Pre_GI: SWBIT SVG BLASTP

Query: NC_005126:4824500 Photorhabdus luminescens subsp. laumondii TTO1, complete genome

Lineage: Photorhabdus luminescens; Photorhabdus; Enterobacteriaceae; Enterobacteriales; Proteobacteria; Bacteria

General Information: This strain was isolated on Trinidad and Tobago. It is a symbiont of the nematode Heterorhabditis bacteriophora. Bioluminescent bacterium. This organism is unusual in that it is symbiotic within one insect, and pathogenic in another, the only organism that is known to exhibit this dual phenotype. Enzymes are then released by the bacteria that result in rapid degradation of the insect body, allowing both bacteria and nematode to feed and reproduce. During this period Photorhabdus luminescens releases bacteriocidal products, including antibiotics and bacteriocins, that prevent infection of the larva by competitive microbes. The result is promotion of Photorhabdus luminescens-nematode interactions that result in continuation of the symbiotic relationship. In order to engage in a symbiotic relationship with the nematode and a pathogenic one with the insect larva, the bacterium encodes specific factors that encourage both. These include a large number of genes that code for secreted toxins and enzymes, as well as genes that encode products for the production of antibiotics and bacteriocins. Secretion of these products occurs by an array of systems including type I, type II, and type III secretion systems. The type III system is closely related to the Yersinia plasmid-encoded type III system. Genes that promote symbiotic relationships are also encoded on genomic islands on the chromosome including some that affect nematode development. Virulence genes appear to be active during exponential growth. Symbiotic genes appear to function during stationary phase (post-exponential) growth. The switch from one state to another is controlled. Photorhabdus luminescens is capable of giving off light, a complex process that requires the products of the lux operon.

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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.