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More than 15 species of Borrelia have been associated with human disease, and other species are responsible for similar diseases in animals. B.burgdorferi is the cause of Lyme disease. Other members of the genus cause relapsing fever, an illness with intermittent fevers and little else. The relapsing fevers differ in their specific vector and geographic distribution. The human body louse is the vector for B.recurrentis, but the remainder of the relapsing fevers are linked to several ticks and species of Borrelia;these are discussed together here as B. hermsii, themost common causeof relapsingfeverin North America.
Borrelia are long(10 to 30μm), slender (0.2 to 0.5μm) spirochetes containingmultiple(7 to 20) axial flagella. In contrast to Treponema and Leptospira, its spirals form loose, irregular waves. The basic organizational structure of the cell and its motility conform to that of the other Gram negative spirochetes, but unlike the others, Borrelia are readily demonstrated by common staining methods like the Giemsa or Wright stains. Borrelia are microaerophilic and have been successfully grown in liquid or semisolid media contain-ing N-acetylglucosamine and long-chain fatty acids.
The outer membrane of all Borrelia species contains abundant outer membrane proteins and lipoproteins. In some species these surface proteins have been observed to vary antigenically at a frequency too high to be explained by simple mutation. Experiments with B. hermsii have demonstrated up to 40 antigenically distinct variants of the same protein arising from a single cell. The genetic mechanism for this antigenic variation involves recombination between the distinctive linear plasmids found in manyBorrelia species. Multiple copies of the genes for these proteins are present. Some genes express the protein while others are “ silent” because they lack crucial promoter sequences. When structural sequences from a silent gene are transferred by recombination to an expressing gene on another plasmid, the protein expressed is altered in a which may make it antigenically different. This mechanism resembles that described for trypanosomes and gonococcal pili .
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