Pre_GI: SWBIT SVG BLASTP

Query: NC_008261:3014373 Clostridium perfringens ATCC 13124, complete genome

Lineage: Clostridium perfringens; Clostridium; Clostridiaceae; Clostridiales; Firmicutes; Bacteria

General Information: The species type strain, originally isolated from a human gas gangrene patient. Causative agent of gas gangrene. 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. Known opportunistic toxin-producing pathogens in animals and humans. Some species are capable of producing organic solvents (acetone, ethanol, etc,), molecular hydrogen and other useful compounds. This organism is a causative agent of a wide spectrum of necrotic enterotoxicoses. It also causes such animal diseases as lamb dysentery, ovine enterotoxemia (struck), pulpy kidney disease in lambs and other enterotoxemias in lambs and calves. It is commonly found in the environment (soil, sewage) and in the animal and human gastrointestinal tract as a member of the normal microflora. It is a fast growing (generation time 8-10 min) anaerobic flesh-eater. Active fermentative growth is accompanied by profuse generation of molecular hydrogen and carbon dioxide. It is also oxygen tolerant which makes it an easy object to work with in laboratories. C. perfringens have been developed and the species became a model organism in clostridial genetic studies. Known isolates belong to five distinct types (A, B, C, D, and E) that are distinguished based on the specific extracellular toxins they produce. Known isolates belong to five distinct types (A, B, C, D, and E) that are distinguished based on the specific extracellular toxins they produce. All types produce the alpha toxin (phospholipase C). Type A strains that cause gas gangrene produce alpha toxin, theta (hemolysin), kappa (collagenase), mu (hyaluronidase), nu (DNAse) and neuraminidase which are all the enzymatic factors aiding the bacterium in invading and destruction of the host tissues. Type C strains produce alpha toxin, beta toxin and prefringolysin enteritis. In addition to alpha toxin, Type B strains produce beta toxin, types B and D produce the pore forming epsilon toxin and type E strains produce iota toxin.

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BLASTP Alignment.txt

Subject: NC_004668:2762464 Enterococcus faecalis V583, complete genome

Lineage: Enterococcus faecalis; Enterococcus; Enterococcaceae; Lactobacillales; Firmicutes; Bacteria

General Information: This strain is one of the first vancomycin-resistant strains isolated. This isolate came from a blood culture derived from a chronically-infected patient in 1987 from Barnes Hospital in St. Louis, Missouri, USA. This strain was found to lack the cytolysin gene and a surface adhesin, Esp, that contributes to urinary tract infections. Mobile genetic elements make up one quarter of the genome. This genera consists of organisms typically found in the intestines of mammals, although through fecal contamination they can appear in sewage, soil, and water. They cause a number of infections that are becoming increasingly a problem due to the number of antibiotic resistance mechanisms these organisms have picked up. Both Enterococcus faecalis and Enterococcus faecium cause similar diseases in humans, and are mainly distinguished by their metabolic capabilities. This opportunistic pathogen can cause urinary tract infections, bacteremia (bacteria in the blood), and infective endocarditis (inflammation of the membrane surrounding the heart), similar to infections caused by Enterococcus faecium. Hospital-acquired infections from this organism are on the rise due to the emergence of antiobiotic resistance strains. Enterococcus faecalis produces a cytolysin toxin that is encoded on various mobile genetic elements, pathogenicity islands, and conjugative plasmids. The cytolysin aids in pathogenesis, possibly by causing destruction of cells such as erythrocytes, which allows access to new nutrients for the organism.