For those who have not seen it yet, I highly recommend the blog, Spirochetes Unwound.
Although entries are not posted often at the SU site, they are informative, science-based, and ask important questions. Occasionally, people give interesting responses, too.
This post from 2009 discusses the Barthold mouse experiment (E. Hodzic, S. Feng, K. Holden, K.J. Freet, and S.W. Barthold. (2008). Persistence of Borrelia burgdorferi following antibiotic treatment in mice. Infection and Immunity 52(5):1728-1736) and this comment follows:
"Maybe you know this, but something analogous has been seen in syphilis post-treatment. However, I'm not sure but I don't think there was any truly positive identification of treponemes in the papers I read on this, which were mighty old. Just morphological identification via electron micrography, which is rather tentative.
If I may, how does some ten-minute trial of one or two agents really dismiss the whole "abx-refractory lyme disease" model, when four or five agents are routinely used for years (with mixed success) in treating M. avium complex in man, when diverse bacterial taxa form biofilms that are highly abx refractory in vivo, when chlamydiae in monocytes are rendered highly abx refractory (Gieffers 2001), and when diverse taxa are rendered abx-refractory in vitro by treatments as simple and diverse as starvation, heat shock, pH shock, etc? Everyone ought to admit that there is no truly convincing case for or against this highly politicized model, and take a balanced view of it like you do. Granted, it's clear that this syndrome is not a classical bacteriosis, if "classical" means it can be steamrolled by a brief treatment with agents that mash the putative miscreant in glass on growth-permissive media. The question is whether that is the only sort of bacteriosis that exists.
SCID mice are especially susceptible to developing severe inflammation when infected with B. burgdorferi. Nevertheless, inflammation was not detected in the SCID mice
But, in addition to what you already stipulated, it's also worth mentioning that human refractory lyme (assuming it actually is an infectious disease) might well be mediated by the adaptive IS - if so, a SCID mouse obviously won't hunt."
- Eric J. Johnson
That's an interesting comment.
Hey Eric, come on over here and write some more comments like this...
I wonder which Eric J. Johnson this is?
Risk factors for HIV-1 shedding in semen
Risk factors for HIV-1 shedding in semen are discussed based on an investigation in 149 men of factors that may be compartment-dependent, the genitourinary tract of the male being immunologically different from blood. Systemic and local genitourinary tract factors influence risk of shedding. Findings indicate that measures of systemic virus burden alone may not be reliably predictive of infectivity of semen.
Author: Collier, Ann C., Corey, Lawrence, Zeh, Judith, Krieger, John N., Hooton, Thomas M., Koutsky, Laura A., Johnson, Eric J., Coombs, Robert W., Ross, Susan O., Cent, Anne, Dragavon, Joan, Speck, Carl E., Lee, Willa, Sampoleo, Reigran T.
Publisher: Johns Hopkins University Press
Publication Name: American Journal of Epidemiology
Naaaaaw... you don't think so, do you?
I'm not so sure, either...
Addendum: If you are interested in the interaction between NKT cells and Lyme disease Borrelia, you may also want to see this post on SU... it includes a video of green glowing NKT cells in liver tissue.
Monday, April 4, 2011
2 Blog Log: Spirochetes Unwound
Tags: analysis, article, bacteria, barthold, biofilms, blog, borrelia, causation, chronic lyme, controversy, lyme disease, mice, paper, pcr, persistence, questioning, research, spirochetes