Sarbatori Fericite!

Fie ca sarbatorile de anul acesta sa va umple sufletul de bucurie, incredere, speranta si iubire. Iar Mosul sa va aduca cele mai dorite si neasteptate cadouri voua si celor apropiati!!

Tura cu biseptol si clindamicina

Tocmai pe tura asta m-am bucurat ca am scapat de scamele din ochi. Ameteli si oboseala am avut tot timpul, dar parca totusi am simtit o imbunatatire.Dupa 4 saptamani am repatat analizele generale si hemoleucograma mea este varza + analizele la ficat. Leucocitele sunt 2500 si neutrofile, limfocite arata cam la fel de prost. Doctorul m-a rugat sa opresc tura si sa trec pe naturiste si putine antibiotice pana imi revin la normal. Am apucat sa fac doar 4 saptamani din 6 si sunt tare dezamagita. Sincera sa fiu, ma batea gandul sa continui, dar am dureri si in zona rinichilor de vreo 2 sapt si m-am gandit sa nu dau in altele. Chiar speram sa duc tura asta la bun sfarsit fara nici un fel de probleme. Mi-au mai scazut leucocitele asa de rau pe tura de cefort.Dar am terminat 1 luna de cefort si am facut pauza 10 zile. Mi-am repetat apoi leucograma si leucocitele erau in limita normala. Acum sper sa imi revin pe tura asta mai usoara si sa prind forte noi pt alte ture serioase de antibiotic.

Anaplasma

ScienceDaily (Nov. 29, 2012) — Bacteria that cause the tick-borne disease anaplasmosis in humans create their own food supply by hijacking a process in host cells that normally should help kill the pathogenic bugs, scientists have found. This bacterium, Anaplasma phagocytophilum (Ap), secretes a protein that can start this process. The protein binds with another protein produced by white blood cells, and that connection creates compartments that siphon host-cell nutrients to feed the bacteria, enabling their growth inside the white blood cells. The finding defies conventional wisdom about most bacteria, which try to avoid this cellular process. Called autophagy, the process allows a cell to digest parts of itself to produce energy when it is experiencing starvation. But that digestive feature also is enacted by the immune system to help clear away certain intracellular pathogens, including those that cause salmonellosis or shigellosis. The Ap bacterium, however, launches and then manipulates the autophagy process to its own advantage. "This study shows how bacteria subvert natural processes," said Yasuko Rikihisa, professor of veterinary biosciences at Ohio State University and lead author of the research. "They are creating their own food supply through a cellular mechanism that hurts other infectious bacteria. And because this process doesn't cause inflammation, they do it very gently, becoming an insider that eventually kills the host cell." The finding could help identify new targets for drugs to treat this infection, which is a rare but emerging infectious disease that can be lethal for the elderly and people with compromised immune systems. The current first-line treatment is the antibiotic doxycycline. Also known as human granulocytic anaplasmosis, the disease affects more than 1,000 people per year in the United States, up from just 348 reported cases in 2003, according to the Centers for Disease Control and Prevention. It is transmitted to humans by tick bites primarily from the black-legged tick and the western black-legged tick. The study appears online this week in the early edition of the Proceedings of the National Academy of Sciences. The Ap bacterium secretes substances to perform a process resembling mating to infect host cells, primarily the granulocyte class of white blood cells that fight off invading pathogens. Rikihisa's lab previously identified a protein called Ats-1 that is secreted by Ap bacteria during this process. In this new study, the researchers found that once inside the host cells, Ats-1 binds to another protein called Beclin 1, which is part of a system of molecules involved in the earliest stages of the autophagy process. The scientists observed that when the two proteins bind, they create little bubbles known as vesicles. Through a series of experiments, the researchers determined that these bubbles were in fact autophagosomes -- bubble-like compartments that are formed as a cell prepares to undergo autophagy. They were able to confirm this by imaging the vesicles to determine that they had the tell-tale double membrane characteristic of autophagosomes, and by testing for the presence of other compounds that serve as markers of the initiation of the cell-digesting process. Under normal circumstances, autophagosomes contain the nutrients that are meant to be digested and recycled for other uses -- but in this case, the bacteria take those nutrients to promote their own growth. That Ats-1 could start this process on its own represents a rare power for a single protein. "We believe this is the first bacterial protein that has been found to do this," said Rikihisa, also an investigator in Ohio State's Center for Microbial Interface Biology and Comprehensive Cancer Center. "Ats-1 initiates an early stage of the autophagosome, then picks up nutrients from the main body of the host cell and closes the layers." Most of the action of bacterial growth takes place inside a special compartment that typically doesn't contain many nutrients. But after the Ap bacterial protein starts this process of producing autophagosomes that can encase nutrients, these bubbles fuse with the compartment, creating a steady supply of food at the site of bacterial replication and growth. The researchers showed this by further imaging the bubbles to determine that an autophagy marker protein could be found both inside and outside of the bacterial growth compartments. They also showed that infected cells did not contain any lysosomes, which are cell parts that perform the actual digestion and degradation of foreign bodies during autophagy. An experiment in mice deficient in the Beclin 1 protein showed that infection levels were much lower if mice had low levels of this protein -- confirming its role in binding with Ats-1 and producing autophagosomes to promote infection. In cell cultures, the researchers also showed that when Ats-1 was overproduced, bacteria grew 10 times more effectively than they did in cells in which an unrelated protein was overproduced. All of this activity allows the bacteria to remain hidden from the immune system because the induction of autophagy is considered a normal cell function and it does not produce any inflammation, which would recruit infection-fighters to the scene. Instead, the Ap bacteria set themselves up comfortably inside granulocytes and steadily grow for a few days until they rupture their host cells and generate a strong immune response -- which makes an infected person sick. In one final experiment, Rikihisa and colleagues blocked autophagosome production in Ap-infected cells using an experimental drug called 3-MA. With that process blocked, bacterial growth declined dramatically. 3-MA is toxic to humans, but its effectiveness in blocking the infectious properties of Ap in cells suggests that its structure could serve as the basis for a safe small-molecule drug, Rikihisa said. "A similar compound could be a potential treatment to inhibit bacterial growth," she said. Clarifying the power of Ats-1 in inducing autophagy also suggests that this protein could be an important tool in further studies of this complex cell process that remains poorly understood, she added. This work was supported by a grant from the National Institutes of Health. Co-authors include Hua Niu and Qingming Xiong of Ohio State's Department of Veterinary Biosciences; and Akitsugu Yamamoto of the Nagahama Institute of Bioscience and Technology and Mitsuko Hayashi-Nishino of Osaka University, both in Japan.

Protomyxozoa Rheumatica

Protomyxozoa Rheumatica is a parasite discovered by hemotologist, Dr Steven Fry. He believes the organism may cause numerous neurological diseases, including ALS. The following is Part I of the transcript of a recent interview with Steven Fry, MD. Please do not expect your physician or other health care provider to know about what is covered here. You will not even find most of this information on Dr. Fry's lab's website. Understand that it will be some time before some of the remaining studies that test "causation" are completed and this information is more widely known and used. Interview Braman: What I’d like to do by way of outline is: If you can just share a little bit about how you came to get into this rather unique field, what you are currently doing, what you are finding from the testing that you are doing, and what you are seeing in terms of patient outcomes -- just kind of an overview. And then in part two I’d like to move into what you are seeing and finding relative to the lifestyle effect on these conditions and the lab findings that you are doing -- so kind of a part 1 and a part 2. Fry: Okay. So, I first got into this area -- well, let me backtrack a little bit and give you my background. I have a bachelors degree in Microbiology, a masters degree in Molecular Biology, then I went to medical school, then I did a transition internship, then I did two years of surgical pathology, and ended up in general practice. And while I was in general practice, I got intrigued by those patients who were perfectly healthy, and then would go on a trip, or something would happen, and they would develop a flu-like illness, and they would develop what we now call chronic fatigue syndrome. Then the real breakthrough was about seventeen or eighteen years ago when I had one of my patients who had fibromyalgia, which is very similar to chronic fatigue syndrome -- in many ways I feel like they are the same disease, or the same disease entity. She gave me a book written by Henry Scammell, I think the title was ‘Why Arthritis’, [probably actually “The Arthritis Breakthrough” by Henry Scammell with Thomas McPherson Brown, MD] it was on the best sellers list in the early 90’s. It talked about Thomas McPherson Brown, the rheumatologist, who was one of the chief rheumatologists at Washington University. He was using antibiotics -- primarily tetracyclines -- to treat autoimmune disease. So she brought me this book, and I was a little hesitant, but I read the book and I was really impressed by it, and I said, “What’s the harm here putting her on minocycline? I mean I put teenagers on minocycline for acne.” So you know, the risk benefit ratio was huge in that sense. And I started her on minocycline, and she got amazingly better on a course minocycline. Her fibro got better, her lupus got better, and so I started to pursue that, and with more and more patients I started to use tetracyclines for therapy. And then finally I started -- you know, there was a network of physicians who worked with Dr. Brown’s former technique, and I got on, I guess, a group that was referring patients through that -- I was one of the few in the southwest doing it. And I started getting patients with lupus, and rheumatoid arthritis, and one thing led to another, and I would start doing patients with MS [multiple sclerosis]. And then about eleven years ago I was impressed by an article out of Italy on chronic fatigue syndrome, and I just borrowed money, bought a nice research grade microscope, and started developing some stains. And in about six months I developed a stain that was picking up bacteria attached to red blood cells. I thought it was bacteria at the time, turns out it was. And then we started to see ring shapes that looked very similar to malaria, but it really wasn’t malaria. Anyway, one thing led to another, and it turns out that what we were looking at was actually a variety of different bacteria attached to red blood cells. Now the old coin name would be bartonella, or hemobartonella, and it turns out on a molecular level it was a lot of different kinds of bacteria. And the intracellular bacteria, or intraerythrocytic [inside red blood cells] bacteria that we were looking at really wasn’t bacteria, it was this protozoan [single-celled organisms that include amoebas and the malaria organism] that we’ve discovered. And at first I thought it was babesiosis, and over the years, and a lot of money, and a lot of time, turns out it was actually a malaria-like organism with an extremely complex lifecycle that forms biofilm communities in the blood, it is a blood-loving parasite. And after mapping the genome of it, and we didn’t really name it until we had done that -- it’s probably a new genus, in the phylum [?]. You know, similar to malaria, similar to babesiosis, even more complex genetically, sort of in between a helminth [parasitic worm] and a protozoan. So it’s really a complex organism. And because of the biofilm, and its slower rate of growth, it’s really not that invasive, it’s not like staph, or strep, or malaria. And it hides itself from the immune system, and hides itself from antibiotics, and likes to attach to the surfaces. And over the years I evolved from using simple antibiotics like tetracyclines to more complex formulations that were really geared more towards malaria-like, or protozoa-like organisms. And that seemed to work a little bit better. And then a year and a half ago I was introduced to Colin Campbell's work, John McDougall’s work, and I said, “You know, these patients that they claim are getting much better on a low-fat diet, a whole foods plant based diet, well these are the same patients I’m treating.” So we started to look at that analytical level and saying, “Hey, does this organism that we’re working on basically have a fat requirement?” Well it does. We were able to grow it in a culture, give it fat, and it grows a lot better with fat than without. Actually it doesn’t grow very well at all without any fat. And then we followed patients who went on a low fat diet, and we were able to calculate that the levels of this organism were decreased, sometimes disappearing, on a whole food, plant based, low fat diet. So, in the last year, my practice, I would have to say it is a lot more successful because I’ve combined this dietary lifestyle approach with traditional antibiotics. And that’s where I am today. Does that make sense? Braman: So over what period of time -- what was it, eleven years -- that this has occurred? Fry: Actually, you’d have to say that it’s been about 20 years. About 20 years ago I got interested in fatigue syndrome. Now let me explain something, as I saw these patients and talked to them and got their histories, you know, trying to really dig in to the real core of this whole problem, a lot of these patients with autoimmune disease start with fatigue syndrome. Most people don’t realize it, and other neurologists will acknowledge that, actually I was at a CCSVI [chronic cerebrospinal venous insufficiency] training session, at the neuroimaging center in Buffalo, and we were lectured by one of the leading MS experts -- he’s there, and he agrees, a lot of these MS patients have a prodrome [preceding syndrome] of fatigue, and it is really fatigue syndrome. So I feel that, you know, there is this spectrum of disease, starting with fatigue, that leads to fatigue, joint pain, muscle pain, brain fog, myalgic encephalitis. Then these people go on to develop a really true, full blown arthritis, or lupus, or, ALS [amyotrophic lateral sclerosis – Lou Gehrig’s disease], Parkinson’s, that sort of thing. So the mechanism of the disease is primarily for the neurodegenerative disorders, is a vascular sludging, and most probably vegetations that we can actually see in ultrasounds in these patients, and that is some work that we are very interested in, and we’re probably going to start a collaborative study with one of the centers on that one. Braman: So with what kind of ultrasound, what kind of vegetations are you finding? Fry: Well, they are doing -- this goes back to Paulo Zamboni’s work. I think he’s a vascular specialist at the University of Ferrara in Italy. His wife came down with multiple sclerosis and he wanted to find out what it was and hypothesized it was a vascular problem, and then after a lot of work developed an ultrasound technique and was able to visualize, using ultrasound, a defect in flow in either the deep cerebral veins or the petrosal veins of the brain or the internal jugular veins coming down from the brain. The next step to that was that he was able to show that in patients who had internal jugular vein obstruction or decreased flow he could go in with a balloon catheter and open this up. Some of these MS patients could get improvements and some dramatic improvements in their condition. Of course there’s a relapse rate with this that is actually quite high. But it makes sense if it’s a microorganism that is growing there and you’re kind of, you know, clearing things up -- that would make a lot of sense. So now this has been repeated by Dr. Hubbard, who’s just recently submitted a 265 patient study showing similar results. Actually, that was a 6-month study. So these patients with MS have obstruction in the flow of the brain, and Dr. Hubbard used the word “swamp”. There’s reduced flow, bad flow, backflow. We feel the same way, that the brain is probably a sensitive organ or tissue. So if you change the flow environment in any way, whether it is less oxygenation, less nutrients, you are going to see some subtle changes and thus demyelination. It would be a subtle change, and I want you to know that they have documented remyelination in some of these patients where they have done this balloon procedure. So here is a model of MS. In MS the researcher Roy Swank showed that patients with MS who are on a low fat diet, basically did not die of MS, and if they were on a regular diet they died of MS. And I think John McDougall was associated with the study, also out of University of Oregon, a five year study which should be near completion. I don’t know if he’s going to talk about it at ACAM meetings this week. I’m going to make sure I see that lecture, and I’m just curious to see if that data has been completed and if it shows the same thing that Roy was able to show. So if you tie in that concept with our concept it makes a lot of sense. Now another interesting point, if we want to talk about MS and neurodegenerative disease, is that MS, there are about 75 papers dating back to the 1880‘s where physicians and laboratorians have discovered a malaria-like organism in patients with MS. There are 75 papers. There is a review article, a medical hypothesis, a two-part article that discusses this, and actually used antimalarial drugs in the 1920’s and early 1930’s in MS patients with significant improvement. But there was so much malaria in the U.S. at that time that they concluded that they really probably just had underlying malaria, and that was the cause of their MS. So if you put all the dots together it is a very fascinating argument if you believe that, in effect, this agent could be the underlying cause. Braman: Wow! Now when you were talking about vegetations and ultrasound, can you actually see vegetations on the ultrasound image? Fry: Yes, and when you see these vegetations, some are valves, and actually they categorize the type of vegetations. Or actually, they don’t use the word vegetations as Zamboni does, and I use that vegetation concept or idea. But there are growths, or filaments, or webs, or other structures that they see, that certainly aren’t normally found in the vasculature. And if you look at Zamboni’s work -- there is one you can see online -- Paolo Zamboni, you can pull it up, and there is an ultrasound and you can see the valve moving, but also you see a lot of other smaller and filamentous type material. Actually we have seen in blood samples filamentous material similar to that in patients with chronic fatigue. I think it is the same thing, and what we are seeing in the blood are really material that has just detached from the vasculature in long linear strands. Braman: And has there been any work using -- you mentioned using a balloon to help clear things up -- what about things like thrombolytics [“clot-busting” or dissolving medications]? Fry: Well, you know, thrombolytics are used in therapy on patients with proven vascular obstruction with clot. Now if you want to think of lumbrokinase as a thrombolytic -- you know, a lot of the alternative medicine folks out there are using lumbrokinase, serrapeptidase, and other agents like that to whittle away at these diseases. And of course you know Dave Berg who advocates a lot of this thinking, that it’s really...I think Dave’s old way of thinking about it is, some agents, whether it’s infection or say a heavy metal like mercury or something like that was, whether it was a virus or bacterial agent -- chlamydia or whatever -- was stimulating this coagulation phenomena producing a coagulation disorder. And of course he’s got the ISAC panel that he used to use to determine what type of coagulopathy these patients had and whether or not they had a hereditary disposition. Now if you throw in this concept that these patients might have gross obstructive disease with a biofilm-forming protozoan, then it’s sort of...kind of brings all this thought together. So really in these patients they have -- for instance, in the CSF of fibro patients, they have brain fog -- I think that’s due primarily to sluggish flow either through some obstructive process due to these vegetations that I’m talking about, or even just the viscosity issue with a larger microorganism forming biofilm communities in the circulatory system. To really mainstream [medicine] this is a radical concept, but the idea of biofilm communities elsewhere is no longer a radical concept. But I think a hematopoetic biofilm community of protozoans is a radical concept. But -- you know -- we have pictures. And, you know, the pictures are pretty astounding, pretty amazing. I developed this hypothesis years ago, that this is a biofilm problem, modified for additional techniques, and... there was, right in front of us. It was always there. And again, I’m not the first to report it either. Braman: And so the biofilm -- they’re a web, or fibers, or sludgy blood? Fry: Well, actually, not quite. Basically a biofilm...when we think of biofilm, bacterial biofilms... in training back in the ‘70s when I went to undergraduate school we called it “the slime layer.” And microbiologists have known about slime layers and syncytial microbes for a long, long time. And the best analogy would be to think of a slug that you see crawling around, and you know that slimy stuff on there, it’s a similar material. It’s a mixed mucopolysaccharide, there is hyaluronic acid in it. And actually the biofilm is a very complex structure with a lot of function attached to it. And so DNA is the -- I think the “rebar” for biofilm. DNA is not only an informational molecule, it is also a structural molecule. So with this rebar of DNA, that’s basically a grid system. Secreted are mucopolysaccharides, peptides, that sort of thing. So it is able through the biofilm -- it can actively transport nutrients in and export noxious byproducts from metabolism out. The only problem is that it also excludes antibiotics and drugs. Also biofilms prevent the microorganism from being even seen by the immune system, and we think that is what’s going on with these patients. So if you have ever heard of the Jarisch-Herxheimer [clinical worsening due to the infectious agent dying off] reaction, we think what is going on in a Jarisch-Herxheimer in these patients.... I mean usually when you treat these patients with drugs, say a lupus patient with Plaquenil, they feel terrible initially and it flares up their disease. So what’s going on in that particular situation, I believe, is that the drug is getting to the organism somewhat and weakens it enough so that its antigens are exposed on the surface, and system can see this enough to produce a profound inflammatory response. And I think that is what the Jarisch-Herxheimer actually is. It’s not necessarily cellular death; it’s really the cytokines produced by the immune system trying to destroy the pathogen, but it can’t really get at it very well. And a real limitation to therapy is this Jarisch-Herxheimer reaction or inflammatory response. And, possibly, if we found the greatest drug in the world to kill this microorganism, the use of this drug would be limited because of this profound inflammatory response once you start to get at that organism. Braman: How are you currently treating this and what results are you seeing? Fry: Well I’m actually pretty conservative, I’m really kind of the McPherson Brown… you know, go slow, steady, conservative approach. Let’s not get people so debilitated they can’t go back to work. Almost all of these patients are low in Vitamin D. So the first thing I start patients on is Vitamin D. Some patients start Vitamin D -- they get ill when they start, then they start feeling better. So, in terms of nutrition, vitamin D. And then I put them on a low-fat diet. And the amazing thing -- the majority of my patients who initiate an ultra low-fat diet have a Herxheimer reaction. So we can actually explain that now because we’ve weakened the microorganism. It probably needs fat because of this high energy requirement to produce this biofilm in a harsh host environment, and as we restrict fats it weakens the organism, the immune system can see it, and we get a flare. A lot of my patients have a flare reaction, or Herxheimer reaction, when they change their diet to a low-fat diet. And then I start with tetracyclines -- usually doxycycline or minocycline. I like those two because it hits a lot of other microorganisms at the same time. They’re pretty safe, they’re inexpensive, and both drugs are also antimalarial drugs. They’re used prophylactically and for application for treatment around the world for malaria. So they actually have antiprotozoal activity that most people aren’t aware of. Then I proceed to azithromycin because that seems to work in some patients. It’s a safe drug. You can take it for long periods of time without major problems. And then on to more of the traditional antimalarial drugs like Plaquenil in combination with tetracyclines -- that’s been done for a long, long time. I think the hesitancy in the rheumatology community for minocycline or tetracycline: 1) is they’re not sure how it’s working, and 2) these patients have a flare or Herxheimer reaction that’s very hard to manage. And that may be one of their observations, not really understanding the underlying mechanism and what’s going on there. I thought for a long time these patients may have had babesiosis because it seemed to look like it in the microscope and I was using azithromycin and atovaquone and patients have profound Herxheimer reactions on that combination, but once they get through it they seem to actually do very well. And we’re always looking at other drugs in the laboratory, and that’s another story -- what drugs seem to work in the lab. I don’t think our model of disease is developed enough...we use microtiter plates, we’re able to culture it. I just don’t think our model of disease is good enough yet to make great conclusions as to invitro [in the lab] sensitivity. I’m pretty sure that people have different strains of this microorganism. One drug might work on one person, and not on another person. So I suspect that there are really significantly different strains of this organism out in the community. Braman: So you are able to culture this and grow this in the lab? Fry: Oh, no, we can grow it. There is no question we are growing it. So we’re growing it quite well, it’s just that I’m not really happy -- there are a lot of technical issues with drug sensitivity. A lot of these drugs require second order kinetics. They have to go through the liver, so it is just a matter of time and money to really get serious about doing drug sensitivity studies. But we have some interesting data created now, and confirmed by PCR [polymerase chain reaction – a technology for measuring very specific DNA sequences] so.... Really what we developed is a biofilm assay for this organism, I mean, that’s really what we’re measuring now. And those studies are really backed up by PCR, quantitative PCR. Braman: So are you actually able to eradicate it in people, or is it an indefinite...? Fry: We cannot eradicate it in patients, as far as we know, and we cannot eradicate it completely in the test tube yet with any known agents that could be delivered in therapeutic doses. Now we have some patients who are feeling very well, who, where by our normal procedure, we can’t find evidence of disease, but if we go through a sample and keep looking, and looking and looking we can find some. Most patients that are ill, with our technology it’s very easy to detect disease. These patients that are doing much, much better, who are on a low fat diet, we’re able to find it, though rarely in those patients. So I cannot say that we have eradicated it in any patients. My patients who do great, who are on a low fat diet, if they start eating a regular American diet again, they relapse. So I have not cured anybody. Part II Braman: So how does it compare…give me some kind or picture or sense of what percentage of people with what conditions are you finding this in, and how does that compare with normal, or people who don’t have these conditions? Fry: Well, that’s an excellent question, and that is actually the purpose of the Phoenix Study. We’re trying to go through IRB approval for this study, a 390 patient study. Ninety patients consisting of 30 with CFS, 30 with MS, and 30 with ALS, compared to 300 normal controls. Now we find this organism profoundly in everybody with autoimmune disease. Now you have to consider the spectrum of autoimmune disease. That includes diabetes [type 1], MS, probably ALS, autism is considered an autoimmune disease in some circles, lupus, rheumatoid arthritis, sclerodermas, sarcoidosis, chronic fatigue is acknowledged as a possible autoimmune disease, I am sure it is, and fibromyalgia. So we have a lot of people out there with chronic inflammatory disease who I think have this. I think we’ve got now probably 20 or 25 different categories where we are able to isolate this organism. Where we are fully convinced that this is the cause of their disease because when we are able to knock down this microorganism in their blood, their symptoms resolve, and sometime resolve dramatically. So we have a cause-and effect confirmed by microscopy and PCR in these patients. So we think that is the cause of their disease. Now the question is, what is the incidence or prevalence of this microorganism in the community. We think it is very high. In that study we recruited 300 normal controls. Now our criteria, this is probably the most difficult part of the study, recruiting patients who are perfectly healthy with no complaints. I think the older our patient population gets it’s going to be much, much more difficult to find individuals who really do not have chronic headaches, chronic fatigue, chronic joint pain, and a lot of these other symptoms. And they have to be perfectly healthy with no complaints, on no medication, and no history in the past of having any of these autoimmune diseases. So it is a really tough challenge. So, if we believe that mosquitos are a prime vector, and we have proven mosquitos carry it, mosquitos are all over. We actually have this kind of ballpark guess, you know, in the population, we think 10 to 20 percent per decade of life is the increase or acquisition level of this micro-organism in the community. So we think a lot of normal people have it, but maybe genetically inclined to where in their immune systems handle it, maybe diet and exercise play a role, their own immune systems and their genetics play a role in this. So if it is true that this is the cause of lots of cardiovascular disease, when you talk to a cardiologist they say “Hey, the event that caused this cardiovascular disease we think happens by the time people hit the age of thirty.” And if this is the same phenomena then that may be right. It may be our estimate of 10 to 20 percent per decade, is too low. Maybe it is higher. But we think it is a ubiquitous pathogen all over the world. Braman: All over the world? Fry: Yes. Braman: And you said that you have pretty much proved that it is found in mosquitos, and/or transmitted by mosquitos? Fry: I can’t say transmitted. That’s a whole ‘nother study. I would need some animals to do that study. That requires money; animals are pretty expensive. If you want to get it published, you’ve got to do it the right way. I think we were going to look at four Guinea Pigs for four months; that was around $10,000 for that little study, just for the animals from an animal resource at the nearby university. We actually did the study. We went down to an area in the Phoenix metropolitan area where a lot of people are getting chronic fatigue, I know, cause I’ve been taking care of patients here in the community for the last twenty years. We then caught, I think we caught about 20 or 30 mosquitoes. 81 percent of the mosquitoes, two different species of mosquitoes, were PCR positive for protomyxoa. That is the name of the organism. So mosquitoes certainly have it—now whether they are transmitting it, you know, and whether they are a vector or not, that’s a whole ‘nother issue. And I don’t know how transmissible it is by a mosquito bite. Braman: Is there any indication of any other source, or transmission? Fry: We suspect, oh, I have a number of patients who really seem to get sick after what looks like water or food contamination. And then I’m convinced that ticks are certainly a vector. Two out of two ticks that we’ve tested were positive by PCR. We now have a nurse in upstate New York. We’re going to start a one hundred tick sample study, hopefully we’ll get a hundred ticks from the area of upstate New York. We’re actually going to run a number of different vector borne disease assays looking for babesiosis, ehrlichiosis, anaplasmosis, rocky mountain spotted fever by PCR, and protomyxoa by PCR, and survey that population of ticks. This will all probably be from the same general area in upstate New York. So we will get a larger tick study in that one area to see if they actually carry it. Braman: And has the, what you called protomyxoa, is that an internal name or has this been officially recognized in some standard process as a new bug? Fry: That is a, we think it is at least a new genus. It’s maybe a higher order, and we can find nothing similar to it that is close enough genetically, so actually that is the name we developed. It was a scientific name we developed or came up with. Protomyxoa is Greek for “slime forming protozoan”. And we call it protomyxoa rheumatica because we think it is associated with the autoimmune or rheumatic disorders. We have not submitted our DNA database, or our DNA map to the international registry for IP [intellectual property] reasons. We are a private diagnostic laboratory; this is our technology, and we just haven’t done that yet. We are protecting our trade secrets and technology. Eventually this will get out; that’s our plan, that’s our intention. We plan to partner with one of the major institutions for validation. It just takes time and money. Braman: So how far away do you think you are from this hitting mainstream knowledge and use? Fry: Well, one of the problems is publications. We have a very small publication. We presented this information at the 2009 Biofilm Meetings. And we had no problem getting our abstract accepted. We’ve submitted this article really in fuller form to four mainstream peer-review neurology journals—this is a study in ALS; that is one of our main interests. And they have declined to review it, or they’ve rejected it. And one of my colleagues is the former editor of one of these journals, the former president of one of the national societies, he says, “Look, this is too political, too new, really a radical concept.” And actually the CCVI information showing obstructions in MS patients is now considered a very radical concept. So it is just going to take time, and we realize that. So now we are looking at lesser journals, reconstructing that small paper to get that out. And of course, larger studies we have on the books, we are trying to get IRB [institutional review board – a system for ensuring the ethical guidelines are followed in medical research] approval for a number of studies right now. And that takes time and money. But we just keep plugging away at it. We are almost done, we are using one of the larger IRB’s, institutional IRB’s available for groups like ours. And we have a consultant with them, and we are designing a study, and it is pretty much, it’s almost done, it has some rough edges to clean up. Then we’ve got to pursue additional funding to make that project happen. But that is in collaboration with two neurologists in the Phoenix metropolitan area. Braman: So you are getting some uptake in the traditional system? Fry: Sure, yeah, and I have some of my colleagues that are patient, they’re open-minded. And, you know, when you show someone one these pictures, that we get from some of these patients, it’s really pretty amazing. It’s hard to believe it’s there, it is hard to believe these patients are alive with that kind of infection. But if you understand the underlying disease process, you can understand why they are still alive with a disease like this. They are not well, they don’t feel very good, but, you know, they are able to stay alive. And we believe this is chronic inflammatory disease. Braman: So have you sequenced the DNA of this organism yet? Fry: Actually we’ve mapped the genome and filed an IP on that, but we’ve mapped the genome, yes. And that is how we know where we can place it phylogenetically, and know it is new, and know it is unique. Braman: Interesting. So if you have gotten to the step of actually sequencing the whole genome, you know you are dealing with an actual bug. Not just in pictures, as impressing as that might be. But if you have the DNA in hand, and it is consistent, and it is mapped, then you know you have a “critter”, if you will.... Fry: Right, and so really the gold standard in microbiology today is the molecular signature, well, we have that now. And not only do we just have a signature for a portion of the genome, we have the entire genome mapped. At least, an isolate from one patient. And with that information we know it is unique, it’s not like anything else. Actually it is probably close to a couple other organisms, but not close enough to say that it’s probably in the same order, same phylum, but not the same order. And really, this type of organism we think is a little different than what we are used to dealing with genetically. And it is just a unique organism. It’s a slime forming complex protozoan, trying to become a helminth [parasitic worm], trying to become a worm. And that may suggest why it is really resistant to a variety of different medications. It’s a tough bug. It has a lot of gene sequences that are very, very similar to human. And that is probably the confounding aspect to it. Because it has resiliency of human tissue, and it has similar requirements. And this is probably an organism that developed over the eons and borrowed genes from it’s hosts. And, you know, kept some that it liked, and discarded some it didn’t like. And of course it’s got it’s own genetic information, and it’s, you know, it’s progenitor with some ameba, or some protozoan in the past. But it is a little more complex than say, malaria or babesiosis genetically. Actually it is sort of in-between, again, a helminth and a malarial type organism. Braman: And has this been.... you mentioned you have found it in mosquitos and ticks. Do we have any reason to think that this may be in people’s dogs and cats, or cattle and chickens, in this country? Fry: Actually, we did a study on one of my employees, the spouse works in a veterinary lab, and we were able to get random samples. And, dogs have it. And actually, the older the dog is the greater likelihood of having this organism. Younger dogs don’t have it, the older dogs have it. And so we think the same thing we will find in humans. Younger humans don’t have it, older humans do. So, that was a small study, about eight or nine dogs, one cat. Actually, we looked at one cat, one cat did not have it, the cat was two years old. But the dogs, the older dogs had it, the younger dogs didn’t. Braman: Interesting. Now if this.... If everything “pans out” if you will, and gets out there, this would be a phenomenal impact on health and healthcare. Fry: We think so. Braman: What do you see in the future for this, and I mean, how do you think this is going to impact healthcare. Fry: Well, for most patients, most of the healthcare dollar is spent on taking care of chronic inflammatory disease. Diabetes, cardiovascular disease, the autoimmune diseases, you know—we think the mechanism is again, slugging or clotting. So for instance, in the type-two diabetic, you might like my model of why a low fat diet works. And I’ve seen it in my practice. So patients with type two diabetes, non-insulin dependent diabetes, if you put them on a low fat diet, their diabetes gets better, and sometimes they can go off their medication completely. So our model of this disease is that vascular slugging, and deposition of plaque occurs, and I said the word plaque, and this is what biofilm communities do, they form sludge, or plaque, or growths. And this is producing slugging and clogging up the small vasculature and capillaries leading into these, into the islet cells [cells in the pancreas that produce insulin]. So if you sort of clean.... You know, the islet cells aren’t dead. If you clean things up, if you restore flow, then you get endocrine function again, and you get insulin production again. And I think that is the phenomenon that we are seeing in these patients who go on an ultra low-fat diet. Now in the type-one diabetic, I think what they do—you know, if you talk to type-one diabetics, and I’ve actually seen this in my practice, usually they have this flu-like prodrome before they go into crisis, and they develop insulin dependent diabetes. I think those individuals probably get this organism, and it basically strokes out their islet cells, and they lose insulin functioning, insulin capability, completely. And so if we look at this, maybe we can vaccinate people against this organism, and then we may be able to eradicate diabetes, we may be able to eradicate cardiovascular disease, we may be able to get rid of autoimmune disease. That would extend the natural lifespan for many, many years in humans. So that is the implication of this, we think. And we get surprised all the time with new information. So here we have a ubiquitous micro-organism that seems to accumulate as time goes on, and it really wasn’t a problem when life expectancy was probably in the 40’s and 50’s, which wasn’t too long ago. But now, as we have older populations that are in their 60’s, 70’s, and 80’s, they are dying of heart attacks, they are dying of strokes, they are dying really of autoimmune disease. And so now this organism becomes a much bigger factor as the population ages. And it becomes really more important, so... I mean earlier humans were dying of infectious diseases primarily, now humans are dying from other diseases, and we think this organism could be the underlying cause. So it has a lot of implications for healthcare. For example, what if we started treating autoimmune disease patients more aggressively with anti-malarial drugs and diet. If you could really make the rheumatologists and the neurologists believe that, hey, this is the cause.... So listen to what Roy Swank [MS research who showed that a plant-based low-fat diet was of large benefit to many MS patients] says, lets put everybody on a low fat diet, lets emphasize that, why don’t we try them on a course of minocycline or doxycycline. You know, minocycline is already in the literature worldwide for treating MS, ok, this is not something new. What if we got a little more aggressive with some of the chloroquines, the problem again with practitioners who have tried this in the past, I’m sure, is this Jarisch-Herxheimer reaction. Braman: So on a scale of potential impact this could be huge. I mean this could be one of the biggest medical breakthroughs in what, the last century...? Fry: Well, it’s possible, but only time will tell. We are very convinced this organism exists, we are very convinced that we can alter its disease course. Again, when we show a dramatic reduction in this by PCR and by visualization in the blood stream, we see clinical improvement in patients, sometimes dramatic. So here we have an organism cause-and-effect with intervention, and if we’re right, then a lot of people have this disease, and, you know, we really just call it “chronic inflammatory disease”. We don’t really know what the underlying cause is. Well this could be a new cause. So it has wide implications. It is just a matter of time, and work, and money to get these publications out and these studies done. And then to win over our critical colleagues to get this published. I mean here, you know, the fellows who review papers and all this—you know, it’s a club. And when you come up with a radical concept, they have to protect their turf and their journals, and their way of thinking about things. I remember talking to Barry Marshall before he got his Nobel Prize years ago, and he went through a lot of flak from saying that H. pylori [bacteria] was the cause of ulcers. Not a radical concept, but in those days it was. And when I was introduced to Barry’s work in what was it, ‘80 or ‘81, I think that he was kind of frustrated, but people started to listen to him. So any new concepts are difficult. The thing is, if you put it in perspective, and you put all this information together—I mean physicians, writers, and researchers have been saying this for over 100 years—you know, this is not a new idea. This has been out there a long time. Braman: They have been saying what for one hundred years? Fry: Well, you know, at least in the case of MS, writers have been saying that it was a malaria-type organism for over one hundred years. So, I’m not the first one to say that a process like this is going on. Braman: Right... Fry: Yeah, it is just that we have done a lot more in developing techniques to basically get a high yield on anybody that has this organism to say they have it. And that is the main focus of our laboratory, coming up with more tests to define the organism for clinical diagnostics and clinical therapeutic purposes. Braman: I remember—I don’t know if I mentioned it to you before—but there was one point where I was seeing as a patient a nurse who used to run research projects for a major medical university. And she became ill. She saw all the specialists. Nobody could help her. So she started looking, and eventually figured out some fairly alternative stuff that made it so she could function. So when she came to see me, we ran a bunch of tests, and again, I had been looking at a lot of other stuff for years trying to help people, and dig beyond just the typical. And I found a lot of evidence for chronic infectious agents, and/or coagulation issues. And I still remember—I used to process the specimens myself, I would draw it, I would process it, I would separate it, etc.—I was stunned that this lady’s test came back negative for the things we were testing. But what really stunned me was that after I spun her blood and went to separate it, it was stringy. I mean it was literally, visibly stringy. Fry: Yeah, and that stringy stuff is not clot, it’s protomyxzoa in filaments. We’ve seen it, too. And we’ve actually taken that stringy stuff from blood and looked at it under a microscope, done a PCR analysis, and that’s actually a linear biofilm community, filamentous, of protomxzoa. There are actually other organisms embedded in there, but it is primarily protomyxzoa. So what you are seeing is this organism. I have to tell you, I was talking to a patient in the summer. He wasn’t my patient, someone else’s CFS patient, a real sick fellow. And he said “Yeah, when they draw my blood all these stringy things come out. The nurse just said it was a clot.” And I said, “No, that’s probably this micro-organism, that filaments are there.” So you can imagine that in the vasculature, you know, getting in the way, producing chronic inflammation, reducing flow, and that can make you pretty sick, tired and exhausted. Braman: Is there anything else that you think would be helpful for people to understand about what you are doing? Clinical pearls, perspective...? Fry: Well, one of the things that I find very detrimental overall, and this is very controversial in the alternative community, is that a lot of practitioners are prescribing mineral supplements. Magnesium, ok, and it seems to make people better for a little while. But magnesium is a major component of biofilm, so we feel and observe that when patients are taking magnesium supplements I can never get them any better with antibiotics or any sort of therapy, and when I take them off their supplements eventually they seem to start getting better. And so magnesium as a supplement to these ill patients dramatically enhances the biofilm forming capability, and basically you are building armor around this micro-organism. So in the short term, when you give magnesium to these biofilm communities you hide them even more from the immune system, so you get a relief that is less inflammation. But in the long term you are building up slugging, more biofilm, and enriching that community, which makes it harder and harder to get rid of. So again, this is very controversial, I get a lot of criticism for this. But I think in the long-haul I’m going to be proven correct in this analysis—that the supplements really aren’t good for people. And I don’t know if this is a pearl or not, but that is just one observation. Braman: Oh, absolutely. Fry: Yeah, I observe that clinically, and then becoming a biofilm educated microbiologist, I sort of put it together, and now there are actually a couple of studies that confirm this in biofilms, exactly that. So what the magnesium does is it stabilizes the DNA and actually becomes an integral portion of it. There is a biochemistry behind it. Braman: Very interesting. Any other pearls or insights? Fry: No, just need more time and more money (laughs) for our studies and eventually we will get there. Right now, we’ll primarily support it by revenue coming in from our laboratory running these tests, and we’ve had a few very generous individuals that have helped out somewhat. We just got a small grant actually from the Coulter Foundation. And they are watching us now, and hopefully that will grow a little bit. But again, we have to produce some data, and of course we have to go through IRB approval to generate data on large numbers of patients. We are working on that and hopefully we can stay ahead of the game and keep the funding and the project going. And I think we will. I think there is enough interest now in the community to where doctors have been sold on this idea, they are very curious, they want to order these tests on the patient, and we can show them photographs and DNA data that show they, indeed, have an infectious agent. And the question is the frustration with therapy. It’s very difficult to treat, and it is hard for most practitioners to convince their patients to change their diet. So that is a big stumbling block. So I think eventually that diet is helpful, but we are going to have to come up with a drug that works where people won’t have to diet. And then a method, of course—the linchpin is a method of reducing their inflammation during therapy. And this is the hardest thing to get patients to go through. Some patients start to flare, and then they say, “That’s it, I’m done. I don’t want any part of this.” So, it’s an obstacle. Braman: So how do you spell protomyxzoa? Fry: Ok, so it’s p-r-o-t-o-m-y-x-z-o-a, protomyxzoa. And that’s Greek. And that’s our name. We filed that with the patent office in connection with the gene sequence. And we are probably going to file that within the next 12 months in the international databases. We could be wrong; I don’t think we are. It’s just I’ve got some very good people working with me. We have three different technologies now, with actually a fourth one coming online soon, that say this is what it is and it makes a whole lot of sense. And if you go back and pore through the literature there is a lot of supporting research done on what we are saying. And now we have this macroscopic evidence that’s pretty amazing, and that puts the puzzle together. And again, the traditional techniques for looking at blood, traditional molecular techniques for analyzing blood, don’t work. This is the big struggle over the last decade. And getting this technology together it was not obvious. Braman: And why don’t the traditional techniques work? Fry: That is intellectual property. Braman: Oh, ok. Fry: That’s the trick. There are a number of tricks, and it took a long time to figure out the tricks. We can reliably now detect this organism in people that have it. We’re very convinced of that. And we are actually coming up with better ways. The real problem is going to be, if you are getting a patient a lot better and can’t find it through the techniques we develop, do they still have disease, when can you stop therapy? And that is our goal right now in therapeutic diagnostics, that’s where we are going with this. But the diet is huge, lifestyle modification, diet, exercise, get in the hot tub, get in the steam room, get rid of all the sugar, you know, the high fructose corn syrup, get rid of the fatty diets. And some of these patients have dramatic improvements with lifestyle changes. I have people who don’t want to take antibiotics. They change their lifestyle, they do get better. So you folks are on the right track. Braman: And you said steam rooms and saunas. Are you finding those helpful? Fry: Yeah well, you know, the ancient Romans, the American Indians, the Swedes had this figured out a long time ago. This disease has been around forever, and you know, it is like my handyman who is in his late 60’s says: “Well, why do you do the hot tub everyday?” cause it makes me feel a whole lot better, okay. So I think that this organism probably has an intolerance for heat. And we know that when we heat the body up we get vasodilation, that probably improves blood-flow, and also it probably has an effect on the immune system. It probably blunts some of the inflammation. So that is another adjunct that I recommend my patients do one of those modalities, and it seems to help. Braman: Excellent. Fry: Again, that’s lifestyle modification. Braman: Absolutely. Hey, I want to thank you so much for taking the time to do this. Fry: No problem. Braman: I’m excited about this. I think it’s fabulous, and I think it’s the kind of thing we need to do in looking at things from multi-modal perspectives, and putting the pieces together. Fry: You know I’ve tried to stay open minded here and tried to fit this all into a model, and it seems to fit.

Update - Sfarsitul turei 5

Azi e ultima zi a celor 5 saptamani de azitromicina, zinnat si tinizol. M-am smtit asa si asa. Oboseala, slabiciunea,ameteala si scamele din ochi nu prea imi dau pace. Mai am si insomnii, iar daca iau 1 mg de melatonina, ma trezesc beata a 2-a zi. Microscopia arata la fel ca celalalte 2. Nici o schimbare. Afzelii, Garinii si bartonella tot acolo sunt. Am descoperit ca daca iau fluconazol imi reduce ameteala. Nu de tot, dar intensitatea e mult mai scazuta decat in mod normal. Asa ca am introdus si fluconazolul dupa ce am citit despre beneficile lui in tratarea neuroboreliozei Am introdus si ulei de nuca de cocos, seara, o lingura inainte de culcare. Nu stiu daca ma auta sau nu. Dimineata ma trezesc foarte slabita si am in permanenta probleme pe partea stanga, mana si piciorul sunt mereu amortite. Ma deranjeaza foarte tare pt ca sunt stangace si parca nu mai am putere sa fac treburile cu mana stanga. Am mai citit de stephania root pt ameteli, probleme cu vederea si cu auzul. Inca nu am incercat-o pt ca e tinctura si nu o pot lua cu tinizolul. Pt ca ma simt oricum mai bine decat acum 6 luni am cautat sa-mi gasesc un job (jobul dinaninte l-am pierdut din cauza bolii).Am fost la un interviu saptamana aceasta si l-am luat, incep de maine incep munca. Sa ma ajute Dumnezeu sa rezist! Trebuie sa muncesc ca sa-mi pot cumpara tratamentul. Acum urmeaza cateva zile de pauza, iar apoi incep clindamicina cu biseptolul.

Cine a descoperit Babesioza

Babesiosis (pronounced buh-BEEZ-e-OH-sis) is named for Dr. Victor Babes, a Romanian pathologist who in 1888 identified the disease in cattle that had fever and blood-tainted urine. Until the mid-20th century, the disease was known only in wild and domestic animals, which can be infected by more than 100 different Babesia species

Lyme Protest

https://www.facebook.com/worldwidelymeprotest

Infectia Chlamydophila pneumoniae in SM

http://www.davidwheldon.co.uk/ms-treatment1.html

Noutati despre bacterie

Cercetatori de la Scoala Commonwealth University de Medicina au identificat "cheile" și "ușile" la bacterie responsabilă pentru o serie de boli cu transmitere prin muscatura capusei. Aceste constatari pot indica cercetatorii spre dezvoltarea unui vaccin unic, care protejeaza intreaga familie impotriva acestor bacterii care cauzeaza boli la oameni, animale domestice și animale salbatice. Supraviețuire acestor bacterii depinde de capacitatea lor de a invada celulele umane sau animale. Și aceasta trebuie să se facă într-un mod foarte precis. Bacteriile folosesc un set specific de "chei" pe suprafețele lor de a debloca ușile specifice " intrari in celulele gazda. Prin intelegerea modului in care aceste bacterii invadeaza celulele, cercetatorii sunt capabili sa identifice potentiale tinte pentru a bloca răspândirea infecției, iar de acolo, dezvoltarea de vaccinuri sigure si eficiente. Cercetatorii au raportat ca o proteina numita ompA pe suprafața de Anaplasma phagocytophilum este important pentru invadarea celulele gazdă. Anaplasma phagocytophilum este o bacterie care infecteaza oamenii Anaplasmataceae de a provoca anaplasmoza granulocitara. Aceasta este a doua cea mai comuna boala transmisa de capusa după boala Lyme în Statele Unite, și este, de asemenea prezenta în Europa și Asia. Echipa a identificat, de asemenea, reziduu de zahăr special, pe suprafetele de celulele gazdă la care se leaga ompA. "Cu alte cuvinte, am identificat atât o cheie cat so o ușa care să promoveze infecția cu Anaplasma", a declarat cercetatorul Jason A. Carlyon, Ph.D., profesor Departamentul de Microbiologie si Imunologie, în Scoala VCU de Medicina. "Aceste constatari sunt importante, deoarece datele noastre, pot să stabilească o direcție de dezvoltare a unui vaccin unic, care protejeaza membrilor intreagii familii de bacterii care cauzeaza boli la oameni, animale domestice și animale salbatice", a spus el. Potrivit Carlyon, regiunea de ompA care mediaza infecție este împărțită între bacteriile Anaplasmataceae. Experții au înregistrat o creștere constantă a incidenței infecțiilor umane cauzate de căpușe transmise agenti patogeni în ultimii ani. Multe bacterii transmise de capuse sunt patogene si sunt considerate "agenți patogeni noi", pentru că a fost d recent descoperit că acestia pot infecta oameni. Mai mult decât atât, dovezile sugereaza ca multe dintre aceste infectii merg nerecunoscute, semnificând faptul că prevalența bolilor umane cauzate de agenți patogeni Anaplasmataceae este chiar mai mare, a spus Carlyon. Infecții de animale transporta o povară economică semnificativă, costa SUA 100 milioane dolari pe an, in industria cu bovine, a adăugat el. Constatările studiului VCU-a condus, de asemenea, au fost evidențiate într-un comentariu care a aparut in acelasi numar al revistei, scris de doi experți în domeniu, inclusiv Guy H. Palmer, DVM, Ph.D., director, președinte Creighton și profesor Regents în G. Paul Allen Scoala pentru sănătatea animală globală, la Universitatea de Stat de la Washington Colegiul de Medicina Veterinara, si Susan M. Noh, Ph.D., de asemenea, cu Universitatea de Stat de la Washington Colegiul de Medicina Veterinara. Pentru acest lucru, VCU a depus un brevet. În acest moment, drepturile din SUA și străine sunt disponibile, iar echipa cauta parteneri comerciali pentru a dezvolta în continuare această tehnologie. Carlyon a colaborat cu VCU Scoala de Medicina cercetatori Nore Ojogun, Ph.D.; Kahlon Amandeep, Ph.D.; Matei Troese J., Ph.D., si Rachael Thomas J., Ph.D., toate colegii fostul post-doctoral în Departamentul VCU de Microbiologie si Imunologie si de laborator Carlyon lui; Stephanie A. Ragland, tehnician de laborator fostului Departamentului VCU de Microbiologie si Imunologie, Lauren VieBrock, student absolvent in cadrul Departamentului VCU de Microbiologie si Imunologie, ambele, de asemenea, in laboratorul Carlyon lui; Juliana E Masttronunzio, Ph.D., post-doctoral fellow la Universitatea Yale Scoala de Medicina, si Erol Fikrig, MD, Waldemar. Von Zedtwitz profesor de medicina si epidemiologie și patogeneza microbiene la Scoala de Medicina Yale University, si cercetatorul cu Institutul Medical Howard Hughes , și șef de secție de boli infecțioase, și Naomi J. Walker, tehnician cu Universitatea din California Scoala de Medicina Veterinara, și Dori L. Borjesson, Ph.D., profesor de la Universitatea din California Scoala de Medicina Veterinara. Acest studiu a fost sustinut de un grant de la National Institutes of subventii de sanatate R01 AI072683, R01AI072683-04S1, și R21 AI090170 (la Carlyon) și R01 AI141440 (la Fikrig). Citometrie de flux și VCU comun de resurse Facilitatea Imaging este susținută, în parte, prin finanțarea de la NIH-NCI Cancer Support Center 5 Grant P30 CA016059.

Minociclina induce boli autoimune

http://www.ncbi.nlm.nih.gov/pubmed/19153345 http://rheumatology.oxfordjournals.org/content/40/3/329.full http://dermatology.jwatch.org/cgi/content/full/2007/525/2 http://www.jabfp.com/content/15/3/239.full.pdf

Sfarsitul rundei IV

Am terminat si cu tura 4 de antibiotic, cefort. Nu pot spune ca a fost o tura usoara. Primele 2 saptamani faceam frisoane si temperatura 39 grade dupa fiecare injectare. Au trecut aceste reactii, dar ma intepa toata pielea foarte rau dupa administrare.Senzatia de intepaturi si mancarimi ale pielii trecea dupa 2 ore. Am avut si dureri graoznice de ochi in primele 2 saptamani, dar au trecut. In final am ramas cu oboseala si ameteli. Mai am si acele scame in ochi. Analizele au iesit cam prost pe ficat si in plus leucocite foarte scazute + eozinofile crescute. Dezamagita total, asteptam sa ma simt mai bine. Microscopia e neschimbata, iar pe partea de simptome am scapat de durerile articulare, dar oboseala si ameteliile ma omoara. Urmeaza o tura cu minociclina de care mi-e extrem de frica. Am citit de reactii foarte urate pe aceasta tura. Nu cred ca voi scapa de starea asta de betie in curand. Am incercat sa iau ulei de nuca de cocos si parca ma simt si mai rau de cate ori il iau.Am zis ca poate ma ajuta sa nu fac candida si sa nu mi innegreasca dintii.Candida nu am facut, dar dintii s-au innegrit.

Tratamentul de lunga durata in Lyme

http://news.brown.edu/pressreleases/2012/08/lyme

INFLUENTA PARAZITILOR ASUPRA STARII DE SANATATE

Stiai ca organismul tau este colonizat de o multume de paraziti care mananca zilnic din tine? Vrei sa accepti sau nu, realiatea este ca toti avem in noi diferite specii de paraziti care ne consuma substantele nutritive si ne expun unor boli infioratoare. Toti oamenii au? Fara exceptie! Iti aduc la cunostinta ca oamenii de pe planeta se impart in 2 categorii: 1. Oameni care se detoxifica(periodic) de paraziti. 2. Oameni care NU se detoxifica de paraziti Asadar nici NU se pune problema organismului neinfestat. Suntem cu totii mult prea expusi, cu atat mai mult in aceste vremuri cu aer poluat, apa murdara si mancare infestata. Partea buna este ca… …daca ai un stil de viata sanataos si echilibrat, care-ti asigura un sistem imunitar puternic, corpul tau este capabil sa tina cat de cat sub control majoritatea parazitilor cu care te infestezi, INSA daca nu ai grija de sanatate, ai toate sansele ca mai devreme sau mai tarziu parazitii sa-ti produca o gramada de boli. Legatura dintre Paraziti si BOLI Dupa mai multe experiemente, cercetatoarea Hulda Clark a ajuns la concluzia ca multe din bolile cu care se confrunta omenirea in zilele noastre sunt produse de un anume parazit. Ea a scris si despre aceste descoperiri revolutionare in cartea “Vindecarea tuturor formelor de cancer” – pe care v-o recomand chiar daca nu aveti cancer. Cercetatoarea a descoperit in experimente ca: + organismele TUTUROR pacinetilor bolnavi de cancer erau supraincarcate cu parazitul Fasciolopsis buskii (un vierme plat). + TOTI pacientii cu boli de piele erau supra-infestati cu viermi cilindrici(oxiuri,limbrici etc). + TOTI pacientii cu acnee rosacee erau puternic infestati cu parazitul Leishmania. + TOTI diabeticii aveau trematodul pancreatic al bovinelor – Eurytrema. + TOTI cei care sufera de migrene au nematodul Strongyloides. + personele cu ASTM au ascarizii in plamani. + Multe persoane care fac infarct au viermi in inima(foto 2). + Parazitii care ajung la creier produc BOLI PSIHICE, in special schizofrenia + Persoanele care transpira excesiv noaptea sunt supra-infestate cu ascarazi. Si lista poate continua… Asadar Hulda Clark tras concluzia ca parazitii reprezinta o componenta esentiala in producerea a 90% din bolile cu care oamenii se confrunta in ziua de astazi. De ce sunt parazitii periculosi? Parazitii colonizeaza de obicei colonul si intestinul subtire al oamenilor, unde pot produce boala chron sau polipi, insa pot ramane si inofensivi daca gazda are un sistem imunitar puternic si o flora intestina echilibrata. Partea proasta incepe atunci cand parazitii reusesc sa treaca din intestine in restul organismului si se instaleaza in alte organe, incep sa apara bolile. Trecerea din intestine in alte organe se poate realiza pe fondul unei flore intestinale dezechilibrate, si DOAR in conditiile in care organismul este infestat cu alcool izopropilic. Insa Atentie! Parazitii nu pot supravietui in alte organe in afara de intestin, decat in prezenta ALCOOLULUI IZOPROPILIC (un produs secundar al industriei petrolului, folosit ca solvent). CUM ajunge alcoolul izopropilic in corpul tau? Foarte simplu, deoarece e o substanta la care suntem cu totii expusi in aceste vremuri. El se gaseste in: majoritatea sampoanelor(si patrunde prin piele in corp), in sucurile din comert, in produsele cosmetice, in apa de gura, in fixativul pentru par, in toate produsele pentru barbierti, in cafeaua decofeinizata, in cerealelel prelucrate, in diferite medicamente…si lista continua. Mai mult decat atat, specia comuna de bacterii clostridium produce alcool izopropilic in intestinul tau. Ideea e ca suntem atat de expusi incat chiar NU avem cum sa ne ferim. Asta e realitatea, oricat de infiorator ar suna. Insa vestea buna este ca Dumnezeu ne-a lasat in natura exact leacurile de care avem nevoie, pentru a ne curata periodic organismul de paraziti. Programul 100% natural de eliminare a parazitilor – Are la baza 3 PLANTE: + PELINUL (capsule sau ceai) + CUISOARELE(recomand cuisoare intregi, inlocul capsulelor) + Tinctura din COAJA NUC NEGRU Aceste 3 ingrediente luat impreuna au potentialul sa omoare majoritatea speciilor de paraziti care-ti colonizeaza corpul. Mai mult este 100% NATURAL , iar ingredientele le poti gasi la oricare magazin naturist ( mai putin tinctura de nuc negru, care se gaseste mai rar in magazine, insa se gaseste lejer pe internet). Dureaza 3 saptamani ! Iata programul pe cele 3 saptamani: * Dupa cum vezi tratamentul are 2 FAZE: 1. Faza de inceput (deparazitarea) - in care se face tratament intesiv pentru a elimina parazitii si oualeacumulate. 2. Faza de mentinere - in care se ia 1 data/saptamana tratamentul, pentru a preveni o noua supra-infestare – pe care ar fi bine s-o tineti regulat, toata viata. Adica: 0data in fiecare saptamana vei lua 2 lingurite de tinctura de nuc negru, 7 capsule de pelin si 7 capsule de cuisoare(aprox 3 lingurite de cuisoare intregi). Simplu, nu? Respectand aceste principii vei ajuta ENORM corpul in lupta cu parazitii, la care suntem cu totii expusi in fiecare zi. Alte remedii care ajuta in lupta cu parazitii: 1. Usturoiul Desi este cunoscut pentru calitatile anti-parazitare, anti fungice, anti bacteriene si de antibiotic natural pe care le are, beneficiile usturoiului merg mult mai departe de atat. Eu de exemplu in ultimii 2 ani n-am luat niciun medicament alopat, indiferent ca am avut ferba 39-40. De fiecare data cand racesc imi fac un suc de lameie si mananc cativa catei de USTUROI. In acesti 2 ani n-am fost racit niciodata mai mult de 3 zile, iar trratamentul nu a dat niciodata gres. 2. Argila Un alt supliment MIRACULOS. Si nu exageraz deloc. E unul din cele mai bune remedii pentru paraziti, insa are multe alte benefiii. Curata intreg oganismul de toxine si metale grele, purifica sangele, detoxifica ficatul, detoxifica intestinele, echilibreaza glandele endocrine, ajuta flora intestinala, are efect anti-depresiv si anti-stress, repara leziuniile din intreg tubul digestiv( de la gingivita, rosu in gat, gastrita, intestin iritabil…pana la hemoroizi), si foarte multe alte beneficii. Administrare: Desi se gaseste si sub forma de capsule, eu recomand argila pulbere sau granule – care se lasa intr-o cana cu apa de seara pana dimineata. Dimineata se amesteca si se bea apa argiloasa tulbure. Nu uita ca Dumnezeu ne-a facut din tarana. 3. Nuca de cocos Este plin internetul de articole despre beneficiile antiparazitare, antibacteriene si in special antifungice ale uleiului de cocos. Se poate consuma ulei de cocos natural, insa eu recomand nuca de cocos intreaga pentru rezultate mai bune. Tin minte ca am citit pe un forum despre unu baiat relativ sanataos, care a decis sa faca o cura de 2 saptamani cu ulei de cocos, deoarece auzise ca este sanatos. In timpul celor 2 saptamani ii s-a intamplat de 2 ori sa defecheze un pumn de viermi. Groaznic asa-i? ) 4. Seminte CRUDE de dovleac Aproximativ 50 de seminte de dovleac dimineata pe stomacul gol, era cura importiva parazitilor recomandata de regretatul Valeriu Popa. Acest remediu are capacitatea sa omoare cele mai comune specii de paraziti. 5. Fibrele vegetale Este esential sa elimini regulat materiile fecale. Constipatia(=neeliminarea fecalelor la mai mult de 48 de ore) duce inevitabil la dezvoltarea si inmultirea parazitilor, deoarece le oferi mediul perfect pentru devzoltare. Mai multe despre fibre am scris in articolul despre Detoxifierea Colonului 100% Natural. 6. Probioticele si Prebioticele Flora intestinala este bareiera dintre parazitii, bacteriile daunatoare si virusii din intestin si restul organismului. O flora intestinala echilibrata si sanatoasa va lasa doar nutrientii necessari sa treaca in organism , blocand orice altceva. Pentru a mentine aceasta flora sanatoasa este esential sa consumam regulat probiotice si prebiotice. * Probioticele sunt bacterii benefice precum cele dn intestin, care se se gasesc in produsele fermentate, in special IAURTUL si KEFIRUL. Atentie! Iaurtul facut de casa bate la orice ora d.p.d.v calitativ, orice iaurt din comert. Asadar mai bine cumpara lapte proaspat de la tarani si pune-l la prins, decat sa-ti dai banii pe cele din comert, facut exclusiv pentru a produce cat mai multi bani, si atat. * Prebioticele sunt alimentele care hranesc bacteriile benefice din flora intestinala: cicoarea, napul, ceapa cruda, usturoiul crud, sparanghelul, taratele de grau, fasolea si mazarea, spanacul si legumele cu frunze verzi, banana, ovazul etc. Dupa cum vezi prebioticele se gasesc intr-o gama larga de alimente, asa ca ai de unde alege. 7. Vitamina C Vitamina C joaca un rol esential in functionarea optima a organismului, cu atat mai mult in eliminarea eficienta a parazitilor. ATENTIE! Vitamina C de calitate NU se gaseste in capsule, ci in gradina! Vitamina C e un micronutrient format din: Rutina, Bioflavonoide, Factorul K, Factorul J, Factorul P, Tyrosinasa, Ascorbinogen,Acid ascorbic. Suplimentele din farmacii cu Vitamina C contin doar acid ascorbic, in timp ce in Vit. C din natura are TOATE componentele. Stiai ca ardeiul verde contin cel putin triplu vitamina C fata de citrice? Macesele 1500-2000 mg Vit. C /100g Arderiul verde 1600-1800 mg Vit. C/100g Catina 670 mg Vit. C /100g Patrunjelul 150 mg Vit. C /100g Kiwi 120-180 mg Vit. C /100g Coacazele 55-215 mg Vit. C /100g Portocala 53 mg Vit. C /100g *Ideea e ca, exista destule surse de vitamina C in natura! Nu e nevoie sa optezi pentru capsule. 8. Altele: Eu le-am prezentat mai sus pe cele mai comune si mai accesibile, insa asta nu inseama ca sunt sigurele. Mai au proprietati antiparazitare: * Argintul Coloidal * Samburii de grephuit si de lamaie * Aloe vera * Propolisul * Pau d’Arco * MMS (Mineral Miracle Solution) * Iodul (Sub forma de iodura de potasiu sau Solutie lugol) Si lista poate continua… Rotirea alimentelor Ca orice organism viu, parazitii au capacitatea de a se adapta in timp si de a deveni imuni la alimentele sau plantele care ar fi trebuit sa-i omoare. De aceea, nu vei avea rezultate consumand doar usturoi in fiecare zi sau doar se minte de dovlea in fiecare zi. Cea mai inteleapta alegere este ROTIREA ALIMENTELOR. Adica o saptamana consumi multa nuca de cocos, in urmatoarea semintele de dovleac, apoi treci la argila si asa mai departe… Astfel nu numai ca parazitii nu pot dezvolta rezistenta, dar vei fi capapil sa omori o gama mult mai larga de specii, deoarece nu toate speciile mor de la acelasi aliment. Oricum reginul HULDEI CLARK este punctul de plecare , deoarece cele 3 componente(nucul negru, pelinul si cuisioarele) sunt o combinatie care omoara majoritatea speciilor de paraziti…in mai putin de 3 saptamani

Borrelia burgdorferi adjutant in vaccinurile gripale

Declaratia unui cercetator: "Am scris un articol despre vaccinuri anul trecut în lista de Sănătate Publică. Am găsit brevete în care Borrelia burgdorferi a fost enumerate ca fiind folosit ca adjuvant in vaccinul brevet de gripa special. Nu știu dacă acest vaccin a fost adus pe piață sau nu. Toate vaccinurile conțin adjuvanți, care acționează pentru a stimula agresiv / ingreuna sistemul imunitar pentru a face vaccin mai eficient. Particule de metal, cum ar fi aluminiul sunt utilizate în prezent, dar mai mult, se folosesc agenți patogeni suplimentari în vaccinuri ca adjuvanti in afara patogen pentru care este de fapt vaccinul . Am găsit, de asemenea, in cercetare, în care Borrelia burgdoferi este studiata ca adjuvant în vaccinuri mucoasei nazale și un vaccin pentru Chlamydia trachomatis. L-am întrebat Dr. Garth Nicolson dacă utilizați Bb ca adjuvant în vaccinuri ar provoca boli, iar el a confirmat că aceasta ar putea provoca cu siguranta boli autoimune. El a spus că nu a fost conștient de vre-un vaccin prezent pe piata care contine Bb. Știm cu toții efectele pe termen lung ale BB pentru sistemul nostru imunitar. Primirea Bb în vaccinuri va garanta pe termen lung boala cronica, etiologia, care cel mai probabil nu va fi niciodată determinată. Am o teorie pe care eu nu pot dovedi încă. Teoria ce m-a condus la această cercetare și alte brevete. M-am întrebat de ce există atât de mulți oameni care au test pozitiv pentru boala Lyme / BB, care nu au fost muscati de capuse. M-am întrebat dacă s-ar putea ca Bb a fost deja utilizat în vaccinuri pe care oamenii le-au primit ani în urmă, când au fost tineri. Asta e ceea ce ma determinat prin aceasta cercetare. Poate că știe că CDC Bb a fost folosit în vaccinuri de ani în urmă, la fel ca și virusul simian 40, care provoaca leucemie a fost cunoscut de Merck au fost în celulele renale de maimuta, care au fost utilizate pentru a dezvolta vaccinuri de poliomielita care au fost administrate la 40 de milioane de oameni de ani în urmă. Acum avem o epidemie de leucemie. Hmmmm. Imaginați-vă că si Merck cu bună știință a comercializat vaccinul în acest fel. Bayer a lansat un medicament pentru hemofilicii care conținea HIV. Medicamentul a fost interzis in SUA, dar apoi Bayer a vandut in 2 sau 3 țări din Europa în loc. Este într-adevăr atât de exagerata sa cred ca Big Pharma ar comite astfel de atrocități din nou și din nou pentru profit? Dacă Bb a fost deja utilizată în vaccinuri, s-ar explica acțiunile inumane și înșelătoare ale CDC în toți acești ani. Cu alte cuvinte, știm postura CDCs pe LD se datorează actual de dezvoltare a vaccinurilor Lyme pentru profit. Cu toate acestea, ar putea postura CDC și este eșecul orchestrată în criteriile de diagnostic să fie, de asemenea, rezultatul unei anterioare, Public Health Service / risc vaccin Militar / farmaceutice, care ar duce la multe manifestări neurologice ale bolii pentru profit, de etiologii ale care se pretinde a fi necunoscut? (MS, ALS, Parkinson, ETC) Big Pharma a fost demonstrată în multe instanțe de a comite astfel de acte criminale, deci nu cred că teoria mea este în afara liniei. Pur și simplu nu am putut să-l documenteze - încă"

Formation of ‘dormant’ Borrelia stages

Leandro Lemgruber1, Christiane Brenner2, Misha Kudryashev3, Yuri Abud4, Celso Sant’Anna4, Reinhard Wallich2, Freddy Frischknecht1 1. Department of Infectious Diseases - Parasitology, University of Heidelberg Medical School, Germany 2. Institute for Immunology, University of Heidelberg Medical School, Germany 3. Center for Cellular Imaging and Nano Analysis (C-CINA), Biozentrum, University of Basel, Switzerland 4. Laboratório de Biologia, Diretoria de Programa, Inmetro, Brazil email: leandro.lemgruber@med.uni-heidelberg.de Keywords: Video-microscopy, cryo-electron microscopy, cryo-immunolabeling, immune-scanning electro microscopy Spirochetes of the genus Borrelia are the causative agents of Lyme disease, a tick-borne zoonosis mainly found in North America and in Europe [1]. Even after antibiotic treatment some patients may go on to develop persistent Lyme disease symptoms. The mechanism of bacterial survival in the presence of the hosts’ immune system is still poorly understood. One possible explanation for this clinical observation is the formation of Round Bodies (RB), a pleomorphic stage formed when spirochetes are exposed to unfavorable conditions [2]. Here we used GFP-expressing B. burgdorferi to characterize this transformation process, exposing the spirochetes to different culture conditions. Using video-microscopy, we were able to follow the conversion of the spirochetes into RBs under unfavorable conditions, with the GFP signal concentrated in a round spot. Cryo-immunolabeling and quantitative fluorescent analysis showed that this is not caused by a leaking of the GFP fluorescence but by a concentration of GFP into a single spot. Although RBs are observed in cultures under normal conditions, their number increased when spirochetes were exposed to adverse conditions. This transformation can be reversed, since bacteria induced to form RBs can be re-transformed back to spirochetes. Live/Dead assay showed that these RBs were viable even after several days under adverse conditions. Negative staining and cryo-tomography [3] observations showed that this transformation led to a detachment of the outer membrane and formation of vesicles that are secreted by the bacteria. When examined through scanning electron microscopy, the bacterial surface was covered with small vesicles. Previously, it was shown that Borrelia spirochetes could evade the hosts’ immune response via differential expression of outer surface proteins. We applied immunofluorescence and immune-scanning electron microscopy [4] to analyze the pattern of distribution of major surface proteins, i.e. OspA, OspB, OspC, p39 and p83, on the helical forms of spirochetes and RBs. OspA was detected over the whole surface of the spirochetes, while OspB, OspC, p39 and p83 were distributed in a scattered manner. When we observed the RBs after 6 or 24 hours in adverse condition, OspA now presented a scattered distribution, as did OspB. However, we did not detect the presence of OspC, p39 and p83, although the level of protein expression was not altered during RB induction, as analyzed by western blot. Immuno-SEM showed that the bacteria shedded these surface proteins in vesicles, when they are in adverse conditions. References [1] Radolf JD et al., Nat Rev Microbiol 10 (2012), p. 87. [2] Brorson Ø et al., Proc Natl Acad Sci USA 106 (2009), p. 18656. [3] Kudryashev et al., Mol Microbiol (2009), p. 1415. [4] Sant’Anna et al., Histochem Cell Biol (2005), p. 87. [5] The authors gratefully acknowledge funding from the German Research Foundation (DFG), the Cluster of Excellence CellNetworks from the University of Heidelberg, European Research Council (ERC).

GcMAF

http://www.gcmaf.eu/info/

Sindromul de Oboseala Cronica

Viral infection ruled out as cause of ME Published on Tuesday 18 September 2012 00:00 VIRUSES have nothing to do with chronic fatigue syndrome (CFS), despite earlier evidence of a link, a study has shown. The new findings deepen the mystery surrounding the cause of the debilitating condition, also known as myalgic encephalomyelitis (ME). Scientists dismissed previous claims that two viruses, known as XMRV and pMLV, may underlie CFS. “The bottom line is we found no evidence of infection with XMRV and pMLV,” said Dr Ian Lipkin, a member of the research team at Columbia University in New York City. “These results refute any correlation between these agents and disease.” In 2009 and 2010, separate studies found the two viruses in the blood of CFS patients, raising hopes of identifying an easily treatable cause of the condition. But since then, other investigators have been unable to confirm the results.

Raspandirea capuselor datorita incalzirii globale

http://newswatch.nationalgeographic.com/2012/09/07/disease-spreading-ticks-on-the-move-as-climate-changes/

Un nou virus de la capusa

http://www.nytimes.com/2012/09/04/health/research/new-tick-borne-heartland-virus-has-scientists-puzzled.html?_r=1&partner=rss

Curcumina

http://www.eurekalert.org/pub_releases/2012-08/gmu-tsu081612.php

Doze mari de vitamina C??!!

http://www.lymeneteurope.org/info/vitamin-c-a-lyme-patient-s-friend-or-foe

lyme vs sifilis

It appears that the Lyme spirochete and the spirochete that causes syphilis are only about fifty percent similar genetically, and that the syphilis bacterium completely lacks the additional 838 plasmid genes of the Lyme bacterium. Since the plasmid genes are the genes which code for all of the transmembrane proteins and OSP lipoproteins, it appears that Borrelia, at least from a genetic standpoint, has a greater range of antigenic variation than the treponemes. This could suggest to some that the Lyme spirochete is more evolved, more advanced, and better equipped to deal with host immune systems. Se pare că spirochetele Lyme si spirochetele care provoacă sifilisul sunt doar aproximativ cincizeci la sută similar genetic, și că bacteria sifilis nu are complet plasmida suplimentara 838 a bacteriei Lyme. Deoarece genele plasmida sunt genele care codifica toate proteinele transmembranare și lipoproteinelor OSP, se pare că Borrelia, cel puțin din punct de vedere genetic, are o gamă mai largă de variație antigenică decât treponemele. Acest lucru ar putea sugera faptul că la unele spirochete Lyme sunt mai evoluate, mai avansate, și mai bine echipate pentru a face față sistemelor imunitare gazdă.

scheme de tratament din alte tari

In UK te poti trata de borrelia intr-o clinica privata aflata langa Londra. Recent am intrat pe forumul pacientilor tratati de aceasta clinica si am aflat schemele de tratament. Ca sa faci testele si sa te consulte un doctor acolo ajung la 5000 lire, apoi tratamentul ajunge la 13000 lire. Incluse sunt 3 luni de cefort 2 g/ zi, apoi antibiotice orale cu naturiste. Antibioticele orale preferate sunt: doxiciclina 200 - 400 mg zi timp de 4- 4 luni + niste naturiste pt spargerea chisturilor, sau amoxacilina cu claritromicina + naturiste pt cateva luni si poate 1 luna cu rimfapicina. Pe langa aceste tratamente se ma prescriu fel si fel de infuzii cu vit C si altele. Nu am nimic impotriva tratamentelor naturiste, dar chiar daca il combina cu antibiotice tratamentul lor e f slab comparativ cu cel din Romania,Ungaria, Germania sau SUA.Doxiciclina luata 3 luni, 400 mg/zi e egal cu zero daca nu e combinata cu un tinidazol. Ma bucur ca nu am ajuns sa dau banii pe acolo si ca am posibilitatea sa ma tratez in Romania. Cu 13000 lire te tratezi cativa ani buni in Romania si mult mai bine decat in UK. Alt lucru pozitiv este ca in Romania se foloseste DFM -ul si in UK nu. Multi dintre ei nu stiu ce co-infectii au. Am scris toate astea pt cei care se trateaza in Romania si cred ca in alte tari tratamentul este mai bun. Clar in UK nu pare prea adecvat pt a combate bacteria.

Sfarsitul rundei 3 antibiotic

Am incheiat si runda 3 de antibiotic cu rifampicina si tavanic. M-am simtit mai bine decat la runda 2, dar scamele in ochi au devenit foarte intense si am avut dureri in umeri, spate si piciore. Durerile nu mi-au trecut nici acum in pauza, dar scamele din ochi s-au mai diminuat.

Sper sa fac intravenos a 4 a tura dearece durerile in articulatii sunt insuportabile si ametelile, problemele cu vederea nu imi dau pace.

Sunt foarte descurajata de rezultate. Speram sa-mi revin cat de cat sa fiu in stare sa muncesc, dar vad ca rezultatele bune se lasa asteptate.

Lyme arma biologica

http://rense.com/general69/lyme.htm

Sfarsitul rundei a 2-a

    S-a terminat si runda a 2- a de tratament. Am avut si zile bune si rele, dar mai multe rele. Au mai trecut durerile de spate si de picior, dar a ramas slabiciunea, tremuratul in picioare si problemele de respiratie cu palpitatii si dureri in partea stanga a pieptului si sub coaste. In ultimele 3 zile de tratament am facut o gripa foarte urata de am stat vreo 2 zile in pat. Chiar a fost gripa caci toti din casa au avut-o.

Acum sunt in prima zi de pauza si ma ustura ochii foarte rau, am ameteli, slabiciune , tremurat in picioare si nelipsita problema cu respiratia. 

Oare dupa cate ture de antibiotic ma voi simtii normal? 

Lyme si co-infectii

Lista simptomelor pentru Lyme si coinfectii

http://www.lyme-symptoms.com/LymeCoinfectionChart.html

Care o fi oare adevaraul?

http://www.x-rx.net/blog/2010/06/open-letter-to-ilads-from-a-former-member.html

Protocol antibiotic pentru Lyme

Antibioticele folosite in tratarea Lyme

http://www.canlyme.com/guidelines[1].pdf

puterea otetului de mere in diferite afectiuni

http://healthnews.benabraham.com/html/wonderdrug_for_chronic_ailment.html

Medicatia ajutatoare

Lista cu vitaminele si medicamentele ajutatoare in perioada tratamentului antibiotic.

1. Betaserc
2. Omeran
3. Laptisor de matca
4. Cucurmin
5. Silimarina
6. Ginkgo Biloba
7. Suc Aloe Vera
8. L-Carnitine
9. Vit C
10. Complex multivitamine si minerale
11. Complex B
12. B12
13. Sarsaparilla
14. Devil's claw
15. Probiotice

a doua tura de antibiotic

Tratamentul meu este prescris pe 4 luni dupa care trebuie sa vin in Romania sa repet testele si sa vad care e continuarea. Toate antibioticele si vitaminele au fost cumparate din Romania. Aici nu aveam nici o sansa sa-mi prescrie cineva atatea antibiotice.

Dupa prima tura am avut 7 zile pauza si apoi am inceput 28 zile cu doxiciclina, ciprobay si tinizol.

Durerea de cap mi-a trecut de la prima tura de tratament. Dar scapi de unele si dai de altele. In continuare am probleme de respiratie, dureri in piept, dureri de spate si de picior stang. Incerc sa fac exercitii in fiecare zi, treburi casnice si imi scot cainele la plimbare. Deci ma mentin activa, dar imi este foarte greu deoarece durerea este constanta. Sa nu mai vorbesc de ameteala!!

Sunt in a 2-a zi din seria a 2-a si va voi tine la curent cu progresul meu.

As aprecia daca cineva a avut acelasi simptome ca ale mele sa ma sfatuiasca cu sa scap de ele.

prima tura de antibiotic

Prima tura de antibiotic azitrox + tinizol. Primele 4 zile m-am simtit ca o stafie. Nu aveam echilibru, nu simteam ca picioarele imi ating pamantul, dureri groaznice in piciorul stang, partea de sus si coapsa. Apoi am inceput sa am probleme cu respiratia.  Parca nu-mi ajungea aerul. Desi luam toate vitaminele si beam mai mult de 3 litri de apa pe zi tot nu reuseam sa ameliorez starea in care ma aflam.M-am speriat de problema cu respiratia si am facut o radiografie pulmonara care a iesit perfecta.Apoi am inceput cu dureri groaznice de spate.

In a 3-a saptamana de tratament a trebuit sa ma intorc in UK, desi dorinta mea era sa raman in Romania sa ma tratez pana imi revin cat de cat la normal.

Intoarsa aici mi-am gasit un alt doctor de familie care mi-a acceptat diagnosticul si mi se fac analize de sange lunare pt monitorizarea ficatului si rinichilor. Doamne ce norocoasa sunt sa gasesc un asemenea doctor. Problema e ca aici nu stiu sa trateze Lyme. Este o clinica langa Londra care este exagerat de scumpa si mai e un doctor de familie prin Tara Galilor care a fost amentat ca i se ridica licenta daca mai trateaza de Lyme.

Am vazut pe internet ca lumea se vaita de Romania ca sunt doctori ignoranti, dar aici este de 10 ori mai rau. Mi-a placut ca in Romania s-a mediatizat totul si s-a informat publicul. Aici nu se face asta. Aici se poate spune ca se trateaza totul cu ignoranta. Medicamentul miracol pt orice este paracetamolul si daca nu merge cu el, atunci direct antidepresant sa te mai calmezi putin.

Eu am venit in Romania si am avut adevaratul diagnostic si tratament in 2 saptamani. In UK nu au reusit in 6 luni si nu reuseau in veci cu testele pe care le au. Aici nu se face WB decat daca Elisa iese pozitiv. Oricum in Bucuresti si Elisa mi- iesit pozitiv ceea ce dovedeste ca se foloseste o calitate superioara celor folosite in UK.

Cum a inceput totul

Cum a inceput totul........

Totul a inceput in noiembrie 2011. Conduceam in drum spre casa si la o intersectie am intors capul spre dreapta pentru a ma asigura, iar cand l-am intors sa ma uit in fata nu am mai vazut nimic. Totul a devenit negru, nu mi-am mai simtit mainile si picioarele si am crezut ca voi lesina. Am reusit sa trag pe dreapta sa-mi revin si am reusit sa conduc pana acasa tremurand si cu vederea afectata. Din aceasta zi nu mi-am mai revenit. Ameteli si dureri de cap constante. Dupa o luna am inceput sa am mioclonii. Imi sarea capul, mana, piciorul si nu puteam dormi toata noaptea. Am facut control la ORL, specialist de migrene, neurolog, RMN, ecograf, analize de sange pt boli autoimune. Totul era perfect. Concluzia a fost ca sufar de depresie.Desi mi se dadusera o groaza de antidepresante sa tratez migrena si nimic nu a mers, acum vroiau sa incerc cu unele mai puternice si doze mai mari. Singurul care ma ajuta in durea de cap si maxilare era lyrica in doza minima si nu am vrut sa-l schimb.

Incercand sa gasesc pe internet ce boala as putea avea am vazut o poza cu eritemul migrator si mi-am adus aminte ca l-am avut in urma cu 2 ani, iar doctorul de familie mi-a zis ca e tinea corpis si mi-a dat o crema. Am avut 2 teste Elisa pt Lyme si au iesit negative. Eu locuiesc in UK unde este foarte greu sa ai o programare cu un specialist sau sa ceri sa ai un anumit test. Oricum am reusit sa am un Elisa la privat si unul in spital, pluse o punctie lombare. Toate negative ca de obicei.

Fiind sigura ca am Lyme si stiind ca am fost in foarte multe locuri de risc am decis sa ma intorc in Romania si sa-mi fac testele. Am ajuns in Bucuresti in mai 2012, dupa 6 luni de chin. Starea se inrautatise foarte mult dupa punctia lombara. Aveam dureri de cap oribile si nu-mi mai simteam piciorul stang. Imi era foarte greu sa merg si trebuia sa fiu insotita de cineva in permanenta. Ma simteam beata 24/7.

Analizele au fost pozitive pt garini si burgdorferi plus bartonella.In final aveam diagnostic si primisem tratamentul potrivit.