Lyme disease, the fastest-growing vector-borne disease with over 476,000 new cases each year, can sometimes be mistaken for an autoimmune disease. While Lyme disease has many overlapping symptoms with autoimmune diseases like lupus, Multiple Sclerosis, and rheumatoid arthritis, Lyme is a bacterial infection. Though it is not an autoimmune disease, Lyme does impact the immune system, so much so that downstream autoimmune conditions can arise.
What is Lyme Disease?
Named for Lyme, Connecticut where a cluster of cases was discovered in the 1970s, Lyme disease is a bacterial infection transmitted by the bite of a black-legged tick. These ticks are most common in New England, the upper Midwest, and along the East and West coasts, but cases of Lyme disease have been reported across the U.S. and in many countries around the world. Ticks tend to live in moist, shady areas like long grasses, stone walls, leaf piles, beach dunes, shrubs, and the woods. Anyone who spends time outside is at risk for a tick bite. And because ticks can be as tiny as a poppyseed and their bites don’t hurt or itch, many people never know they were bitten. In early-stage Lyme disease, symptoms are usually flu-like (fever, fatigue, aches, chills, swollen lymph nodes). Some, but not all, Lyme patients get an erythema migrans (EM) rash, which can look like a bulls-eye but also can take other shape. As the disease progresses, the spirochete bacteria can spiral into cells, tissue, and muscle, affecting every system of the body and, in some cases, getting into the joints (Lyme arthritis), heart (Lyme carditis), and the central nervous system (neurological Lyme disease).
Lyme is easiest to treat when it is diagnosed early, but some 10-20% of people who are treated immediately still go on to experience persistent symptoms. Still others aren’t diagnosed until the infection has progressed, and their illness becomes chronic. Lyme disease diagnosis and treatment can also be complicated by other tick-borne diseases (co-infections).
Mechanisms of Immune Invasion
Lyme disease can affect every system of the body, including the immune system. Utpal Pal, Ph.D., professor in veterinary medicine at the University of Maryland, discovered that a protein produced by the Lyme disease bacteria, borrelia Burgdorferi, disables one of the body’s first immune responses.i This means that Lyme disease immediately affects the immune system, and this is also one of the reasons that Lyme disease can relapse. In "Conquering Lyme Disease: Science Bridges the Great Divide," Brian A. Fallon, MD and Jennifer Sotsky, MD note, “B. burgdorferi has the ability to produce proteins that bind to and inactivate a key component of the immune system, called complement. The production of complement inactivators has the net effect of markedly decreasing the destructive capacity of the antibodies against the spirochete.”ii
Immune System Response
Not only can the Lyme disease bacteria disable part of the immune response, it can also deceive the immune system. Borrelia burgdorferi are smart, tricky bacteria that can evade antibiotics, cross the blood-brain barrier that is otherwise supposed to protect the central nervous system from infection, and cause a short-lived and weakened immune response. This can lessen the body’s chance of fighting recurring or new infection (Lyme or otherwise). As noted in a UC Davis study on mice, the Lyme disease bacteria “cause structural abnormalities in ‘germinal centers’—sites in lymph nodes and other lymph tissues that are key to producing a long-term protective immune response.”iii
Immune System Dynamics in Lyme Disease
In addition to a non-specific and weakened initial response to the bacterial invasion of Lyme disease, the body’s immune system can also become overreactive as a result of Lyme. This can cause the immune system to overreact to other invaders, and also can lead to inflammation. As Richard I. Horowitz, MD says in How Can I Get Better? An Action Plan for Treating Resistant Lyme & Chronic Disease, “The three I’s of Lyme disease—infection, inflammation, and immune dysfunction—are the biological triad responsible for many commonly observed symptoms.”iv Persistent inflammation and immune overreaction can keep Lyme patients in a chronically ill state, whether or not their infection is cleared.
Debunking Autoimmunity and Lyme Disease
While persistent inflammation and immune dysregulation are autoimmune-style reactions, their derivation in Lyme disease is bacterial infection. Lyme disease can, however, cause autoimmune conditions such as Lyme arthritis. Neurological Lyme disease may also in part be autoimmune in origin as well.
Boosting the Immune System
Though Lyme disease can seriously affect the immune system, there are ways you can counteract the effects. Since there is no set protocol for Lyme disease, your Lyme Literate Medical Doctor (LLMD) can determine exactly how your own immune is impacted (by evaluating your symptoms and likely running some tests) and the best ways to treat that dysfunction. They may make suggestions such as certain immune-boosting vitamins or supplements, certain dietary changes (many Lyme patients follow the “Lyme disease diet”), treatment of sleep disturbances, exercise as tolerated, and adjunct therapies.
Conclusion
When you have Lyme disease, your immune system is up against an intelligent and elusive bacterium. However, all hope is not lost! As your infection clears, your immune system can start to repair itself. With immune support guided by your LLMD, fighting Lyme disease—and winning—is certainly possible.
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The above material is provided for information purposes only. The material (a) is not nor should be considered, or used as a substitute for, medical advice, diagnosis, or treatment, nor (b) does it necessarily represent endorsement by or an official position of Global Lyme Alliance, Inc. or any of its directors, officers, advisors or volunteers. Advice on the testing, treatment or care of an individual patient should be obtained through consultation with a physician who has examined that patient or is familiar with that patient’s medical history.