Lyme Disease and Its Clinical Spectrum Essay

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Lyme disease, or tick-borreliosis, is a natural focal disease transmitted by ticks. It is characterized by skin, joints, nervous and cardiovascular systems lesions and often assumes a chronic, relapsing course. The causative agent of borreliosis is Borrelia burgdorferi, Borrelia garinii and Borrelia afzelii, which are the most pathogenic for humans (Cardenas-de la Garza et al., 2019). Transmission is transmitted by tick bite (inoculation). However, the possibility of infection is not excluded by contact with the feces of the tick on the skin, with subsequent absorption by scratching.

Clinical symptoms appear at the different stages of the disease. Penetrating in the human body, borrelia in the place of introduction causes the formation of the primary effect, that is, papule, erythema mite. Then they enter different organs and tissues via the hematogenous route, where they are adsorbed on cells, interacting most actively with the galactocerebroside of neuroglia membranes (Cardenas-de la Garza et al., 2019). There arise perivascularly infiltrates consisting of lymphocytes, macrophages, plasmocytes, and diffuse infiltration of damaged tissues by these elements. Borrelia and formed immune complexes lead to the development of vasculitis and vascular occlusion.

In the later stages of the disease borrelia, they provoke the development of immunopathological processes of considerable importance for the pathogenesis of neuroborreliosis and chronic arthritis. Among these patients, those with HLA-DR2 and HLA-DR4 genotypes are the most frequent (Shapiro & Wormser, 2018). In the early stages of the disease, specific antibodies are produced, the titer of which increases in the progression of the disease. The immune response is most pronounced when the joints are affected in the later stages. With effective therapy and recovery, the level of antibodies is normalized (Shapiro & Wormser, 2018). Prolonged persistence of antibodies or their appearance in high titers at late stages indicates the persistence of the pathogen even in the absence of clinical manifestations.

References

Cardenas-de la Garza, J. A., la Cruz-Valadez, D., Ocampo-Candiani, J., & Welsh, O. (2019).. European Journal of Clinical Microbiology & Infectious Diseases, 38(2), 201-208. Web.

Shapiro, E. D., & Wormser, G. P. (2018). Jama, 320(7), 635-636. Web.

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