Pre_GI: SWBIT SVG BLASTP

Query: NC_004311:1096649 Brucella suis 1330 chromosome II, complete sequence

Lineage: Brucella suis; Brucella; Brucellaceae; Rhizobiales; Proteobacteria; Bacteria

General Information: A swine isolate. Causes brucellosis, infectious abortions, fevers. They are highly infectious, and can be spread through contact with infected animal products or through the air, making them a potential bioterrorism agent. Once the organism has entered the body, it can become intracellular, and enter the blood and lymphatic regions, multiplying inside phagocytes before eventually causing bacteremia (spread of bacteria through the blood). Virulence may depend on a type IV secretion system which may promote intracellular growth by secreting important effector molecules. This organism is a swine-specific Brucella. It causes infectious abortions in animals and a systemic, febrile (feverish) illness in humans. Brucella suis is considered a potential bioterrorism agent and was the first pathogenic organism to be weaponized by the USA.

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Subject: NC_008599:128431 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.