Topic: Are co-infections curable? If so, why does it take so long??
CD57
Frequent Contributor (1K+ posts)
Member # 11749
posted
Hello- Newish to this board and wondering about some things. I understand that the co-infection (erlichia, bart, etc) bacteria/protozoa are not as crafty/sophisticated as Bb with regards to hiding from the immune system/abx, so.....they are curable. Right?
But....why does it seem like it takes so long to get rid of them.....and why does it also seem like most people relapse? These are just straightforward little critters, shouldn't we be able to kill them pretty easily???
And one more question on this topic, oh wise ones.....why is there "herxing" at all when killing these guys, since they don't release toxins like Bb when dying? Shouldn't we just be feeling better on treatment?
trying to make my way through the weeds here....gotta lot to learn!
Posts: 3528 | From US | Registered: Apr 2007
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TerryK
Frequent Contributor (5K+ posts)
Member # 8552
posted
Your questions would best answered by an LLMD (lyme literate Medical Doctor).
I'm not a doctor but I do believe that most co-infections are curable with the exception of some viruses which can go into remission but will always be present thus not "cured". My understanding is that many of us have a varitable "soup" of infections. Not only do some of us get infected with more than one TBI (tick borne illness) but our immune systems are compromised from years of infection with a bug that is good at disabling the immune system and thus we have picked up other infections as well. The interactions between these infections complicate treatment. The more infections, the more complex our illness and the longer it takes to identify and get rid of disease causing infections.
There are many strains of some of the TBI's and establishing effective treatment is often a trial and error process. For example, what is called bartonella is not the common cat scratch fever but is a bartonella like organism (BLO) that requires different treatment than cat scratch fever. Very little to no research is going into solving the puzzle of these illnesses which means it takes longer to figure out how to treat them. So, to answer your question, no they are not straight forward bugs, if they were, *maybe* the IDSA would have already figured them out.
And to answer your last question as to why there is herxing at all when killing co-infections - according to Dr. S's new book on babesia, some doctors think that babesia may have toxins similar to Bb. For all we know, there could be other infections that make toxins too. Also, many of the treatments for co-infections use abx that also kill Bb.
I'm sure I've left some things off but others will come along and respond I'm sure. Most importantly, I encourage you to consult with an LLMD and ask your questions. Terry
Posts: 6286 | From Oregon | Registered: Jan 2006
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CD57
Frequent Contributor (1K+ posts)
Member # 11749
posted
up -- thanks Terry! Anyone else want to weigh in on this?>
Posts: 3528 | From US | Registered: Apr 2007
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
While some biofilms are useful--sewage treatment plants, for instance, rely on them to remove contaminants from water--they are estimated to be involved in 65% of human bacterial infections : when microbes band together in a biofilm they are 1,000 times more resistant to killing by antibiotics, biocides and disinfectants than free-floating bacteria. ndvB gene is required for the production of periplasmic glucans, glucose polymers that prevent antibiotics from reaching sites of action.
structures for survival under unfavourable growth conditions (protection and dispersion) (endo)spores : mainly in Gram +ve genera (Bacilli(aerobic rods), Clostridii, Thermoactinomyces and Desulfotomaculum (anaerobic rods), Sporosarcina (aerobic cocci)) but also Gram -ve (Coxiella burnetii).They arise in 6�8 hrs after post-logarithmic phase in culture growth ... biofilm 1
Neither strain died in the experiment. We observed a form of biofilm-formation of large Borrelia burgdorferi bundles[b] (see cover; unpublished), which likely served to protect Borrelia bacteria from complement. This may be analogous to attack of the complement system on tumors,where the outer cell-layers are attacked, but the inner layers protected (128).
This mechanism has also been documented elsewhere (76). MMPs (68, 75, 129)enable the spirochetes to invade tissues and when they are able to grow into a larger population, they may be able to shield each other by forming a form of biofilm. Because there was a very large amount of bacteria, the majority of the cells were not attacked. In a physiological sense this may partially explain the difficulty in treating persistent long-term infections. Transfecting a serum sensitive B. garinii strain with a plasmid containing OspE from a serum resistant 297 strain, increased the serum resistance of the B. garinii strain (V).This suggests that in in vitro cultured B. garinii spirochetes, the expression of OspE-proteins is suppressed.
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