Query: NC_009715:873280 Campylobacter curvus 525.92 chromosome, complete genome Lineage: Campylobacter curvus; Campylobacter; Campylobacteraceae; Campylobacterales; Proteobacteria; Bacteria General Information: Gastrointestinal clinical isolate. Members of this genus are one of the most common causes of bacterial gastroenteritis (campylobacteriosis). Members of this genus are one of the most common causes of bacterial gastroenteritis (campylobacteriosis). Usually the symptoms are abdominal pain, fever, diarrhea, and cramps, but the illness can sometimes be fatal and some infected individuals develop a syndrome (Guillain-Barre) in which the nerves connecting the spinal cord to the brain are damaged. C. jejuni is the main cause of campylobacteriosis, but other species can also cause infection, including C. coli, C. upsaliensis, and C. curvus.Campylobacter curvus.This species was originally isolated from the human oral cavity in cases of gingivitis; however the role it plays in periodontal disease is unclear. This organism has also been isolated from cases of gastrointestinal disease, and occassionally from abscesses.
- Sequence; - BLASTN hit (Low score = Light, High score = Dark) - hypothetical protein; - cds: hover for description
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.