Clostridium perfringens toxinotype NEW

@article{pmid33843463,

title = {Pathogenicity and virulence of Clostridium perfringens},

author = {Iman Mehdizadeh Gohari and Mauricio A Navarro and Jihong Li and Archana Shrestha and Francisco Uzal and Bruce A McClane},

doi = {10.1080/21505594.2021.1886777},

issn = {2150-5608},

year  = {2021},

date = {2021-12-01},

urldate = {2021-12-01},

journal = {Virulence},

volume = {12},

number = {1},

pages = {723--753},

abstract = {Clostridium perfringens is an extremely versatile pathogen of humans and livestock, causing wound infections like gas gangrene (clostridial myonecrosis), enteritis/enterocolitis (including one of the most common human food-borne illnesses), and enterotoxemia (where toxins produced in the intestine are absorbed and damage distant organs such as the brain). The virulence of this Gram-positive, spore-forming, anaerobe is largely attributable to its copious toxin production; the diverse actions and roles in infection of these toxins are now becoming established. Most  toxin genes are encoded on conjugative plasmids, including the pCW3-like and the recently discovered pCP13-like plasmid families. Production of  toxins is highly regulated via processes involving two-component regulatory systems, quorum sensing and/or sporulation-related alternative sigma factors. Non-toxin factors, such as degradative enzymes like sialidases, are also now being implicated in the pathogenicity of this bacterium. These factors can promote toxin action  and, perhaps , and also enhance  intestinal colonization, e.g. NanI sialidase increases  adherence to intestinal tissue and generates nutrients for its growth, at least . The possible virulence contributions of many other factors, such as adhesins, the capsule and biofilms, largely await future study.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29866424,

title = {Expansion of the Clostridium perfringens toxin-based typing scheme},

author = {Julian I Rood and Vicki Adams and Jake Lacey and Dena Lyras and Bruce A McClane and Stephen B Melville and Robert J Moore and Michel R Popoff and Mahfuzur R Sarker and J Glenn Songer and Francisco A Uzal and Filip Van Immerseel},

doi = {10.1016/j.anaerobe.2018.04.011},

issn = {1095-8274},

year  = {2018},

date = {2018-10-01},

urldate = {2018-10-01},

journal = {Anaerobe},

volume = {53},

pages = {5--10},

abstract = {Clostridium perfringens causes many different histotoxic and enterotoxic diseases in humans and animals as a result of its ability to produce potent protein toxins, many of which are extracellular. The current scheme for the classification of isolates was finalized in the 1960s and is based on their ability to produce a combination of four typing toxins - α-toxin, β-toxin, ε-toxin and ι-toxin - to divide C. perfringens strains into toxinotypes A to E. However, this scheme is now outdated since it does not take into account the discovery of other toxins that have been shown to be required for specific C. perfringens-mediated diseases. We present a long overdue revision of this toxinotyping scheme. The principles for the expansion of the typing system are described, as is a mechanism by which new toxinotypes can be proposed and subsequently approved. Based on these criteria two new toxinotypes have been established. C. perfringens type F consists of isolates that produce C. perfringens enterotoxin (CPE), but not β-toxin, ε-toxin or ι-toxin. Type F strains will include strains responsible for C. perfringens-mediated human food poisoning and antibiotic associated diarrhea. C. perfringens type G comprises isolates that produce NetB toxin and thereby cause necrotic enteritis in chickens. There are at least two candidates for future C. perfringens toxinotypes, but further experimental work is required before these toxinotypes can formally be proposed and accepted.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}