Pre_GI: SWBIT SVG BLASTP

Query: NC_006142:140853 Rickettsia typhi str. Wilmington, complete genome

Lineage: Rickettsia typhi; Rickettsia; Rickettsiaceae; Rickettsiales; Proteobacteria; Bacteria

General Information: This genus, like other Rickettsial organisms such as Neorickettsia and Anaplasma, is composed of obligate intracellular pathogens. The latter is composed of two organisms, Rickettsia prowazekii and Rickettsia typhi. The bacteria are transmitted via an insect, usually a tick, to a host organism, in this case humans, where they target endothelial cells and sometimes macrophages. They attach via an adhesin, rickettsial outer membrane protein A, and are internalized where they persist as cytoplasmically free organisms. Transovarial transmission (from mother to offspring) occurs in the invertebrate host. Rickettsia typhi causes murine typhus and is an obligate intracellular pathogen that infects both the flea vector and hosts such as human, rat, and mouse. In the flea vector, the bacterium penetrates the gut epithelial barrier and is found in the feces which become infective.

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BLASTP Alignment.txt

Subject: NC_010673:388442 Borrelia hermsii DAH, complete genome

Lineage: Borrelia hermsii; Borrelia; Spirochaetaceae; Spirochaetales; Spirochaetes; Bacteria

General Information: This strain was isolated from a case of relapsing fever in western Washington, USA. Borrelia hermsii is the causative agent of tick-borne relapsing fever in the western United States and Canada. Borrelia then multiplies rapidly, causing a generalized infection throughout the tick. While feeding, the tick passes the organism into a mammalian host through its infectious saliva. Relapsing fever is characterized by a period of chills, fever, headache, and malaise, an asymptomatic period, followed by another episode of symptoms. This cycle of relapsing is due to changes in the surface proteins of Borrelia, which allow it to avoid detection and removal by the host immune system. This antigenic variation is the result of homologous recombination of silent proteins into an expressed locus, causing partial or complete replacement of one serotype with another. These plasmids carry genes involved in antigenic variation and pathogenicity.