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Animal Connection Challenges
Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
There are accidents such as snakebites, encounters with sharks at beaches or with big cats or other wild animals such as wolves or bears that can cause problems for humans. What is certainly even more serious is the exposure to insects such as mosquitoes, in particular in tropical regions. Over 1 million people worldwide die from mosquito-borne diseases every year, making those diseases a serious threat to human health. Mosquito-initiated diseases include malaria, dengue, encephalitis and yellow fever. Another potentially serious condition is Lyme disease, which is caused by Borrelia, a genus of bacteria of the phylum Spirochete. Lyme borreliosis is a zoonotic,a vector-borne disease transmitted primarily by ticks and by lice368 that first infest rodents and then deer before jumping on humans and dogs. The genus is named after the French biologist Amédée Borrel (1867–1936).
Health effects and the baby boomers — adolescence and early adulthood
Published in J. Mangano Joseph, Low-Level Radiation and Immune System Damage, 2018
Syphilis is another notifiable disease representing a sexually transmitted organism (the spirochete Treponema pallidum). Syphilis is also curable with penicillin if the medication is administered in the primary stage (usually a genital sore) or secondary stage (skin eruption and inflammation of several organs). If allowed to progress to a later stage, syphilis can damage the heart and central nervous system, and may even cause blindness. In 1994, about 81% of primary and secondary syphilis cases were reported in persons 15 to 39 years old, according to the CDC.
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.
Detection of pathogenic Leptospira in ornamental water fountains from urban sites in Cali, Colombia
Published in International Journal of Environmental Health Research, 2019
Kevin Escandón-Vargas, Javier Andrés Bustamante-Rengifo, Miryam Astudillo-Hernández
Leptospirosis is a zoonosis with global distribution particularly affecting tropical countries and resource-poor communities, caused by species of the spirochete genus Leptospira. Thirty-five species (13 pathogenic, 11 intermediate, and 11 saprophytic) have been described to date (Bourhy et al. 2014; Lehmann et al. 2014; Thibeaux et al. 2018). While the pathogenic and the intermediate Leptospira species are considered the infectious group capable of causing disease in humans and animals, the saprophytic species are considered environmental bacteria that do not cause disease. Infection occurs either by direct contact with urine of reservoir animals or indirectly via contaminated water or moist soil. The leptospiral carriage in animal reservoirs’ renal tubules leads to urinary shedding of leptospires in the environment (Levett 2001; Bharti et al. 2003). Pathogenic Leptospira enter the body via cut or abraded skin, and mucous membranes.