Pre_GI: SWBIT SVG BLASTN

Query: NC_010117:1461502 Coxiella burnetii RSA 331, complete genome

Lineage: Coxiella burnetii; Coxiella; Coxiellaceae; Legionellales; Proteobacteria; Bacteria

General Information: This strain (RSA 331; Hentzerling) is associated with acute Q fever and was isolated from the blood of an infected patient in northern Italy in 1945. This organism is widely distributed in nature and can cause infections in reptiles, birds, and mammals. It causes Q fever, or 'query' fever, an atypical pneumonia first associated with abattoir workers in Australia. Transmission may be through insect vectors such as ticks that have bitten an infected wild or domesticated animal, or through an aerosol produced by domesticated animals such as sheep or cattle. The presence of a plasmid is believed to be associated with virulence and pathogenicity, however C. burnetii isolates containing plasmid QpDG are avirulent in guinea pigs and plasmidless isolates have been associated with endocarditis in humans. Coxiella burnetii has a developmental life cycle, and can grow vegetatively through binary fission, or asymmetrically and produce a spore-like cell. The spore-like cell may enable the organism to exist extracellularly for small amounts of time. This bacterium is an obligate intracellular pathogen. It is endocytosed by a host cell, a macrophage for example, and lives and replicates inside the phagolysozome, a unique property of this organism. The genome encodes proteins that have a higher than average pI, which may enable adaptation to the acidic environment of the phagolysozome. The chromosome also contains genes for a number of detoxification and stress response proteins such as dismutases that allow growth in the oxidative environment. The type IV system is similar to the one found in Legionella, which may be important for intracellular survival. This organism produces numerous ankyrin-repeat proteins that may be involved in interactions with the host cell. The genome has 83 pseudogenes, which may be a result of the typical genome-wide degradation observed with other intracellular organisms and also has a group I intron in the 23S ribosomal RNA gene.

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BLASTN Alignment.txt

Subject: NC_009089:1 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.