Myositis Autoantibodies in Patients with Suspected Post-Treatment Lyme Disease Syndrome

Abstract

Most patients suffering from Lyme disease are effectively treated with antibiotics. In some patients, however, problems persist for a long time despite appropriate therapy. The term post-treatment Lyme disease syndrome (PTLDS) is currently used for this condition in scientific literature. The pathogenesis is still not precisely known, but the involvement of immunopathological mechanisms is assumed. In our study, we analyzed the presence of autoantibodies including myositis-specific (MSA) and myositis-associated autoantibodies (MAA) in patients with laboratory proven history of Lyme disease and with clinical symptoms of PTLDS. A total of 59 patients meeting the criteria for PTLDS were enrolled in this study. The control group consisted of 40 patients undergoing differential diagnosis of neurological disorders without clinical and/or laboratory-proven history of Lyme disease. The presence of autoantibodies was determined by immunoblot methods and positive samples were further tested for serum creatine kinase (CK) and myoglobin levels. The presence of myositis autoantibodies was detected in 18 subjects with suspected PTLDS (30.5%), but only in 5% of control subjects exhibiting no evidence of Lyme disease history. The difference was statistically significant (p = 0.002). The subsequent biochemical analysis of muscle-damage markers in positive subjects found a mild elevation in six MSA/MAA-positive PTLDS patients. The study detected raised MSA/MAA autoantibodies formation in the group of PTLDS patients raising the question about their involvement in the pathogenesis of this syndrome.

Concurrent Infection of the Human Brain with Multiple Borrelia Species

“…The question of what defines the distribution of spirochete species in brain tissues remains unanswered but is one of increasing importance as the number of human Borrelia infections increases. The possible pathological effect of persistent forms of Borrelia detected in the present study is also discussed from the point of view of the potential induction of an immunopathological reaction associated with chronic inflammation and/or autoreactive immune response, where non-replicative structures can be recognized as long-term antigenic stimuli [13].…”

“…Persistence of Borrelia or associated co-infections, immune dysregulation leading to inflammation or autoimmunity, and/or disrupted central neural pathways [11] leading to central sensitization, among others, have been postulated. If PTLDS is due to or is independent of microbial persistence or other causes remains a topic of debate [12,13]. However, the ability of LD spirochetes to colonize multiple host tissues has been confirmed [14].…”

Antigenicity and immunogenicity of different morphological forms of Borrelia burgdorferi sensu lato spirochetes

“…However, in the more recent literature, do not relying on mimicry phenomenon, autoantibodies against a wide range of different autoantigens have been described in patients with LD or PTLDS. Specifically, it concerns antibodies against endothelial cell growth factor 62 , matrix metalloproteinase-10 63 , apolipoprotein B-100 64 , anti-ganglioside autoantibodies 65 , anti-phospholipid antibodies 66 , anti-nuclear and myositis-specific/associated autoantibodies 13 , 14 .…”

A causal link between autoantibodies and neurological symptoms in long COVID

“…Although the root cause(s) of PAIS remain unclear, a wealth of data supports an autoimmune etiology of PAIS 3,[14][15][16][17][18][19][20][21][22][23] . For example, AABs have been found in ME/CFS [24][25][26] , chronic Lyme disease 27,28 , and LC 3,[14][15][16][17][18][19][20][21][22][23] , some of which target GPCRs and GABA receptors involved in neuronal pathways relevant to neurological symptoms.…”