Query: NC_010103:1777000 Brucella canis ATCC 23365 chromosome I, complete sequence Lineage: Brucella canis; Brucella; Brucellaceae; Rhizobiales; Proteobacteria; Bacteria General Information: Etiologic agent of canine brucellosis. 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 bacterium is the causative agent of canine brucellosis. The main sources of infection are vaginal fluids of infected females and urine in males. The most significant symptoms are late abortions in bitches, epididymitis in males and infertility in both sexes, as well as generalized lymphadenitis, discospondylitis and uveitis. Human contagion is not frequent, although it has been reported, and is easily treated. B. canis can be differentiated from the other species of the genus Brucella (except B. ovis) in that it forms rugose colonies.
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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.