Guest guest Posted December 29, 2008 Report Share Posted December 29, 2008 > fyi thought many on this list might find this of interest. lyme can > minaifest in many ways so if you are diagnosed with RA should test for > lyme. see below for info on what using anti-TNF therapy can do to lyme > bacteria. i'm quite certain they contribute to proliferation of all > bacteria since they disarm the immune system. > > > *Research Op-Ed and Commentaries* > > In this section, key articles are summarized and commentary is > provided. This section also serves as an opportunity for specific > topics to be reviewed in detail. Contributions to this section by > scientists, researchers, and/or physicians are welcome and will be > reviewed for inclusion by members of our Center Research Staff and by > members of the Center's Scientific Advisory Board with expertise > specific to the commentary or review. > > *Persistence of Borrelia burgdorferi in mice after antibiotic therapy.* > > Two studies have recently been published which reveal that Bb may > persist in the mouse despite antibiotic therapy. These studies > support much earlier work by Straubinger et al in the dog model (1997) > and Bockenstedt et al (2002) in the mouse model. Bockenstedt et al > (2002) showed that Bb persistence can occur after antibiotic treatment > and that these spirochetes could be acquired by ticks (xenodiagnosis) > but that the infected^ ticks could not transmit infection to naïve > hosts -- suggesting that the spirochetes were attenuated in that they > had become non-infectious. Straubinger et al (1997) had shown that > even after 30 days of antibiotic treatment, Bb spirochetes could be > demonstrated in 3/12 dogs by culture, and DNA could be demonstrated by > PCR in 9/12 dogs long after treatment. > > More recently, Hodzic et al from UC in California reported in > Antimicrob Agents Chemother. (2008;52(5):1728-36) a study which > examined the effectiveness of antibiotic treatment using ceftriaxone > or saline for 1 month. Mice were treated either early in the > infection (3 weeks) or later (4 months). Tissues were tested by > immunohistochemistry, PCR, culture, transplantation of allografts, and > xenodiagnosis at 1 and 3 months after treatment. Tissues from the > mice treated with antibiotics were culture negative, but tissues from > some of the mice remained PCR positive and intact antigen-positive > organisms with spirochetal morphology were visualized in collagen-rich > tissues. Xenodiagnosis demonstrated that uninfected larval ticks > after feeding on the antibiotic-treated mice were able to acquire > spirochetes (confirmed by PCR) and then transmit these spirochetes to > naïve SCID mice which became PCR positive but culture negative. This > study therefore demonstrated that antibiotic treatment in the mouse > model does not result in eradication of the Bb spirochetes and that > some of these spirochetes were infectious, although attenuated in > activity. > > Yrjanainen et al from Univ of Turku in Finland reported in _J > Infectious Disease_ (2007; 195(10):1489-96) a study which examined > whether anti-tumor necrosis factor-alpha would have a beneficial > effect on Bb-infected mice. C3H/He mice were infected with B. garinii > A218 or B. burgdorferi sensu stricto N40. In study 1 (with B. garinii) > and in study 2 (with Bb SSN40), 2 weeks after infection, 10 mice were > treated with ceftriaxone only for 5 days and 10 mice were treated with > anti-TNF-alpha only. In another group of 10 mice, anti-TNF was added > simultaneous to the ceftriaxone at 2 weeks after infection while in > another group of 10 mice anti-TNF was added at 6 weeks after infection > (ie, 4 weeks after ceftriaxone). Finally, a fifth group of mice was > treated with saline as a sham treatment. For the group that received > ceftriaxone only, no samples were positive by culture or by PCR at 2 > weeks after infection. However, among those mice treated with > anti-TNF-alpha either at 2 weeks or 6 weeks after infection, > spirochetes grew from one-third of the mice. Contrary to earlier > findings by Bockenstedt et al (2002) in which the spirochetes detected > after antibiotic treatment were attenuated in activity, the recovered > spirochetes in this study did not appear to be attenuated, as > ceftriaxone sensitivity rates, plasmid profiles, and virulence rates > were similar to those of bacteria used to infect the mice. This study > demonstrated that a portion of B. burgdorferi-infected mice still have > live spirochetes in their body, which are activated by anti-TNF-alpha > treatment. > > *Commentary*. These two studies demonstrate that Bb spirochetes can > persist in the mouse after ceftriaxone therapy. The Finish study was > remarkable in that culture and PCR were negative after ceftriaxone > but, after additional treatment with anti-TNF-alpha, viable > spirochetes were recovered. TNF is a pro-inflammatory cytokine which, > when blocked, typically results in a reduction in clinical > inflammation; for this reason, such treatment is used for patients > with rheumatoid arthritis. To the surprise of the authors, viable > spirochetes were recovered in these PCR- and culture-negative mice > after TNF blocking treatment was given. Also interesting is that > anti-TNF treatment did not result in the expected finding of a > reduction of joint swelling. > > The Finnish study was the first study to demonstrate that > immunomodulatory treatment of animals infected with Bb could convert > them from culture negative to culture positive. The California study > was remarkable in that only tick-feeding was capable of extracting > infectious but non-replicating attenuated spirochetes; without having > done that step of xenodiagnosis and then transferring the tick to feed > on naïve SCID mice, the authors' conclusion would have been that > infectious spirochetes do not persist in the mouse model as culture > was negative. The authors further concluded that negative culture > and PCR can not be relied upon as markers of treatment success. > > We do not know the extent to which these findings can be translated to > the human situation. Nevertheless, the activation of infectious > spirochetes after anti-TNF therapy in mice should alert clinicians to > the possibility that anti-cytokine therapy may result in a similarly > increased risk of activating latent infection among patients with a > history of treated Lyme disease. At this point, we do not know > whether attenuated spirochetes are capable of inducing > illness-symptoms in mice or humans; while it is possible that > spirochetal mRNA may be producing surface lipoproteins that stimulate > systemic symptoms, this hypothesis needs to be tested in the next > phase of this important research. > > *BAFallon, MD* > > *from http://www.columbia-lyme.org/research/keyarticles.html* > > Happy Holidays! > > Jim M. > President > CANADIAN LYME DISEASE FOUNDATION > A Federally-registered Charitable Organization > www.canlyme.com <http://www.canlyme.com> > > PLEASE NOTE: > Nothing contained in this document is to be considered as medical advice. > Please consult your doctor for medical advice. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 30, 2008 Report Share Posted December 30, 2008 Can anyone translate the below into something short/sweet/understandable/the bottom line? I have no idea what anti-TNF therapy is and my brain is not working well enough today to comprehend the below. I have Lymes’ (and was diagnosed with RA) and was on Minocin for just under three years. I’ve toyed with the idea of MMS and Marshall Protocol; actually did the Schardt protocol; feel pretty great; now the below has me worrying. El _____ From: rheumatic [mailto:rheumatic ] On Behalf Of Sauve Sent: Tuesday, December 30, 2008 1:54 AM rheumatic Subject: rheumatic Re: Lyme disease info and anti-TNF meds > fyi thought many on this list might find this of interest. lyme can > minaifest in many ways so if you are diagnosed with RA should test for > lyme. see below for info on what using anti-TNF therapy can do to lyme > bacteria. i'm quite certain they contribute to proliferation of all > bacteria since they disarm the immune system. > > > *Research Op-Ed and Commentaries* > > In this section, key articles are summarized and commentary is > provided. This section also serves as an opportunity for specific > topics to be reviewed in detail. Contributions to this section by > scientists, researchers, and/or physicians are welcome and will be > reviewed for inclusion by members of our Center Research Staff and by > members of the Center's Scientific Advisory Board with expertise > specific to the commentary or review. > > *Persistence of Borrelia burgdorferi in mice after antibiotic therapy.* > > Two studies have recently been published which reveal that Bb may > persist in the mouse despite antibiotic therapy. These studies > support much earlier work by Straubinger et al in the dog model (1997) > and Bockenstedt et al (2002) in the mouse model. Bockenstedt et al > (2002) showed that Bb persistence can occur after antibiotic treatment > and that these spirochetes could be acquired by ticks (xenodiagnosis) > but that the infected^ ticks could not transmit infection to naïve > hosts -- suggesting that the spirochetes were attenuated in that they > had become non-infectious. Straubinger et al (1997) had shown that > even after 30 days of antibiotic treatment, Bb spirochetes could be > demonstrated in 3/12 dogs by culture, and DNA could be demonstrated by > PCR in 9/12 dogs long after treatment. > > More recently, Hodzic et al from UC in California reported in > Antimicrob Agents Chemother. (2008;52(5):1728-36) a study which > examined the effectiveness of antibiotic treatment using ceftriaxone > or saline for 1 month. Mice were treated either early in the > infection (3 weeks) or later (4 months). Tissues were tested by > immunohistochemistry, PCR, culture, transplantation of allografts, and > xenodiagnosis at 1 and 3 months after treatment. Tissues from the > mice treated with antibiotics were culture negative, but tissues from > some of the mice remained PCR positive and intact antigen-positive > organisms with spirochetal morphology were visualized in collagen-rich > tissues. Xenodiagnosis demonstrated that uninfected larval ticks > after feeding on the antibiotic-treated mice were able to acquire > spirochetes (confirmed by PCR) and then transmit these spirochetes to > naïve SCID mice which became PCR positive but culture negative. This > study therefore demonstrated that antibiotic treatment in the mouse > model does not result in eradication of the Bb spirochetes and that > some of these spirochetes were infectious, although attenuated in > activity. > > Yrjanainen et al from Univ of Turku in Finland reported in _J > Infectious Disease_ (2007; 195(10):1489-96) a study which examined > whether anti-tumor necrosis factor-alpha would have a beneficial > effect on Bb-infected mice. C3H/He mice were infected with B. garinii > A218 or B. burgdorferi sensu stricto N40. In study 1 (with B. garinii) > and in study 2 (with Bb SSN40), 2 weeks after infection, 10 mice were > treated with ceftriaxone only for 5 days and 10 mice were treated with > anti-TNF-alpha only. In another group of 10 mice, anti-TNF was added > simultaneous to the ceftriaxone at 2 weeks after infection while in > another group of 10 mice anti-TNF was added at 6 weeks after infection > (ie, 4 weeks after ceftriaxone). Finally, a fifth group of mice was > treated with saline as a sham treatment. For the group that received > ceftriaxone only, no samples were positive by culture or by PCR at 2 > weeks after infection. However, among those mice treated with > anti-TNF-alpha either at 2 weeks or 6 weeks after infection, > spirochetes grew from one-third of the mice. Contrary to earlier > findings by Bockenstedt et al (2002) in which the spirochetes detected > after antibiotic treatment were attenuated in activity, the recovered > spirochetes in this study did not appear to be attenuated, as > ceftriaxone sensitivity rates, plasmid profiles, and virulence rates > were similar to those of bacteria used to infect the mice. This study > demonstrated that a portion of B. burgdorferi-infected mice still have > live spirochetes in their body, which are activated by anti-TNF-alpha > treatment. > > *Commentary*. These two studies demonstrate that Bb spirochetes can > persist in the mouse after ceftriaxone therapy. The Finish study was > remarkable in that culture and PCR were negative after ceftriaxone > but, after additional treatment with anti-TNF-alpha, viable > spirochetes were recovered. TNF is a pro-inflammatory cytokine which, > when blocked, typically results in a reduction in clinical > inflammation; for this reason, such treatment is used for patients > with rheumatoid arthritis. To the surprise of the authors, viable > spirochetes were recovered in these PCR- and culture-negative mice > after TNF blocking treatment was given. Also interesting is that > anti-TNF treatment did not result in the expected finding of a > reduction of joint swelling. > > The Finnish study was the first study to demonstrate that > immunomodulatory treatment of animals infected with Bb could convert > them from culture negative to culture positive. The California study > was remarkable in that only tick-feeding was capable of extracting > infectious but non-replicating attenuated spirochetes; without having > done that step of xenodiagnosis and then transferring the tick to feed > on naïve SCID mice, the authors' conclusion would have been that > infectious spirochetes do not persist in the mouse model as culture > was negative. The authors further concluded that negative culture > and PCR can not be relied upon as markers of treatment success. > > We do not know the extent to which these findings can be translated to > the human situation. Nevertheless, the activation of infectious > spirochetes after anti-TNF therapy in mice should alert clinicians to > the possibility that anti-cytokine therapy may result in a similarly > increased risk of activating latent infection among patients with a > history of treated Lyme disease. At this point, we do not know > whether attenuated spirochetes are capable of inducing > illness-symptoms in mice or humans; while it is possible that > spirochetal mRNA may be producing surface lipoproteins that stimulate > systemic symptoms, this hypothesis needs to be tested in the next > phase of this important research. > > *BAFallon, MD* > > *from http://www.columbia <http://www.columbia-lyme.org/research/keyarticles.html*> -lyme.org/research/keyarticles.html* > > Happy Holidays! > > Jim M. > President > CANADIAN LYME DISEASE FOUNDATION > A Federally-registered Charitable Organization > www.canlyme.com <http://www.canlyme. <http://www.canlyme.com> com> > > PLEASE NOTE: > Nothing contained in this document is to be considered as medical advice. > Please consult your doctor for medical advice. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 31, 2008 Report Share Posted December 31, 2008 anti-TNF therapy is using any biologic like enbrel or remicade etc. the study says that using these when you are infected with lyme bacteria can make it spread. which makes sense since the anti-TNF meds suppress your imm systm, doing nothing for the cause of the arthritis symptoms. monique Can anyone translate the below into something short/sweet/ understandable/the bottom line? I have no idea what anti-TNF therapy is and my brain is not working well enough today to comprehend the below. I have Lymes' (and was diagnosed with RA) and was on Minocin for just under three years. I've toyed with the idea of MMS and Marshall Protocol; actually did the Schardt protocol; feel pretty great; now the below has me worrying. El Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.