Can Lyme disease trigger Autoimmune diseases?
Evidence about the links between Lyme disease and autoimmune illnesses has been established by doctors and researchers. Although 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 read about autoimmune disorders, how Lyme disease can cause them, and how Lyme disease may be misdiagnosed or incorrectly diagnosed because of similarities of some autoimmune disorder symptoms to those of Lyme disease.
An immune system disease is an autoimmune disease that results in either abnormally high or abnormally low immune system activity levels. When the body's natural defence system can't distinguish between your cells and alien cells, it causes an autoimmune response and unintentionally attacks healthy cells, resulting in an autoimmune disease. 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 60-100 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
- Chronic fatigue syndrome (some professionals classify it as an autoimmune condition)
Understanding the immune system: systemic autoinflammatory diseases 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 show 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 affected by autoimmune illnesses. B-cells or T-cells are involved in these processes. By exposing the body to pathogens (such as 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 caused by ticks.
The innate immune system is another type of immune system. SAIDs affect this immunological system. The physical barriers (such as skin, hair, and mucous membranes), active and passive defence 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, present at birth. Inflammation, which occurs when immune cells (leukocytes) reach the location and release 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 defence and the latter produces specialized cells to combat particular foreign invaders.
Both SAIDs and autoimmune diseases 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
Symptoms of autoimmune and autoinflammatory diseases include inflammation, enlarged lymph nodes, rashes, and fevers. (Notably, several of these symptoms are also typical signs of illnesses carried by ticks, such as Lyme.) Although researchers have recorded at least one case of SAID—adult on-set Still's disease or AOSD—that was presumably induced by Lyme illness, this article mostly focuses on autoimmune diseases and how they resemble, vary from, and interact with Lyme disease.
What causes an autoimmune disorder?
A majority of scientists concur that environmental factors cause autoimmune disorders. Foods (like gluten-containing goods), toxins (from hair dyes, tobacco products, and more), and viral or bacterial illnesses are a few examples that may be such environmental factors.
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, dermatomyositis, rheumatoid arthritis (RA), psoriatic arthritis, and spondyloarthritis have all been linked to or mimicked by Lyme disease, according to studies (SpA).
Misdiagnosis of Lyme disease or complication of autoimmune diseases?
As already mentioned, there is evidence linking autoimmune disorders like Lyme to one another. According to research, Lyme disease can either cause or present as an autoimmune disease or 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 duration for which it is left untreated.
Lyme disease is notoriously difficult to diagnose because its symptoms overlap with those of so many other illnesses, including autoimmune diseases. The inflammatory condition 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 disease is diagnosed with RA without the Lyme being diagnosed 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, commonly known as Lyme borreliosis, is a zoonotic illness caused by the Spirochaetaceae family member Borrelia burgdorferi sensu lato (B. burgdorferi s.l.). Because the symptoms of Lyme disease may resemble those of various systemic disorders with musculoskeletal symptoms, differential diagnosis of the condition is frequently challenging. In addition, a misdiagnosis may occur because of the high incidence of antibodies against borrelia in the general population.
A wide range of clinical indications of Lyme disease, such as signs of articular, neurological, circulatory, cardiac, and ophthalmic involvement, may be present. It should be emphasized that many autoimmune illnesses, including systemic lupus erythematosus, have symptoms similar to these. Given the need to distinguish the primary pathology and choose a management approach, the connection between these two pathologies in clinical practice is of great importance.
Early stages of Lyme disease 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 may play a role in the de novo emergence of chronic autoimmune illnesses. Because the symptoms of Lyme disease can mirror those of numerous other illnesses and have been connected to numerous autoimmune disorders, the confluence of these two diseases may be of clinical interest to rheumatologists.
Multisystemic Lyme disease 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 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 Lyme disease or subsequent autoimmune reactions and illnesses.
There is compelling evidence that patients with antibiotic-resistant Lyme disease 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 patients with Lyme arthritis. Immune system activation depends heavily on MHC class II molecules. The immune system is affected by polymorphisms 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 affected by the second way that MHC class II molecules govern the ontogenetic selection of 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.
According to studies, there are some similarities between the musculoskeletal symptoms of Lyme disease and rheumatoid arthritis. 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 explored the connection between particular HLA-DR serotypes and people with Lyme disease who are more likely to develop chronic arthritis. HLA-DR4 was more prevalent in patients with chronic arthritis and was the only serotype that significantly correlated with treatment-resistant Lyme arthritis in a study of 130 patients with diverse Lyme disease symptoms. Overall, HLA-DR4 or -DR2 was present in 89% 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.
The preclinical stage of an autoimmune disease 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 manifestations. 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 effect of infection.
The key is early detection
Timely, precise testing is essential to avoid a false-positive result 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 various symptoms that characterize autoimmune disorders. One of the most severe connective tissue systemic disorders, systemic lupus erythematosus, has several atypical variations (with respect to onset and course) that are resistant to rigorous treatment.