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If only more researchers reviewed Dr. Brown’s work! 😳
(Please excuse the choppy cut and paste. The following quotes are highlights from the article. Although some excerpts may seem to flow, large parts of the article are missing.)
Researchers’ discovery may explain difficulty in treating Lyme disease
http://medicalxpress.com/news/2015-06-discovery-difficulty-lyme-disease.html“Northeastern University researchers have found that the bacterium that causes Lyme disease forms dormant persister cells, which are known to evade antibiotics. This significant finding, they said, could help explain why it’s so difficult to treat the infection in some patients.“
“In other chronic infections, Lewis’ lab has tracked the resistance to antibiotic therapy to the presence of persister cells
Dx: Diffuse Systemic Sclerosis/SLE overlap, Raynaud's June 2013, Lyme August 2013
AP: Azithromycin (Teva) 250mg BID, May 2014, Clindamycin 600mg every 8 hours for 2 weeks July 27, 2015 - Aug 10, 2015
Minocycline (Teva generic) 100mg BID November 20, 2014
Meds: LDN 3.5 mg, Prednisone 5 mg (discontinued), Aspirin 81mg, Liposomal Artimisinin 50mg QID x 3 weeks, 4th week off, rotating (discontinued May 2015, restarted 2016 7 days per month), Daily Nystatin, 2 tabs BID, as a preventative measure
SupplementsNice find Calida!
Re-inventing the wheel indeed 😀 😀 😀 And, yes, surprising how relevant Dr Brown’s approach is consistently found to beBe well! Lynnie
Palindromic RA 30 yrs (Chronic Lyme?)
Mino 2003-2008 100mg MWF - can no longer tolerate any tetracyclines
rotating abx protocol now. From Sep 2018 MWF - a.m. Augmentin Duo 440mg + 150mg Biaxsig (roxithromycin). p.m. Cefaclor (375mg) + Klacid 125mg + LDN 3mg + Annual Clindy IV's
Diet: no gluten, dairy, sulphites, low salicylates
Supps: 600mg N-AC BID, 1000mg Vit C, P5P 40mg, zinc picolinate 60mg, Lithium orotate 20mg, Magnesium Oil, Bio-identical hormones (DHEA + Prog + Estrog)Thanks, Calida! This follows on nicely from other research conducted at Hopkins, in MD, last year looking at various abx to treat persister forms of borreliosis and definitely second Lynnie’s comment above!
viewtopic.php?f=1&t=12520&p=78033&hilit=persister#p78033
As is my way (apologies in advance!), however, I have some niggling (probably annoying) questions and hope you don’t mind me raising these.
Northeastern University researchers have found that the bacterium that causes Lyme disease forms dormant persister cells, which are known to evade antibiotics. This significant finding, they said, could help explain why it’s so difficult to treat the infection in some patients.
Well, it’s not a new thing that persistent forms of borrelia exist and research has been done, over and over, to demonstrate how borrelia shape-shifts…but that research has been largely ignored and relegated to the fringe science stratosphere. Here’s a youtube (2007) to watch in real time how the spiral forms ball up quickly into resistant cyst forms when under attack by penicillin.
https://www.youtube.com/watch?v=lVmCa70bAxE
I’d kind of like clarification of what the researchers mean by “persisters.” Do they mean cell wall-deficient forms, cystic forms, blebs, biofilm, etc? Lyme Literate docs have known and have been treating these forms for years with combination protocols to target the various forms of borreliosis.
Nearly 10 years ago, when I first got so sick from Lyme that triggered my RA, I saw an amazing LLMD and, later that first year, he tried me on long pulses of high dose abx, explaining the life cycle of the bug and why these type of pulses work. However, it’s not all that clear whether the researchers in the new study are talking about low dose, every other day pulses or long pulsed doses. Lyme is such a different bug from the mycoplasma that Dr. Brown was treating and the longer pulses tend to be formulated to the life and reproductive cycle of the spirochete, so that the 2 -3 week heavy hits of high dose combination abx are used and then the patient has a washout for a week or so. I did this in my first year and, geez-louise, was it rough going! Each time, I experienced massive die-off and increasing hypersensitivity issues. It’s not an easy protocol to go through…much harder than the pulses used by Dr. Brown for mycoplasma (I’ve done both types of pulsing – ugh) that are geared to treating hypersensitive rheumatic tissues and keeping herxing to a minimum.
Not hitting Lyme heavy and hard can present with serious long-term probs, as shared by Dr. Eva Sapi at the ILADs conference back in 2012. She and her students had run studies (in vitro) on low dose doxycycline for Lyme and they reported with enlarged, microscopic visuals in their presentation how the treatment pushes borrelia deeper into resistant biofilm forms.
This leaves hypersensitive Lyme/rheumatics in quite a quandary….is the answer to go with high dose combos and risk increasing tissue hypersensitivity with elevated inflammation or is it better to go with low dose combination therapy? This may be the bigger question for we rheumatics. Certainly seems that combination antibiotic (and other) therapies are needed for chronic Lyme and these need to be carefully designed to prevent resistant forms to hit them from all angles, as well as to target any coinfections passed by the wretched bugs….and, ultimately, treatment needs to be a balance of killing the bugs, but not the patient. Not an easy balance to strike in complex cases.
“It hasn’t been entirely clear why it’s difficult to treat the pathogen with antibiotics since there has been no resistance reported for the causative agent of the disease,” explained University Distinguished Professor Kim Lewis, who led the Northeastern research team.
There have been numerous in-vitro (test-tube) and in-vivo (animal) studies published in the past…here’s one study, but there are plenty out there:
http://www.jneuroinflammation.com/content/5/1/40
The research was supported by grants from the Lyme Research Alliance and the National Institutes of Health.
Dr. Brian Fallon, who is a medical advisor to the Lyme Research Alliance and heads up the Columbia Lyme research center in NYC (the org that helped to co-fund this research), is well-respected on both sides of the controversy as an objective researcher. He has done masses of research on Lyme persistence and here is one Finnish article posted on their site describing how Lyme reactivates in mice who have been infected with Lyme and treated with the antibiotic, ceftriaxone, and that these mice revert to seropositivity when later administered an anti-TNF agent (like Humira or Enbrel). Not saying this is a bad thing, but it may be an important part of the puzzle, because Lyme loves immune-suppression, so when the body’s natural defenses are shut down, this may be a good time to hit those little devils! The researchers mention a chemotherapeutic agent (Mitomycin C) that works to kill the bug, but also harms the host as it’s so toxic. In any case…what I mean to say is that this persister phenomenon is nothing new in the Lyme Literate world…researchers all over the world have been trying to figure out this problem for decades now…it’s just here in the US where it’s finally getting some attention:
http://www.columbia-lyme.org/research/keyarticles.html
The second approach, which Lewis noted is much more practical, involved pulse-dosing an antibiotic to eliminate persisters. The researchers introduced the antibiotic a first time, which killed the growing cells but not the dormant persisters. But once the antibiotic washed away, the persisters woke up, and before they had time to restore their population the researchers hit them with the antibiotic again. Four rounds of antibiotic treatments completely eradicated the persisters in a test tube.
If only test-tube results could be replicated in humans and other mammals. Test tubes can identify what is going on, which is wonderful, but unfortunately there are variables, in-vivo, that just don’t make it that simple. E.g. antibiotics have a very difficult time penetrating joints, so bugs remain holed up there in all that lovely inflammation they’ve created.
This is the first time, we think, that pulse-dosing has been published as a method for eradicating the population of a pathogen with antibiotics that don’t kill dormant cells,” Lewis said. “The trick to doing this is to allow the dormant cells to wake up.
Biofilm colonies are another huge problem. Some bugs may leave those colonies, but some might remain safe in that yeuky slime. Cystic forms can remain in the body for decades with the host being completely unaware they have Lyme, because these forms have reduced outer surface proteins that cleverly cloaks their existence from immune surveillance (and testing). 🙄
He added: “This gives you an idea that you could, in principle, establish a similar regiment for treating patients for this and other chronic diseases.”
Well, there is certainly potential there, but as I discovered through hard personal experience, when the Lyme bugs gets deeply embedded in tissues where abx can’t reach, it’s much trickier than just treating with a pre-determined number of pulsed abx. Hmmm…are they talking about one antibiotic or a combination approach?
“What we came up with was the pulse-dosing regimen, which worked beautifully,” Lewis explained. “I think this could be very useful, especially for antibiotics for which resistance doesn’t rapidly develop.”
It could, but patient experience of chronic Lyme is very different from test-tube studies and experienced LLMDs have already been doing this for years with combination protocols.
Though the researchers identified the presence of these persister cells, they also note in their paper that the mechanisms by which the persisters are able to survive remain unknown. More work in this area will be required, they wrote.
Definitely more work in this area is needed and this is a good first step, if it means that the “post Lyme syndrome” term will finally be realized for what it is – chronic persistent Lyme disease. Once this distinction has been confirmed by researchers that the IDSA approves of (ahem), it’s possible that more research will go into effective ways to really help chronic Lyme patients, because right now the landscape is pretty bleak. The IDSA is just about set to revise their Lyme treatment guidelines and they’ve finally agreed to allowing a “consumer representative” onto the panel discussions. But, hey…guess what? That person is from Nebraksa and has no prior knowledge of Lyme disease! Introducing Jane Rips, who has a background in raising funds for cancer research. Bearing in mind that “reported cases” of Lyme is a loaded statement, as few docs report Lyme and a good majority of those with Lyme don’t even know they have it for varying lengths of time and may never get diagnosed as testing is so poor…but guess how many cases of Lyme in Nebraska were reported to the CDC in 2013?
http://www.cdc.gov/lyme/stats/chartstables/reportedcases_statelocality.html
Calida, forgive my commentary…I’m no expert, but 10 years of struggle to regain my health from chronic Lyme has caused me to question research. I’ve learned enough from my incredible LLMDs to be skeptical of all research, even research that appears to be moving in a positive direction. We want to believe and keep the hope that the paradigm shift we’ve all be dreaming of will occur and, perhaps it is tiny increments when, one day, a critical mass in Lyme awareness is reached…until then, let’s keep the faith!
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