Pre_GI: SWBIT SVG BLASTN

Query: NC_004668:3156247 Enterococcus faecalis V583, complete genome

Lineage: Enterococcus faecalis; Enterococcus; Enterococcaceae; Lactobacillales; Firmicutes; Bacteria

General Information: This strain is one of the first vancomycin-resistant strains isolated. This isolate came from a blood culture derived from a chronically-infected patient in 1987 from Barnes Hospital in St. Louis, Missouri, USA. This strain was found to lack the cytolysin gene and a surface adhesin, Esp, that contributes to urinary tract infections. Mobile genetic elements make up one quarter of the genome. This genera consists of organisms typically found in the intestines of mammals, although through fecal contamination they can appear in sewage, soil, and water. They cause a number of infections that are becoming increasingly a problem due to the number of antibiotic resistance mechanisms these organisms have picked up. Both Enterococcus faecalis and Enterococcus faecium cause similar diseases in humans, and are mainly distinguished by their metabolic capabilities. This opportunistic pathogen can cause urinary tract infections, bacteremia (bacteria in the blood), and infective endocarditis (inflammation of the membrane surrounding the heart), similar to infections caused by Enterococcus faecium. Hospital-acquired infections from this organism are on the rise due to the emergence of antiobiotic resistance strains. Enterococcus faecalis produces a cytolysin toxin that is encoded on various mobile genetic elements, pathogenicity islands, and conjugative plasmids. The cytolysin aids in pathogenesis, possibly by causing destruction of cells such as erythrocytes, which allows access to new nutrients for the organism.

Subject: NC_010161:2050816 Bartonella tribocorum CIP 105476, complete genome

Lineage: Bartonella tribocorum; Bartonella; Bartonellaceae; Rhizobiales; Proteobacteria; Bacteria

General Information: This organism was isolated from the blood of wild rats and from fleas obtained from wild rats. Transmission of these organisms is often through an insect vector. Once in a host, this intracellular pathogen is internalized by an actin-dependent mechanism, and primarily targets endothelial cells, although other cells can be infected. The proliferation of the vascular endothelium (bacillary angiomatosis) is characterisitic of Bartonella infection and results in multiplication of the bacterium's host cells. Infected macrophages are stimulated to release vascular endothelial growth factor (VEGF) and interleukin 1 beta, both of which promote angiogenesis. Endothelial cells are also stimulated to grow and divide by direct contact with bacterial cells. In addition, programmed cell death (apoptosis) of endothelial cells is inhibited, combatting a common mechanism eukaryotic cells use to deal with bacterial infection. Other pathogenicity factors include pili and outer membrane adhesins for attachment to host cells. This organism is genetically related to Bartonella elizabethae which was isolated from a case of endocarditis in a human.