posted
I've read one case report about this, but it didn't play out like this stragegy.
First off, I'm usually not into alternatives as everyone can probally tell from my posts. I stick pretty closly to what the ILADS have to say.
However, when I come accross something that may be in the middle between Duck, and ILADS, I find it interesting because though the ILADS system does work for a lot of Lyme patients, it takes a long damned time, and we often relapse years later.
So, since I'm big on science, I actually think this makes sense. What do you guys have to say?
An alternative therapy that may have some legitamate logic with things like fact to base the theory.
We all know that Borrelia can induce tolerance within the immune system, and that it causes permanent infection without antibiotics, even the Ducks admit that. The rest of us know that it can become permanent, or nearly permanent even though we do use antibiotics.
Read this. Perhaps Borrelia change the immune system just like parasitic worms that live in the body for years-and by using steroids, which made patients worse, we had always assumed immunosupression didn't work. But, what if we used the wrong immunosuppressive, and we take away the ability of Borrelia to change the immune sytem, impair its abiltiy to hide, then hit it with antibiotics.
I'd like to see the results of some trials on this, as, if they can get some data on how this drug affects the immune system in a specific way, and then they can show borrelia does the same thing, and this this drug would kinda competivly inhibit Borrelia's ability to change things....... I think it actually has some promise.
(Datum: 13.4.2006)
Isabel Diterich, Immunomodulation and new therapeutic strategies in Lyme borreliosis, Dissertation (Dr. rer. nat.), Universit�t Konstanz, 2003.(im Cache) 7 Summary If infection with Borrelia burgdorferi is not treated adequately with antibiotics in an early stage, it may lead to Lyme borreliosis (LB), a chronic multisystemic disorder which is difficult to cure. In some cases the pathogen survives in spite of antibiotic treatments. It is challenging to understand why Borrelia are often not eradicated, although being recognized by the host's immune defense and occasionally inducing a strong inflammatory reaction. Thus, it remains an area of debate how this pathogen persists in human tissues. This question was addressed in the present thesis, examining possible immune evasion mechanisms of Borrelia.
Blood cells from patients suffering from persistent LB released significantly lower levels of pro-inflammatory cytokines (TNF� and IFN�) in response to either Borrelia lysate or to lipopolysaccharide (LPS) in comparison to cells from healthy volunteers. In blood from healthy volunteers Borrelia lysate led to strong production of anti-inflammatory IL-10 and G-CSF, while inducing only low levels of proinflammatory IFN�, compared to LPS. Similar to endotoxin tolerance, different Borrelia preparations desensitized human blood monocytes on re-stimulation with either stimulus. Borrelia-specific stimuli induced cross-tolerance towards heterelogous stimuli such as lipopolysaccharid (LPS) and lipoteichoic acid (LTA) in human monocytes. Toll-like receptor (TLR) 2 but not TLR4 was required for Borrelia-induced tolerance and cross-tolerance, as shown in experiments with knock-out mice. PBMC tolerized by Borrelia lysate exhibited reduced TLR2-mRNA levels. Further, IL-10 was identified as a key mediator involved in tolerance-induction by Borrelia lysate. Combination of Filgrastim treatment with Ceftriaxone in a late stage LB-patient who failed standard antibiotic therapy led to successful eradication of the pathogen and complete regression of symptoms. The mouse model of Borrelia infection was set up and characterized in order to study the therapeutic effects of Filgrastim in vivo. Treating immunocompetent and immunodeficient SCID mice with Filgrastim, as an immunosupportive therapy of LB did not attenuate the characteristic ankle swelling induced by Borrelia infection. Regular application of Filgrastim led to an enhanced elimination of Borrelia from various organs in SCID mice. In immunocompetent mice this effect was less pronounced. In summary, we propose that Borrelia modulate the host's immune system in order to evade clearance in the immunologically competent host. Tolerance could represent the mechanism inhibiting host response thereby enabling survival and persistence of the pathogen. Promising results were obtained testing a novel treatment strategy for late stage LB, a combination of Filgrastim as an immunosupportive therapy with antibiotics. The respective clinical trial based on these findings was recently started.
Posts: 559 | From Cary, NC | Registered: May 2006
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Aniek
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posted
I don't understand most of this. But, I when researching reactive arthritis, I remember multiple people mentioning that the current way of managing symptoms of people with RA are immunosuppresants that reduce length of life.
This was mentioned by people who were using minocylcine to reduce RA and other arthritic symptoms.
Is this a similar immunosuppresant? Sorry if I'm completely off track.
I blame Lyme for my total inability to understand science. My new theory is that the cognitive symptoms hit during chemistry my sophomore year of high school and disappeared as soon as I dropped the class
-------------------- "When there is pain, there are no words." - Toni Morrison Posts: 4711 | From Washington, DC | Registered: Mar 2004
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posted
Ok, here is the whole darned thing, after reading a bit, and only a couple of pages at that, I can't wait to read this entire thing.
I'm rather giddy! I feel like a physicist in the early 10920's reading Einsteins work for the first time. Simply amazing. THIS IS A TRULY REVOLUTIONAIRY IDEA.
And, he is basically saying, well what about this. How does Borrelia continue to live, there are all kinds of conflicting studies, some studies showing a strong inflamatory response in vitro, but thats impossible to explain everything about Borrelia because we have all these other studies finding borrelia later on, so something else might be going on, it has to, because the current theory DOES NOT EXPLAIN THE INCONGRUINCY OF DATA.
FINALLY, someone who actually thinks like a scientist!!
This is what I've been searching for, and NEVER could understand.
Why did the ducks, who are supposed to be scientists, never say, OK, we got some of it right, but not the whole thing. WHY?
But, what did they do, they never asked that question. Cudos to this professor, even if it turns out that your theory is wrong, I still say that this is the most origninal idea concerning Lyme Disease that I've heard in a very long time.
If HE IS RIGHT, He deserves the NOBEL in Medicine. I for one am going to try to contact this guy, I still can't believe we havn't heard of this before.
posted
My mistake. He is not saying anything about using immunosupressives. He is talking about using a drug that prevents infection durring cancer treatment. He thinks that this drug restores immune competence agaisnt Borrelia kinda like durring the early stages of LB, and if one does this, Lyme gets a lot easier to cure.
I think I've read something about this before, but from someone using a far less targeted therapy. Truth is, I've even thought about something like this, but, this guy is much further along than I ever was, prolly cuz he doesn't have a Lyme Brain.
Here is an abstract that explains this idea in a simpler way, and in a shorter way so you don't have to read the 101 page dissertation.
Diterich I. 2003. Immunomodulation and new therapeutic strategies in Lyme borreliosis.
Experimental Therapy of Lyme borreliosis with Granulocyte Colony-Stimulating Factor (Filgrastim)
Isabel Diterich, Carolin Rauter, Albrecht Wendel and Thomas Hartung
Biochemical Pharmacology, Faculty of Biology, University of Konstanz
submitted to Wien Klin Wochenschrift
5.1 Abstract
Therapy of late stage Lyme borreliosis (LB) is difficult due to the limited success of antibiotic treatment in some cases.
Here, we report an anecdotal observation of a late stage LB patient, who was successfully treated by a combination therapy of the cephalosporin antibiotic Ceftriaxone plus Filgrastim. As the patient became free of any symptoms with this new regimen, we were interested to investigate the effects of Filgrastim treatment of LB in more detail.
Based on this case and on our recent report, that Borrelia modulate the host's immune response impairing their elimination (30), we raised the hypothesis that Filgrastim might restore the pathogen-induced dysfunction of immune competence. In order to study the therapeutic effects of Filgrastim in Borrelia infection we carried out experiments in two different mouse models.
We first assessed the ankle swelling of Borrelia-infected immunocompetent disease-susceptible C3H/HeN mice treated with Filgrastim compared to placebotreated controls and found that treatment had no beneficial effect on the pathology, i.e. joint swelling. In the next experiment the bacterial load was determined by quantitative real-time PCR. Less spirochetes were found in the bladder and in the ankle of Filgrastim-treated C3H/HeN mice compared to the placebo-treated. In severe combined immunodeficiency (SCID) mice infection again resulted in severe arthritis in both groups, however, the numbers of Borrelia were less in all organs tested of the Filgrastim-treated group. Taken together, the positive effects of Filgrastim treatment in the patient case as well as in mice prompted us to propose a clinical study on immunosupportive therapy of LB.
V�it�skirjassa tutkittiin my�s syit� Borrelioosin kroonistumiseen eli Borrelia bakteerin selviytymist� elimist�ss� immunij�rjestelm�n toiminnasta huolimatta. Tutkimuksessa havaittiin BB:n kykenev�n muuttamaan immuunij�rjestelm�n toimintaa vaikuttamalla sek� tulehdusta hillitseviin ett� -lis��viin mekanismeihin:
We investigated whether Borrelia modulate the host's immune system in order to persist. Blood cells from patients suffering from persistent Lyme borreliosis released significantly lower levels of pro-inflammatory cytokines (i.e. TNF? and IFN?) in response to either a Borrelia-specific stimulus or to lipopolysaccharide (LPS) incomparison to the cells from healthy volunteers (30). Based on their findings in patient specimens, others have also described Borrelia as an immunomodulator, supporting the hypothesis of Borrelia-induced immundysregulation (91), (92). In line, Borrelia seem to influence the balance between the pro- and anti-inflammatory immune response. We and others found that Borrelia not only induce proinflammatory cytokines, but also lead to a strong formation of IL-10, which is an important down-regulator of the pro-inflammatory immune response (30, 46, 84).
.............. 4.5 Discussion
Understanding the immunopathology of LB is still a major challenge. Although inducing strong immune activation, e.g. in phases of arthritis, the causative agent of LB persists and leads to a chronic pathology in the immunocompetent host. Noteworthy, the inflammatory episodes in LB are typically self-limiting and the site of manifestation often changes e.g. between different joints.
These phenomena suggest counter-regulatory anti-inflammatory mechanisms and the long phases of latency indicate phases of immune evasion.
We recently proposed a possible mechanism for survival of Borrelia in the immunologically competent host: Since our ex vivo experiments with whole blood from patients with LB revealed a significantly reduced capacity to release TNF? and IFN? in comparison to blood cells from healthy controls, we postulated that Borrelia modulate the host's immune system in order to evade immune clearance (30). There are few reports about Borrelia acting as an immunomodulator (91, 92, 115). We found further evidence for Borrelia-induced immunomodulation by demonstrating, that Borrelia induce a stronger anti-inflammatory cytokine-response than endotoxins from various other Gram-negative bacteria (30).
.............. Taken together, in this study we characterized Borrelia-induced desensitization in human monocytes which is cross-reactive to LPS and to LTA and IL-10- and TLR2-dependent. Based on this ability of Borrelia to render cells hyporesponsive we propose that this might mirror a mechanism how this human pathogen avoids elimination and persists in the host leading to chronic disease.
Posts: 559 | From Cary, NC | Registered: May 2006
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posted
I don't think the concept is completely new.
For example Buhner's protocol is based on the same idea. (see Buhner: Healing Lyme, p.71f.: "Immune Modulation and Support")
Btw Mrs Diterich is a SHE.
Posts: 71 | From germany | Registered: Mar 2006
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Dave6002
Frequent Contributor (1K+ posts)
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posted
That's almost 100% certain that the chronical infection of Bb is due to its suppression of host immune system.
Even at the beginning of the infection, it depends on the immune suppresson of Tick bite. Without Tick bite, Bb couldn't establish successful infection.
I agree that immune-supportive therapy would be a breakthrough in Lyme therapy.
Cytokines, such as TNFa, interferon, GCSF, interleukins etc. play important roles in immune system modulations.
In the Salt/Vitamin C therapy, they implied that impproving immune system is critical.
Why don't we reapeat the experiments by including Filgrastim (GCSF) in our abx therapy.
In Stephan's book Healing Lyme, immune modulation is a big topic and several main herbs like Cat's Claw have significant immune modulation function.
Posts: 1078 | From Fairland | Registered: Apr 2006
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quote:Originally posted by 777: I don't think the concept is completely new.
For example Buhner's protocol is based on the same idea. (see Buhner: Healing Lyme, p.71f.: "Immune Modulation and Support")
Btw Mrs Diterich is a SHE.
Good point. I said the same thing. Of course its not new.
The thing that IS new is that he seems to be advocating a SPECIFIC WAY to do this.
What's more is that he is a legitamate, respected scientist who published in major journals.
He believes in chronic Lyme, as any, REAL scientist would if they READ the freaking science. IT didn't make sence, one report goes one way, another goes another way.... how can they both be researching the same damned thing.
Ahhhh, just as with Newton when Einstein came along, we found out that well, Newton was incomplete.
So, have other people suggested immune problems. Yes, of course. The difference here is that this scientist has found a way to explain this scientifically in a much more quantitative way, as opposed to the qualitative method we all knew to be true, but the point is that work like this is much more likely to be broadly accepted by the scientific community.
Here is one paper they published on this. Apparently, they are in the process of publishing their clinical trial.
Infect Immun. 2003 Jul;71(7):3979-87. Related Articles, Links
Borrelia burgdorferi-induced tolerance as a model of persistence via immunosuppression.
Diterich I, Rauter C, Kirschning CJ, Hartung T.
Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Konstanz, Germany.
If left untreated, infection with Borrelia burgdorferi sensu lato may lead to chronic Lyme borreliosis. It is still unknown how this pathogen manages to persist in the host in the presence of competent immune cells. It was recently reported that Borrelia suppresses the host's immune response, thus perhaps preventing the elimination of the pathogen (I. Diterich, L. Harter, D. Hassler, A. Wendel, and T. Hartung, Infect. Immun. 69:687-694, 2001). Here, we further characterize Borrelia-induced immunomodulation in order to develop a model of this anergy. We observed that the different Borrelia preparations that we tested, i.e., live, heat-inactivated, and sonicated Borrelia, could desensitize human blood monocytes, as shown by attenuated cytokine release upon restimulation with any of the different preparations. Next, we investigated whether these Borrelia-specific stimuli render monocytes tolerant, i.e. hyporesponsive, towards another Toll-like receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-positive bacteria, or towards the TLR4 agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli was induced. Furthermore, using primary bone marrow cells from TLR2-deficient mice and from mice with a nonfunctional TLR4 (strain C3H/HeJ), we demonstrated that the TLR2 was required for tolerance induction by Borrelia, and using neutralizing antibodies, we identified interleukin-10 as the key mediator involved. Although peripheral blood mononuclear cells tolerized by Borrelia exhibited reduced TLR2 and TLR4 mRNA levels, the expression of the respective proteins on monocytes was not decreased, ruling out the possibility that tolerance to Borrelia is attributed to a reduced TLR2 expression. In summary, we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts.
PMID: 12819085 [PubMed - indexed for MEDLINE]
Posts: 559 | From Cary, NC | Registered: May 2006
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posted
Well, I don't know if we should start taking this medicine yet, though it is already approved by the FDA, and on the market.
Of course, educate yourself on this idea, bring it to the attention of your LLMD. Ask him to talk to this professor. Maybe your LLMD thinks it a good idea, and may try it on a few patients to see if it works, BUT, I think we need to see what some LLMD's think about this as they see a LOT of Lyme.
I for one have a treatment regamine that currently works. However, I plan on bringing this info to my doctor as I think it is something that we should definatly look into.
Posts: 559 | From Cary, NC | Registered: May 2006
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Dave6002
Frequent Contributor (1K+ posts)
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posted
Immune suppression of Bb is just one side of multiple faced demon: Lyme is a desease of a complex of multiple agents including Bb, Bart, Babs etc. and probably there is no ring-leader here.
That's why monotherapy might never work; Lyme is the biggest imitator; long term abx therapy is required; too many herx reactions; too many relapses...
Admit or not, basically we don't know how to efficiently cure Lyme: we are all guinea pigs.
Just focus on one agent but not all the agents at the same time probably is the cause of our frustrations.
Restoring immune system will target all infectious agents in our body and probably would be more efficient.
For a complex disease, the answer is an army of therapeutics.
Posts: 1078 | From Fairland | Registered: Apr 2006
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luvs2ride
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Member # 8090
posted
Building up the body so it can do the job God intended it to do is what alternative care is all about.
It doesn't require a scientific brain and it isn't new. It is commonsense.
I do love and support the idea of science studying natural medicine.
BTW, I am rapidly moving into full remission of all symptoms especially the arthritis. I will keep posting as to how permanent my recovery proves to be.
Sorry it is not scientific, but it is a real life experience.
-------------------- When the Power of Love overcomes the Love of Power, there will be Peace. Posts: 3038 | From america | Registered: Oct 2005
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posted
As far as I got it Mrs Diterich tested the protocol on one human being and two mice (or one mouse & one control mouse) for her dissertation in 2003. A clinical study was announced there, but nothing seems to be published about that yet.
posted
Think other useful research has come from this author and collaborators, so it would be advisable to keep an open mind on the idea.
Not quite ready to jump into this treatment myself yet, but hoping they do proceed with larger scale studies of immune modulator + antibiotic. It is always encouraging when a researcher admits that the disease can be chronic even after supposedly sufficient abx were taken. These are the only researchers who are going to help us find a solution. The ones who say "post lyme syndrome" are never going to help us, since they don't even recognize the problem.
It is definitely true that taking abx forever is not the best solution. Unfortunately, it is all we have now. Need better ideas.
As someone else pointed out, we have a soup of pathogens, so one combo of drugs isn't going to fix the whole thing.
A while back I posted some abstracts on immune modulation. There was discussion at the time about the side effects of these drugs and other potential hazards.
But still worth keeping an eye on this.
Posts: 8430 | From Not available | Registered: Oct 2000
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oxygenbabe
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posted
I recall a letter to one of the prominent journals about treating late stage lyme in a patient with rocephin and then he relapsed; they added in G-CSF (granulocyte stimulating factor), at least I think they did, or maybe it was IVIG, but I think it was the former, gave another course of rocephin and he got well. A similar idea perhaps.
If you have coinfections not sure how that would work.
Posts: 2276 | From united states | Registered: Jun 2004
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Marnie
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Member # 773
posted
Pro and Con:
Filgrastim is used to treat neutropenia (a low number of neutrophils), stimulating the bone marrow to increase production of neutrophils.
(Neutrophils are the most abundant of the WBCs and contain calprotectin which binds zinc.)
Neulasta� (pegfilgrastim) is prescribed to reduce the risk of infection (initially marked by fever) in patients with some tumors receiving chemotherapy that may decrease the number of infection-fighting white blood cells.
Rare cases of a ruptured spleen and sickle cell crises have been reported in postmarketing experience with Neulasta�. Report symptoms of abdominal or shoulder tip pain to your doctor immediately.
In rare cases, serious allergic reactions can occur, causing a rash, shortness of breath, wheezing, dizziness (a drop in blood pressure), swelling around the mouth or eyes, fast pulse, or sweating.
Sometimes these symptoms could come back within days after stopping treatment for the allergic reaction. If you get these symptoms at any time, stop using Neulasta� and call a doctor or get emergency care right away.
If you have an allergic reaction during the injection of Neulasta�, stop the injection right away. In a clinical study, mild to moderate bone pain occurred in 31% of the patients in the study taking Neulasta� and in 26% of the patients taking a placebo injection.
In most cases, bone pain was controlled with a non-narcotic pain reliever, such as acetaminophen.
Other common side effects reported by patients in the study taking either Neulasta� or placebo were consistent with the underlying cancer diagnosis and its treatment with chemotherapy, with the exception of bone pain.
While not reported in patients receiving Neulasta�, rare events of adult respiratory distress syndrome have been reported in patients receiving the parent compound, NEUPOGEN� (Filgrastim).
However...I do believe immune support is absolutely needed via nutrients.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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posted
Thanks for all the reply's on this topic. I'll have to go back and read what you're referring to Lou.
Marnie, thanks for posting that infomation regarding the posited drug combo.
Sure, we all need a good nutrional program, but I have to dissagree with your premise concerning the best way to tackle this problem.
I still have yet to finish the 101 pages, but the reason I feel her research holds promise is that she identifies in a quantitative way exactly how Lyme seems to be effecting the immune system, so if one is to throw everything but the kitchen sink in terms of herbs and such at this problem, then we may do some good, but what are the other consequences of adding so many different variables.
Though this drug may not be the final answer, I think the premise she is proposing is profound.
The reason this is such a profound premise deals with the issue of immune dysfunction. Several academics have tried to debunk that this even occurs because a couple HIV patients had case reports indicating regular 14 day IV therapy worked for them, so the imune component must not happen in Borrelia.
So, while our side has indeed proposed this kinda thing occurs, Dr. B has talked about it for a long time, what this researcher has done is to show why that it may not matter as much in severe immune deficiency because the objects needed for Borrelia to do its whole immune disregulation thing aren't available anyways- which would explain why those 2 AIDS patients may not have had a complicated case of nuero Lyme.
She prooved this theory with an immune disfunction far greater than AIDS, she used Bubble Boy syndrome, or Severe Combined Immune Dificiency syndrome.
So, thats why this is so important. My point is that this is indeed a real disease, and these things DO happen, but to find acceptance, we need to be able to explain these occurances in a quanitative way that can be reproduced. I have a feeling her experiments can be reproduced, though, of course, time will only tell.
IN the academic artilces we have published concerning Lyme diseaese, our LLMD's that is, we have proposed several mechanims for the survival of Borrelia, but we have never used this in peer reviewed literature, except with perhaps the CD-56 subset, but even with that, we don't have the rigorous animal models and placebo group that she has demonstrated, and repeated in the labratory.
So, she may well find that this whole thing leads to a dysfunction of the CD-56 subset after pilling together all the pieces of the biochemical pathways, but we need to cheer her on.
She is adding a powerfull voice to the reason Borrelia persists, and I think Drug therapy is a more appropriate stategy if it is designed to target the exact nature of the immune disfunction. And that is not because I just love drugs, truth is, I don't care what we use, or she uses, even if its some food or herb. The key is finding something that works like a lock and key, and that is the reason one should use a "drug" for this problem if its proven effective.
Unil then, sure, a balanced diet trying to help eliminate some of these imbalances is wonderful, but we are always left with a guess and check system.
I for one, plan on finishing this disertation. After I'm done reading this, I'll post whether or not I still think its a wonderful idea to use this drug.
As for now, I'm happy she is at least thinking like a scientist.
What is the world coming too?? I mean gosh, females doing science, WTF?
That was a joke by the way, hope all you ladies laughed (my point was that this woman is doing this amazing science, and all the other men couldn't figure it out, sad for us guys, but bravo ladies) Posts: 559 | From Cary, NC | Registered: May 2006
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oxygenbabe
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posted
Hey Lymescience she might even be open to a phone call from you and 'interview'. Scientists like their work to be noticed.
Posts: 2276 | From united states | Registered: Jun 2004
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posted
thats a good idea oxygenbabe, I think I may try to do just that.
If she agrees, I'll post the interview on Lymenet.
I hope that is good enough for her, if she speaks english that is, that her interview would only be posted on a internet forum, but then again, maybe one of the powers that be would pick it up and repost in the Lyme Times or something....
Good idea, THANKS!
Posts: 559 | From Cary, NC | Registered: May 2006
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oxygenbabe
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posted
Well, you might be able to get it published somewhere, you know. Perhaps some site like immunesupport.com might be interested, who knows. Take notes and tape the interview. You can tell her also how many members are on this board (I have no idea how many) and also tell her you are featured in an upcoming documentary. That should do it. And in fact, it would be nice if the documentary includes forward-looking work, that's why I suggested on here they talk to some of the scientists who are working on this. Janet Wais, Mario Phillipe, and whoever at Yale (I think it's Yale?) that is attempting to develop a vaccine that repels tickbites, period. THat documentary needs some hope. Then it can be used for good funding of further research. Good luck and I'll be interested to see it. There's no doubt that borrelia plays havoc with the toll-like receptors. I just think its coinfections that get us. I'm planning to call Eva Sapi sooner or later, because of her recent work documenting 6 bugs in ticks in southern connecticut.
Posts: 2276 | From united states | Registered: Jun 2004
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Truthfinder
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posted
At this point, any respected scientist or researcher who comes up with a new, plausible perspective on treating this disease is welcome sight.
I get a little tired of reading about another new study on tick control, you know? Granted, that is important but doesn't do anything for those of us who are pretty much past the tick problem. It helps to know there are those out there - usually in foreign countries - doing real research on treatment.
I do wonder how co-infections might factor into this equasion?
Tracy
-------------------- Tracy .... Prayers for the Lyme Community - every day at 6 p.m. Pacific Time and 9 p.m. Eastern Time � just take a few moments to say a prayer wherever you are�. Posts: 2966 | From Colorado | Registered: Dec 2005
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posted
Tracy, she discusses co-infections in her dissertation, which is long, and says they are key to this disease as well. So far, it seems to me to be one of the most complete academic compillation regarding the real science of Lyme Disease.
She uses both sides of this debate, and while seeding some points, comes down on the side of persistant infection and she points to many ways this can happen.
Beautifully written!
Posts: 559 | From Cary, NC | Registered: May 2006
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oxygenbabe
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posted
Okay, I've read this. First of all, the patient she's talking about is the one I remember the letter about--the one treated with IV rocephin and G-CSF (that turns out to be brand name Filgastram), and got better, without relapsing. That was a letter in a journal a while back.
Secondly, I've always wondered and wish they would study how mice become thoroughly infected and then clear the infection. If they could figure that out maybe that would help us.
Anergy over time is a definite aspect of LD, but, I don't know...I wonder about the model of SCID-deficient mice, because I'm not sure that presents a good analogue with humans.
I do think it makes sense to give immune boosters with antibiotics, herbs, whatever you are doing to treat LD. That could be IVIG, as some docs do, or perhaps G-CSF. I know that G-CSF has helped cleaer Crohn's disease as well.
Hope they do more research like this in humans, just add in G-CSF to antibiotics. In fact, considering that was successful a while back, I'm surprised no other docs have tried it.
Posts: 2276 | From united states | Registered: Jun 2004
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janet thomas
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posted
What is the world coming too?? I mean gosh, females doing science, WTF?
Yeah, you made me laugh, hard, I'm a female Lymie with a BA in biology and board certification as a Medical Technologist.
So I think I'll read her dissertation. I relapsed after being almost well and am searching for new information. Thanks.
-------------------- I am not a doctor and this is not medical advice but only my personal experience and opinion. Posts: 2001 | From NJ | Registered: Mar 2005
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JRWagner
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Member # 3229
posted
What's a female????
Seriously, I THINK I remember...
A friend of mine with Lyme for 12 years who has done over two years of IV ABX, and Hyperbaric Oxygen, Rife, etc. has low Neutrophils...he has done this treatment...absolutely no help...to him...at all, plus it can be dangerous, as the literature states...if one has undetected cancer, this drug can contribute to the cancer's spread.
Who knows? Very interesting paper though...
Peace, love and wellness, JRW
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