Query: NC_010120:144000 Neisseria meningitidis 053442, complete genome Lineage: Neisseria meningitidis; Neisseria; Neisseriaceae; Neisseriales; Proteobacteria; Bacteria General Information: Causes septicemia and meningitis. The second of two pathogenic Neisseria, this organism causes septicemia and is the leading cause of life-threatening meningitis (inflammation of the meninges, the membrane surrounding the brain and spinal cord) in children. This organism typically residies in the nasopharynx cavity but can invade the respiratory epthelial barrier, cross into the bloodstream and the blood brain barrier, and cause inflammation of the meninges. Pathogenicity factors include the surface proteins (porins and opacity proteins), and the type IV pilus (which is also found in Neisseria gonorrhoeae). Pathogenicity factors include the surface proteins (porins and opacity proteins), and the type IV pilus (which is also found in Neisseria gonorrhoeae). This organism, like Neisseria gonorrhoeae, is naturally competent, and protein complexes at the cell surface recognize the uptake signal sequence in extracellular DNA, an 8mer that is found at high frequency in Neisseria chromosomal DNA.
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General Information: This strain was isolated in the USA from the soft tick Ornithodoros turicatae. Borrelia turicatae is the causative agent of tick-borne relapsing fever in the southwestern USA. Ticks become infected with Borrelia while feeding on an infected mammal, usually a rodent or squirrel. Borrelia then multiplies rapidly, causing a generalized infection throughout the tick. While feeding, the tick passes the spirochete into a mammalian host through its infectious saliva. Relapsing fever is characterized by period of chills, fever, headache, and malaise, followed by an asymptomatic, followed by another episode of symptoms. The 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.