The Tipping Point.....When you've fallen into the autoimmune bucket.

Infections play a significant roll in the development of autoimmune diseases. As I've mentioned before, the immune system begins to fatigue and ultimately fails to function normally. Multiple factors can contribute such as environmental exposures, toxins and genetics. The notion that infections are the culprit for the downward spiral can be found peppered throughout immunology and rheumatology research. Lyme disease and other tick-borne illnesses fit well within this mold.

As the immune system fails, it no longer recognizes "self" and begins producing auto-antibodies which perpetuate the cycle and continue to damage cells. This damage triggers inflammation which drives all autoimmune disorders creating  a vicious cycle of symptoms.

Autoimmune disorders play a major role in a person's ability to heal. Certain genetic markers that determine the body's ability to detox, methylate and break down inflammatory markers contribute. MTHFR, COMT, CBS, SOD, VDR are some of these relevant genetic markers. Genomix is a wonderfully relevant genetics testing company. I use them often to test patients.

Specific markers, HLA-DR4 and subsets within are strongly linked to a process called "molecular mimicry" . There are multiple avenues by which a pathogen can create autoimmunity in a host and this is one of them. Molecular mimicry occurs when a pathogen carries amino acid sequences similar to self-peptides leading to cross-reactivation of auto-reactive T and B cells. The pathogen acts as a self "mimic" . As a result, the activated T and B cells are also cross reactive with self and cause direct damage to its own cells.

An example of molecular mimicry is the development of Rheumatic fever following a streptococcal infection. Multiple studies show myosin to be the major autoantigen in the heart. When exposed to strep, cross reactivity between proteins of the streptococci and the "self" proteins occur causing an autoimmune response.

Another pathway is via epitope spreading where a persisting infection/antigen leads to an ongoing immune response causing tissue damage. When this occurs, further antigens are released and are taken up by antigen-presenting cells or APCs.  Antigen-presenting cells contain antigen complexes with histocompatibility complexes on their surfaces. Examples of these APCs are dendritic cells, macrophages and B cells. These in essences are accessory cells that assist in breaking down antigen proteins, creating peptides and presenting them on the cells surface so that T cells may  recognize them and ingest them. In a chronic or persistent infection scenario, eventually the  immune response becomes dysfunctional and serves its own cells on a silver platter for T cells to attack. 

Persistent Lyme disease via molecular mimicry and epitope spreading are shown in multiple human and animal models. Specifically, T-cells respond to the outer surface protein A of  Borrelia Burgdorferi and higher incidence of cross reactivity occurred with those that had the HLA markers. Outer surface protein A also  cross reacts with central nervous system proteins, creating neurological inflammation. This could explain why some people recover from the symptoms of Lyme disease and others develop chronic inflammatory driven illnesses that in many cases lead to  infectious triggered autoimmune encephalopathy and other autoimmune conditions despite antibiotic treatment.

I realize the subject matter is rather heavy for a Monday morning but bare with me. It's important to understand what is occurring in your body if you suffer from Lyme or other persistent infections. Many if not most symptoms described are interconnected and stem from the same process.  Knowing how the body may respond and understanding the nature of the antigen drives treatment options and ultimately determines if you will recover.  I utilize a barrage of antibiotic combinations while teasing in herbals, dietary restrictions and other modalities that will drive down inflammation, detox and alkalinize the body and temper T cell function ultimately treating the entire process. If treatment focus is just upon " killing the bug",  you've already lost the battle....