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Borreliella burgdorferiRANK: SpeciesTAXONOMY: Bacteria -> Spirochaetes -> Spirochaetia -> Spirochaetales -> Borreliaceae -> Borreliella -> Borreliella burgdorferi OVERVIEW: Borrelia burgdorferi is a bacterial species of the spirochete class of the genus Borrelia. B. burgdorferi exists in North America and Europe and is the predominant causative agent of Lyme disease in the United States. Borrelia species are considered diderm (double-membrane) bacteria rather than gram positive or negative. B. burgdorferi is one of the few pathogenic bacteria that can survive without iron, having replaced all of its iron-sulfur cluster enzymes with enzymes that use manganese, thus avoiding the problem many pathogenic bacteria face in acquiring iron. Lyme disease is a zoonotic, vector-borne disease transmitted by the Ixodes tick (also the vector for Babesia). The infected nymphal tick transmits B. burgdorferi via its saliva to the human during its blood meal. In order for a successful infection, the vertebrate host reservoir must cultivate enough bacteria that can be circulated throughout the blood, so that B. burgodorferi can be transmitted through Ixodes blood feeding. Additionally, the bacteria itself must withstand the molting and life cycle of the Ixodes tick and successfully transinfect a host for B. Burgdorferi to spread to humans.Clinical presentation of Lyme disease may include the characteristic bull's-eye rash and erythema chronicum migrans (a rash which spreads peripherally and spares the central part), as well as myocarditis, cardiomyopathy, arrythmia, arthritis, arthralgia, meningitis, neuropathies, and facial nerve palsy. After the pathogen is transmitted, it will acclimate to the mammalian conditions. Borrelia burgdorferi will change its glycoproteins and proteases on its plasma membrane to facilitate its dissemination throughout the blood. While infecting, B. burgdorferi will express proteins that will interact with endothelial cells, platelets, chondrocytes, and the extracellular matrix. This interaction inhibits proper function of the infected areas, leading to the pathological manifestations of Lyme disease. In response, the host will emit an inflammatory response to fight off the infection.Borrelia burgdorferi, also, expresses at least seven plasminogen binding proteins for interference of factor H at the activation level. This is part of a complement system evasion strategy that leads to downstream blocking of immune response. |