Archive for the ‘research’ Category

Persistent Borrelia Infection in Patients With Ongoing Symptoms of Lyme Disease

http://www.mdpi.com/2227-9032/6/2/33

Persistent Borrelia Infection in Patients with Ongoing Symptoms of Lyme Disease

Marianne J. Middelveen 1, Eva Sapi 2OrcID, Jennie Burke 3, Katherine R. Filush 2, Agustin Franco 4, Melissa C. Fesler 5 and Raphael B. Stricker 5,* OrcID

Published: 14 April 2018
(This article belongs to the Special Issue Lyme Disease: The Role of Big Data, Companion Diagnostics and Precision Medicine)

Abstract
Introduction: Lyme disease is a tickborne illness that generates controversy among medical providers and researchers. One of the key topics of debate is the existence of persistent infection with the Lyme spirochete, Borrelia burgdorferi, in patients who have been treated with recommended doses of antibiotics yet remain symptomatic. Persistent spirochetal infection despite antibiotic therapy has recently been demonstrated in non-human primates. We present evidence of persistent Borrelia infection despite antibiotic therapy in patients with ongoing Lyme disease symptoms. Methods: In this pilot study, culture of body fluids and tissues was performed in a randomly selected group of 12 patients with persistent Lyme disease symptoms who had been treated or who were being treated with antibiotics. Cultures were also performed on a group of ten control subjects without Lyme disease. The cultures were subjected to corroborative microscopic, histopathological and molecular testing for Borrelia organisms in four independent laboratories in a blinded manner. Results: Motile spirochetes identified histopathologically as Borrelia were detected in culture specimens, and these spirochetes were genetically identified as Borrelia burgdorferi by three distinct polymerase chain reaction (PCR)-based approaches. Spirochetes identified as Borrelia burgdorferi were cultured from the blood of seven subjects, from the genital secretions of ten subjects, and from a skin lesion of one subject. Cultures from control subjects without Lyme disease were negative for Borrelia using these methods. Conclusions: Using multiple corroborative detection methods, we showed that patients with persistent Lyme disease symptoms may have ongoing spirochetal infection despite antibiotic treatment, similar to findings in non-human primates. The optimal treatment for persistent Borrelia infection remains to be determined.

healthcare-06-00033-g001

Figure 1  (A) Top left:  Darkfield microscopy of blood culture showing live spirochete and spherules.  Magnification 400x.  (B) Botom left:  Fieterle silver stain culture fluid from Case 10 showing live spirochetes  Magnification 1000x.  (D) Bottom right:  Typical dermal filaments from patient with Morgellons disease.  Magnification 100x

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For more:  https://madisonarealymesupportgroup.com/2017/08/25/sleeper-cells-the-stringent-response-and-persistence-in-the-borreliella-burgdorferi-enzootic-cycle/

https://madisonarealymesupportgroup.com/2017/08/18/drexel-prof-lyme-persists/

https://madisonarealymesupportgroup.com/2016/12/21/dr-zhang-on-persisters/

https://madisonarealymesupportgroup.com/2017/05/10/chronic-lyme-disease-a-case-definition-at-last/

https://madisonarealymesupportgroup.com/2018/04/13/chronic-lyme-post-mortem-study-needed-to-end-the-lyme-wars/

LD & The Brain – Podcast With Dr. Bransfield

Episode 23: Lyme Disease and the Brain

Cindy Kennedy, FNP, is joined by Dr. Robert C. Bransfield, M.D., F.A.P.A., who discusses Lyme disease and the brain, including the connection between Lyme disease and mental health and how Lyme disease and co-infections can cause cognitive impairments, sleep disorders and various psychiatric issues.

Dr. Bransfield is a graduate of Rutgers College and the George Washington University School of Medicine. He completed his psychiatric residency training at Sheppard and Enoch Pratt Hospital. He is board certified by the American Board of Psychiatry and Neurology in Psychiatry. 

Dr. Bransfield’s primary activity is office-based private practice of psychiatry with an emphasis upon treatment resistant cases. In addition, Dr. Bransfield is the Associate Director of Psychiatry and the Chairman of Quality Assurance at Riverview Medical Center in Red Bank, N.J.

He has held teaching appointments at Hahnemann Medical College and Eastern Virginia Medical School. He has taught in many settings to physicians, mental health professionals and the public. He has performed research, and has a particular interest in psychopharmacology, a unified theory of mental health and illness, the link between microbes and mental illness, Lyme and other tick-borne disease, violence, and the link between microbes and violence.

Dr Bransfield has authored and co-authored a number of publications in peer-reviewed literature, other medical publications and books. He has held a number of administrative positions for various organizations involved with a number of health, mental health and community related activities.

Dr Bransfield has been active in political advocacy on a national, state and local level. He has appeared on network and regional television, radio and various publications.

Transcript of Episode 23: Lyme Disease and the Brain

https://madisonarealymesupportgroup.files.wordpress.com/2018/04/lwle23.mp3

Cindy K.: This is Cindy Kennedy your host and we are on the Living with Lyme today. We have the great honor of having Dr. Robert Bransfield with us. He is well versed and considered an expert in the area of Lyme and other tickborne diseases and the treatment of neuropsychiatric symptoms. He’s active in political advocacy on national state and local levels. He’s also been an author and a speaker. He has notable publications in peer-reviewed literature. We’ve had a lot of technical issues today but we finally have him and I’d like to welcome Dr. Bransfield. How are you today?

Robert B.: Good Cindy. It’s good to be here.

Cindy K.: Oh it is. It is. I’m so thankful because your expertise goes beyond the scope of anything I can imagine. I’m sure the information that you and I are going to talk about are going to be very, very helpful to a lot of people. So, my question to you is, we know that Lyme is certainly underdiagnosed and undertreated. I think for most healthcare professionals that a psychiatric presentation is highly unlikely and they wouldn’t consider Lyme and all the symptoms that go along with it. Can you give your experience on that?

Robert B.: Yes. What happens is many of the doctors who have capability, experience, credentials for treating early infectious disease invariably have very little training in psychiatry. So, you may find that patients go to infectious disease doctors, rheumatologists and they haven’t had much current experience with psychiatry. When I ask them, “What’s your training in psychiatry?” They may say that 40 years ago they did a one-month rotation in a state psychiatric hospital and that might be the extent of their psychiatric training. So, they have difficulty seeing the connection between the physiological process that occurs that impacts the brain that then results in psychiatric symptoms.

Cindy K.: You know Dr.-

Robert B.: You can tell their training may go back to the old Freudian theories and it’s hard for them to understand the physical basis to the mental symptoms that we see.

Cindy K.: Dr. Bransfield, hold on one second. Don’t speak so close to the phone because it’s hissing a little bit. So, I’m sorry. I’m going to go back to the point where I asked you, what is your experience with these doctors not understanding that there can be psychiatric presentations?

Robert B.: I think many doctors just lack the training in understanding the physiology as how mental illnesses are caused by brain inflammation. Many doctors who treat earlier cases of Lyme disease have knowledge in infectious disease but they don’t have knowledge or extensive knowledge in psychiatry. Some have only had maybe one-month rotation decades ago when they were in medical school and have not kept current with current physiology, understanding as how brain processes can cause mental symptoms. So, I think that’s a big problem is the disparity, the gap between infectious disease in psychiatry.

Cindy K.: Is there any certain type of patient that comes to you with particular psych issues that would prompt you to immediately think “Geez, could this be Lyme?”?

Robert B.: Yes. The more common cases often it’s progressive. So, the mental symptoms keep getting worse and a particularly common case would be someone who is partially treated for Lyme disease. The partial treatment may be enough to help some of the … or major part of musculoskeletal symptoms, but not enough to help the cognitive and the neuropsychiatric and some of the neurological symptoms. So, that’s the case. It can go under the radar for diagnosis since it’s not your migratory arthralgia, your type of presentation that most people would recognize Lyme disease.
So, this typical case is someone who’s symptoms keep getting worse with time and you give a treatment that works for a while and then they keep getting worse. It’s a combination. It’s a multisystem illness and you have to look at all the different ways it presents and every patient is all but different but you see invariably fatigue, multiple cognitive impairments, multiple psychiatric symptoms, anxiety, depression, irritability and sleep disorders and then neurological symptoms, neuropathy. So, it spans almost every system in the body.

Cindy K.: Do certain co-infections exaggerate psychiatric symptoms or would you see a particular psychiatric symptoms more often with say babesia?

Robert B.: So, invariably when we look at the more severe psychiatric cases we find co-infections. It may be that when someone has Lyme alone maybe that’s not as bad. When co-infections are present, it’s not an additive effect. It’s an interactive effect. So, when you add to infections, they interact in a way that can magnify the degree of severity. So, we babesia, bartonella, mycoplasma and these are opportunistic viruses. Probably other things that we aren’t really testing for chlamydia, rickettsia, ehrlichia, the more severe cases often have multiple co-infections.

Cindy K.: Now you said I’m thinking to myself and we had a discussion a little earlier about someone that I know having an onset which looks to be Parkinsonian and of course that goes along with when your body is not really … it’s breaking down in some sorts that you get depression. So, when you’re talking out psychiatric issues, is it something that’s kind of insidious that leads you? Is there a rapid onset of say dementia that would trigger some sort of a concern because maybe it’s not in the family, maybe again it wasn’t something that … it just came up very quickly. Is that something you’d see?

Robert B.: Sometimes. I think the more common case seems to be someone who has infection more in the body there’s an immune reaction. Rather than adaptive immunity and the infection’s gone, you see with these infections persistent inflammation and autoimmunity and disease progression. Now there are some cases where … these are the cases I think where there’s infection in the brain rather than infection in the body provoking the immune system which causes mental symptoms. The cases where there’s clear infection in the brain, those can appear as a more rapidly progressive dementia case. We used to call these pre-senile dementia but this can be a relatively young person and it’s a very rapid downhill course even with a fair amount of antibiotics that may just slow it down. These are very difficult cases.
Fortunately, they’re the minority but they’re very tragic when we see them and invariably on an autopsy then you can find borrelia in the central nervous system, but your average run-of-the-mill cases more rather than neuroborreliosis more Lyme encephalopathy where we have it in the body and it can affect the brain. So, you don’t have to have spirochetes inside the brain to get mental symptoms from Lyme disease. You can have it in the body and has that immune effects and that orders neural functioning because the cytokines and certain antigens from the infection can cause the blood brain barrier and cause mental symptoms. That’s why it can be episodic. Someone can be good in the morning and then several hours later be very impaired.

Cindy K.: I understand that oral antibiotics is not a great way to treat complications that are arising in the brain. It typically doesn’t cross the blood brain barrier. That you need to use more IV or possibly intramuscular injections. Is that true?

Robert B.: Right. If it’s actually in the brain, that might be true although it’s more an issue of how high a blood level you can get with antibiotics. If someone’s GI tract tolerates it, then you may be able to do it with orals and it might be effective. I think you do see more use of orals proportionally now than used to be the case whereas before in the earlier era of the Lyme epidemic, people would start out more with IV. One hesitation about that is if you start with a very aggressive antibiotic treatment, you might get a neuropsychiatric Herxheimer reaction where someone could have an exacerbation of their neuropsychiatric including suicidality. That could provoke a suicide attempt. So, I find it’s often better to gradually ramp up the treatment so that there isn’t too much of a Herxheimer reaction that could be destructive to the patient.

Cindy K.: This is an interesting question and I don’t have an answer. If you’re bitten by a tick that’s infected and it’s on the upper portion of your body, say you found it in your scalp versus something on a lower limb behind your knee. Does that trigger more neurologic per se?

Robert B.: Yes.

Cindy K.: It does.

Robert B.: Yes. There was one study done where they looked at the different quadrants of the body, because some of it’s dissemination through the blood but some of it’s local spread. In part this is why children may have more severe … one of the reasons why children may have more severe symptoms is because their … what happen is a tick would first get on the lower part of the body, work their way up until there’s some constriction. Then they would attach there. So, children are closer to the ground or their brains are closer to the ground than adult. There may be a three-foot trip instead of a six-foot trip to get up the length of an adult. So, when the ticks are attached, more in the head and neck region and that’s a common place where they are attached. You see that in deer also. They could be in the hairline, above the hairline. It does seem they do have more of the CNS symptoms when the attachment is closer to the brain.

Cindy K.: What type of neuro symptoms do children have versus adults? Is there any difference?

Robert B.: Yes. Well, one difference can be they invariably don’t have a reference point of what it’s like to not have symptoms. They don’t know what healthy is. So, if you’re an adult and at the age of 30 you get an infection, you know what you were like before the date of that infection then you may struggle to try to function at the level that you used to be at. So, you know what should be but a child who is developing doesn’t have that reference point. So, that’s a major problem. You invariably see a lot of tantrums, irritability, low frustration tolerance. It can be like behavior problems, obsessiveness, aggressive outbursts, difficulty with school. Some of it, it can look somewhat like attention deficit disorder but it qualitatively is different. There is a difference between Lyme and attention deficit disorder although some of the symptoms overlap.

Cindy K.: I did read an interesting story about a young boy who was very obsessive about being on his bicycle. It just came on very quickly. If he wasn’t eating in school or sleeping, he had to be on his bicycle. They were saying this child is obsessive compulsive. That’s all it is and the mom wouldn’t settle for that. It went on and went on. One doctor finally laid out all the paperwork, went through with a fine tooth comb and did find that he had a tick bite sometime prior and wasn’t treated. When they tested him, he was Lyme positive. They treated him and that compulsion to be on the bike just went away. I find that-

Robert B.: That was the famous case of bicycle boy with Andy Pachner. That goes back 30 years ago.

Cindy K.: Oh it does.

Robert B.: So, that case as a 30-year-old case and that was one of the earlier recognitions of the psychiatric manifestations of Lyme disease. Then that was also published in the magazine in Washington DC and that was included in the case histories. It was around ’87 or ’88 that that was published. So, that’s a 30-year-old case. So, this isn’t anything new to connect the psychiatric symptoms with Lyme disease. This has been around for a while and there’s been expanding recognition with many journal articles. Yet even with that, it’s … so for the rank-and-file doctor to catch on and see that connection.

Cindy K.: That might be a very hard one. Let’s talk about the nitty-gritty, because the vast majority of the people that are suffering are suffering with certain types of problems. I think we need to hear about why these problems are occurring. I’m going to start first with brain fog, that horrible inability to process things, to feel like you’re on your game. It commonly goes with that horrific fatigue. Where is that coming from?

Robert B.: Well bran fog is supported what we call sickness syndrome. Sickness syndrome, you could replicate it and it’s replicated when people have interferon treatment or when they get the cold or the flu and their inflammatory … part of their immune system is activated. So, lupus patients call it lupus fog. Fibro patients call it fibro fog. That fog, the best way to compare it is go take 100 mg of Benadryl in the morning and then go back your daily activities and see how you feel. So, it’s that fog that’s a thought like your brain is sluggish. Now you can see why it’s called the terrible triad. Terrible triad can be nonrestorative sleep, cognitive impairment and fatigue. So, the three can go together.
Now brain fog can be akin to like mental fatigue. Mental fatigue and physical fatigue have some similarities where there’s a sluggishness, the slowness and fatigue in the body is a lack of physical energy unrestored by rest. Compared to exhaustion, exhaustion you ran a marathon and now you’re exhausted because you expanded some energy whereas fatigue you wake up after 12 hours of sleep and you feel like you ran a marathon even though you did not. So, it’s that both cases that lack of physical energy. It’s a very frustrating symptom.
I think overall it’s very hard. People get the symptoms and they wish they didn’t have them. They can’t explain them. They can’t understand them. Their family can’t understand it. Just stop it and everybody wishes it would work that way. Then their doctors don’t understand it. Your insurance company doesn’t want to understand it. It’s baffling but there is a very clear explanation for it. It takes more complicated model and then we can understand it very clearly.

Cindy K.: You can’t just draw blood. See, that’s the thing. You can’t just draw blood that shows this particular issue, can you?

Robert B.: Well, this is a complex disease. You can’t use a simple diagnostic model to explain a complex disease. You have to use a complex model to explain a complex disease. Now it’s not that simple that you could just do one simple test. The reality if you look at the history of medicine, diseases that are simple have all been discovered, well understood well explained. What is left that is still at the leading edge of discovery in medicine are the more complex diseases that require more complex formula. If people keep using the simple “Let’s just do a blood test. If it’s positive, you have it. If it’s negative, you don’t.”
As long as you approach a complex disease in that way, you’ll be going around in circles never understand it, never solve it. You have to shift to a different model and recognizing the full complexity, there may be multiple interactive co-infections, multiple immune reactions and multiple manifestations. Now probably looking forward, there’s more in the way of gene testing and particularly these more sophisticated DNA testing for microbes. As that gradually gets online, I think that we can understand this much better. How you have a mix of infectious agents and then once this disease takes hold, orders what genes are turned on and turn off in our body. Often you’re looking at immune system genes. Then that correlates with the symptoms. That’s the model you need. Anything short of that is futility.

Cindy K.: Right. The other things that people experience are confusion or memory or word find issues. That lack of ability to concentrate or you’re reading something and you’re reading it five times and you still can’t remember. Is that also a process of that inflammation that happens as your body is trying to recover itself from an infection?

Robert B.: Yes. I think you can break it down in a couple areas. One is executive functioning and another is slow processing. Maybe slow processing … I’ll talk about that first. It’s easier to understand. Now think of a computer that has a slow processor. Invariably that’s a white line is more of a white matter dysfunction in the brain. When you do a MRI you see white matter hyperintensities. You see changes with the SPECT scan.

Cindy K.: What does that mean?

Robert B.: So, white matter is more the inside of the brain that has to do with processing. It is making the connections whereas something like Alzheimer’s is more of a gray matter disease where memory content is lost. So, if someone doesn’t remember the thing grandchildren that’s more a gray matter disease, but slowness of processing is white matter. So, invariably one way to compare it is in a Peanuts cartoon where when the adults are talking it’s wah, wah, wah, wah and the person is sitting there and they hear the words but they’re not digesting the content. So, it’s slow processing going in and going out, both. So, if it’s slow that helps.
Often a person can keep up with the conversation. So, like in a lecture hall in school, they’re not able to keep pace and digest the content. They can’t process it fast enough. Think of it like an assembly line. So, that’s going in but also going out. On going out, you can see that because a person’s struggling with word finding problems. You can see how they’re groping to correct, that they’re trying to solve. That type of thing. That’s what you’re seeing.

Cindy K.: [inaudible 00:22:37] I got nervous there. I see that you were trying to replicate what [crosstalk 00:22:42].

Robert B.: That’s why it works. So, it’s obvious and also if you explain something and you talk too fast, a person will just sit there with a blank expression on their face. You can see that they’re not really grasping what they’re saying. They need that slowness and-

Cindy K.: Is that because of inflammation though or do we not know?

Robert B.: [crosstalk 00:23:11] exactly but somehow it’s the connections are slow. Probably invariably inflammation is contributing to that. I first ran into that. I worked in a mental health clinic in North Carolina and there were these loggers that were there. I think looking back a lot of them had Lyme disease. It was a low-budget clinic and the consultation rooms are very small. You’d be in a tiny consultation room looking at someone maybe a foot or two in front of you and you’d say to them, “How are you doing today?” Then they’d look with a blank expression and say, “Who? Me?” A lot of them did this. It was very puzzling why they did that.
We tried to explain it and at the time we never could, but looking back I think the lot had Lyme disease. By saying, “Who? Me?” they were buying time to collect their thoughts. They couldn’t just answer because they weren’t processing fast enough. So, that’s the processing speed part of it. Then the other part is executive functioning. Executive functioning is the capacity to create sustained, monitor, regulate, goal-directed behavior. So, it’s when looking at the cognitive side of Lyme disease, it can be confused with Alzheimer’s. It can be confused with attention deficit disorder. It has unique qualities different from other cognitive impairments. In some ways it has more similarities to postconcussion syndrome.
With executive functioning, it’s hard to plan, prioritize, multitask. It’s hard to work and chew gum at the same time so to speak. Time management becomes poor. It’s hard to keep organized. People make careless mistakes. They [crosstalk 00:25:17] in the refrigerator and the milk in the cabinet. That goes with difficulty multitasking, getting sidetracked.
Then another part too can be the sensory hyperacuity, the excessive sensitivity to sound, light touch, smell, sometimes vibration. So, that there can be the sensory overload and the person deem it very flooded and emotionally react to the dog barking, noise and then they can’t hear themselves think. They get overwhelmed and then they become night owls, because only then can they hear themselves think. Then they stay up at night and they get sleep deprived. The sleep deprivation doesn’t help. So, all those things are a common vicious cycle of the disease progression that’s driven by these conditions.

Cindy K.: Now you just mentioned something that’s real important and we see a lot. My particular first symptom was a sleep disorder. I was waking 17 times that I could count at night but yet on a sleep study the sleep neurologist said to me, “You know what? You’re waking up like 30 times in an hour and I’ve never seen this before.” So, I was never getting restorative sleep. What cause that?

Robert B.: There’s a lot of different issues. Sometimes trouble falling asleep can increase the symptoms. There can be nightmares. There can also be … normally with healthy sleep, you get cycles of deep sleep in the beginning of the night which helps with your immune functioning. Then you get REM sleep towards early morning hours and then you’re recovered. One study looked at sleep patterns of Lyme patients and 100% of Lyme patients had sleep disorders. So, a lot of times one of the first things they attack is the sleep disorders.
Now I’ve also seen sleep apnea. It can be common. You can see narcolepsy with some patients. Cataplexy besides the nightmares. The anxiety and the depression that can be a part of Lyme disease can contribute to the sleep disorders. There’s multiple facets to it. So, it’s often can be … and the pain can be contributory. A person will lie in one position and we’re in pain. The pain interferes with their ability to sleep. So, the nonrestorative sleep when that perpetuates because sickness syndrome is often state where you curl up in a ball and you sleep and your body diverts it’s energy inside.
When that is effective, then it helps you recover, but if you’re never really sleeping, you’re never recovering. Sometimes getting the sleep better is more critical I think sometimes than antibiotics, because you play such in two ways. One is with narrowed immune system and the other is with whatever antibiotic a doctor thinks might work. Who’s smarter, your immune system or us as doctors trying to pick which antibiotic? An immune system is smarter. So, doing everything you can to help the body heal is a first step.

Cindy K.: What type of medicines are best for these people with sleep disorders since they’re so many of them and they affect the brain in a variety of different ways? What have you found to be the best to aid in sleep?

Robert B.: Well, all of your FDA approved sleep meds invariably help someone fall asleep and stay asleep longer, but none of the FDA except for one and that’s [inaudible 00:29:18]. None of the FDA approved sleep meds actually improve quality of sleep. So, by sleeping longer then there’s some improvement. So, there are certain meds particularly a couple of the antidepressants that we know improve deep sleep, sleep architecture. Those are sometimes one of the first things we try to distract them. Remeron, a couple of doxepin so those can promote more that deep sleep that is more critical, but of course you can’t have quality of sleep unless you also fall asleep. So, you want to look at can the person fall asleep, can they stay asleep, do they have an early-morning awakening and do they have good quality of sleep and then you break it down.
For instance, falling asleep is there trouble to turn of your head, is there trouble to calm down your emotions, is there difficulty relaxing your body, is there difficulty actually feeling sleepy and that would determine which approach we would take in treatment.

Cindy K.: We’re also battling adrenal issues and sometimes your time becomes your … you have such a hard time getting up in the morning and getting going and then you’re struggling. Then supper time happens and then all of a sudden you’re revving up.

Robert B.: That goes with the circadian rhythm. The theory there is you get the deep sleep and the deep sleep not only helps with immune functioning, but it also promotes the secretion of growth hormone which is the master hormone and help set circadian rhythm.

Cindy K.: Do you feel the severity of symptoms relate to the length of the time that they’ve been infected?

Robert B.: Yes. One of every occurs although you do see some people who have a very rapid progression of the symptoms. More commonly, when I see the psych symptoms, that’s usually a few years after infection. That doesn’t happen early. You can get brain fog. You can get some of the cognitive impairments earlier but the depression, the panic attacks, the various anxiety symptoms, aggressiveness, those things it usually several years later. A lot of times when people don’t make the connection, neuropathy, that’s often a later symptom. So, even though some people progresses quicker than others, my average patient that I see has been infected 5, 10, 15, 20 years sometimes longer.

Cindy K.: Yes. See, there’s just so much. A lot of people are unhealthy to begin with, because they’ve got other co-infections. I’m sorry no comorbidities such as diabetes or hypertension or cardiac especially as they get older. So, it can get most confusing. So, I do have one other question that I want to ask you. Then, I have a couple of other quick questions. In terms of the vascularity changes that happen, are people with Lyme more prone to have TIA which is a transient ischemic attack?

Robert B.: I haven’t seen that much although that may be more in Europe where there’s some .. one way to think of how Lyme affects the brain is where it’s neuroborreliosis in the brain, Lyme encephalopathy in the body affecting the brain and then the third way can be vascular. It does affect the vascular system. People can [inaudible 00:33:26] a part of that but when people have that vascular form, there’s vasculitis or it’s impacting the vasculature that some people for instance they get aneurysms. So, when they have that vascular form, I think it can but that does seem more common with European strains than what we see here. For some reason, in fact Carolina there’s what’s called the stroke belt. What is it in South Carolina where there’s more that there? You’d wonder is there a local pathogen that may be contributes to some vascular anomaly. Also with vascular disease, you can’t just think of Lyme. You could also think of dental spirochetes. That’s playing a role there chlamydia. So, it’s a number of other infections not just Lyme and looking vascular issues.

Cindy K.: Yeah. No wonder why this is so complicated. Well, I’ll tell you this has been a wonderful learning lesson from you. It’s very complex and we run the gamut of people having the sleep issues, the anxiety, the depression, the anger, the rage that can occur with this. So, again it’s very complicated and thank God for people like you that can invariably look at this at a whole different way. I know that you’re helping other people to understand this and teaching people to be open to this type of psychiatric neuro changes that can happen. So, now we’ve got a couple of fun things. Okay?

Robert B.: Okay.

Cindy K.: All right. So, what ticks you off?

Robert B.: What ticks me off? Okay.

Cindy K.: Got to be something.

Robert B.: I guess when someone has an answer before they even think about your question.

Cindy K.: Okay. I hope I didn’t do that.

Robert B.: [inaudible 00:35:39].

Cindy K.: I hope I didn’t do that.

Robert B.: No. I found that you can … I see relevant to Lyme disease where you think something and someone has like they don’t even think. They don’t process it. They have already made knee jerk answers without really thinking or the context. That’s part of why they end up in the controversy.

Cindy K.: Okay. That’s absolutely true. The second thing. So, I look at it. I had Lyme disease. Now I’m able to be a facilitator for education and that’s basically having lemons and turning it to lemonade. So, what has been your lemonade?

Robert B.: I wasn’t really looking for Lyme. Lyme kept finding me whether I wanted to deal with it or not. Being a doctor, I think it’s been very gratifying to help people and particularly helping people in ways where they otherwise would not have had help before. That’s a lot more gratifying than doing something that’s a rubber stamp assembly line part of medicine that anybody could do. So, I think it’s good to feel that I’ve had some impact on helping advance understanding in a piece of medicine that previously wasn’t well understood.

Cindy K.: I’ll tell you I hope that more people are going to think about this. I think that it’s unfortunate that the Lyme community is small. It’s not as broad. Medical schools aren’t really putting this as part of their education or it is but very limited. So, thank you so much for this talk, this interview. It’s been most enlightening. I hope that everyone out there listening has enjoyed Dr. Bransfield. He’s just super, super knowledgeable. I thank you and I want to say I hope that I meet you sometime soon. Again, thank you. You al-

Robert B.: Okay, thank you.

Cindy K.: Yes. You all have been listening to Living with Lyme another episode. This is Cindy Kennedy, nurse practitioner and I want to encourage you to reach out and subscribe to the website so you can stay connected http://www.livingwithlyme.us. Everybody have a great day. Come back and listen real soon.

 

Chronic Lyme Post-Mortem Study Needed to End the Lyme Wars

https://www.lymeneteurope.org/info/chronic-lyme-post-mortem-study-needed

Chronic Lyme Post-Mortem Study Needed

post-mortem-1200x624

Editorial by Tom Grier

Key Words:

  • Antibody: A protein produced by a white-blood-cell to attack bacteria and viruses.
  • Titer: Another word for level, as in level or amount of antibody measured in the blood.
  • Seronegative: Despite an infection there is an absence of antibodies in the blood or serum of the patient.
  • Spirochete: A spiral bacteria in the same family of bacteria as Syphilis.
  • Borrelia burgdorferi: The spirochete bacteria that causes Lyme disease.
  • Erythema Migrans: A red expanding rash on the skin caused by an infected tick bite. An EM rash is diagnostic for Lyme disease even in absence of a positive test.
  • Antigen: Refers to a foreign substance in our blood that is capable of causing an immune response.

There isn’t a disease in the past 100 years that has polarized the medical community more than Lyme disease. From the very beginning, it was misunderstood. In the early 1970’s, two concerned mothers, Polly Murray and Judith Mensch, were convinced that the epidemic of juvenile rheumatoid arthritis (JRA) cases they were seeing in their neighborhoods in Old Lyme, Connecticut, were being contracted as a result of some kind of environmental exposure rather than a genetic disorder. After the state health department admitted that the JRA incidence rate in that area was at least eight times the national average, they somewhat reluctantly decided to investigate the observations of these two woman. Murray and Mensch had to present actual patient case histories they had collected before an investigation was started.

In 1975, a rheumatologist named Dr. Alan Steere first described in medical literature these abnormal cases of JRA as a new type of arthritic disorder. He coined the term “Lyme Arthritis”. This led to an immediate misunderstanding of Lyme disease, which was incorrectly thought of as strictly an arthritic disease for many years.

Six years later, in 1981, the actual cause of Lyme disease was discovered to be a new species of spirochetal bacteria transmitted to humans from the bite of infected deer ticks. Almost ten years after Steere’s description of Lyme disease as an arthritic disorder, it was now becoming recognized that Lyme disease was in fact much more than just a new type of arthritis. Lyme disease was now recognized as being equally capable of causing severe and devastating neurological disorders. [Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme Disease: Meningitis, cranial neuritis, and radiculoneuritis. Neurology 1985;35:47-53]

Dr. Willy Burgdorfer was the first to isolate the spirochetal bacteria from the midgut of Ixodes Scapularis (deer ticks) gathered from the Shelter Island area, located near the coast of New York and New Jersey.

Shortly after the cause of “Lyme Arthritis” was discovered to be a bacteria, articles appearing in medical literature quickly assumed that the Lyme spirochete was similar to other bacterial infections. Many treatment studies based their protocols of antibiotic treatment on other bacterial infections, such as strep throat. The conclusions from most early studies having short patient follow-up concluded that you could expect Lyme disease to respond to 10-14 days of antibiotics. The antibiotics tested in the test tube and deemed to be effective at that time included erythromycin, tetracycline, and penicillin.

From the very beginning, treatment failures were seen in virtually every antibiotic study done. The longer the patient follow up, the higher the incidence of treatment failure. The medical community blamed early treatment failures on the older antibiotics erythromycin, tetracycline, and penicillin, and determined that these antibiotics were not very effective at curing Lyme disease. Ignored was the fact that the newer antibiotics were also consistently failing to prevent relapses of active infection. Since these early treatment studies, the concept that two weeks of antibiotic therapy is adequate treatment for Lyme disease has remained ingrained in the medical community’s collective consciousness. [The Long-Term Follow-up of Lyme Disease: A Population-Based Retrospective Cohort Study. Authors: Shadick NA; Phillips CB; Sangha O et al. Ann Intern Med 1999 Dec 21;131(12):919-26]

*Data presented by Dr. Nancy Shadick at an International Lyme Symposia showed that patients in the Nantucket Island study followed for up to 5.2 years after initial antibiotic treatment had ever-climbing relapse rates. Relapse rates in patients receiving two weeks of IV Rocephin (ceftriaxone) could expect a relapse rate to exceed 50% after five years.

Other factors that contribute to relapse post-treatment seem to include length of infection before diagnosis, choice of antibiotic, and severity of symptoms at time of evaluation.

While from the very beginning there have been thousands of patients who have complained of still being sick and symptomatic despite supposed adequate antibiotic treatments, most of the medical community has ignored the patient’s observations and labeled them as being cured – despite the fact that they still have most of the same symptoms that brought them to their doctors in the first place. So, what determines a cure if the patient still has the symptoms of the disease? In many cases, it is not the patient’s disability that determines the disease state, but rather the presence or absence of natural immune factors or antibodies. The problem is that antibodies are not a direct measurement of active infection.

How could this have happened? Part of the problem was the newly emerging science and technology of antibody serology testing known as ELISA tests (Enzyme-Linked Immunosorbent Assay).

[ELISA tests look for an enzymatic color change that indicates the presence or absence of Lyme antibodies in a patient’s serum. If you still see a color change when a patient’s serum is diluted with 512 parts water, then it is said a patient has a dilution titer of 1:512. Note: Higher titer numbers do not have any correlation to how sick a patient is feeling. In fact, a high number indicates the presence of lots of immunity. A patient with a high titer is better able to fight the infection than someone who is producing low numbers of antibody or has a borderline or even negative titer.]

Not only was it clear that ELISA tests were quick and easy to develop, but they were cheap and easy to administer. The convenience of ELISA tests was a powerful enticement to both doctors and patients. Let’s face it, taking a 10 cc vial of blood is more convenient and inexpensive than having several brain, skin, bladder, or heart biopsies costing thousands of dollars done. The problem from the very beginning was that it was assumed and generally accepted these tests were a better diagnostic tool than patient evaluations based on symptoms and a response to treatment.

It was erroneously accepted that absence of antibodies in the blood meant no infection was present anywhere in the patient’s body. Even more disturbing was the incorrect assumption that the drop in antibody levels during treatment indicated a microbiological cure. Thus, many studies concluded that patients were cured if they eventually tested negative for Lyme antibodies. Both assumptions were and continue to be incorrect.

On paper, it certainly looks good for a doctor if he can tell a patient that, based on the test, they are negative for Lyme disease. However, in reality a more accurate statement would be that the patient is simply negative for the presence of those antibodies for which that particular test is sensitive for. Absence of antibodies does not mean the patient cannot have active infection.

ELISA tests can vary greatly from lab to lab. Since each lab holds a patent on their particular test, they are all competing to say they have the best test. It is a competitive business and certain buzz words, such as specificity, sensitivity, efficacy, and accuracy, are used to try to outsell one’s competitors lab tests.

This gives rise to many methods of testing efficacy implemented by competing labs in order to say that their test is better than the competition’s. This is usually based on predetermined laboratory standards. Unfortunately, laboratory methods of determining an ELISA test’s efficacy and accuracy does not directly correlate to accuracy in determining infection in a human being.

If a laboratory tests its’ ELISA on 100 test tubes of an identical known sample and, simultaneously, on 100 test tubes of distilled water (the control group), and picks up 99 of the 100 samples and only one of the control samples, they can claim their test is 99% accurate. It had a 1% rate of false negatives and a 1% rate of false positives. (The lab chooses what dilution titer it accepts as positive. For one lab it maybe 1:256, while for another it may be as high as 1:1024)

A 99% sensitivity sounds great, and most doctors and lay people would determine that this ELISA test is 99% effective and accurate. But these tests cannot tell you if a patient who is infected but makes no antibodies (seronegative patients) has active Lyme disease. Also, there is evidence that in humans with high titers, the tests can still be as high as 55% inaccurate.

What if I told you that some manufacturer’s tests are sensitive to only one of the antibodies we produce to the Lyme bacteria, and it is an antibody that is rarely elevated in late Lyme? What if I told you this test only had moderate sensitivity and requires highly positive serum to have a reagent color change? What if I told you that out of over 100 different Lyme ELISA tests by different labs, each was slightly different? What would you think if I told you that each lab holding a patent on an ELISA test presents data in such a way to make their test appear to look better than the competition in order to increase their profit? And, what would you say if I told you that many medical institutions are actually corporations that own patents on these Lyme tests, and that the reputations of these institutions and the researchers who developed them are all on the line if their test is found to be fallible?

What are the consequences to the reputations of these institutions if patients who say they are still sick after treatment are denied treatment because of these fallible tests? What if a patient becomes disabled or dies? The admission that the Lyme bacteria is alive and sequestered in some seronegative patients is not welcome news to the developers of these tests. But, rather than do the type of autopsy and tissue studies that would truly compare these tests, the manufacturers have chosen to manufacture patient studies that compare their tests to other equally bad serum tests. If a carpenter has a yard stick 29 inches long and he tests its precision with another yardstick 29 inches long, it will always appear that his yardstick is accurate.

How do laboratory claims to the efficacy of these tests actually stand up in the real world for the diagnosis of Lyme disease? Hundreds of labs and ELISA tests were evaluated by independent sources and were found several times to be less that 65% accurate. (This was based on triple-paired identical positive serum samples that were sent to 516 labs across the United States.) In some cases, some labs were far below this average. Without even arguing that some Lyme patient’s blood can be antibody negative despite an active infection, the patient whose blood is highly positive runs as much as a 45% chance or higher of still testing negative with an ELISA test. So they can have loads of antibody and still test negative simply by virtue of the lab’s inability to deliver consistently accurate results.

Now consider this. By today’s diagnostic criteria, if you test negative by ELISA, you don’t have Lyme disease. But, if you do test positive, you still do not have Lyme disease until you also test positive by Western Blot. A recent study shows that the Western Blot can be less than 50% accurate. So, statistically, if the ELISA test is 65% accurate and a Western Blot is 50% accurate, multiplying these probabilities gives less than a 33% chance of testing positive using the two tiered testing approach.

The biggest problem for Lyme patients today is that the medical community still by and large makes the same two incorrect assumptions about blood-based testing. This includes the more recent PCR DNA blood tests, which have the same pitfalls as antibody serologies in that the absence of infection of the bloodstream does not mean absence of infection in the body. Two important points to remember about antibody and PCR testing are:

  1. The absence of antibody (or bacterial DNA) does not prove absence of infection and
  2. the drop in antibodies (or the absence of Bb DNA) does not guarantee that a patient is cured or that the patient won’t relapse from active infection.

Example: Let’s consider that antibodies or bacterial DNA in the patient’s serum are like hailstones you see during a hailstorm. Standing in your yard with a five-gallon pail for several seconds, you don’t collect a single hailstone. What can you conclude? The absence of hail stones in your small bucket doesn’t exclude the fact that it could have been hailing in your yard. You can use a larger bucket and increase your odds, but what if the hailstorm is just in one corner of your yard? Likewise, a small 10 cc vial of blood may be inadequate to find an infection that isn’t even in the blood.

A very important observation is that there is a history in medical literature of symptomatic seronegative Lyme patients who have received aggressive long-term antibiotic therapy and still have been culture positive for active infection post-therapy. Tests can be and are fallible, and infection can persist despite lengthy and aggressive antibiotic therapy.

Other persistent infection studies have shown the presence of Borrelia burgdorferi antigens, bacterial particles, bacterial DNA/RNA, and the presence of the bacteria in tissue biopsies of patients despite antibiotic therapy. Using staining techniques that are sensitive for spirochetes, researchers have found the bacteria in tissue biopsies from living patients as well as sequestered in patient’s tissues at autopsy. All of these methods are a much more direct measurement of the presence of Lyme bacteria than antibody blood tests. But they are impractical tests for the average doctor to perform on a daily basis.

Why can infection be present in the body without the immune system making measurable antibodies? Once an infection has left the bloodstream, a patient may not make enough antibodies to test positive. Once the infection has found a safer place in the body to hide, it can avoid the immune system and also avoid any antibiotics that are mainly circulating in the blood. Here is a list of mechanisms of immune escape:

  • Bb can be coated by human blocking antibody and become invisible to killer immune cells.
  • Bb can coat it self with B-cell membrane and cloak itself in human proteins.
  • Bb can find places like inside joints and tendons where it is sequestered from the immune system and even antibiotics.
  • Bb can go metabolically inactive.
  • Bb can hide in the brain, heart, bladder, and possibly skin cells. It is motile so it seeks out survivable places.
  • Bb may have another form that lacks cell wall and therefore lacks many of the antigens the human immune system would use to attack.
  • Bb may hide inside some human cells.

Without infection being in constant contact with the blood-borne immune system, the body shuts off antibody production. Antibody levels will fall despite the fact that the infection is still sequestered deep in the body, such as the brain, tendons, heart, nerves, bladder, eyes, and joints. How do we know this? Patients who have been repeatedly seronegative for antibodies have been culture positive for the Lyme bacteria. Patients who have been aggressively treated with antibiotics have been culture positive for the Lyme bacteria. Despite repeated negative Lyme antibody tests, these patients still had symptoms – symptoms that, in most cases, responded to extended antibiotic therapies. [See references]

Because the medical community has by and large refused to accept a patient’s symptoms as proof of infection and have continually based their diagnosis of Lyme disease on Lyme serologies, there has been an ever growing schism between so called “chronic Lyme patients” and a medical community that refuses to accept their claims of still having active infection post-treatment. In many cases, not only are serologies used to determine the diagnosis, but the drop in antibodies is often used to indicate a biological cure.

It has been the variable nature of the disease and its’ wide range of symptoms, and the reliance on unreliable tests that has given rise to two different camps concerning the diagnosis and treatment of Lyme disease. Let’s discuss the evolution of these two opposed paradigms of diagnosis and treatment in the next section.

The Need For A Post-Mortem Lyme Study

The medical community is unevenly divided into two opposing camps on three major issues concerning Lyme Disease:

  • What constitutes a proper diagnosis of Lyme disease?
  • What constitutes proper treatment for patients with Lyme disease who have symptoms that persist beyond four weeks of antibiotic therapy?
  • What role should Lyme tests play in both diagnosis and treatment?

The first camp on the diagnosis and treatment of Lyme disease:

The first camp, which I will call Camp A, represents the majority of the medical community and is spearheaded by researchers from Yale Medical, the American College of Physicians (ACP), and several other major medical institutions. In general terms, this camp believes that Lyme disease is best diagnosed through the use of two consecutive serology tests; the ELISA test followed by a confirming Western Blot. This is known as two-tiered testing. With very little opposition from the medical community, two-tiered testing has now become the diagnostic standard of most major medical centers.

Camp A also maintains that Lyme disease, despite the stage or severity, is usually cured with just a few weeks of oral antibiotics. This is by far the most popular position within the medical community and the health insurance industry at this time.

How does Camp A make a diagnosis of Lyme Disease?

In the past, a history of a tick bite followed by a bull’s-eye skin rash or erythema migrans rash was diagnostic of the disease, but a diagnosis based on the rash and symptoms alone has come under increasing attack by several advocates of two-tiered testing, including Yale Medical [See Yale Medical Report] and the ACP.

A video training tape by the ACP is quite explicit that, in the absence of an erythema migrans (EM) rash, the diagnosis must be made by dual serologies and more than two weeks of antibiotics is almost always unnecessary. In one of the video scenarios, the tape suggests to treating physicians that patients who insist that they have persistent symptoms post-treatment should be referred to psychiatrists. The logic of this psychiatric referral stems from the premise that, since antibiotics are accepted as curative, any persistence of symptoms has to be purely psychological. So if a patient doesn’t feel better post-treatment, send them to a shrink!

The second camp on the diagnosis and treatment of Lyme disease:

The second camp, often referred to as “Lyme advocates,” which I will call Camp B, believes that most of the persistent symptoms post-antibiotic treatment are caused by persistent infection. This camp maintains that antibody serologies are poor at detecting a spirochetal bacterial infection that has sequestered in deep tissues and is no longer found within the bloodstream. They believe spirochetes that have found sequestered, or privileged, sites tend to hide in the body and are poorly detected by any means. As proof of their position, this camp offers numerous studies which have shown persistence of Borrelia infection post-antibiotic treatment. Listed below are several of these published cases of persistent infection in humans and animals post-treatment as confirmed by either culture or tissue biopsy and stain:

Schmidli J, Hunzicker T, Moesli P, et al, Cultivation of Bb from joint fluid three months after treatment of facial palsy due to Lyme Borreliosis. J Infect Dis 1988;158:905-906

Liegner KB, Shapiro JR, Ramsey D, Halperin AJ, Hogrefe W, and Kong L. Recurrent erythema migrans despite extended antibiotic treatment with minocycline in a patient with persisting Borrelia burgdorferi infection. J. American Acad Dermatol. 1993;28:312-314

Waniek C, Prohovnik I, Kaufman MA. Rapid progressive frontal type dementia and death with subcortical degeneration associated with Lyme disease. A biopsy confirmed presence of Borrelia burgdorferi post-mortem. A case report/abstract/poster presentation. LDF state of the art conference with emphasis on neurological Lyme. April 1994, Stamford, CT*

Lawrence C, Lipton RB, Lowy FD, and Coyle PK. Seronegative Chronic Relapsing Neuroborreliosis. European Neurology. 1995;35(2):113-117

Cleveland CP, Dennler PS, Durray PH. Recurrence of Lyme disease presenting as a chest wall mass: Borrelia burgdorferi was present despite five months of IV ceftriaxone 2g, and three months of oral cefixime 400 mg BID. The presence of Borrelia burgdorferi confirmed by biopsy and culture. Poster presentation LDF International Conference on Lyme Disease research, Stamford, CT, April 1992 *

Haupl T, Hahn G, Rittig M, Krause A, Schoerner C, Schonnherr U, Kalden JR and Burmester GR: Persistence of Borrelia burgdorferi in ligamentous tissue from a patient with chronic Lyme Borreliosis. Arthritis and Rheum 1993;36:1621-1626

Lavoie Paul E MD. Protocol from Rakel’s: Explains persistence of infection despite “standard” courses of antibiotics. Lyme Times-Lyme Disease Resource Center 1992;2(2): 25-27 Reprinted from Conn’s Current Therapy 1991

Masters EJ, Lynxwiler P, Rawlings J. Spirochetemia after continuous high dose oral amoxicillin therapy. Infect Dis Clin Practice 1994;3:207-208

Pal GS, Baker JT, Wright DJM. Penicillin resistant Borrelia encephalitis responding to cefotaxime. Lancet I (1988) 50-51

Preac-Mursic V, Wilske B, Schierz G, et al. Repeated isolation of spirochetes from the cerebrospinal fluid of a patient with meningoradiculitis Bannwarth’ Syndrome. Eur J Clin Microbiol 1984;3:564-565

Preac-Mursic V, Weber K, Pfister HW, Wilske B, Gross B, Baumann A, and Prokop J. Survival of Borrelia burgdorferi in antibiotically treated patients with Lyme Borreliosis Infection 1989;17:335-339

Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the Lyme Disease spirochete, Borrelia burgdorferi from ceftriaxone in vitro. J. Infect Dis 1992;166:440-444

Haupl TH, Krause A, Bittig M. Persistence of Borrelia burgdorferi in chronic Lyme Disease: altered immune regulation or evasion into immunologically privileged sites? Abstract 149 Fifth International Conference on Lyme Borreliosis, Arlington, VA, 1992 *

Lavoie Paul E. Failure of published antibiotic regimens in Lyme borreliosis: Observations on prolonged oral therapy. Abstract presented at the 1990 Lyme Borreliosis International Conference in Sweden.*

Fried Martin D, Durray P. Gastrointestinal Disease in Children with Persistent Lyme Disease: Spirochetes isolated from the G.I. tract . 1996 LDF Lyme Conference Boston, MA, Abstract*

Neuroboreliosis: In the journal Annals of Neurology Vol. 38, No 4, 1995, there was a brief article by Dr. Andrew Pachner MD, Elizabeth Delaney BS, and Tim O’Neill DVM, Ph.D. The conclusion of the article was simple and concise: “These data suggest that Lyme neuroboreliosis represents persistent infection with B. burgdorferi.” The study used nonhuman primates as a model for human neuroborreliosis, and used a special PCR technique to detect the presence of Borrelia DNA within specific structures of the brains of five rhesus monkeys. The monkeys were injected with strain N40Br of Borrelia burgdorferi, and later autopsied for analysis.

(For further information, please refer to the compendium of references to the persistence or relapse of Lyme disease at http://www.geocities.com/HotSprings/Oasis/6455/lyme-links.html)

Abstract summaries:

Abstract # D654 – J. Nowakowski, et al. Culture-Confirmed Treatment Failures of Cephalexin Therapy for Erythema Migrans. Two of six patients biopsied had culture confirmed Borrelia burgdorferi infections despite up to 21 days of cephalexin (500 mg TID) antibiotic treatment. · Abstract # D655 – Nowakowski, et al, Culture-confirmed infection and reinfection with Borrelia burgdorferi. A patient, despite antibiotic therapy, had a recurring Erythema Migrans rash on three separate occasions. On each occasion it was biopsied, which revealed the active presence of Borrelia burgdorferi on two separate occasions, indicating reinfection had occurred.
Abstract # D657 – J. Cimperman, F. Strle, et al, Repeated Isolation of Borrelia burgdorferi from the cerebrospinal fluid (CSF) of two patients treated for Lyme neuroborreliosis. Patient One was a twenty year old woman who presented with meningitis but was seronegative for Borrelia burgdorferi. Subsequently, six weeks later Bb was cultured from her CSF and she was treated with IV Rocephin 2 grams a day for 14 days. Three months later, the symptoms returned and Bb was once again isolated from the CSF. Patient 2 was a 51 year old female who developed an EM rash after tick bite. Within two months she had severe neurological symptoms. Her serology was negative. She was denied treatment until her CSF was culture positive nine months post-tick bite. She was treated with 2 grams of Rocephin for 14 days. Two months post-antibiotic treatment, Bb was once again cultured from her CSF. In both of these cases, the patients had negative antibodies but were culture positive, suggesting that the antibody tests are not reliable predictors of neurological Lyme Disease. Also, standard treatment regimens are insufficient when infection of the CNS is established and Bb can survive in the brain despite intravenous antibiotic treatment.
Patients with ACA shed Bb DNA post-treatment: Aberer E. et al. Success and Failure in the treatment of acrodermatitis chronica atrophicans skin rash. Infection 24(1):85-87 1996. ACA is a late stage skin rash usually attributed to Borrelia afzelii, it is sometimes mistaken for scleroderma. Forty-six patients with ACA were treated with either 14 days of IV Rocephin or thirty days of oral penicillin or doxycycline and followed up for one year. Of those treated with IV, 28% had no improvement, and 40% still shed Bb antigen in their urine. Of the oral group, 70% required retreatment. Conclusion: Proper length of treatment for ACA has yet to be determined. Logigian EL, McHugh GL, Antibiotics for Early Lyme Disease May Prevent Full Seroconversion but not CNS Infection. 1997

ABSTRACT # S66.006 Neuloogy Symposia, NEUROLOGY 1997; A388:48 In this study, 22 late-stage neurological patients who met the Centers for Disease Control (CDC) criteria for Lyme disease were studied over a three year period. Eighty-five percent of seronegative patients who still had active disseminated infection had been treated within one month of tick bite. This means that early antibiotic treatment may make you test negative, but you still progress to develop encephalitis. Without antibodies your brain has no natural immunity or local immune system to fight the infection, so withdrawing antibiotics causes the infection in the central nervous system (CNS) to go unabated. Patients who go on to develop brain infections despite antibiotics, may have suppressed antibody production thus worsening any remaing active infection in the central nervous system.

Valesova H, Mailer J, et al. Arthritis: A three year follow-up: Long-term results in patients with Lyme disease followed for three years after two weeks of IV Rocephin. Infection 24(1):98-102, 1996. This study represents another of the problems with author’s bias interpretation of data. Thirty-five Lyme arthritis patients were treated with a two week course of IV Rocephin. They were then followed for three years. At the end of the study, six patients had complete relapses, nineteen had marked improvement, four had new Lyme symptoms, and the rest were lost to follow up. The authors conclusion: “The treatment results for this group of 35 Lyme arthritis patients are considered successful.”

Let’s look at the above figures mathematically, based on the 29 patients out of 35 who were contacted and assessed:

19 improved = 65 %
6 relapsed = 20 %
4 worsened = 15 %

Does a total of 35% of patients still suffering sound like successful treatment to you? This is a treatable disease, but you have to treat it! What if a doctor’s child was one of the 35%? Do you think they would continue to go untreated as suggested by the ACP? How many patients have to relapse before treatment is considered unsuccessful? Six patients – or 20% – had complete relapses, yet the conclusion of the study was that, in general, treatment was considered successful! We get better cure rates for tuberculosis.

Animal vs. Human Studies:

Support for the theory that Borrelia burgdorferi can find safe havens in sequestered sites despite antibiotic therapy comes from several animal model studies. However, only a few human cases have yet been published. This is because the tissue studies that are required almost demand that they be done in a post-mortem exam. (See Stanek and Appel’s work on skin biopsies verses post-mortem exam of deep tissues in Lyme infected and antibiotic treated beagles)

Abstract # D607 – M.J.G. Appel, The persistence of Bb in Dogs after antibiotic treatment. Seventeen Beagle puppies were infected with Bb from infected ticks, eleven were treated for four weeks with either Doxycycline or amoxicillin in doses according to weight. Six were control dogs. 1/11 had Bb isolated from skin, but 7/11 dogs had Bb isolated from other tissues during post-mortem. All of the persistent infected pups had persistent arthritis. Conclusion: Skin biopsies are not predictive of persistence of infection. Also the standard excepted four week course of antibiotic treatment in dogs is not sufficient.

To date, no major multi-center post-mortem Lyme disease study has ever been done on humans. Without this type of post-mortem study, the debate between the two disagreeing camps will almost certainly continue.

Results from the European Alzheimers study done by Dr. Judit Miklossy suggests that post-mortem exams should not only look for persisting spirochetes in deceased Lyme patients, but should also look for spirochetes in the brains of deceased dementia patients as well.

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

Miklossy Judit. Alzheimer’s disease a spirochetosis? Neuro Report 1993;4:841-848 Thirteen out of thirteen Alzheimer patients had spirochetes in the brain. None of the age-matched control subjects had evidence of spirochetes in their brains. This study suggests that there is a correlation between an Alzheimer’s dementia and CNS spirochetosis in Swiss patients. In other words spirochetes might contribute to a CNS dementia similar to Alzheimer’s disease. (This is not to suggest that all Alzheimer’s is caused by spirochetes, but even if a small percentage of dementia can be prevented by antibiotics then further studies are justified. None are currently being done! ?

To do this type of tissue study of sequestered spirochetal infections takes nearly heroic efforts in time, costs, and diligence. Yet the few times that these types of studies have been applied to humans have suggested that Borrelia burgdorferi can indeed survive and thrive within the human body despite a complete course – or even several courses – of antibiotic therapy.

_______________

More on Grier:  https://madisonarealymesupportgroup.com/2016/12/19/microbiologist-tom-grier/

Lyme on the Brain, part 1: https://madisonarealymesupportgroup.com/2010/08/09/tom-grier-lyme-lecture-outline/
Lyme on the Brain, part 2: https://madisonarealymesupportgroup.com/2010/08/18/lyme-on-the-brain-part-2-by-tom-grier/
Lyme on the Brain, part 3: https://madisonarealymesupportgroup.com/2010/08/29/lyme-on-the-brain-by-tom-grier-part-3-b-lecture-notes/
Lyme on the Brain, part 4: https://madisonarealymesupportgroup.com/2010/08/30/lyme-on-the-brain-by-tom-grier-part-4-lecture-notes/

https://madisonarealymesupportgroup.com/2016/08/09/dr-paul-duray-research-fellowship-foundation-some-great-research-being-done-on-lyme-disease/

https://madisonarealymesupportgroup.com/2018/03/25/a-brief-history-of-neuroborreliosis-research-dementia-an-inside-look-at-two-researchers/

https://madisonarealymesupportgroup.com/2011/09/21/lab-tests-for-lyme-disease-by-tom-grier/

Psychiatric Drugs Create Violence & Suicide, School Shootings & Other Acts of Senseless Violence

Since many with Lyme/MSIDS are misdiagnosed with mental disorders, we need to seriously heed this report.

https://www.cchrint.org/pdfs/violence-report.pdfhttps://www.cchrint.org/pdfs/violence-report.pdf  Citizens Commission on Human Rights International A Mental Health Industry Watchdog

March 2018

Psychiatric Drugs:  Create Violence & Suicide, School Shootings & Other Acts of Senseless Violence 

From the FDA Adverse Event Reporting System’s 484 prescription drugs, 31 were disproportionately associated with violence, 25 of which are psychotropic drugs.

  • Prozac 10.9 times
  • Paxil 10.3 times
  • Luvox 8.4 times
  • Effexor 8.3 times
  • Pristiq 7.9 times
  • Zoloft 6.7 times

For following stimulants taken for ADHA

  • amphetamines 9.6 times
  • Strattera 9 times

Of 409 Official Psychiatric Drug Warnings:

  • 49 warned of self harm, suicide or suicide ideation
  • 27 warned of violence, mania, psychosis, hostility, aggression or homicidal ideation
  • 43 warned of death or increased risk of death
  • 35 linked emotional problems to the drugs
  • 17 warned of addition or withdrawal effects

David Kirschner, Ph.D., a New York Psychologist has evaluated 30 murderers and almost all had been in short term and psychoactive drug-oriented treatment before they killed.

Kirschner states,

“Most of the young murderers I have personally examined had….been in ‘treatment’and were using prescribed stimulant/amphetamine type drugs before and during the killing events.  These medications did not prevent but instead contributed to the violence by disinhibiting normal, frontal cortex control mechanism….And so, despite ongoing congressional debates regarding stricter gun control laws vs. improved access to mental health treatment, our concern should be about the quality of mental health care, not just a societal safety net insuring treatment for all children and young adults.”

According to the report there are currently 8 million American children & adolescence prescribed psychoactive drugs with a 200% increase in number of mass shootings per year from 2008 to 2012.

Professor Healy estimates that 90 percent of school shootings, over more than a decade, were linked to SSRI antidepressants (e.g., Prozac, Paxil, Zoloft, etc.).

“We’ve got good evidence that the drugs can make people violent and you’d have to reason from that that there may be more episodes of violence,” Dr. Healy stated.  Further, “What is very, very clear is that people do become hostile on the drugs.

The report states it is misleading to believe the theory that the patient becomes violent due to stopping the medication due to numerous studies showing that drug withdrawal can actually do it and can last from several months to years regardless of tapering off slowly.

Psychiatric Drugs are abused.

In 2014, 10,574 died from heroin overdose while 15,778 died from psychiatric drug overdose.

Police are at Risk.

Police spend more time with mental disturbance calls than traffic accident, burglary, or assault calls.  A 2009 study classified 36% of officer-involved shootings in North America as “suicide by cop,” a term describing a person with mental illness on prescribed drugs who inflicts self-harm or commits heinously violent crimes purposely compelling officers to use deadly force.  NewOne6 in Oklahoma states,

“Suicide by cop is happening so often that one study called it a rising tide that must be stopped.”

United Nations Health Rights Special Rapporteur Dr. Dainius Puras stated,

“Mental health policies and services are in crisis—not a crisis of chemical imbalances, but of power imbalances. We need bold political commitments, urgent policy responses and immediate remedial action.”

Dr. Thomas Dorman, an internist, said,

“Clinicians should first of all remember that emotional stress associated with a chronic illness or a painful condition can alter the patient’s temperament. In my practice I have run across countless people with chronic back pain who were labeled neurotic. A typical statement from these poor patients is ‘I thought I really was going crazy.’”  The last thing a person needs is a drug that masks and exacerbates the problem.

It’s important for health professionals to recognize physical disease as these physical diseases may worsen or actually cause a patient’s mental disorder.Dr.

Mary Ann Block, a best-selling author, including Just Because You’re Depressed Doesn’t Mean You Have Depression, also said,

“Many doctors don’t do physical exams before prescribing psychiatric drugs…This is not how I was taught to practice medicine. In my medical education, I was taught to do a complete history and physical exam. I was taught to consider something called a ‘differential diagnosis.’ To do this, one must consider all possible underlying causes of the symptoms.”

This information is critical now and even more so for Lyme/MSIDS patients as doctors MUST consider pathogen involvement in ANY mental disorder.

Here’s a few examples:

https://madisonarealymesupportgroup.com/2017/06/30/child-with-lymemsidspans-told-by-doctors-she-made-it-all-up/

https://madisonarealymesupportgroup.com/2017/10/01/panspandas-steroids-autoimmune-disease-lymemsids-the-need-for-medical-collaboration/

https://madisonarealymesupportgroup.com/2017/10/08/misdiagnosed-how-children-with-treatable-medical-issues-are-mistakenly-labeled-as-mentally-ill/

https://madisonarealymesupportgroup.com/2017/10/03/treat-the-infection-psychiatric-symptoms-get-better/

https://madisonarealymesupportgroup.com/2017/04/11/hidden-invaders-infections-can-trigger-immune-attacks-on-kids-brains-provoking-devastating-psychiatric-disorders/

https://madisonarealymesupportgroup.com/2016/08/09/a-bartonella-story/

https://madisonarealymesupportgroup.com/2018/03/09/aggressiveness-violence-homicidality-homicide-lyme-disease/

Bb Can Cause Infectious Myelopathy

https://www.ncbi.nlm.nih.gov/pubmed/29613895
Continuum (Minneap Minn). 2018 Apr;24(2, Spinal Cord Disorders):441-473. doi: 10.1212/CON.0000000000000597.

Infectious Myelopathies.

Grill MF.

Abstract
PURPOSE OF REVIEW:
This article reviews bacterial, viral, fungal, and parasitic pathogens associated with myelopathy. Infectious myelopathies may be due to direct infection or parainfectious autoimmune-mediated mechanisms; this article focuses primarily on the former.
RECENT FINDINGS:
Some microorganisms exhibit neurotropism for the spinal cord (eg, enteroviruses such as poliovirus and flaviviruses such as West Nile virus), while others are more protean in neurologic manifestations (eg, herpesviruses such as varicella-zoster virus), and others are only rarely reported to cause myelopathy (eg, certain fungal and parasitic infections). Individuals who are immunocompromised are at increased risk of disseminated infection to the central nervous system. Within the last few years, an enterovirus D68 outbreak has been associated with cases of acute flaccid paralysis in children, and emerging Zika virus infection has been concurrent with cases of acute flaccid paralysis due to Guillain-Barré syndrome, although cases of myelitis have also been reported. Associated pathogens differ by geographic distribution, with myelopathies related to Borrelia burgdorferi (Lyme disease) and West Nile virus more commonly seen in the United States and parasitic infections encountered more often in Latin America, Southeast Asia, and Africa. Characteristic CSF and MRI patterns have been identified with many of these infections.
SUMMARY:
A myriad of pathogens are associated with infectious myelopathies. Host factors, geographic distribution, clinical features, CSF profiles, and MRI findings can assist in formulating the differential diagnosis and ultimately guide management.

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**Comment**

Myelopathy is a neurologic deficit related to the spinal cord which can be caused by trauma (spinal cord injury) or inflammation (myelitis).  Inflammation can be caused by numerous things including pathogens such as Borrelia burgdorferi (Bb), the causative agent of Lyme Disease, as well as numerous viruses that can also be a part of the Lyme/MSIDS symptom picture which can be transmitted directly from ticks or activated due to the reaction of the body to the tick bite.  Much research is needed in this particular area.

Myelopathy is typically a clinical diagnosis with patients complaining of weakness, clumsiness, muscle atrophy, sensory deficits, bowel/bladder symptoms, sexual dysfunction, altered tons, spasticity, and hyperreflexia among other symptoms.  https://en.wikipedia.org/wiki/Myelopathy  Treatment depends upon the underlying cause.  If infectious, pathogen specific antibiotics, and/or things to reduce inflammation are in order.

Personal response:  While I was not diagnosed with myelopathy specifically, one of my hallmark symptoms was spinal and occipital pain.  After ruling out Chiari:  https://madisonarealymesupportgroup.com/2016/04/02/chiari/ and regularly seeing an upper cervical chiropractor for structural malalignment, MSM helped me tremendously.  Please read about MSM here:  https://madisonarealymesupportgroup.com/2018/03/02/dmso-msm-for-lyme-msids/

Make sure to discuss all treatment options with your health care provider.

 

 

BBA57 Found to Help Bb Evade Immune System

https://www.ncbi.nlm.nih.gov/pubmed/29610317

Proc Natl Acad Sci U S A. 2018 Apr 2. pii: 201718595. doi: 10.1073/pnas.1718595115. [Epub ahead of print]

Plasticity in early immune evasion strategies of a bacterial pathogen.

Bernard Q, Smith AA, Yang X, Koci J, Foor SD, Cramer SD, Zhuang X, Dwyer JE, Lin YP, Mongodin EF, Marques A, Leong JM, Anguita J, Pal U.

Abstract

Borrelia burgdorferi is one of the few extracellular pathogens capable of establishing persistent infection in mammals. The mechanisms that sustain long-term survival of this bacterium are largely unknown. Here we report a unique innate immune evasion strategy of B. burgdorferi, orchestrated by a surface protein annotated as BBA57, through its modulation of multiple spirochete virulent determinants. BBA57 function is critical for early infection but largely redundant for later stages of spirochetal persistence, either in mammals or in ticks. The protein influences host IFN responses as well as suppresses multiple host microbicidal activities involving serum complement, neutrophils, and antimicrobial peptides. We also discovered a remarkable plasticity in BBA57-mediated spirochete immune evasion strategy because its loss, although resulting in near clearance of pathogens at the inoculum site, triggers nonheritable adaptive changes that exclude detectable nucleotide alterations in the genome but incorporate transcriptional reprograming events. Understanding the malleability in spirochetal immune evasion mechanisms that ensures their host persistence is critical for the development of novel therapeutic and preventive approaches to combat long-term infections like Lyme borreliosis.

_____________

**Comment**

So it’s recognized that Borrelia Burgdorferi is capable of causing persistent infection in “mammals,” but evidently, according to the CDC/IDSA/NIH, not humans.  

This would be humorous if it didn’t kill people.

 

 

Canadian Citizen Scientists Helping With Tick Surveillance

PMCID: PMC5872229
PMID: 29498648

Citizen Science and Community Engagement in Tick Surveillance—A Canadian Case Study

Abstract

Lyme disease is the most common tick-borne disease in North America and Europe, and on-going surveillance is required to monitor the spread of the tick vectors as their populations expand under the influence of climate change. Active surveillance involves teams of researchers collecting ticks from field locations with the potential to be sites of establishing tick populations. This process is labor- and time-intensive, limiting the number of sites monitored and the frequency of monitoring. Citizen science initiatives are ideally suited to address this logistical problem and generate high-density and complex data from sites of community importance. In 2014, the same region was monitored by academic researchers, public health workers, and citizen scientists, allowing a comparison of the strengths and weaknesses of each type of surveillance effort. Four community members persisted with tick collections over several years, collectively recovering several hundred ticks. Although deviations from standard surveillance protocols and the choice of tick surveillance sites makes the incorporation of community-generated data into conventional surveillance analyses more complex, this citizen science data remains useful in providing high-density longitudinal tick surveillance of a small area in which detailed ecological observations can be made. Most importantly, partnership between community members and researchers has proven a powerful tool in educating communities about of the risk of tick-vectored diseases and in encouraging tick bite prevention.

_______________

**Comment*

Please know that according to an independent Canadian tick expert John Scott, climate change has nothing to do with the spread of ticks and the pathogens they carry:  

https://madisonarealymesupportgroup.com/2017/08/14/canadian-tick-expert-climate-change-is-not-behind-lyme-disease/  “The climate change range expansion model is what the authorities have been using to rationalize how they have done nothing for more than thirty years. It’s a huge cover-up scheme that goes back to the 1980’s. The grandiose scheme was a nefarious plot to let doctors off the hook from having to deal with this debilitating disease. I caught onto it very quickly. Most people have been victims of it ever since.”
“This climate change ‘theory’ is all part of a well-planned scheme. Even the ticks are smarter than the people who’ve concocted this thing,” he says.
“Climate change has nothing to do with tick movement. Blacklegged ticks are ecoadaptive, and tolerate wide temperature fluctuations. On hot summer days, these ticks descend into the cool, moist leaf litter and rehydrate. In winter, they descend into the leaf litter, and are comfortable under an insulating blanket of snow.Ticks have antifreeze-like compounds in their bodies, and can tolerate a wide range of temperatures. For instance, at Kenora, Ontario, the air temperature peaks at 36°C and dips to –44°C, and blacklegged ticks survive successfully.
“Ticks are marvellous eco-adaptors. They will be the last species on the planet. Do you see how silly this theory of climate change is as a way to rationalize what’s happening. It’s all a red herring to divert your attention,” he explains. “In simple terms, the feds have diverted our attention by saying ‘let’s worry about ticks and climate change, put all our funding there and we will solve the problem of Lyme disease’.”

Similarly to the latest fashion trends from Paris driving fashion across the world, the phrase “climate change,” is the latest angle in Science to obtain grants that is driving research.  

This research is not helping patients in the least.  

https://madisonarealymesupportgroup.com/2017/01/28/sit-down-science/  How research is being manipulated to fit industry agendas.

https://madisonarealymesupportgroup.com/2017/01/02/fake-science/ Exactly how this manipulation occurs.

https://madisonarealymesupportgroup.com/2017/07/08/global-warming-numbers-fudged/

https://madisonarealymesupportgroup.com/2017/01/13/lyme-science-owned-by-good-ol-boys/

https://madisonarealymesupportgroup.com/2017/08/04/science-for-sale/

https://madisonarealymesupportgroup.com/2017/12/05/bought-documentary-on-pharma-vaccines-gmos/