Pre_GI: SWBIT SVG BLASTN

Query: NC_004668:241352 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_008710:621822 Borrelia turicatae 91E135, complete genome

Lineage: Borrelia turicatae; Borrelia; Spirochaetaceae; Spirochaetales; Spirochaetes; Bacteria

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.