Query: NC_017062:996197 Rickettsia typhi str. B9991CWPP chromosome, 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. This organism causes murine typhus and is an obligate intracellular pathogen that infects both the flea vector and hosts such as human, rat, and mouse. R. prowazekii, and genomic comparisons demonstrate colinearity and similarity to the genome of that organism except for two independent inversions near the origin and terminus. In the flea vector, the bacterium penetrates the gut epithelial barrier and is found in the feces which become infective.
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General Information: This strain (82-40) was isolated from the blood of a human patient who was having a renal transplant and is the best characterized isolate of this species.. The ratio of bloodstream infection to diarrheal illnesses for C. fetus is nearly 400-fold higher than for C. jejuni, indicating its marked propensity for invasive disease compared to C. jejuni. Causes infertility, infectious abortions in cattle, opportunistic human pathogen. This organism causes infertlity and infectious abortions in domesticated sheep, goats and cattle. It is an opportunistic pathogen in humans which can severely affect immunocompromised patients. Initially the bacterium can cause gastroenteritis, and then spread systemically throughout the blood (bacteremia) and cause septicemia, meningitis, and other systemic infections. This layer is essential for host colonization, and prevents complemented-mediated immune responses by inhibiting complement C3b binding.