Friday, 9 December 2011


In some genetic backgrounds of mice, acute inflammation is sufficient to fight off infection and resolve disease. In other mouse strains, the pathogens, or in this case the bacteria, get past TLR-induced inflammation and remain symptomatically undetectable in cells and tissues (Barthold, etc); Barthold et al. have found that no matter how severe or mild the disease in any of the genetically inbred strains of mice, there was no more inflammatory disease when the bacteria were eliminated. If bacteria find a new disguise, and then come out of hiding, does the process start over again, resulting in chronic, or relapsing remitting, symptoms of inflammation, until the pathogen finds a new disguise or a new hiding place? Or, even if the Borrelia remain dormant, does exposure to a different pathogen that also produces TLR agonists re-trigger the expansion of latent pro-inflammatory cells that were initially stimulated by Borrelia TLR binding proteins?

From Dr Karen Newell Rogers presentation at 2011 Lyme and Tick borne Diseases National Conference details here


  1. I found what Barthold had to say to be notable, too. I wrote about this at the end of an entry I posted about the conference on Wednesday:

    I hope Columbia University and/or the LDA will make slides of the presentations available somewhere online, because I want to learn more.

  2. I think Barthold has come up with one or two things that support ILADS view as opposed to IDSA but I was very dissappointed in his presntation at IOM Workshop I felt he held a lot back and never even mentioned his Rhesus monkey studies - you don't have a link to that research do you Camp. Thanks for the link to your recent post one to read soon.

  3. Joanne, I'm not sure which studies you mean?

    There are a pile of them on PubMed.


    Barthold is also not the only researcher to work with non-human primates and Borrelia. AR Pachner and MT Philipp have done a lot of work in this area, too.