Pre_GI: SWBIT SVG BLASTP

Query: NC_006570:1526071 Francisella tularensis subsp. tularensis Schu 4, complete genome

Lineage: Francisella tularensis; Francisella; Francisellaceae; Thiotrichales; Proteobacteria; Bacteria

General Information: This subspecies is virulent in humans, and the strain is a clinical isolate that is also virulent in an animal model. Originally isolated from a human case of tularemia in 1951. There are a large number of insertion sequences including a mariner element, which is a transposon typically found in eukaryotes and is the first instance of this element to be found in a microbe, which may have acquired it during transit through one of the insect vectors. Causative agent of tularemia. This organism was first identified by Edward Francis as the causative agent of a plague-like illness that affected squirrels in Tulare county in California in the early part of the 20th century. The organism now bears his name. The disease, which has been noted throughout recorded history, can be transmitted to humans by infected ticks or deerflies, infected meat, or by aerosol, and thus is a potential bioterrorism agent. This organism has a high infectivity rate, and can invade phagocytic and nonphagocytic cells, multiplying rapidly. Once within a macrophage, the organism can escape the phagosome and live in the cytosol. It is an aquatic organism, and can be found living inside protozoans, similar to what is observed with Legionella.

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BLASTP Alignment.txt

Subject: NC_007797:914500 Anaplasma phagocytophilum HZ, complete genome

Lineage: Anaplasma phagocytophilum; Anaplasma; Anaplasmataceae; Rickettsiales; Proteobacteria; Bacteria

General Information: Isolated from a patient in New York, USA, in 1995. This organism is a tick-borne (Ixodesspp.) obligate intracellular pathogen that infects humans and causes human granulocytic anaplasmosis as well as infecting several other types of animals. This organism produces a number of pathogenic factors that aid virulence. These include specific adhesins for neutrophils, virulence factors that inhibit both phagosome-lysozome fusion and production of reactive oxygen species that would normally kill the bacterium. The bacterium also inhibits programmed cell death of the neutrophil (apoptosis) and induces expression of interleukin-8, which causes neutrophil chemotaxis, thereby increasing the spread of the bacterium throughout the host organism.