Query: NC_012563:4101000 Clostridium botulinum A2 str. Kyoto, complete genome Lineage: Clostridium botulinum; Clostridium; Clostridiaceae; Clostridiales; Firmicutes; Bacteria General Information: This strain was isolated from a case of infant botulism in Kyoto, Japan in 1978. This organism produces one of the most potent and deadly neurotoxins known, a botulinum toxin that prevents the release of acetylcholine at the neuromuscular junction, thereby inhibiting muscle contraction and causing paralysis. In most cases the diseased person dies of asphyxiation as a result of paralysis of chest muscles involved in breathing. The spores are heat-resistant and can survive in inadequately heated, prepared, or processed foods. Spores germinate under favorable conditions (anaerobiosis and substrate-rich environment) and bacteria start propagating very rapidly, producing the toxin.Botulinum toxin, and C. botulinum cells, has been found in a wide variety of foods, including canned ones. Almost any food that has a high pH (above 4.6) can support growth of the bacterium. Honey is the most common vehicle for infection in infants. Food poisoning through C. botulinum is the most frequent type of infection caused by this bacterium. The wound botulism that occurs when C. botulinum infects an individual via an open wound is much rarer and is very similar to tetanus disease. There are several types of botulinum toxin known (type A through type F), all of them being neurotoxic polypeptides. The most common and widely distributed are strains and serovars of C. botulinum that produce type A toxin.
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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.