Pre_GI: SWBIT SVG BLASTP

Query: NC_009882:167350 Rickettsia rickettsii str. 'Sheila Smith', complete genome

Lineage: Rickettsia rickettsii; Rickettsia; Rickettsiaceae; Rickettsiales; Proteobacteria; Bacteria

General Information: This strain was isolated from from a patient with Rocky Mountain spotted fever. Causative agent for Rocky Mountain Spotted Fever. This genus, like other Rickettsial organisms such as Neorickettsia and Anaplasma, are obligate intracellular pathogens and is composed of two groups, the spotted fever group, and the typhus group. The latter is composed of two organisms, Rickettsia prowazekii and Rickettsia typhi. The bacteria are transmitted via an insect, usually a tick, to a host organism, in this case humans, where they target endothelial cells and sometimes macrophages. They attach via an adhesin, rickettsial outer membrane protein A, and are internalized where they persist as cytoplasmically free organisms. Rickettsia rickettsii was first identified by Dr. Howard Rickets as the causative agent of Rocky Mountain Spotted Fever, which was originally named for its geographic distribution at the time, it is now known to be widespread throughout the North American continent. This bacterium is an obligate intracellular pathogen that infects primarily the vascular endothelium, and occasionally smooth muscle tissue. This bacterium is an obligate intracellular pathogen that infects primarily the vascular endothelium, and occasionally smooth muscle tissue. It is passed to the human host from a tick bite, and the tick acts as both a natural reservoir and a vector for disease transmission. Once the organism is endocytosed by the host cell, it quickly escapes the phagozome, and replicates intracellularly, causing cell death and tissue damage. The disease is characterized by a spotted rash and has a high mortality rate if left untreated.

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BLASTP Alignment.txt

Subject: NC_009089:117980 Clostridium difficile 630, complete genome

Lineage: Peptoclostridium difficile; Peptoclostridium; Peptostreptococcaceae; Clostridiales; Firmicutes; Bacteria

General Information: This strain is the epidemic type X variant that has been extensively studied in research and clinical laboratories. It produces both toxin A, and B. Causative agent of pseudomembranous colitis. This genus comprises about 150 metabolically diverse species of anaerobes that are ubiquitous in virtually all anoxic habitats where organic compounds are present, including soils, aquatic sediments and the intestinal tracts of animals and humans. This shape is attributed to the presence of endospores that develop under conditions unfavorable for vegetative growth and distend single cells terminally or sub-terminally. Spores germinate under conditions favorable for vegetative growth, such as anaerobiosis and presence of organic substrates. It is believed that present day Mollicutes (Eubacteria) have evolved regressively (i.e., by genome reduction) from gram-positive clostridia-like ancestors with a low GC content in DNA. Some species are capable of producing organic solvents (acetone, ethanol, etc,), molecular hydrogen and other useful compounds. This species is now recognized as the major causative agent of pseudomembranous colitis (inflammation of the colon) and diarrhea that may occur following antibiotic treatment. This bacterium causes a wide spectrum of disease, ranging from mild, self-limiting diarrhea to serious diarrhea and, in some cases, complications such as pseudomembrane formation, toxic megacolon (dilation of the colon) and peritonitis, which often lead to lethality among patients. The bacteria produce high molecular mass polypeptide cytotoxins, A and B. Some strains produce only one of the toxins, others produce both. Toxin A causes inflammatory reaction involving hypersecretion of fluid and hemorrhagic necrosis through triggering cytokine release by neutrophils. Alteration of intestinal microbial balance with antibiotic therapy and increased exposure to the bacterium in a hospital setting allows C. difficile to colonize susceptible individuals. Moreover, it has been shown that subinhibitory concentrations of antibiotics promote increased toxin production by C. difficile.