Lyme Borreliosis as a Trigger for Autoimmune Disease

Abstract

Lyme disease (LD), also known as Lyme borreliosis, is a zoonotic disease caused by the Gram-negative bacteria Borrelia burgdorferi sensu lato belonging to the Spirochaetaceae family. Differentiating LD from other systemic disorders that present with musculoskeletal symptoms is challenging, and the presence of antibodies to borrelia in the general population may contribute to misdiagnosis. Moreover, long-term exposure of the host's immune system to spirochetes can contribute to the development of chronic autoimmune disease de novo. We report a 35-year-old woman with a combination of LD and systemic lupus erythematosus (SLE), and in this case, LD was the most likely trigger for SLE. We also performed a literature review and summarized the previously reported cases with a combination of LD and autoimmune disease.

Comparison of the Efficacy of Longer versus Shorter Pulsed High Dose Dapsone Combination Therapy in the Treatment of Chronic Lyme Disease/Post Treatment Lyme Disease Syndrome with Bartonellosis and Associated Coinfections

“…Borreliosis can cause numerous disabling rheumatologic, cardiologic, neurologic, and psychiatric complications, mimicking a broad range of chronic illnesses with constitutional symptoms, including chronic fatigue syndrome/M.E. [ 330 ], fibromyalgia [ 331 ], neuropsychiatric as well as autoimmune diseases [ 42 , 66 , 67 ]. The quality of life of those living with CLD/PTLDS has been reported to be worse than that of those living with congestive heart failure, diabetes, and rheumatoid arthritis [ 190 , 332 ], secondary to infection, inflammation, and immune dysfunction resulting in disabling symptoms [ 42 ].…”

“…Horowitz has identified a precision medicine model that has identified up to 16 factors likely responsible for chronic persistent symptomatology in patients suffering from CLD/PTLDS, referred to as MSIDS (Multiple Systemic Infectious Disease Syndrome) [ 50 ]. These include multiple overlapping sources of inflammation (borreliosis and chronic co-infections including Bartonella , leaky gut with dysregulation of gut microbiota, multiple food sensitivities with or without mast cell activation, environmental toxicity [heavy metals, mold], vitamin and mineral deficiencies, and sleep disorders) [ 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 ] with downstream effects of inflammation, including mitochondrial dysfunction [ 62 ], hormonal dysregulation [ 63 , 64 ], Postural Orthostatic Tachycardia Syndrome (POTS) with dysautonomia [ 65 ], autoimmunity [ 42 , 66 ], neuropsychiatric symptoms [ 67 ], liver dysfunction [ 68 , 69 ] and resistant pain syndromes [ 70 ]. Patients oftentimes have multiple overlapping etiologies responsible for their chronic fatiguing, musculoskeletal, and neuropsychiatric symptoms [ 71 ].…”

COVID-19 Infection: The Virus and Its Origin, the Variants, the Immune Defense, the Multiorgan Autoimmune Reactions, and the Targeted Treatments

“…Similarly, bacterial and parasitic infections can trigger autoimmune diseases as seen in reactive arthritis (ReA), rheumatic fever (RF) and Lyme disease (LD) [132] [133] [134]. For example, there were cases of LD patients who developed SLE a couple of months after they were treated for the bacteria Borrelia Burgdorferi infection.…”

“…Microscopic skin lesions were shown without pronounced lymphocytic infiltrates. Indirect immunoassays showed antinuclear antibodies (ANA), anti-nRNP, compliment C3 and C4, and lupus anticoagulant [134].…”

Lyme Disease and Post-treatment Lyme Disease Syndrome: Current and Developing Treatment Options

“…While Lyme disease has several clinically approved treatments, PTLDS suffers from the limited options of only therapeutics directed toward symptom management rather than attacking the disease. Recent studies show that PTLDS may be due to the development of an underlying autoimmune condition after treatment with antibiotics [ 8 , 9 ]. Furthermore, reports of Lyme disease have expanded in the last decade, showing marked spread into previously non-endemic areas [ 1 ].…”