Medical science and other branches of science are biased and political. A researcher, an investigator(s) has to walk on eggshells when their findings bump up against beliefs of mainstream beliefs espoused by the experts. They have to fall in line with political correctness if they hope to see their research published, and if they want to keep their jobs as academic researchers. .
The research findings published in the PNAS, Proceedings of the National Academy of Science this month entitled Borrelia burgdorferi peptidoglycan is a persistent antigen in patients with Lyme arthritis appears to be excellent science.
The research moves the ball forward in our understanding of chronic inflammation associated with Lyme disease. Political correctness and conformity with mainstream thinking corrupts the paper from the start seriously damaging the credibility of the authors. Immediately the terms postinfectious Lyme arthritis and posttreatment Lyme disease are used and they poison the broth.
The preponderance of scientific evidence, overwhelming and mounting evidence supports the understanding that Lyme bacteria persist in the face of the standard antibiotic therapies discussed.
The finding that peptidoglycan (PPG), the crosslinking molecules which comprise cell walls in gram-negative and gram-positive bacteria are a major determinant of persistent Lyme arthritis is new information that moves the ball forward.
Borrelia spirochetes have a double outer membrane and lack PG cell walls. However, PG molecules are present internally, inside the outer membrane (cell envelope) providing support to the spirochetes.
The fragments of PG are call muropeptides.
We learn Bb, Lyme processes a unique PG structure. And we learn these fragments are highly immunogenic – incite an excessive immune response or cytokine response likely responsible for clinical manifestations of Lyme arthritis.
Perhaps the peptide fragments do cause an autoimmune response. Although the theory is discussed at length this is not what the research shows. Lyme related joint inflammation is directly caused by unique Lyme PGs.
A variety of experiments, controlled experiments using a variety of bacteria with different PGs, a variety of clinical diagnoses, mice, humans, joint fluid and serum support the findings. The findings are based on a great deal of animal and human research.
Antibodies were developed against Lyme specific PGs. These antibodies could be the basis for a new, more accurate diagnostic test.
From recent research we know that Lyme biofilms and planktonic round forms cause more inflammation than spirochete forms. We know these are the most antibiotic tolerant forms or resistant forms.
The article at length discusses issues related to diminished bacterial recycling of PGs compared with gram negative bacteria.
Two theories are proffered as to how Lyme PG persists after “curative therapy” with a short course of doxycycline or Rocephin. The authors suggest that these mechanisms account for the persistence of symptoms lasting weeks or months.
But Lyme arthritis lasts for years. Biofilm forms are impervious to standard antibiotic therapies.
Somehow the authors suggest that immune suppressive therapy should be considered rather than additional antibiotics.
We have heard catchy phrases like “persistence of evidence or evidence of persistence." The issue has prevsiously be settled.
Good science can easily self-destruct with the unforced errors all for the sake of political correctness.