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Health effects and the baby boomers — middle age
Published in J. Mangano Joseph, Low-Level Radiation and Immune System Damage, 2018
In the late 1980s, another new disease caught the eye of the public and health professionals. Reports mostly from the northeast U.S. described a condition called Lyme disease, named for the Connecticut town with an unusually high incidence. Unlike CFIDS, the cause of Lyme disease was quickly uncovered. Ticks, which had picked up a bacterium called Borrelia burgdorferi from infected deer, bit and infected unsuspecting individuals. The disease that often ensued usually consists of a rash in the shape of a bulls-eye, malaise, fever, neurological problems, joint pain, headache, and stiff neck. Fortunately, antibiotic treatments often prove effective if the disease is spotted in time.
Evidence for a Role of Infections in the Activation of Autoreactive T Cells and the Pathogenesis of Autoimmunity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
J. Ludovic Croxford, Stephen D. Miller
Lyme arthritis is a multi-system disease resulting from infection by the spirochete, Borrelia burgdorferi, following a tick bite. Early symptoms occur within days and include secondary skin lesions, mild hepatitis and cardiac disease. The main symptoms appear months after the initial infection, and include large joint inflammation, swelling and pain, similar to rheumatoid arthritis. Most infected people can be treated with a course of antibiotics, whereby the spirochete is eliminated, as determined by PCR.53 However, around 10% of patients are resistant to treatment, and even though the spirochete is eliminated, chronic joint inflammation persists. A current hypothesis suggests that this may be due to autoimmunity. The majority of antibiotic-resistant individuals with Lyme arthritis express the HLA-DR1*0401, 0404, 0101, 0102 alleles.54 A number of spirochete T cell epitope specificities arise in the early phase of infection.55 In late stage disease, CD4+Th1 cells and serum IgG specific for the Borrelia burgdorferi outer surface protein A (OspA) are detected in the synovial fluid of Lyme arthritis patients concomitant with prolonged attacks of arthritis.55,56 Interestingly, T cell responses specific for OspA154-173 were rare in antibiotic-treatable cases of Lyme arthritis compared to resistant Lyme arthritis patients, suggesting that this epitope may be involved in the pathogenesis of disease.55 A possible mechanism of autoimmune pathogenesis by this epitope, is molecular mimicry between the foreign OspA epitope and an unknown self-tissue epitope. Computer searches determined that OspA165-173 shared sequence homology with a human protein epitope, leukocyte function-associated antigen 1αL326-345 (LFA-1αL326-345).57 Interestingly, T cells from antibiotic-resistant Lyme arthritis patients displayed Th1-type responses to both OspA165-173 and LFA-1αL326-345 confirming cross-reactivity between the spirochete and self-epitopes.57 Although LFA-1α is not joint-specific, it is expressed by lymphocytes, which may be present in the joints following spirochete infection. Current thinking suggests that the large number of IFN-γ secreting OspA-specific T cells activate APCs in the joints, which may phagocytize apoptotic T cells and present LFA-1α. Following eradication of the spirochete infection, APC presenting LFA-1α may cross-activate OspA-specific T cells, which then presumably mediate joint damage. Although the present evidence is suggestive for a role of molecular mimicry in the pathogenesis of Lyme arthritis, further elucidation of the pathogenic role of LFA-1α specific T cells is required.
Modelling the effects of habitat and hosts on tick invasions
Published in Letters in Biomathematics, 2018
Two tick species, I. affinis and A. maculatum, are concurrently expanding their ranges into the Mid-Atlantic region of the US and have been observed invading in different geographic patterns, and with different genetic signatures (Nadolny et al., 2015).Ixodes affinis has been implicated in the sylvatic cycle of Borrelia burgdorferi, the agent of Lyme disease, while A. maculatum is a known vector of numerous pathogens of medical and veterinary importance, including Rickettsia parkeri, the agent of Tidewater spotted fever (Oliver, 1996; Teel, Ketchum, Mock, Wright, & Strey, 2010). Ixodes affinis is generally found in disturbed forested habitat and is a generalist tick species that feeds on small mammals and birds during immature life stages, and medium and large mammals during the adult stage. This tick species exhibits genetically well-mixed populations that are likely created and maintained through short-distance dispersal events throughout the contiguous forested habitat that is abundant in the Mid-Atlantic (Nadolny et al., 2015).