Excerpt:

Borrelia burgdorferi stimulates a strong inflammatory response
during infection of a mammalian host. To understand the
mechanisms of immune regulation employed by the host to control
this inflammatory response, we focused our studies on
adrenomedullin, a peptide produced in response to bacterial
stimuli that exhibits antimicrobial activity and regulates
inflammatory responses by modulating the expression of
inflammatory cytokines. Specifically, we investigated the effect
of B. burgdorferi on the expression of adrenomedullin as well as
the ability of adrenomedullin to dampen host inflammatory
responses to the spirochete. The concentration of adrenomedullin
in the synovial fluid of untreated Lyme arthritis patients was
elevated compared with control osteoarthritis patient samples. In
addition, co-culture with B. burgdorferi significantly increased
the expression of adrenomedullin in RAW264.7 macrophages through
MyD88-, PI3-K-, and p38-dependent signaling cascades.
Furthermore, the addition of exogenous adrenomedullin to B.
burgdorferi-stimulated RAW264.7 macrophages resulted in a
significant decrease in the induction of pro-inflammatory
cytokines. Taken together, these results suggest that B.
burgdorferi increases the production of The role of adrenomedullin in Lyme disease.

Excerpt:

IDSA knows that chronic Lyme exists

The IDSA is aware that chronic Lyme exists. We know this because
members of the 2000 and 2006 Lyme disease guideline panels wrote, in
research articles and patents, that chronic Lyme exists.

Evidence about the existence of chronic Lyme borreliosis has increased
since the 2006 LD guidelines were published.

Scientists in California recently reported that not only can Bb persist
in mice despite treatment with ceftriaxone, but the Borrelia can also
infect other ticks and mice. (1) This study buttresses previous
studies that showed that Borrelia can persist in mice (2, 3), dogs (4,
5, 6), and ponies (7).

Studies have also shown that Bb can persist despite antibiotic
treatment in the following human cells, tissues, organs, and body
fluids:

* Fibroblasts (8; Mark Klempner, an IDSA LD guideline panel member in
2006, is an author of this study)

The study was published in the May issue of Arthritis & Rheumatism (http://www3.interscience.wiley.com/journal/76509746/home).

Led by John D. Carter of theUniversity of South Florida, the study involved blood and synovial tissue analysis from 26 patients who had chronic uSpA or Chlamydia-induced ReA. Synovial tissue samples from 167 osteoarthritis patients were used as controls. Samples were analyzed to assess chlamydial DNA and the 26 subjects were asked if they had any known exposure to Chlamydia trachomatis or Chlamydia pneumoniae and if so, the infection was documented in relation to the onset of their uSpA. They also underwent a physical exam that included evaluation of swollen and tender joints and other symptoms of SpA. The results showed that the rate of Chlamydiainfection was 62 percent in uSpA patients, significantly higher than the 12 percent seen in control subjects.

It is believed that as many as 150,000 cases of Chlamydia trachomatis-induced ReA may appear in the U.S. each year compared to about 125,000 new cases of rheumatoid arthritis. This is a low estimate since it does not include cases resulting from Chlamydia pneumoniae. “Thus, Chlamydia-induced ReA represents a considerable burden on the health care systems of the U.S. and other nations, and its impact on those systems may well be significantly under recognized,” the authors state.

Most women with genital Chlamydia trachomatis infection have no symptoms at the time of the initial infection; this was also true of the patients in the study who had DNA evidence of Chlamydia. For Chlamydia pneumoniae, as many as 70 percent of acute infections are asymptomatic and, even when there are symptoms, definitive identification of the organism is rare. The authors point out that relying on identification of a symptomatic infection may therefore result in routine underdiagnosis or misdiagnosis of Chlamydia-induced ReA.

They add that because ReA is a type of SpA and patients with ReA do not present with the classic combination of symptoms of arthritis, conjunctivitis/iritis and urethritis, it is reasonable to believe that Chlamydia trachomatis plays a role in causing uSpA, which may in fact be ReA. They conclude that although there is no diagnostic test for Chlamydia-induced ReA, testing for chlamydial DNA in the synovial tissue of patients thought to have ReA may be the most accurate way of diagnosing the condition.

Article: “Chlamydiae as Etiologic Agents in Chronic Undifferentiated Spondylarthritis,” John D. Carter, Hervé C. Gérard, Luis R. Espinoza, Louis R. Ricca, Joanne Valeriano, Jessica Snelgrove, Cynthia Oszust, Frank B. Vasey, Alan P. Hudson,Arthritis & Rheumatism, May 2009.