumatological and neurovascular diseases. He has also published papers providing new insights as to a potential infectious (Bartonella spp.) cause of osteoarthritis and also, a case of arthritis associated with hypermobility that was likely caused by Bartonella spp.
- What advances have been observed in recent years in the realm of Bartonella?
- What are common symptoms of Bartonella?
- How is Bartonella transmitted?- Might Bartonella lead to autoimmunity?
- Can Bartonella be a trigger for PANS?
- Might Bartonella be a contributor to osteoarthritis?
- Is there a connection between Bartonella and hypermobility or EDS?
- Does Bartonella contribute to MS?
- What is the connection between Bartonella and SIBO?
- Can Bartonella act as a trigger for MCAS?
- Is Bartonella activation observed in those with COVID?
- What is the state of the art in Bartonella testing?
- What is Babesia odocoilei?
- What agents are most helpful in the treatment of Bartonella?
- Is there a place for herbs and other natural interventions in Bartonella treatment?
- Should pets be considered as a potential source of exposure to Bartonella?
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May 24, 2023
Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast. They are not a full replacement for the discussion. Timestamps are provided to facilitate finding portions of the conversation. Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed. Please Contact Me with any corrections.
[00:00:01] ANNOUNCER: Welcome to BetterHealthGuy Blogcasts, empowering your better health. And now, here's Scott, you're BetterHealthGuy.
The content of this show is for informational purposes only and is not intended to diagnose, treat or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.
[00:00:35] SCOTT: Hello, everyone, and welcome to episode number 185 of the BetterHealthGuy Blogcasts series. Today's guest is Dr. Bob Mozayeni. And the topic of the show is Unraveling Bartonella.
Dr. Bob Mozayeni is an expert in translational medicine, the science and art of advancing medical science safely and efficiently. He is the Chief Medical Officer of Galaxy Diagnostics and a co-founder of the Foundation for the Study of Inflammatory Diseases.
He serves as an advisor to pharmaceutical and nutraceutical companies and serves on an Institutional review board specializing in nutraceutical products for pain management. He is the immediate past president of ILADS, the International Lyme and Associated Diseases Society, where his goal was to advance the science of translational medicine.
In late 2019, Dr. Mozayeni launched TLab, a research and clinical laboratory engaged in research using advanced microscopy to understand better the pathogenesis of disease in inflammatory conditions associated with persistent infection.
He has research and clinical expertise with regard to autoimmune diseases and the effects of chronic infection and inflammation on vascular physiology and neurovascular conditions seen commonly with autoimmune and neurovascular diseases.
With a strong foundation in the basic sciences and evidence-based medicine, he analyzes complex medical cases using a combination of basic scientific principles and clinical experience along with the balance of the evidence base.
Dr. Mozayeni has published numerous papers on immunology and cerebrovascular blood flow hemodynamics. He has been actively researching and publishing his work on chronic rheumatic diseases and their relationship to persistent human Bartonella infection.
Of note, chronic persistent Bartonella infections are strongly associated with neurovascular diseases. Dr. Mozayeni is uniquely qualified in the combined areas of chronic persistent endovascular infections and related rheumatological and neurovascular diseases.
He has also published papers providing new insights as to a potential infectious cause of osteoarthritis and a case of arthritis associated with hypermobility that was likely caused by Bartonella.
And now, my interview with Dr. Bob Mozayeni.
[00:03:02] SCOTT: This is an episode I have wanted to do for some time. I'm very excited about our discussion today. Dr. Mozayeni and I collaborated on an article in the Townsend Letter in 2015. I'm looking forward to discussing the latest on the topic of Unraveling Bartonella.
We talked about doing this podcast a few years ago. And I would jokingly email him on Thanksgiving Day for the past couple of years and suggest how grateful I and we would all be to have him on the podcast. Many of the questions for today's talk have come directly from listeners and from participants in the Facebook group Breaking Down Bartonella. Thank you to those that submitted questions for our talk today. And thank you, Dr. Mozayeni, for being here.
[00:03:42] DR. MOZAYENI: Yeah, my pleasure, Scott. And I'm glad we finally got to do this. Crazy busy few years. Things are looking I think better than ever for patients who have these issues and need to get better.
[00:03:55] SCOTT: Since the article that we worked on eight years ago, what has been the most significant difference in our understanding of Bartonella as a contributor to chronic illness or in terms of how treatment is approached? What do you see as the biggest differences between unraveling Bartonella today as compared to when we collaborated on that article eight years ago?
[00:04:17] DR. MOZAYENI: To touch on a few of the biggest cites, or changes, or developments, they include the very substantial advancement of testing not just for Bartonella but for other co-infections. We're starting to see a lot of it being co-associated with Babesia. Even though, historically, people don't think that Bartonella is as likely to be tick transmittable, for some reason, there seems to be a co-association with Babesia.
And it's continuing to confirm our original thinking that much of what the public would define as Lyme disease is really is often not Borrelia but might be a mixture of these other infections. I think we're getting a more nuanced appreciation of what I call #lyme really is. We have a medical definition, a scientific definition, and we have a public definition. And much of the controversy and confusion has been around the fact that people are using different definitions when they use the word Lyme disease.
For a patient, it's sort of like I don't feel well. The closest thing I can come up with when I do my search is that I have Lyme disease. That becomes a public definition. And whereas the physicians and medical scientists trying to study this bristle at that because they're trying to work with a very narrow definition.
But if you don't define a study narrowly, a term narrowly in a clinical trial, then you don't make progress and it's not publishable. Whereas the patients have a general set of issues that they're classifying as Lyme disease, again, that I call #lyme.
We're getting a better idea of what the spectrum of infections really is in these patients. And we're getting a better idea of who is more likely to get sick. For example, I always tell patients that there's a difference between the infection and how it causes disease and the host response and how that causes disease.
And this is a debate that's not new. It's a debate between Louis Pasteur and his colleague, Beauchamp. And so, really, we have to keep in mind that it's the net interaction between the microbe and the host response that defines the disease.
[00:06:28] SCOTT: In the realm of Lyme and co-infections, it's been my opinion for many years that Bartonella is often a more significant challenge or contributor than Borrelia or even Babesia. Obviously, the more of these you have, they kind of become more synergistic and lead to more significant presentations.
But in terms of the impact on our health, which of the chronic vector-borne pathogens do you feel is the biggest contributor to chronic vector-borne illnesses?
[00:06:57] DR. MOZAYENI: That's a tough question to answer, again, because the host response varies. But if we breakdown the characteristics of the different major co-infections, Borrelia, Bartonella, and Babesia, Babesia often will sequester fibrin and plug up small blood vessels. Bartonella can do that too. It will infect the endothelium and other cells and activate an epithelial proliferation that can also obstruct the normal blood flow. Both of those can infect red cells and white cells. That can also affect the circulation.
And Borrelia is a biofilm producer also. I mean, they all are. Well, we also know, for example, Bartonella can damage collagen. We have really great microscopic images of Bartonella in colonies sitting on collagen fibers that are damaged. And we're seeing a strong association, which needs to continue to be studied formally. But every time we test a patient who's had these really red, ugly-looking stretch marks. Every time we've looked with a biopsy, they've turned out to be from Bartonella.
And we need a large – a greater N in the study to be able to say that it's always there. But whenever we've had a patient with a Bartonella history and red stretch marks, we found Bartonella on skin biopsies. I think that they all contribute substantially.
We could speculate about one of the long-term effects. For example, if Bartonella is damaging collagen, then could it be contributing to other connective tissue diseases? Could it be damaging the vascular system? Could it be potentially a cause of aneurysms? We don't know these answers. But this is the sort of stuff I think about, which keeps me up at night.
[00:08:45] SCOTT: Bartonella has been called a hidden modern-day epidemic. How common do we think Bartonella infection is in the chronically ill population as compared to the "healthy population"?
[00:08:59] DR. MOZAYENI: Well, the funding really hasn't been there to study the prevalence in the healthy population. Usually, what we learn is sort of ad hoc based on what we find in patients who are sick. I don't want to generalize and say that this infection is highly prevalent. But in our patient mix of people with chronic symptoms, it seems to be very prevalent.
Regardless of which infection you find and document even with hard evidence, you've then have an additional challenge to try to establish that it, in fact, is the cause of the symptoms that the patient has.
For all the great testing we may have in our developing, we still don't have a way to connect the finding to the symptoms. And this, again, is one of the reasons for the controversies. But if you rule out all other possibilities, then this is the – however implausible you're left with these pieces of information. I always emphasize trying to get hard molecular evidence of an infection.
The biggest change in my mind about this whole field is that we're realizing – only because we now have better choices, we're realizing that serology, antibody testing, is woefully inadequate for chronic persisting infections. And the acute infection, a change in antibody titer is very helpful to helping make a diagnosis. But in a chronically ill patient, an antibody titer doesn't really tell you much.
And many, many of my physicians' patients, people I know, are often – just assume that if the antibody is present, so is the infection. And I remind them of things like tetanus vaccines where the goal is to produce antibodies without an infection. Again, the appreciation the antibody testing is limited in chronic infections I think is one of the biggest developments over the last few years.
[00:10:50] SCOTT: Besides Lyme disease, what are some of the illnesses or labels that people may have received that could actually be the result of an underlying infection with Bartonella?
[00:11:01] DR. MOZAYENI: It can present in any different ways. And so, there's some patients who may carry low level of it and not be sick. But the range is quite substantial. From joint pain, skin lesions of different kinds. All the way up to a full-blown neuropsychiatric illnesses including schizophrenia and psychosis. And even, worst case scenarios, suicide.
Many of the symptoms get classified as psychiatric. But, again, psychiatry is a field that's emerging and becoming a bit more of a science than it has been. And so, I think that we need to have psychiatrists trained in internal medicine and improve the care of patients across the spectrum. Plus, when a patient has a neuropsychiatric problem, they end up in a certain kind of institution that's less familiar with these sorts of issues. Yeah.
And I wanted to go back briefly and say that the – back to the antibody question, which I think is part of the reason why these problems exist, is that the antibodies can cross-react. And we often see false positive IgM Western blots and Immunoblots for Borrelia, for Lyme, when a patient has Bartonella.
And so, we treat and monitor. And the antibodies to the borrelia go away when we treat the Bartonella. And so, there's this whole question of like what are the antibodies really reacting to? And that's confusing the field even further. Again, emphasizing the need for molecular diagnostics.
[00:12:33] SCOTT: Well, would you characterize Bartonella as having more physical symptoms or more mental-emotional symptoms? I mean, we know that anxiety, and OCD, and Bartonella rage, and those kinds of things, it seems to me that Bartonella is one of those infections that can really impact us more on a mental-emotional realm than some others.
[00:12:54] DR. MOZAYENI: Yes. Babesia, by sequestering and fibrinous, can obstruct blood flow, capillary blood flow. A lot of the symptoms that we see are attributable to the circulation, the microcirculation.
I know this is one of your questions later is about the blood-brain barrier. I think that people have been overly emphasizing that. If they have brain symptoms, they assume that it's on the other side of the blood-brain barrier. And most of the times, I think it may not be. Because approaches that address the neurocirculation and microcirculation seem to be very important.
And I think the role of the circulation in the brain, it sounds like even a stupid thing to say. But I really don't – because I actually came at the field of Bartonella from my work in neurovascular diseases. Even though I was trained where they discovered Lyme disease, that's not how I got into Bartonella and chronic persistent Lyme. It was from the field of neurovascular medicine.
I worked extensively with US neurologists and European neurologists who were very good at this. I learned some surprising things that the study of vascular medicine and the grants for the study of vascular medicine in the brain go to the Heart, Lung, and Blood Institute and not to the Neurology Institute of the NIH.
In the US, the neurologists are more imaging-oriented. And in Europe, they're hemodynamically oriented. Neurovascular hemodynamics is, as a culture, as a science, and as an expert, awareness is anchored in European – in international neurology where they all learn how to do their own transforming adopter studies.
I think the neurovascular component and, generally, the vascular component throughout the body is the big unrecognized and misunderstood issue. And most of the symptoms that patients have with these infections can be attributable to this. And I tell patients, because it affects the vascular system and the microvascular flow, truly, any symptom is possible with these infections depending on which vessel and which area was affected.
[00:15:04] SCOTT: And would we then say that Bartonella is a contributor to hyper-coagulation?
[00:15:10] DR. MOZAYENI: It can be. Any inflammation can be. It causes endothelial proliferation, which hinders the efficiency of vascular perfusion. We don't have a tool to assess microvascular flow dynamics. People have looked at tools. We were looking at transcranial Doppler, which is being developed still to do that. People have looked at Laser Doppler Flowmetry. There are a lot of tools. But because we have – medicine has been focused on large vessel plumbing, not small vessel plumbing, we haven't had a tool to appreciate the importance of the microvascular flow dynamics.
[00:15:46] SCOTT: And do we find pulsed electromagnetic field mats potentially helpful in that micro circulatory support?
[00:15:53] DR. MOZAYENI: It is the claim. And, potentially, yes. But it'd be great to have a tool where you can reliably measure that in a patient and know if what you're applying is actually working.
[00:16:04] SCOTT: Yeah. Bartonella is commonly referred to as Cat Scratch Disease. What are the most likely ways that Bartonella is being transmitted in your patient population? You alluded to this earlier. I still read articles that suggest that ticks are not considered to be a vector for Bartonella. Not sure if that's true or not. Fleas and lice certainly have been implicated. How are the majority of your patients likely acquiring their Bartonella? And then can Bartonella be transmitted congenitally?
[00:16:35] DR. MOZAYENI: Cat Scratch is the term for the most obvious form of the disease where flea infested cat has flea feces under their nail and they scratch her skin and inoculate the Bartonella from the flea feces under the skin. And you get a local rash on a dermal spread and then ultimately tracking into the lymphatics.
Because Bartonella is also immune suppressive, it kind of dampens its own inflammatory reaction eventually, which is why it becomes unrecognizable after the acute phase. And patients will be pretty mostly better and then people kind of forget that it potentially could persist only to come back years later.
In my experience, the majority of the patients I've seen with Bartonella have gotten it from flea exposure and cats. Bartonella is potentially found in other insects as well. In many insects. It seems to be less prevalent and not that it's impossible to find it in ticks. It's just not as commonly found in ticks.
And whenever these tests were done on ticks, I would just remind us that the sensitivity of the methods may not be adequate enough to discern that it is present there. PCR in vitro can be sensitive. But when you're dealing with the biological mess that you're trying to probe, it may not be as sensitive as we wish it would be.
But, yeah, the majority of them seems to be from cats and fleas and maybe other biting insects. We've had some rare cases where we think patients got it from other kinds of insects. I also had a patient years ago who got Lyme disease from a horse fly bite while jogging on a trail in a completely non-risky area.
In general, it's certainly possible. And Dr. Breitschwerdt published a paper on at least one family case, which was, I would say, a real worst-case scenario. I've had somewhere close to 10 patients over the years become pregnant either before, during or after in infection. And often, we would look at the cord blood at the time of delivery for evidence of Bartonella. But to my knowledge, all of these offspring have done okay.
I think that while it may be prevalent maybe – and who knows if it's actually how transmittable it may be that way, it hasn't been studied. But if it is kind of prevalent, we just don't know is the bottom line. But there might be a way where the developing baby in the womb might have some sort of intrinsic resistance if you will. Maybe not an immune resistance. But it doesn't – I don't think it's always necessarily going to result in a problem.
But the more sensitive the testing gets, the more we're going to begin to notice this. And maybe we'll see some correlations. You kind of wonder about some of the childhood epidemics, like autism and PANS. And not that I'm saying that at all. I'm not saying that those are caused by this. But you kind of wonder. You kind of wonder if there might not be a better answer to why some of these children are the way they are.
[00:19:52] SCOTT: Yeah. I mean, that leads to my next question. We talked about the fact that OCD, anxiety, rage, a lot of these mental-emotional symptoms can be associated to the neurovascular aspects, to the inflammatory aspects. You talked about the host response. So is there an autoimmune component to Bartonella?
And, for example, in PANS, which is also kind of an autoimmune encephalopathy, there is some thought that Bartonella can be a trigger for PANS. What are your thoughts on Bartonella and its contribution to autoimmunity and then Bartonella as a contributor to PANS?
[00:20:29] DR. MOZAYENI: I think whenever you have a persisting infection, you will not specifically stimulate the immune response, which will result in the production of lots of antibodies. Some of which are specific. Some of which aren't. So you kind of get this multi-specificity of an antibody response.
And so, these antibodies could potentially target and trigger receptors, block neurotransmitters from receptors. I think it's entirely plausible that a chronic persistent infection can trigger an auto antibody. And I think autoimmune disease is just a simplistic placeholder that we have for something that – for a root cause that we don't fully understand yet.
But one of my earliest research grant proposals when I was finishing up my residency and doing molecular biophysics postdoctoral fellowship was on the multi-specificity of how one monoclonal antibody could be highly specifically recognizing two entirely different antigens. It is certainly known that that happens. And chronic persisting infection does that.
Another example that people may be more familiar with is Epstein-Barr virus. Non-specifically stimulates antibody production by B cells. And then you can get low-level antibodies to different kinds of infections when someone has Epstein-Barr. And I think similar things can happen when you have Bartonella. The titers usually aren't high. They're low-level. Just an overactive immune system can sort of "spin-off" different kinds of antibodies that may be so-called auto antibodies.
[00:22:00] SCOTT: You have written about the potential role of Bartonella in osteoarthritis. I know Dr. Ty Vincent has talked about a potential autoimmune component of osteoarthritis. How often do you think Bartonella is a potential underlying cause of osteoarthritis? And are there other degenerative conditions that people who might otherwise identify as healthy might experience that could be caused by Bartonella?
[00:22:26] DR. MOZAYENI: I think it would be important to study these. We reported in one case that individual had a highly asymmetric hip arthritis that was a little bit early before that person's age to have that. And so, we, as a team, thoroughly analyze that tissue from that hip. And that individual was noble and stoic enough to insist that they did not want antibiotic therapy before the hip replacement because we didn't want to contaminate the science. If you can believe that.
And then, frankly, that is the standard of care for hip replacement. No one's testing people for Bartonella before they do hip replacements. Hip replacement was done and the person's tissues were extensively studied. And there was an extensive amount of Bartonella found at the immediate – in the bone just immediately under the cartilage mostly.
And so, it fits with the biology of osteoarthritis because there are what we call subchondral cysts that form under the cartilage that we need to now consider could potentially be from Bartonella. Again, we publish one case study and that's not enough to move the dial on how patients should be evaluated or treated.
But I would say, if someone has an atypical arthritis and there's a history of Bartonella, this needs to be considered. I think that that is an interesting example and a model perhaps of what other potential damage or chronic persisting infection with Bartonella can do.
[00:23:55] SCOTT: You talked about the potential impact to collagen when Bartonella is present. What role do you think Bartonella may have in hypermobility syndromes, Ehlers-Danlos, craniocervical instability, other collagen disorders? And have you worked with a patient that had hypermobility or Ehlers-Danlos or CCI that responded to Bartonella treatment and that their more structural symptoms improved?
[00:24:24] DR. MOZAYENI: Yes. We actually published a case in which a veterinarian who had multiple extensive flea exposures to fleas around cats as a child and then later became a veterinary dermatologist acquired hypermobility and was officially diagnosed by an Ehlers-Danlos expert as EDS type 3. And this person also had Bartonella long enough that the initial tests were negative for antibodies to Bartonella until about three months into treatment.
But this person developed hypermobility syndrome. And it was a very useful case example that we published. Because as I treated this person, the high probability resolved. And then the same Ehlers-Danlos expert reevaluated this person and said that it had resolved.
Meanwhile, expert doctors who she was seeing in prestigious Healthcare institutions were telling her that it was genetic even though she was trying to explain to them that she wasn't born with this. We all have a lot to learn. Better to be curious than judgmental.
[00:25:36] SCOTT: I'm surprised – you know years ago we didn't hear about SIBO. And, I don't know, six or eight years ago we weren't talking about mast cell activation. It seems like in the past few years, the Ehlers-Danlos Syndrome, the hypermobility, those things. Whether it's because there's more awareness or there truly is a higher incidence, it seems like that's kind of the area where I'm hearing a lot of people now dealing with these hypermobility, and Ehlers-Danlos, and CCI, and a lot of those types of conditions. I think it's hopeful that you had, at least in this one person, a reversal of that condition through the treatment of Bartonella.
We know that Bartonella can also impact the autonomic nervous system. That it can be a contributor to dysautonomia. Maybe to POTS. How commonly would you suggest that Bartonella could play a role in those that are dealing with POTS?
[00:26:26] DR. MOZAYENI: I would put it the other way. I think POTS is relatively common in Bartonella. But how often you'd see Bartonella in POTS? I strongly suspect you would probably see some sort of chronic inflammatory process. Maybe chronic infection in POTS.
A blood vessel has two determinants of elasticity. One is elastic and the other one is related to the tone of the smooth muscles. I think when you have inflammation, it can affect the tone. But also, if there's abnormality in the collagen metabolism, it may also affect the elasticity.
Generally, patients with high probability syndromes are more prone to POTS. This is something I've heard from patients who've been to POTS clinics where they've been told that. Yeah, hypermobility and POTS is I think a risk factor for POTS. But POTS, I think, is related to inflammation.
And so, one must look for and be on the quest for finding the underlying inflammatory or infectious cause. These inflammatory conditions affect the microcirculation. So they can potentially create a wide variety of symptoms including – and so, if they affect the blood flow of the sympathetic and parasympathetic nervous system, then you can see why it would create a dysautonomia and/or POTS.
[00:27:45] SCOTT: We see a lot of people in the media these days talking about famous people that are now dealing with multiple sclerosis. Can Bartonella play a role in neurodegenerative conditions like MS? And does it potentially play a role in demyelination of the nerves?
[00:28:04] DR. MOZAYENI: What we know about MS is that it's a kind of focal inflammatory and demyelinating condition in parts of the brain. And so, you kind of wonder, "Well, if you had a small vessel inflammatory or infectious process, could it cause something like that?"
I attended a talk once by an MS expert. And when I posed this question, it was answered with almost a semi-humorous, "Oh, are you – it sounds like you're on my grant review committee." So I think that that has been a prevailing idea.
In a neurologist, like psychiatrists, and they take the same board exam. And so, they don't get that much exposure and training in metabolism and in medicine and infectious disease. And I think the testing hasn't been good enough to really discern that. I think that that question is going to become a lot more clear as the better testing spreads.
I also would add, we've had some patients who had been diagnosed with MS. What we do doesn't interfere with the treatments they're receiving. And I always encourage them to stick with their treatments and not kind of digress and think of like a Bartonella or infectious strategy as a substitute for their standard treatment.
But what I can say is in the patients who've had MS who I've seen and have Bartonella and are treated, I don't recall any patient with MS who progressed. I do recall a few who recovered partially or fully. In my view, I think it's very plausible. And I think more research should be done on looking at chronic persisting infections in MS.
[00:29:51] SCOTT: We know that one of the hallmark Bartonella symptoms is sore soles of the feet particularly first thing when getting out of bed in the morning. Listeners were asking about Bartonella as a factor in burning pain in the feet. And is there a specific type of Bartonella that's more prone to creating those burning symptoms? And is that more of a neurological manifestation or more of a small vessel inflammation manifestation?
[00:30:21] DR. MOZAYENI: Yeah. As you said, it's a common symptom. I think all it takes to get heel or foot pain is for some Bartonella to get into the connective tissue. There's a strong connector tissue wall, two pockets of fat, that provide the padding for our heels and the soles of our feet. So if those pockets of connective tissue are inflamed, you're going to have some pain there.
Then the related question is how much of it is neuropathic pain? Meaning that if the nerve is sensitized by having been injured, the normal sensations could potentially be painful. We call it dysesthesia. I have one patient who, when she rubs her thigh, her outer upper thigh, she gets foot pain. There's some sort of cross circuit, short-circuiting there.
One of the things we're now doing is looking at – we've developed a way to look at skin biopsies for nerve demyelination and can actually image it very nicely with the high-resolution microscopy that we do.
So since we now can image a nerve demyelination and quantitate it, the next step will be for us to look at use probes for Bartonella, Borrelia, Babesia on the same tissue to see how they're involved in the demyelination of the peripheral nerves.
And once you – I've always wondered how people with demyelination get more pain sometimes. Nerves travel in a bundle both in non-myelinated and myelinated nerves travel together. The non-myelinated nerves are carrying a pain sensation mostly. And the myelinated carry touch sensation. There are fast fibers. So they carry touch and vibration. Whereas the other, the slow fibers, are the non-myelinated ones. But they travel together.
We have images of the demyelination in nerves right next to the non-myelinated nerve and pain fibers. And so, once you see that, you realize that the electrical signals could potentially be short-circuiting from the myelinated to the non-myelinated fibers and causing pain.
And that's why any kind of touch or pressure could potentially trigger a pain response also in someone who has demyelination. That's one of the common features you see in chronic inflammatory demyelinating polyradiculopathy.
[00:32:58] SCOTT: Rifaximin has been used in the treatment of SIBO. We know that rifaximin is related to Rifampin, which is used in some cases to treat Bartonella. I'm wondering if you have any thoughts on whether or not rifaximin working in those with SIBO could be the result of it addressing Bartonella and Bartonella potentially being a player in SIBO? And then related to that, if Bartonella has the potential to impact the vagus nerve, could this be another way that Bartonella could contribute to SIBO-like conditions? How much do you think Bartonella might contribute to GI conditions?
[00:33:37] DR. MOZAYENI: That's an excellent and well-thought-out question. We actually – for about a period of a year or more, I was hoping that documenting and treating SIBO might be an easier fix for patients who are symptomatic from Bartonella. And I found it was very prevalent in Bartonella. It's almost universal. I started trying to treat for SIBO and then repeat the testing. And more often than not, I would see either no progress or worsening of the gases on the breath test.
Then I work with Dr. Sam Rahbar in Los Angeles and we looked at the broader issue of patients with tick-borne diseases and the prevalence of SIBO. And again, it's quite prevalent. And the working theory that I have is that the gut immune system is affected and may be suppressed by Bartonella. Bartonella gets into all the tissues of the body. And therefore, that might be the reason why people have SIBO. It could also be because of antibiotic use or who knows? But there is a strong co-association with it.
And patients with Bartonella often have difficulty starting clarithromycin, which has kind of may speak to or give us some ideas to why Rifaximin might be helpful. But that's supposedly not very absorbed. But if you have leaky gut, maybe some of it is absorbed. I think there's a strong connection between Bartonella and tick-borne diseases in general. And we actually published about this connection a while ago.
[00:35:14] SCOTT: Mast Cell Activation Syndrome has emerged in the Lyme arena quite prominently in the past maybe seven or eight years. Do you think that Bartonella can be a trigger for Mast Cell Activation Syndrome? And do you find that stabilizing the mast cells is an important component of treating Bartonella?
[00:35:33] DR. MOZAYENI: Great question. I think you've been following along on my work pretty closely.
[00:35:38] SCOTT: I do.
[00:35:40] DR. MOZAYENI: Mast cells are an immune cell, a multi-functioning immune cell and part of a kind of a primordial immune response. They tend to be found in the highest densities in the body in areas that are more likely to be exposed to microbes.
We have them on basically the openings in our body have – the surrounding surface skin is highly dense with mast cells. In the gut, the highest density is at the end of the small intestine where it's near the colon. And the second highest is in the duodenum, where it receives the contents from the stomach. The foods we eat are not sterile, of course. And so, you have the small intestine kind of being protected at both ends by a high density of mast cells.
And so, if it's major role and the primordial immune system was immune – was surveillance and antimicrobial effects, then it makes sense that infections could trigger it.
Also, hot foods like capsicum-containing foods can also trigger mast cells. And some people have allergic-type reactions. There are also alternate pathways for the activation of these mast cells that are not IgE mediated using a receptor called MRGPRX2.
And so, they're these sort of classical and non-classical activation pathways. And so, these mast cells and certainly – are expected to play a role in infection just knowing what we know about their biology.
Now in patients who have mast cell activation, the testing so far seems to show relatively high prevalence of these infections. But how they're exactly related, we don't know. Much of the inflammation that is created is then responsible for more symptoms. Like histamine causes anxiety. Histamine causes blood vessels to be leaky. Histamine has a lot of different side effects in metabolism. It might even compete with adrenaline for metabolism. And also, depends on methylation for metabolism.
There is a big interplay. And I think under-appreciating that everyone has mast cells. And to some degree, with an infection, they're going to get activated whether you call it MCAS because it's severe or if it's mild and it doesn't qualify as MCAS. There's still mast cells and they're still getting activated. I think antihistamines or mast cell therapies in general can be very helpful at least in managing symptoms.
And also, Dr. Theoharides talks about – and I think it's a really interesting insight and observation that mitochondria in mast cells go to the surface and they release their nucleic acids into the circulation. And because mast cells are the mitochondria – our mitochondria are more genetically related to rickettsia, it creates almost a systemic inflammatory reaction.
If there was a ready test for looking at circulating mitochondrial DNA, that might be an interesting thing to look at. But to my knowledge, you don't have a clinical lab test that does that at this time. I think there's a big interplay. And for that reason, also, I think if you treat even with antihistamines, you can help a lot with the symptoms that patients have.
[00:39:09] SCOTT: What is the connection between Bartonella and Morgellons? And how significant of a role do you think Bartonella plays in those dealing with that conditions? It's appeared for many years now to me that the treatment interventions that are focused on Bartonella seem to make the biggest shifts for those that are dealing with Morgellons. I wonder what your thoughts are on that potential connection.
[00:39:31] DR. MOZAYENI: I don't see much Morgellons. And so, I can't really speak to the connection. But I have heard others say that they feel that they're correlated. But that's a tough condition to kind of address for a lot of different reasons. So I don't see a patient in my practice who have that.
[00:39:49] SCOTT: Something tells me that if you had some of those patients with what you're doing, they probably would do fairly well. I guess we'll see.
How has COVID changed the infectious disease landscape? And in those with long COVID, are you seeing more activation of Bartonella infections either in those that maybe never knew they had it? They were essentially asymptomatic. Or those that maybe had it and were previously treated but now have become symptomatic again resulting in potential benefit in revisiting the treatment of the Bartonella?
[00:40:26] DR. MOZAYENI: Yeah. When COVID started, I felt that it was – for those of us who've been dealing with Bartonella particular and generally these persisting infection issues, it just seems that the biology – the pathobiology of the disease seemed to be very familiar, have many familiar components.
I immediately saw it as a vascular inflammatory disease. I recognized it. I immediately saw this as the infection causing platelets to become increasingly activated and cause hypercoagulation syndromes and blood clots. And there's precedent for this too. Because even with influenza, for a few months, there's a higher risk of stroke. And one of the theories about why stroke has a higher prevalence in the spring is because people experience winter viruses and their system is hypercoagulated.
Ever since I've been in private practice, I've always put patients on low-dose aspirin after influenza for three months. And so, to me it was a very obvious pathology. But the severity of it is what – and the suddenness of it is what made it different.
Even now, if a patient has had COVID no matter how mild it was, I usually insist that they take some aspirin. Usually not even a low dose. But like a standard dose. One daily for three months. The risk factors for vascular events goes up substantially for six to 12 months after COVID infection. Most of the disease pathology relates to hypercoagulability and inflammation of the microcirculation.
And right away, we knew. And at the time, I had just started – lucky me. I had just started my term as a vice president. I was trying to get the group to see the advantage that that the skill set of our clinicians, of the advantage of the clinician skill set in managing patients with COVID. But we also had the important question of what's it going to do to our patients?
And so, I'll start with my experience first. None of my patients throughout the period of COVID have been hospitalized for COVID. None of them have died from COVID. When they had COVID – some of them had what you might call long-term, long-haul. But usually not more than four to six months.
At the same time, we were developing our molecular probes where we could both – we could image the blood and other tissues. Along the way, I looked at blood smears from COVID patients. I looked at a skin biopsy from someone who happened to get it. The biopsy collected and sent when they had COVID.
And we also had – and we also were beginning to look at some specific protein probes. Purely on like a research basis. What we found is that the spike protein messenger RNA is expressed in platelets, which explains why they get sticky.
Using some of our molecular probes that were in development at the time, we noticed that the patients who had been treated for Bartonella were doing quite well. When they got COVID, they felt bad again. You might have called them long-haulers. But when we retested them, they had more – they had new evidence for kind of recrudescence of Bartonella in their bloodstream. But then what was interesting is they also responded much more quickly. It was easier to get them well again than when we first started treating them.
[00:43:50] SCOTT: Yeah. I mean, and that could come back to your earlier comment about the terrain, the immune system versus the bug. Because at that point, when they're needing re-treatment, you've already addressed a lot of other aspects that are more terrain and immunomodulatory.
[00:44:05] DR. MOZAYENI: Exactly. And their immune system is recovered to the point where – and this is why I think that you can be healthy without fully clearing Bartonella. The goal is to – it's practical to get you well again and healthy enough to pursue your life's activities and dreams.
So I think as long as you suppress the microbes long enough for the health of the host to come back, you're reestablishing homeostasis. And the goal isn't necessarily to eliminate it completely. And frankly, even if we thought we did, how would you prove that? You can't put every square micron of the body under a microscope and look at it. Even if we have the best available tests, you'll never be able to know for sure if it was fully cleared.
This is a really fascinating topic. But for the most part, I think maybe – in a way, maybe infections were protective of the patients because they didn't – they already were dealing with chronic inflammation. The immune system saw COVID and said, "Yeah, I know inflammation. Maybe I won't react with it so strongly because I'm already dealing with some."
And so, in a way, maybe having these somewhat immune suppressive bacterial infections maybe mitigated the severity of the disease for some of the patients. It's just a theory. But maybe that's why a lot of them did well. Maybe it's because I put everyone on vitamin D. Who knows? But it's been really fascinating to see the research and all of that emerge.
And the with the most amazing thing, and this is the silver lining in COVID, is that it's given everyone in a world an appreciation of chronic persistence symptoms after infection. And the debate comes down to do you think the virus or the bacteria persist? Or is it just the inflammation?
But in patients who died of COVID, they've found active virus, viable virus, in every part of the body. This is a study done at NIH, my pathologist there. And maybe the treatment of – maybe the appreciation of what COVID can do at least helps patients with chronic persistence bacterial infections and get appreciated, at least acknowledged for the fact that they can have persisting symptoms. And then it's still down to a question of is it persisting infection or just the inflammation.
[00:46:36] SCOTT: And, hopefully, COVID brings then more attention, more research dollars and things into exploring potential therapeutic interventions that might then very possibly work well for those people also dealing with chronic Lyme disease and other similar conditions.
I want to talk a little bit now about testing. You are an expert in this realm what is the state-of-the-art testing today for Bartonella? What labs would you generally consider in a patient to explore the potential presence of Bartonella? And how sensitive is Bartonella testing today? Or otherwise stated, how often might a patient have Bartonella but still get a false negative test result?
[00:47:18] DR. MOZAYENI: Yeah. So I'll press this part by saying a few things. One is I was there from the beginning before Galaxy Diagnostics was started. And I continue to work with them as medical directors. So I have that conflict. And then I started working or in the realm of microscopy and imaging using molecular probes. And we created a lab called TLab that I co-founded. And so, I have both experience. But I also have what some would call conflicts. I just want to let everyone know that.
[00:47:48] SCOTT: Your conflicts are welcome here.
[00:47:53] DR. MOZAYENI: And what I find ironic in the healthcare field is like the more you do, the more conflicts you get. And so, I kind of wonder how that's all going to pan out in terms of some of our people who had more experience may have more conflicts. But then their talks don't qualify for CME credits because of conflicts. That's a whole frontier in and of itself.
And then we have – I also have to – there are a lot of labs in this arena. So I also have to be careful that I'm not being any way pejorative toward other labs or what they can do. And then, finally, what we can say about these tests is regulated by the FDA. Claims are regulated. This is a kind of nuanced conversation for all of these reasons.
But let me start with the general principles. When you want to test for an infection, and this is a general trend across the whole field of infectious disease, you want direct molecular evidence. When you have a patient in the ICU who is septic, you have a lot of bacteria in the blood. Therefore, you have a lot of DNA and you can run a sequence analysis and fit the result of what is hurting the patient.
There are labs that do that and they cater more toward the acute severe infection market where there's a lot of like acid in the blood. And so, you don't have to worry as much about sensitivity. With chronic persisting infections, the levels might be low. And so, the methods that you might normally rely on like PCR and sequencing may not be as sensitive as you would like. Because it depends on having enough nucleic acids present.
Every type of test has its advantages and disadvantages. And really, this is what it comes down to is the practitioner and ultimately the patient need to have a really good understanding of what the caveats are with every kind of test. Because every test has caveats.
The caveats of – and we can break them down one at a time. Roughly speaking, there are two classifications, two categories of tests. One is our direct test, which will give you direct evidence of the infection. And our indirect tests, which look at things like antibodies, host response. Those are indirect tests.
The direct tests are what you really want. But then you want them to be sensitive and specific so that you can use them to monitor treatment. In general, I also rely on a set of different tests from different labs because I want the labs to kind of be consistent with each other. If I'm going to be hanging my hat on one diagnosis, I want it to be supported by different angles of testing. And, yes, there are always exceptions.
So let's start with the fact that, in Bartonella, 20% of patients will not have antibodies if they've had Bartonella long time. And usually, in children and teenagers, you find the antibodies, they haven't been alive that long to have lost their antibodies through immune suppression.
But an adult who's had it maybe more than 10, 15, 20 years, 20% may be negative for Bartonella antibodies when they first present. And then – and sometimes it takes three to six months of treatment for you to begin to see the antibodies develop because you're getting rid of this immunosuppressive bacteria.
A lot of the – so not only do you need to know the caveats of testing. You need to know the caveats of the disease that you're testing for. Chronic persistent infection can cause immune suppression that you don't get antibody being produced. And then during treatment, you can get antibody and antigen being produced in the roughly equal amount. And when the two are equal, they precipitate out. And for a window time during a treatment, you may lose the antibodies because of immune precipitation not because you cured the infection.
In general, you want to work with a molecular test, direct detection test. So what are those typically? Those are FISH tests. They're PCR tests. And perhaps the the urine nanotrap antigen test. Because you're detecting the OspA protein. And OspA is from plasmid-derived gene. But that plasmid is highly conserved across Borrelia species. Potentially, you might see it in various Borrelia. Not just Borrelia burgdorferi.
And then you have indirect tests again, which are antibody tests. And then the most indirect are the cytokines. Evidence of inflammation. Briefly, VEGF, vascular endothelial growth factor. Because Bartonella infects the endothelium, it might cause the increased production of vascular endothelial growth factor. But the vessels may also become leaky from inflammation in histamine. So the VEGF levels may drop.
We did a study and published a paper on altitude sickness that we did with the military. And we found that when patients – the patients who became altitude sick had higher VEGF levels before they went to altitude. And that the VEGF levels climbed in all patients went to altitude in all subjects. But then it really crashed and those who became altitude sick.
I think the example there is that if you have a leaky endothelium due to inflammation, your VEGF are produced in high amounts in patches throughout the vascular system and may also leak out of the vascular system. In my experience – and I get asked this question a lot during meetings. But in my experience, VEGF levels are not reliable as to monitor or diagnose Bartonella because they fluctuate a lot.
PCR in theory, in the test tube, in the lab can detect one copy of a nucleic acid. The PCR test for COVID were rated based on the number of virus particles they can detect. And some of them were sensitive to the point where they could detect a few virus particles on a swab.
When it comes to looking for bacteria and/or Babesia, you're dealing with biology much more and you're dealing with a clinical specimen, a blood specimen. And in that mix of tissue, there are a lot of other nucleic acids and there's a lot of interfering factors. Even things as simple as iron in the blood.
PCR techniques are getting better all the time. And Ed Breitschwerdt at NC State has been developing some technology around digital PCR that is finding its way to improve versions and iterations of PCR at Galaxy Diagnostics. Digital PCR is kind of the newer, more sensitive way to look for it.
And then you have this whole other class of testing where you're just trying to visualize using molecular probes like FISH probes. FISH has other limitations. But it doesn't have some of the PCR limitations. Sometimes it can be more sensitive.
When you use a FISH probe, you want to identify a target and you're trying to find either an RNA target or a DNA target. And you're trying to come up with the right sequence of the probe to bind it. And then you build layers of detection on top of that that allow you to very sensitively detect it.
What we said, "Hey, the most prevalent nucleic acid in a microbe is going to be the ribosomal RNA." Because that's what the bug uses to make all of its proteins. If we target the ribosomal RNA with a probe, then we should have much more nucleic acid of that bug than we would if we targeted some gene of that bug.
Then how do we improve the sensitivity? Well, then, we could do a kind of a sandwich assay where there's a probe and something that binds that. And then there's a fluorescent marker that binds that. And with fluorescence, you get an even more sensitivity.
And then what's the best way to look at that? Well, that is using an advanced microscope system like the confocal laser microscope. We kind of stacked the odds of this whole system toward sensitivity. But trying to use a molecular probe, which we would hope would give us good specificity as well. That's the methodology we developed. And it's helped me a lot in managing my patients because I can personally see that I can use it as a guide to see how I'm doing with the treatment.
[00:56:35] SCOTT: And is that sandwiching type approach that you're talking about here, is that what's available now through TLab? Or is that a combination of doing testing with both Galaxy and TLab?
[00:56:48] DR. MOZAYENI: I do a combination of testing especially when you're dealing with a new kind of lab test. And to do that, we had to do all kinds of validations. But it's something that we're going to continue to improve upon. And I'm looking for ways of improving it. One of the things we're starting to look at is doing sequencing. But sequencing isn't as sensitive intrinsically. A lot of it depends on how much nucleic acid you put into the sequencing reaction.
This is kind of the frontier right now. And I don't want to make any claims for it here. What we're trying to do is optimize the performance characteristics of the tests. But also, I rely on sets of tests across track one another. The best-case scenario is if you have a positive FISH result, and you have serology, and you have clinical symptoms that all fit, then that's great.
Sometimes you get – as I said, you get false positive antibodies to other things like Borrelia. So it's important to realize that you might get a false positive IgM on a Borrelia western blot. It's usually IgM. not IgG. And again, IgM in a chronically ill patient has even less value than IgG. Because IgM is an acute-phase antibody. And chronic inflammation tends to create more IgM in general.
I think I would say stay tuned for the papers and ongoing publications to where we could publish and show people the performance characteristics. I will leave it at this. I developed it because I needed a way to monitor patients.
[00:58:24] SCOTT: With TLab and this advanced microscopy work that you're doing, my understanding is that it's not limited to Bartonella. And I could be wrong. But I believe that the discussions increasing around Babesia odocoilei came from some of the work that you were doing putting tests together for Bartonella. So if that is in fact true, can you tell us a little bit about Babesia odocoilei? Is there anything that is done differently relative to treatment of that specific type of Babesia? And are there some other maybe lesser discussed pathogens that you're kind of seeing come up in this work that you're doing with TLab?
[00:59:07] DR. MOZAYENI: A few things here to unpack. One is that the probe methodology and the platform, the imaging, can potentially be done with any nucleic acid probe target. But what's important is that you know the biology and then you understand whether your probe can reach your target. And then you try to validate that the target you're finding is actually really what you think it is.
But in general, if we knew everything – and I had an expert on the biology of any particular microbe or I should say target more generally. It doesn't take much to order a new probe. The hard part is to validate it and to understand its performance characteristics. That's just a general statement.
And, yes, we can do testing for home infections like Babesia and Borrelia. The Borrelia target is different. It's messenger RNA for the OspA. And the Babesia and Borrelia targets are the ribosome RNA.
Now let's talk a bit about Babesia. It's been known to my colleagues and patients that – and generally, the medical community, that Babesia duncani is a West Coast Babesia. Babesia microti is an East Coast Babesia.
So then we've had this dilemma where we see antibodies to Babesia duncani – when we have a Babesia patient in the East, we almost always see Babesia duncani antibodies and not Babesia microti antibodies. I'd say 80%, 90% of the time. Why is that?
If you're exploring different hypotheses, one of them is that Babesia microti has always been thought to be more self-limiting. And maybe it doesn't have a significant persisting form. Babesia microti tends – we believe it doesn't sequester fibrin as much. Whereas the other Babesia do.
Typically, the patient we think has Babesia clinically will have positive duncani serology or not at all. I'd say it's roughly 50-50. And then they will – depending on – you might get a positive FISH result or you might not.
Now we became interested in odocoilei because, talking to labs that do tick testing, we learned that one of them was finding Babesia odocoilei in 25% of the deer ticks they were testing in the Northeast.
And so, we said, "Hmm, if it's that common of ticks, it's got to be – there's somewhere among the patients." So we set out to develop a probe for it. And that's a challenge because the probe sequence that you target can sometimes pick up other babesia as well.
But clinically, we're not good enough to know which treatment to give to which kind of Babesia. There aren't customized or customizable Babesia treatment protocols because we barely had a good one in the first place. There are standard ones that seem to get people better. But the question is whether they work long-term. You know, like the classical azithromycin atopic one protocol.
Then after we started working on the probe, there was a publication regarding a few patients in Canada who had Babesia odocoilei. And then there's another paper a little bit later on finding it again using PCR in ticks. Finding Babesia odocoilei.
So the publications on it are very, very limited right now. But nevertheless, our probe – with our probe, we've been seeing positive results often. And I don't think the target is capable of detecting odocoilei because it was – we chose a sequence that was a little bit – a target sequence that was a little bit more specific to odocoilei. But when you make these probes, you always have to remember that if there's a little bit of a similarity to another Babesia, you may take that up too.
I would say that the probe developed was intended to not miss odocoilei. But the no probe is going to be 100% on target. In some others, you can't identify the microbe from the result of a FISH test because there can be a few nucleic acid differences and the probe can still bind.
[01:03:33] SCOTT: One of the things that I just wanted to point out to listeners was you referred to Borrelia as a co-infection. And so, I think most people traditionally think of borrelia as Lyme disease and then the co-infections of Bartonella and Babesia. I think you and I are probably aligned in thinking of more the Bartonella as maybe the bigger player and the Borrelia and the Babesia as co-infections. Unless I misunderstood your comment there.
[01:04:00] DR. MOZAYENI: It's hard to say because there's a whole thing in medicine called referral bias. Maybe patients get screened for Bartonella before I even see them. I don't want to say that this is – to do this right, you have to do a broad epidemiological study and look at prevalences with a really good diagnostic tool.
We're finally at the point where we potentially could do something like that or like from a technology point of view. But then who would fund them to look broadly?
I just kind of think of all of them as co-infections of each other. But the big thing, the big lesson I've learned is that what most people call Lyme disease isn't necessarily Borrelia. And so, in a way, we're kind of – I think the two sides of the contours are kind of growing closer in terms of how they see the problem. Like one side seeing evidence of persisting inflammation. The better diagnostics are going to help inform how often those patients have persisting infection.
I'm very confident that the science is eventually going to resolve the controversy. And controversies occur in the absence of good data and information. Otherwise, it would be a done deal. And then the only thing left would be how do we optimize the treatment protocols? I think, because we have not had good molecular diagnostics, I don't think any of these protocols have been adequately optimized.
[01:05:26] SCOTT: So let's move in then to our treatment conversation. If you're looking at a patient that has Bartonella, and Babesia, and Borrelia, how do you make a decision on where to start? Are you generally starting more with Bartonella and Babesia and then working with Borrelia later? Are you doing all three of those simultaneously? Is it going to be unique based on the symptom presentation of the patient? What's your thought process there?
[01:05:54] DR. MOZAYENI: So like many of us, we get patients who have been to many other practitioners. And so, they're beginning to develop an idea of what may be going on and what is the dominant thing. So there's always this sort of initial thinking that kind of guides or maybe even colors the initial set of tests. And oftentimes they've had some tests.
What I usually do is just try to initially think about what might have been missed, right? If they had a screening test for Bartonella or they did have an antibody test that was negative, I kind of think about, "Well, can we do a better antibody test? Or can we –"
And so, I try to just make sure that they get the benefit of the best set of tests available. It's the same way like if a gourmet chef was choosing the best ingredients for something, we want to know the tests well enough to know which labs to use for each test and how they come together to help support a diagnosis.
I don't automatically test people for all three. I think if there's a history that's consistent with borrelia, then I would look extensively for that also. Just the set of things I do. But it depends a bit on what they have. And I don't kind of automatically look at all of them.
If they end up on treatment, a lot of times antibiotics that you might use for, say, Bartonella would end up treating borrelia. So you don't always have to have identified every infection. But you try to as much as you can.
[01:07:28] SCOTT: Dr. Zhang has reported on the potential of Daptomycin, Lopinavir, methylene blue, Pyrvinium pamoate, Clotrimazole, a whole number of different things that could potentially be helpful in the treatment of Bartonella. And some of those being more active potentially than what was historically used in Bartonella treatment in the past. My question is what pharmaceutical interventions are you finding most helpful in your patients? And what are some of the agents or tools that you feel hold the most promise?
[01:08:01] SCOTT: Dr. Zhang just certainly did open up a lot of new possibilities. And as a clinician trying to carefully navigate what treatments, not just work, but how they're tolerated. And then I tell all clinicians, like try to get really familiar with the drugs you're using and their side effects. And you need to know them really well.
What has frustrated me is that patients just see some in vitro results and they assume that it's going to work for them clinically. Even though we have a new set of things we can study, people have – and understandably, out of desperation, want to jump the gun and do everything on the list.
I actually don't do that. I try to hold back and I try to focus and just find the simplest protocol that moves the dial forward. And what I find is that if I do a good job diagnostically, then the treatments are – they seem to be more effective and the outcomes are better.
I'm always trying to like rein in the different sets of things. And I'm bombarded constantly, nd it's really the bane of this job, is that you constantly get questions of like, "What about this? What about that?" And so, it can completely obstruct and occupy the time that we need in a patient appointment.
I call this a dichotomous agenda. I feel like I'm getting interviewed by the patient about what do I think about all these things. Instead of what's the right thing for them right now? And it's understandable. But it's anxiety-driven. And yet, I think it's very counterproductive when you're on a diagnostically on a good footing and what you're trying to do is just focus on how to get things started.
Right. I feel like that whole thing is best left to kind of the internet or whatever than trying to discuss every one of these things in an appointment. And this gets even worse as they're getting created because it's not getting better right away. They're automatically going to be searching for other treatment options.
I just want to caution everyone that these are in vitro studies. And having been involved and have worked with some people at the NIH and elsewhere when I was a medical student, there's a whole – this is kind of a quote from one of my mentors. He said, "There's a whole science that has yet to be developed around how to extrapolate in vitro to in vivo clinical treatments."
People underestimate how much it takes to do that. Really, there's a huge leap to say that something that works in vitro is going to work in vivo. And as I said, that's a whole science that I think has evolved a little bit. But it's still an emerging science. Just because you see something work in vitro doesn't mean it's going to help you.
On the other hand, I often feel like giving up on trying to guide the treatment at all. Because what if I'm wrong about what the right treatment is? What if methylene blue is a magic bullet? So I kind of feel like – and this is where I've migrated my practice to just doing the best I can do to give them a diagnostic really accurate consultation and kind of tell them where they are and what I suggest that they do. And then leave it up to them and the treating physician to just try different things. But I try to explain to them that they need a good way to monitor how well things are working.
[01:11:26] SCOTT: And so, in those patients where you still are involved in treatment, is Clarithromycin and Rifabutin still some of the leading tools that have been consistently helpful in your experience? Or are those not your go-tos anymore?
[01:11:40] DR. MOZAYENI: Yeah. For Bartonella, I drew a lot initially from the experience of veterinarians who are treating Bartonella. And in general, they were saying that as if there was more azithromycin resistance than clarithromycin. And there were some other reasons why I thought clarithromycin would be better. I started working mostly with that.
The veterinary community still uses quinolones drugs related to Cipro, like Levaquin. And I think those are potentially very problematic in a patient with chronic joint pain. Because what if they get bad Achilles tendonitis? And so, I am also worried about the long-term side effects of those drugs when they are used long-term.
So then to that, we started adding Rifampin. So one of the protocols that pre-existed for Bartonella was – for a cute cat scratch, the textbooks say use azithromycin if you feel like you need to. But you probably don't really need it. And it'll resolve on its own with or without azithromycin within two weeks.
Well, potential, yes. The cat scratch goes away. The lymph nodes might still be enlarged and tender. The testing has not been there to show these people that it did not go away. It just went dormant.
One treatment that's been out there as an alternative to that has been azithromycin and doxy, or doxy and Rifampin. In the veterinary experience, Dr. Breitschwerdt has lectured on this and said you can soak – this is a quote, "You can soak a dog in a tub of Doxycycline and it will not touch the Bartonella." I generally don't feel that doxy is an effective component of Bartonella treatment.
But doxy is an anti-inflammatory. It inhibits the mitochondrial ribosome. So it can be anti-inflammatory. It can appear like it's treating the infection. But more likely than not, it's only treating the inflammation. That's out there. Some of my colleagues have used Bactrim and Rifampin.
I was using clarithro to which I would then add Rifampin. And here's a problem that very commonly people run into. A patient who's healthy who takes Rifampin probably won't experience much in the way of side effects, for example, in treating tuberculosis, tuberculosis exposure.
Rifampin and Rifabutin also induce the liver to metabolize hormones faster. So they'll accelerate the metabolism of cortisol, estrogen, testosterone, et cetera. So a patient who's adrenally fatigued from chronic illness will do very poorly because of cortisol depletion when they're starting on Rifampin.
And if it's killing off the Bartonella, it also creates inflammation, which requires higher cortisol level. If they're already fatigued and you're giving them inflammation and depleting their cortisol, then you're creating quite a mess by adding Rifampin.
One reason I like clarithromycin is it does sort of the opposite. It actually slows down cortisol metabolism. But in the end, I think the Rifampin wins when you add it. And so, patients who get on Rifampin, they really do need a much better adrenal support even to the point of using a very low dose of physiological dose of hydrocortisone when they get on a Rifampin
And then I run into this whole other thing where, of course, they're going to go search the side effects of Hydrocortisone. And they come back and tell me that they won't do it. They're afraid of it. All of that stuff. And it comes from a complete lack of proper information. And it's information – I call it information poisoning. Because the physiological dose of hydrocortisone is actually vital for life. Your body makes cortisol because you can't live – if you don't have cortisol, you won't make it to 48 hours.
So they're arguing with me over a life vital hormone replacement therapy because they're reading about the side effects of mega doses of steroids in patients with persisting infections who are not diagnosed and treated correctly.
[01:15:32] SCOTT: Yeah. I mean, I would say that in many years now of observing and talking to people, that hydrocortisone is probably one of the more common needle movers that makes people feel significantly better.
[01:15:45] DR. MOZAYENI: Yeah. And pretty quickly. The adrenal insufficiency. And it's not adrenal failure, which is why they pass the standard adrenal failure tests. There's a low-dose adrenal stimulation test developed at Emory. It published years ago that hardly anyone knows about that would look at marginal adrenal insufficiency.
But a chronically ill patient that has been under a lot of stress and they do have not only marginal adrenal insufficiency, their level of illness actually requires higher levels of cortisol. Normal cortisol in a sick patient still can be too low for them, which is why the saliva testing isn't very helpful.
The body adrenal gland makes somewhere between like the baseline and five times the baseline under extreme stress. When your body's under extreme stress, a 2X level of cortisol isn't enough. That's where it gets to be very clinical. And then it's hard to do. There's more conversation. There's more inaccuracy. There's a potential for overdoing it, underdoing it.
But if you underdo the cortisol, people will have amplified symptoms and you'll think they're not getting better when it's just the fact that they don't have cortisol. So it's messy. I think if someone's going to get Rifampin, they and their doctor better really understand this issue.
And then the other thing they run into when you're treating Bartonella is you get a breakdown of the Bartonella. You get immune reconstitution response, which some people would call a Herxheimer. But you also get neutrophils and neutrophil depletion. And sometimes you get a liver enzyme elevation. And then that really freaks everyone out so.
In the middle of Herxing and seeing these lab changes, which are an indication that it's working, the treatment is abruptly discontinued out of fear. I've seen that more often almost – it almost always is the case if I get a patient who went down that road with another practitioner. But their Rifampin was stopped in the middle of the treatment.
The issues with Rifabutin are similar. Rifabutin, Rifampin has a volume of distribution of 0.9 liters. Meaning that a certain amount of Rifampin takes almost a liter to dissolve. Rifabutin is a pharmaceutical term. Volume of distribution. For Rifabutin, that's 49 liters. So it's way more tissue-penetrating.
And some of the patients with neuropsychiatric symptoms, they really seem to meet the Rifabutin for better tissue penetration. Maybe blood-barrier penetration to really see the benefit. But here's a whole other rub with Rifabutin is that it's been associated – clarithro and Rifabutin have been associated in literature and in patients who are sick and were on both with eye inflammation, uveitis. But Bartonella we know can cause uveitis and it can get into the eye.
When Rifabutin is used and it gets into the eye tissue, it can kill the Bartonella that are in the eye and create Herxheimer reaction of inflammation in the eye. This is a paper that needs to be written because the ophthalmologists are aware of chlarithro / Rifabutin as a combination therapy causing a potential complication for uveitis. But that paper never mentioned the possibility of an underlying Bartonella infection that they didn't know about.
[01:18:58] SCOTT: Meaning it's not necessarily a side effect of the drugs. It's the result of the drugs being effective in treating something that they're not considering.
[01:19:09] DR. MOZAYENI: Exactly. Before I give that to any patient, use Rifabutin. I mean, I give them a referral letter. Make sure they go the ophthalmologist. Get a baseline exam and make sure they're plugged in to an ophthalmologist who's ready to stand by and treat them immediately with eye drop steroids and whatever. And if they do that, then it's a manageable problem instead of a major complication. We take a lot of precautions to make sure that's done properly.
Now, enter COVID. Healthcare system wasn't in great shape before COVID broke it. Access to care is bad. Therefore, we want to minimize the dependency of patients as much as possible on acute emergent care.
And I also have found that since whether it's COVID or heightened inflammation from vaccines or whatever, I don't even want to get into it. But we're seeing that their uveitis is harder to control when patients get it. I've backed way off for the time being on using Rifabutin except in really unusual circumstances.
[01:20:13] SCOTT: We touched on the concept of Bartonella persisters. We touched on the fact that Bartonella may contribute to, or create, or participate in biofilm communities. How does that influence the treatment? Are the Clarithromycin/Rifampin, Clarithromycin/Rifabutin combinations, are they effective at getting at some of these persisters?
Do we need to be introducing some of the enzymes? The Boluoke, the Lumbrokinase, Nattokinase, those kinds of things as well to deal with biofilms? How important is considering persisters and biofilms in treating Bartonella successfully?
[01:20:52] DR. MOZAYENI: It's kind of there are stages of treatment. And if you open up those biofilms too quickly too soon, people can get sicker. I view it as a way to potentiate the treatment and help it come to a better closure. And I think the enzymes kind of can cut both ways. The typical patient with these issues needs to draw heavily on principles of integrative and functional medicine while also understanding the microbes and getting to the root cause.
Groups of doctors who are doing more functional and integrative medicine are getting more interested in the infections, which they acknowledge they know very little about. And within the community of doctors treating the persisting infections like Lyme disease, they're doing better at learning integrated and functional medicine.
You have to apply all these different principles to get patients well because they have a lot of a system disturbances, function disturbances. And using enzymes to improve the circulation I think is ultimately pretty important especially for certain microbes that sequester fibrin, the fiber analytics could be important.
Thyroid management is important. I mean, there's so many aspects of it. Then we touched on the adrenal issue, which is important. I think it's a matter of like getting started with something. Getting a little bit better and then adding something else. See if you can get even further.
You have to work very closely, as you know, with these patients for a long period of time and cover all the different angles that can be operating. And this is also why these patients don't – you can't use very simple clinical trials to study them because they – by the time – the longer these infections persist, the more disruption they have in their various functions.
And so, you can't just take a patient with chronic Lyme and just give them an antibiotic and expect a positive result. Because all these issues are not being addressed.
[01:22:42] SCOTT: So with the treatment approach that you have currently, is there a place for methylene blue? Or is that something that you've not found necessarily necessary?
[01:22:52] DR. MOZAYENI: I don't know. My patients who come in on it, I don't – I don't try to get them to stop. I don't really use it. I studied the biofilms of some patients who have been on it. And what's interesting is their biofilms are light blue already without any staining in the laboratory. But it's a light blue.
We know that methylene blue is getting into biofilms. We know it can be a stain of biofilms. To me, it's intriguing that it can stay in the biofilm and be an antimicrobial. It might have a useful role in treating a biofilm community of organisms. But I think it's one of those things where there's some really intriguing in vitro data. But how well that experiments to clinical, we don't know.
And, plus, at higher doses it raises serotonin levels. Maybe people feel better because of that. Again, any of these treatments, if you haven't been tracking with molecular diagnostics and direct detection, you really don't know what you're doing with the treatments.
[01:23:58] SCOTT: I was interested in Dr. Zhang's findings about Pyrvinium pamoate, which is more of an anti-parasitic. I know there's been some discussion in the Lyme community for years around some feeling that Ivermectin was helpful in dealing with Bartonella. Wondering if you find any of the anti-parasitics having a place in the Bartonella landscape.
[01:24:20] DR. MOZAYENI: I am not very familiar with this. And I have not used it for Bartonella. There was a paper on Ivermectin in Babesia. But it's a limited in a study where at least they were able to treat it in a mouse. I think, potentially, for Babesia.
But of what we think of these things being effective for and a lot on like what if – like for example, like Flagyl was in use to treat Borrelia cyst forms. But guess what? It's an anti-Babesia drug. If you've been misdiagnosing someone with Borrelia and they really have babesia and you think that they're not getting better because they have Borrelia cyst forms and you give them Flagyl and they Herx. And you pat yourself on the back and think that you succeeded in the diagnosis. But what you've really done is not realizing that Babesia was there and you just hit it with something that caused a Herxheimer reaction.
So we can talk all day about all these different ideas. But what really is going to clarify the way forward is molecular diagnostics and direct detection. And that applies to any treatment, hyperbaric oxygen. Anything at all that's out there, if people are not tracking the results with molecular diagnostics, they can't really – they can't based on just symptoms and know how well something's working except in the very long-term.
If you do something and symptoms go away after however long it takes, then you can probably conclude that whatever it was and responded to that. But you still don't know what it was you treated. And if you don't know what it was you treated, you've not developed a science around what you're doing either for yourself or for medical science in general.
To me, something scientific is where you actually from – you know enough detail that from the response you can use that insight, that knowledge, that experience and test the study result to guide better your choice of a treatment for the next patient. And trying things randomly and seeing people randomly get better doesn't help you learn anything or about how to improve your treatment for the next patient.
[01:26:26] SCOTT: I want to touch just briefly on antibiotic resistance from two different angles. You had previously discussed an antibiotic-resistant form of Bartonella from the Gulf Coast area. So wondering if there's any updates on that. And then more broadly, antibiotic-resistance, I think people sometimes think that if they're taking an antibiotic and they have Bartonella, it's going to become resistant. Is that common within a single individual? Or does it take longer periods of time within the broader population for antibiotic resistance to be something of concern?
[01:27:01] DR. MOZAYENI: That particular case is in the lower Mississippi. A case we later realized was someone who's just not making antibodies to Bartonella. And yet, the molecular evidence was there for the Bartonella. This person ultimately got well but it took a very – and did really great. But it took much longer to treat. And I think it was because there was immune blind spot. It might have been congenital.
But this person never produced antibodies to Bartonella. So I don't know that it was a resistant strain. I think the host immune response wasn't there or was compromised.
In terms of resistance, people ask me this a lot. I have not ever seen any convincing evidence that this has happened in any particular case. On the other hand, someone's not responding. You tend to consider another strategy. Was that really resistance? We don't know.
The culture systems for Bartonella are difficult. The conditions are difficult. The NC State and Galaxy developed a BAPGM culture medium. And so, potentially, if to the extent that replicates an in vitro clinical environment, you could potentially use that to do sensitivity testing.
With microbes that are hard to grow, we call fastidious microbes, you – it's hard to get a good laboratory in vitro model to look at antibiotic resistance. Again, there, I'm optimistic that over time we're going to start with genetic sequencing to identify the gene changes that are associated with resistance. And then we might see a strain evolve from one that wasn't to one that is resistant. But I haven't seen it be a practical issue at least that I could tell.
[01:28:45] SCOTT: If Bartonella is not commonly eradicated, is there a place for herbal or other natural treatment options longer term? I know there's been conversations around Japanese knotweed and Cryptolepis and a number of other natural tools that can be used. Even allicin. I believe has been discussed. There's a number of companies that have A-BART and BAR-1, 2, 3, and Formula BART, and DesBio Bartonella Series and all of these kinds of tools. What natural options, if any, have you found beneficial for patients? And might it make sense after an antibiotic course to then introduce some of these things for longer-term support?
[01:29:26] DR. MOZAYENI: Yeah, good question. I think it's promising. Because Rifampin and Rifabutin we're kind of difficult and compliance also was difficult. For example, I have one patient who was going to college. He had a really hard time being compliant with the treatment. Not that he didn't want to. It just wasn't working.
I cut him a deal and I said, "Look. Right now, would you at least agree while you're in college to take every day one allicin, one oregano oil, and one curcumin extract? Turmeric." And I said, "I don't know what it's going to do. But I'm about to give up on you. But I don't want to. So we just do this." He said, "Sure. I'll do that." And he's stuck with it.
This was like January of '21. And he said – and I didn't talk to him until like October. When we talked in October, I tested him for Bartonella with a molecular test and it was negative. He said that as he started that, he started feeling better and better. By the time spring came around, he was feeling pretty good. And he had a summer break where he said he felt great and normal. First good summer in years.
And so, that was a lesson to me that sometimes all you need to do is tip the scale, suppress the Bartonella enough for them to regain their health. And I'm always looking for antibiotic-free ways of doing this.
So then there was a little modification to the protocol, which is maybe start with that or start with Clarithromycin if they're not too sick maybe. Or if they are too sick, maybe you just start with the natural antimicrobials then maybe work with Clarithromycin because that has a good safety profile. And then work with the herbal antimicrobials for a while and then see if we really need to add Rifampin or Rifabutin. Again, I'm trying to come up with ways that are more naturopathic where we can really avoid using prescription antibiotics.
[01:31:23] SCOTT: And it sounds like there are some cases where you've been able to do that and that the pharmaceuticals were not necessary in all cases.
[01:31:32] DR. MOZAYENI: No. They're chemicals. And natural products are not chemicals. So they tend to be better tolerated if you know they work. To me, what's really intriguing is to be able to combine molecular diagnostic testing with natural antimicrobials.
[01:31:45] SCOTT: Beautiful. Coming back to the earlier conversation we have about the host response and immune modulation, when we're working with Bartonella, is there a place for transfer factors, low-dose immunotherapy, maybe homeopathy? How do you incorporate some aspect of treatment that is more focused on the host response rather than the bug itself?
[01:32:10] DR. MOZAYENI: Yeah. I am aware of all those things. I don't do those things. And patients still get better. They might do better if I did some of that. I just have a hard time.
I'm trained as a medical scientist. I'm scientifically very progressive. But that same training also makes me very careful and generally skeptical. I think all of those things, there's – in fact, I think one of the areas where medicine could advance is to have a better simpler pathway to validating off-label treatments for all sorts of things.
There's natural product and a lot of these things don't have the deep pockets that the drug development has like from a big pharma company. But we need to identify better which subgroup would really benefit.
One thing we're about to – we have launched at ILADS is what we call a Big Data Initiative, where we're going to start tracking data from – you know about MyLymeData.org. That's patient-driven data. I've spoken with Lorraine Johnson, others, they all see that it's very important for us to get similar data from practitioners.
I've been spearheading that project at ILADS because what you want to do is formulate a large registry where we can see through the collective experience which of these things really works. Because we need to get out of this sort of empirical opinion-based, opinion-driven thing where like if we have any – with any one of these things that you mentioned, if we have 10 consecutive patients who responded who had – and we know the profile of that patient, then we can start looking for the profile of that patient and the next patient that comes along and maybe suggest the same treatment.
This is the vision for big data solving. This complexity of what about all these different treatments that are out there? I find it frustrating that a lot of them make claims around this indirectly. Not officially. But sometimes in the way the product is named, they make you think that it has some validity for a certain purpose. And it may or may not. But it makes one skeptical.
[01:34:22] SCOTT: There's a lot of conversation these days in the Bartonella realm around gallium and also around SOT or Supportive Oligonucleotide Technique. Wondering if you've seen either of those helpful in your patient population.
[01:34:39] DR. MOZAYENI: You know, I hear the same things. I think it's anecdotal. I could tell you this, FISH probes are oligonucleotides. There ae specific tests taken in a laboratory to make sure the FISH probes reach their target. And those conditions are not achievable clinically.
I think that that it's an emerging science. And how the SOT works, it's the same set of issues. It's like how do we know that a patient would benefit from it? And with many patients, it's just like, "I tried everything. I might as well try this." They're just out there trying stuff. And any outcome to them is is preferable to feeling badly. I just find it's the same set of issues around any new emerging idea or treatment.
Now maybe they're cytokines that oligonucleotides can bind, which might reduce the disease severity. Maybe it's helpful in terms of a host response issue. But we have to be careful with the way we use the word treat, right? What are we really treating? The better the diagnostics get, the better the data set, the better we can target all these treatments.
This is the same science that helps pharma companies develop specific drugs for specific treatments is having a better idea of who would benefit from it is very important. And right now, to me it just seems a little bit random.
[01:36:07] SCOTT: What's the average duration of treatment of a Bartonella patient? Maybe what's the longest that you've treated? Do some people need ongoing treatment? What kind of is the end game for patients that are treating Bartonella?
[01:36:23] DR. MOZAYENI: The end game is to get their life back. If you suppress the microbe enough, I think they can do that. As I said, even if we clear the blood completely and it's not detectable and all the antibodies eventually resolve, how long would it take to get there? And what are the relapse rates? I think they all need some sort of monitoring. Maybe after treatment, they need to be on a low level of herbal antimicrobials.
But the end game, and I think is achievable, is that if you suppress these infections adequately and manage the functional medicine aspects of the patient's care, they can regain their health.
[01:36:57] SCOTT: Totally agree. One of the observations that I've had a lot of times is people dealing with Bartonella and they have five cats in their home or other pets that could also have Bartonella and bring in fleas and so on. So I'm just wondering, if someone's treating Bartonella and they have dogs or cats, should they have their dog or cat evaluated and potentially treated for Bartonella as well? And is treating a pet for Bartonella is difficult as treating a human?
[01:37:27] DR. MOZAYENI: What I tell patients – and by the way, there's a whole – you probably know, there's a whole movement called One Health where it's mostly driven by the American Veterinary Medical Association to kind of help everyone appreciate that animal health is intimately tied to human health.
Historically, we've said, well, we don't really know if cats can transmit it. There's some evidence that one infected kitten could transmit it to another just by playing with it. I'll just tell you a short story about a case. I had a patient with rather severe condition. We suspect that it might have been a tick-borne.
They had a cat who had risk factors. I referred them to a veterinarian who was very tuned in and in fact was a leader in our state in this whole issue of tick-borne diseases. The veterinarian was out. The partner saw the cat. Asked if the cat had symptoms. They said, "No. Not really." And she said, "Well, we don't test cats that don't have symptoms."
So then I called my colleague and said, "Hey, your partner said this." And she's like, "Well, yeah, that's our guideline." And I said, "Well, the patient is really sick. I really need you to test the cat."
They drew some blood from the cat. And then this gets back into how do you test the cat? What's the best place to do it? Now Galaxy does veterinary testing too. I think that's where the specimen went. So they came back and said the cat's positive. I said, "Well, are you going to treat the cat? Because I don't want my patient to get sick again." And she said, "Well, we don't treat healthy cats."
And I said, "Well, what about this One Health business?" She said, "Well –" so I checked with Ed Breitschwerdt and he's like, "Yeah, these are the veterinarian experts who are writing these guidelines. We know the guidelines need to be updated. We hope to be able to do that."
And I actually communicated with this particular veterinarian. And so, we had a conversation. It's like, "Yeah, the guidelines could be better. But that's how they are right now." So even I working with a veterinarian who really understood the problem better than most in our own local area couldn't get the cat treated.
When they drew blood from the cat, I asked, "Holly, can I get a tube of blood from your cat to look at?" So we looked at it. Again, as a little like one-time, one-off research thing. And I could not believe how much how positive the test was. And it was so much more than I had seen in any patient that I thought that maybe we made a mistake on the test. We just let it go at that point because we really didn't – we weren't a veterinary lab and I wasn't the veterinarian and I wasn't treating the cat.
What happened the next time I saw the patient is I asked about the cat. And she said, "Oh, it died." I said, "Oh, you're a healthy cat , asymptomatic healthy cat, highly positive for Bartonella died." I said, "What did they die of?" She said multiple organ failure.
I think, honestly, it may be hard and challenging. I mean, you could try to treat the cat. Like veterinarians will use the quinolones, the floxacins, I think because animals don't live as long as humans. Maybe it's safe for them. I just don't like to use those in human patients.
You might find your way to getting a cat treated. But it is the veterinary guidelines that they're not to be tested if healthy and not to be treated if healthy if positive. The safest thing you can do as a patient is to give up your cat for adoption if you really think that's the source. Or you just minimize your contact. Make sure they don't get the fleas. The risky ones are the ones that go indoor-outdoor. Because when they go outdoors, they're hunting rodents. But with a good flea collar, which, technically, if they were indoors, you really don't need. But I think the big risk factor is when they're indoor-outdoor cats. Because they can get Bartonella from hunting rodents and not necessarily from fleas.
And when cats have Bartonella, their blood levels of Bartonella are 500,000 times higher than when a human or a dog gets Bartonella. They are a much more dense reservoir of Bartonella when they get it probably because they're naturally evolved to carry Bartonella with less of a severe impact on their health.
[01:42:01] SCOTT: Before I ask my final wrap-up question, listeners were interested in who you view as the top research scientist, obviously, besides yourself and Ed Breitschwerdt, that we should all be following in the Bartonella space?
[01:42:18] DR. MOZAYENI: Great questions. A lot of good work being done. Even the CDC has been doing some work. The University of Davis, Dr. Bruno Chomel, has been doing a lot. They've been in California. They've also been studying Bartonella and other animals. For example, the seals out in San Francisco Bay. For a while, a lot of them were dying of heart valve infections from Bartonella for unclear reasons.
We did a webinar once through One Health that was international and we had – within 24 hours, I think we had 180 registrants as soon as registration opens. Globally, people in the public health world are very aware of potential and problems associated with Bartonella.
From a public health point of view, you've got the potential for other forms of Bartonella like Trench Fever. Dr. Raoult … in France has been studying Bartonella quintana, Trench Fever. Excellent German physicians like Dr. Dehio who has been publishing a lot of the basic science and the mechanisms for intradermal spread and transmission and the immune suppression that you can get from Bartonella. It's not easy to find these labs. Just go on PubMed and search for Bartonella.
[01:43:31] SCOTT: My last question is the same for every guest, and that is what are some of the key things that you do on a daily basis in support of your own health?
[01:43:40] DR. MOZAYENI: Well, I should be doing a lot more like most of us. I can speak a little bit to how this work on Bartonella and tick-borne diseases has changed what I do and some of the things that I either do or avoid.
I don't golf often. And I'm not that good at it. But I enjoy it. But when I go golfing, I don't chase the balls anymore into the tall grasses. I just spend a few extra bucks on golf balls that I will lose. When I walk on trails, if there's tall grasses growing toward the trail or – I try to not touch the grass because that's where the tick hangs out.
If I go out even around my own house and I'm going into some grasses, or brush, or ground cover that's a little bit higher, I'll spray down – at least from my knees down, I'll spray down my pants with some either DEET-containing or some other insect repellent.
One time I went out to the front of our house where there was just some very loose and well-spaced landscaping shrubbery and mulch just to show an electrician how to change what light I want to change. And, literally, it was a minute or two, I came back and I had a deer tick behind my knee I just happened to touch and feel and remove.
You just can't be too careful. Most of us on the East had a mild winter. I think the ticks are particularly bad this year. I'm more conscientious about just insect bites in general. I used to not worry much about a mosquito bite. I now see the mosquitoes for its potential to transmit other organisms. If they can, in other climates, transmit malaria, why can't they potentially transmit Babesia? We just don't know enough. I've just been you know more and more careful.
Growing up, I was outside all the time. When my kids were growing up, I thought it's a shame they don't spend more time outdoors like I did. And now I'm really thankful that they didn't.
Food-wise, I've become more aware of the importance of low histamines. Fresh usually means lower histamine. Anyone can get less inflammation if they're watching their food and eating fresher foods.
The microbes, the sugars – the sugars will like feed the microbes. So you want to avoid those as much as possible. I used to eat medium or medium rare. And now I eat it medium well. And we've known that meat carries infections. But I think it's really important to cook your food well. But I still eat sushi.
[01:46:10] SCOTT: Dr. Mozayeni, this has been such a great conversation. I joked at the beginning about emailing you on Thanksgiving the last couple of years. And I truly am thankful and grateful for your time today, for this conversation. But much more than that, just thankful for the difference that you make in the world, for the person that you are in helping so many people to improve the quality of their lives. I really think you are a hero and are tremendously contributing to our world. Thank you so, so much.
[01:46:44] DR. MOZAYENI: I really appreciate the sentiment, Scott. We would have done this sooner. But it's been – saying I've busy has been a big understatement. I tell people like if I hit a known – honestly, what I would be doing. Yes, it's very gratifying. But you don't end up doing this because you planned for it. You end up doing it because you find patients coming to you and need the help.
You put all your effort and your energy into trying to figure out how to do that. And to me, that's really the – to me, that's the biggest difference on the two sides of the controversy, is like, "Now if you don't think you can help, that's okay. But just say so." And hopefully, with better data and better testing we're all going to crack the code and make it all more of a medical science as we go forward.
[01:47:30] SCOTT: Totally agree. Again, thank you for all that you do. We appreciate you.
[01:47:33] DR. MOZAYENI: Thank you so much, Scott.
[01:47:34] SCOTT: To learn more about today's guest, visit Translational Medicine Group at TMGMD.com. That's TMGMD.com. TMGMD.com.
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