Query: NC_020064:1150982 Serratia marcescens FGI94, complete genome
Lineage: Serratia marcescens; Serratia; Enterobacteriaceae; Enterobacteriales; Proteobacteria; Bacteria
General Information: This organism was discovered in 1819 by Bizio who named the organism after the Italian physicist Serrati. It was considered a nonpathogenic organism until late in the 20th century, although pathogenicity was noted as early as 1913. Serratia marcescens is an opportunistic human pathogen that is increasingly associated with life-threatening hospital-acquired infections. It is an environmental organism that has a broad host range, and is capable of infecting vertebrates and invertebrates, as well as plants. In humans, Serratia marcescens can cause meningitis (inflammation of the membrane surrounding the brain and spinal cord), endocarditis (inflammation of heart muscle) and pyelonephritis (inflammation of the kidneys). Many strains are resistant to multiple antibiotics. Environmental isolates are noted by production of the red pigment prodigiosin.
Subject: NC_008710:703740 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.