Pre_GI: SWBIT SVG BLASTN

Query: NC_010376:186510 Finegoldia magna ATCC 29328, complete genome

Lineage: Finegoldia magna; Finegoldia; Clostridiales Family XI; Clostridiales; Firmicutes; Bacteria

General Information: It is isolated most frequently from various infection sites, including soft tissue, bone and joint, and diabetic foot infections. This species, formerly Peptostreptococcus magnus, is a commensal bacterium colonizing human skin and mucous membranes. It has been shown to cause valve endocarditic in humans. Gram-positive anaerobic cocci (GPAC) are a major part of the normal human flora colonizing skin and mucous membranes of the mouth and gastrointestinal tracts. In GPAC, Finegoldia magna (formerly Peptostreptococcus magnus) has the highest pathogenicity and is isolated most frequently from various infection sites, including soft tissue, bone and joint, and diabetic foot infections.

- Sequence; - BLASTN hit (Low score = Light, High score = Dark)
- hypothetical protein; - cds: hover for description

BLASTN Alignment.txt

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.