Persistent Antigen Lyme Arthritis: What PG(Bb) May Really Mean

Persistent antigen Lyme arthritis has gained attention following research suggesting that
Borrelia burgdorferi peptidoglycan fragments (PG(Bb)) may drive inflammation
even after antibiotic treatment.

According to Jutras and colleagues, PG(Bb) fragments likely “contribute to inflammation
during infection and in cases of post-infectious Lyme arthritis.” In a mouse model, the
authors found that PG(Bb) alone was sufficient to induce acute arthritis.

Furthermore,

Jutras et al.

suggest that “immune responses to PG(Bb) and autoantigens may contribute to pathology,
even after the infection itself has been cleared.” They propose that differences in disease
severity among patients with Lyme arthritis may reflect variability in immune responses to
PG(Bb).

Author’s note: Jutras and colleagues assume that the infection has resolved.
However, there is currently no reliable test that can definitively confirm that a Lyme
disease infection has been cleared.

Why Does PG(Bb) Persist After Treatment?

A central question raised by the authors is:
How can PG(Bb) material remain in the synovial environment for weeks to months after
appropriate antibiotic therapy?

They propose three possible explanations:

1. PG material may remain after bacterial killing.
2. Macrophages may store PG fragments within intracellular vesicles.
3. PG-containing immune complexes may accumulate in synovial fluid.

Based on these hypotheses, the authors suggest managing persistent antigen Lyme arthritis
with immune-modulating therapies rather than additional antimicrobial treatment.

Proposed Treatments for Persistent Antigen Lyme Arthritis

To dampen immune responses to PG(Bb), Jutras and colleagues recommend
“disease-modifying anti-rheumatic drugs,” primarily hydroxychloroquine or methotrexate.

They further suggest “targeting innate immune responses with medications such as TNF or
NF-κB inhibitors” for patients with persistent inflammatory arthritis.

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The authors also demonstrate that B. burgdorferi releases PG(Bb) fragments
during bacterial growth, raising the possibility that PG(Bb) contributes to the
broader pathogenesis of Lyme disease beyond arthritis alone.

Could Persistent Infection Explain Persistent Antigen?

One critical question remains unaddressed:
Could an active or persistent Lyme infection be driving the continued presence of
PG(Bb)?

The authors do not explore the possibility that ongoing infection could account for the
persistent antigen. Had this been considered, alternative treatment strategies—including
additional or targeted antibiotic therapy—might have been proposed rather than exclusive
reliance on immune suppression.