G09SecL04Tpc2: Difference between revisions
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==Pathogenesis of Lyme Neuroborreliosis (LNB)== | ==Pathogenesis of Lyme Neuroborreliosis (LNB)== | ||
Penetrating the immune system’s first line of defense the skin, Borrelia can cause a local infection at the site of tick attachment. These infections produce easily recognizable marks, referred to as erythema migrans, commonly known as the bulls-eye rash associated with Lyme disease. While other antigens may play a greater role in the beginning of the invasion, OspA has been shown to be more active in the second stage of the infection after the bacteria spreads throughout the body. Affected areas can include the heart, joints, and the nervous system itself. The second stage is when signs of acute Lyme neuroborreliosis (LNB) begin. Symptoms of LNB include meningoradiculitis with inflammation of the nerve roots, radicular pain (Bannwarth’s syndrome), lymphocytic meningitis, in addition to cranial or peripheral neuritis.<ref name=art4>PMID:18097481</ref> | |||
=== The Elusiveness of OspA === | === The Elusiveness of OspA === | ||