Can Lyme disease trigger Autoimmune diseases?
Important findings about the links between Lyme disease and autoimmune illnesses have been established by doctors and researchers. Even while additional research is still required, the evidence that is already available can help both doctors and patients understand and treat their symptoms.
In this article, we'll go over some fundamental knowledge about autoimmune disorders, how Lyme disease may cause them, and how the similarity of some autoimmune diseases' symptoms to those of Lyme disease may result in a missed or incorrect diagnosis.
An immune system illness is an autoimmune disease. Immune system diseases are conditions that result in either abnormally high or abnormally low immune system activity levels. When the body's natural defense system can't distinguish between your cells and alien cells, it develops an autoimmune disease and unintentionally attacks healthy cells. Autoimmune diseases come in more than 80 different types and affect many different body parts.
About 50 million Americans, largely women, suffer from at least 60 to 100 autoimmune illnesses. Among the most typical are:
- Multiple sclerosis
- diabetes type 1
- Psoriasis and rheumatoid arthritis
- thyroid condition
- Addison's illness
- Chronic anemia
- Celiac illness
- Additionally, some professionals classify chronic fatigue syndrome as an autoimmune condition.
Understanding the immune system: Systemic autoinflammatory diseases (SAID) vs. autoimmune diseases
Not all immune system disorders linked to immune system overactivity are autoimmune diseases. The category of systemic autoinflammatory disorders, or SAIDs, is more recent and less well-known. Although they exhibit many of the same symptoms, the innate immune system and the adaptive immune system are two distinct immune systems.
The adaptive immune system, which attacks certain antigens by producing specialized antibodies, is afflicted by autoimmune illnesses. B-cells or T-cells are the cells implicated in these processes. By exposing the body to pathogens (such the COVID-19 virus) through vaccination, the adaptive immune system is stimulated to produce the specific antibodies required to combat the disease. Additionally, this system is used to combat Lyme disease and other bacterial illnesses brought on by ticks.
The innate immune system is the other type of immune system. The immunological system that SAIDs impact is this one. The physical barriers (such as skin, hair, and mucous membranes), active and passive defense mechanisms (such as coughing, sneezing, and fevers), and general immune responses (such as marking harmful foreign invaders for destruction) that keep the body healthy are all part of the innate immune system, which is the immune system that is present at birth. Inflammation, which occurs when immune cells (leukocytes) are sent to the location and begin to assault harmful chemicals, is one of the main types of general immunological responses.
The primary distinction between the innate immune system and the adaptive immune system is that the former provides all-around defense while the latter develops specialized cells to combat particular foreign invaders.
Both SAIDs and autoimmune illnesses make the body attack itself. However, autoimmune disorders are disorders of the adaptive immune system that cause the body to produce antibodies that recognize, remember, and persistently fight off cells from a particular body system, such as the joints (as in rheumatoid arthritis) or the skin. SAIDs are disorders of the innate immune system that cause inflammatory responses without the use of antibodies (as in psoriasis).
Symptoms of both autoimmune and autoinflammatory illnesses might include:
inflammation, enlarged lymph nodes, rashes, and fevers. (Take note that several of these are also typical signs of illnesses carried by ticks, such Lyme.) Although researchers have recorded at least one case of a SAID - adult on-set Still's disease, or AOSD - that was presumably induced by Lyme illness, this article will mostly focus on autoimmune diseases and how they resemble, vary from, and interact with Lyme disease.
What results in autoimmune disorder?
The majority of scientists concur that environmental factors are what cause autoimmune disorders. Foods (like gluten goods), toxins (from hair dyes, tobacco products, and more), and viral or bacterial illnesses are a few examples that come to mind.
Indeed, there is mounting proof that bacterial infections like Lyme disease and others can set off autoimmune illnesses, particularly in people who are genetically predisposed to them. The inflammatory disorders Sjogren's syndrome, dermatomyocitis (DM), rheumatoid arthritis (RA), psoriatic arthritis (PsA), and spondyloarthritis have all been linked to or mimicked by Lyme disease, according to studies (SpA).
Lyme disease misdiagnosis or complication of autoimmune diseases?
As was already mentioned, there is evidence linking autoimmune disorders like Lyme to one another. According to the research, Lyme disease can either cause (or present as) an autoimmune disease, or it can imitate one.
What does this entail for medical professionals and patients? It all boils down to how critical it is to have a prompt and correct diagnosis if you think you may have Lyme disease or another tick-borne illness. The likelihood that Lyme disease will spread to many body systems and perhaps cause an autoimmune reaction increases with the length of time it is left untreated.
Lyme disease is notoriously difficult to diagnose since its symptoms overlap with those of so many other illnesses, including autoimmune diseases. The inflammatory condition rheumatoid arthritis (RA), which is marked by persistent joint pain, is one of the most typical Lyme disease misdiagnoses.
In addition to the arthritic symptoms of Lyme continuing and getting worse, if a patient with Lyme is diagnosed with RA without the Lyme being found and treated, the Lyme can also continue to harm other systems, leading to neurological and mental disorders, cardiac issues, and more. Untreated Lyme disease may occasionally prove lethal.
Lyme disease as a trigger for autoimmune diseases:
Lyme disease (LD), commonly known as Lyme borreliosis, is a zoonotic illness brought on by the Spirochaetaceae family member Borrelia burgdorferi sensu lato (B. burgdorferi s.l.). Since the symptoms of LD might resemble those of a variety of systemic disorders with musculoskeletal symptoms, differential diagnosis of the condition is frequently challenging. Additionally, a misdiagnosis may occur due to the high incidence of antibodies against borrelia in the general population.
A wide range of clinical indications of LD, such as signs of articular, neurological, circulatory, cardiac, and ophthalmic involvement, may be present. It should be emphasized that many autoimmune illnesses, including SLE, have symptoms similar to these. Given the need to distinguish the primary pathology and choose a management approach, the intersection of these two pathologies in clinical practice is of great importance.
Early stages of LD are primarily caused by the presence of live bacteria at the site of inflammation, but later stages of the illness are mostly caused by autoimmune mechanisms, which result in clinical symptoms and the involvement of organs and systems. Spirochete exposure to the host immune system for an extended period of time may play a role in the de novo emergence of chronic autoimmune illness. Since the symptoms of LD can mirror those of numerous other illnesses and have been connected to a number of autoimmune disorders, the confluence of these two diseases may be of clinical interest to rheumatologists.
Multisystemic LD manifests itself in a wide range of ways. It is a sophisticated immune-mediated disease with an infectious and inflammatory etiology.
Spirochete exposure to the host immune system over an extended period of time can result in chronic autoimmune illness. The pathogen causes pro-inflammatory, immunomodulatory, and immunosuppressive effects as a result of the bacterium's interaction with the host. The development of autoimmunity caused directly or indirectly by the pathogen and based on molecular mimicry is one reason for antibiotic-resistant LD or subsequent autoimmune reactions and illnesses.
There is compelling evidence that patients with antibiotic-resistant LD have an immune-mediated mechanism at work. Certain human leukocyte antigen (HLA)-DR alleles, increased joint inflammation, immunological dysregulation of the CD41 Teff:Treg cell ratio, and infection-induced autoimmunity are all linked to this outcome.
Major histocompatibility complex (MHC) class II DR2 and DR4 molecules have been linked in genetic linkage studies of persons with Lyme arthritis. Immune system activation depends heavily on MHC class II molecules. The immune system is impacted by polymorphism in the MHC class II structure's genes in at least two different ways. A class II peptide's ability to bind and, consequently, manifest as a specific class II molecule on an antigen-presenting cell, is first determined by polymorphic amino acid residues on individual class II proteins. The repertoire of CD8+ and CD4+ T cells that identify foreign peptides in the context of MHC class II molecules is impacted by the second way that MHC class II molecules govern the ontogenetic selection of the T-cell receptor specificity in the thymus. According to these results, Borrelia antigens are delivered to CD4 + T cells after being loaded onto MHC class II molecules.
There are some similarities between the musculoskeletal symptoms of LD and rheumatoid arthritis, according to studies. The latter is linked to the HLA system, which encodes class II MHC proteins, particularly the HLA-DR isotype, and contains an autoimmune component.
Studies have looked into the connection between particular HLA-DR serotypes and people with LD who are more likely to develop chronic arthritis. HLA-DR4 was reported to be more prevalent in patients with chronic arthritis and to be the only serotype that significantly correlated with treatment-resistant Lyme arthritis in a study of 130 patients with diverse LD symptoms. Overall, HLA-DR4 or -DR2 was present in 89 percent of individuals with chronic arthritic conditions; however, some patients had both. This suggested that HLA-DR4 and -DR2 may be indicators of rheumatoid arthritis susceptibility.
An autoimmune disease's preclinical stage can become active in response to an infection. Autoantibodies may exist in the preclinical stages for years before an obvious systemic disease manifests itself. Numerous viral pathogens may act as catalysts for the onset of autoimmune disorders' clinical manifestation . Microbes can give a supplementary signal necessary to trigger a pathogenic autoimmune response in addition to activating lymphocytes in response to specific antigens; this is known as the adjuvant impact of infection.
The key is early detection
Timely, precise testing is essential to avoiding a false positive for Lyme disease and any potential repercussions. Even if a patient does not recall having a tick bite or rash, Lyme disease should not be ruled out in cases where the patient exhibits symptoms resembling those of an autoimmune disease. Lyme disease is still a possibility even if the patient has a history of a genetic predisposition to autoimmune illnesses.
However, identifying Lyme disease necessitates more sensitive and specific testing than is normally advised by the CDC, particularly at advanced stages of the illness.
A problem in differential diagnosis and patient treatment is posed by the multisystem involvement and variety of symptoms that characterize autoimmune disorders. One of the most severe connective tissue systemic disorders, systemic lupus erythematosus (SLE) has several atypical variations (with respect to onset and course) that are resistant to rigorous treatment.