Bacterial triggers for lyme and maybe morgellons

[tcmgpt13]

This abstract is a few years old, but I find it interesting as it shows that bacterial infections may be triggers for rheumatic diseases such as reactive arthritis (RA), rheumatic fever and lyme disease. How many others here have had either rheumatic fever as a child or a lot of strep throat infections? Today there are antibiotics which usually prevent full blown cases of rheumatic heart fever from ever developing, but strep throat, which is closely related, is still in the picture for many young children. Do you have a family history of strep infections too? Certainly I never thought about these diseases having a genetic component, but evidently there is one. And since lyme is connected strongly to Morgellons symptoms I felt that at least some here might be interested in reading this:

Bacterial triggers and autoimmune rheumatic diseases.

Girschick HJ, Guilherme L, Inman RD, Latsch K, Rihl M, Sherer Y, Shoenfeld Y, Zeidler H, Arienti S, Doria A.
Pediatric Rheumatology, Immunology, Infectious Diseases, Children's Hospital, University of Wuerzburg, Germany.
Abstract

Autoimmune rheumatic diseases are generally considered as a multifactorial aetiology, mainly genetic susceptibility combined with environmental triggers of which bacteria are considered one of the most prominent. Among the rheumatic diseases where bacterial agents are more clearly involved as triggers are: reactive arthritis (ReA), rheumatic fever (RF) and Lyme disease. The role of bacterial infections in inducing other seronegative spondyloarthritis and antiphospholipid antibody syndrome has been hypothesized but is still not proven. The classic form of ReA is associated with the presence of HLA-B27 and is triggered by the urethritis or enteritis causing pathogens Chlamydia trachomatis and the enterobacteria Salmonella, Shigella, and Yersinia, respectively. But several other pathogens such as Brucella, Leptospira, Mycobacteria, Neisseria, Staphylococcus and Streptococcus have also been reported to cause ReA. RF is due to an autoimmune reaction triggered by an untreated throat infection by Streptococcus pyogenes in susceptible individuals. Carditis is the most serious manifestation of RF and HLA-DR7 is predominantly observed in the development of valvular lesions. Lyme disease is a tick-transmitted disease caused by the spirochete Borrelia burgdorferi. Knowledge is limited about how this spirochete interacts with human tissues and cells. Some data report that Borrelia burgdorferi can manipulate resident cells towards a pro- but also anti-inflammatory reaction and persist over a long period of time inside the human body or even inside human cells.


PMID: 18570749 [PubMed - indexed for MEDLINE]

[sojii]

What about scarlet fever? They're related. I had scarlet fever as a kid and childhood strep.

[fritolay66]

PLoS Pathogens: Autoimmunity as a Predisposition for Infectious Diseases

"Autoimmunity refers to an inappropriate immune response against self-components of the host that results in pathological conditions. Autoimmune diseases are characterized by an activation of autoreactive T and B cells, are associated in some cases with the production of pathogenic autoantibodies against self-molecules, culminating in inflammation and tissue damage. The reasons for the breakdown of tolerance mechanisms leading to autoimmunity are not clearly known. However, a combination of genetic, immunological, and environmental factors plays a critical role in the pathogenesis of autoimmunity."

"During the course of autoimmunity, autoantibodies that can neutralize key components of the immune system that are essential in mounting anti-microbial responses may be produced. These autoantibodies might either exacerbate ongoing infectious diseases or predispose the individual to an increased risk of bacterial, viral, and opportunistic fungal infections."

"Therefore, it can be conceived that the development of neutralizing antibodies against any of these cytokines as a consequence of autoimmunity affects the cellular functions and clearance of pathogens and predisposes the host to infectious diseases."

"These anti-IFN-γ IgG neutralized IFN-γ in whole blood culture, inhibited IFN-γ-dependent phosphorylation of STAT-1 and production of TNF-α and IL-12 by normal peripheral blood mononuclear cells (PBMCs) and macrophages, and inhibited HLA-DR expression in normal monocytes."

HLA-DR - Wikipedia, the free encyclopedia

You will see under "associated diseases" the predisposition to many diseases based on HLA genotypes and the development of autoimmunity.

"In addition, IL-6- deficient mice have been shown to be susceptible to various pyogenic infections, including Streptococcus pneumoniae, Pseudomonas aeruginosa, and Klebsiella pneumoniae."

Interleukin - Wikipedia, the free encyclopedia

Interleukin's have everything to do with TH1 and TH2 responses.

"In view of these findings, we suggest that patients with uncontrolled or repeated infections despite antimicrobial therapy should be considered for screening and evaluating autoimmunity. Although reported examples are of autoantibodies to cytokines, the occurrence of autoantibodies that target either molecules implicated in the recognition of pathogens (such as Toll-like receptors and lectin receptors) or antigen presenting and co-stimulatory molecules cannot be ruled out. Indeed, genetic defects or polymorphisms in pattern recognition receptors and their signaling pathways and susceptibility to infections have been reported."

Yes, indeed. Genetic polymorphisms and susceptability are documented.

"Despite the reports of anti-cytokine antibodies in several malignant or infectious diseases and their low titers in healthy individuals, the high titers are predominant in autoimmune diseases."

Many of us with high titers. I would really like to see which genotypes predominate in the Morgellons community. I would also like to see comparisons of the cytokines and autoantibodies such as CRP, MBP, MMP-9, ACLA, and AGA.

"Therefore, it is probable that autoantibodies are produced as a consequence of infections and these autoantibodies subsequently exacerbate the infectious diseases or, alternatively, a cryptic autoimmunity develops due to unknown reasons that predispose the individual to infections. Infectious agents and vaccines are often thought to be one of the environmental factors that induce autoimmunity either by molecular mimicry, epitope spreading, bystander activation of immune system, or polyclonal activation of immune cells. It is thus likely that in case of chronic persistent diseases such as tuberculosis, a pathogen might trigger the autoimmune process by one of these mechanisms.

Indeed, the majority of patients with autoantibodies and mycobacterial infections originated from disease-endemic areas. Therefore, dissection of underlying causes of autoimmunity such as genetic polymorphisms, gene deficiency, or environmental factors might shed light on these unanswered questions."

Frito