Pre_GI: SWBIT SVG BLASTN

Query: NC_017518:2041282 Neisseria meningitidis NZ-05/33 chromosome, complete genome

Lineage: Neisseria meningitidis; Neisseria; Neisseriaceae; Neisseriales; Proteobacteria; Bacteria

General Information: 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). 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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BLASTN Alignment.txt

Subject: NC_008599:1325155 Campylobacter fetus subsp. fetus 82-40, complete genome

Lineage: Campylobacter fetus; Campylobacter; Campylobacteraceae; Campylobacterales; Proteobacteria; Bacteria

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.