Expansion of the Clostridium perfringens toxin-based typing scheme

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...

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Published inAnaerobe Vol. 53; pp. 5 - 10
Main Authors Rood, Julian I., Adams, Vicki, Lacey, Jake, Lyras, Dena, McClane, Bruce A., Melville, Stephen B., Moore, Robert J., Popoff, Michel R., Sarker, Mahfuzur R., Songer, J. Glenn, Uzal, Francisco A., Van Immerseel, Filip
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.10.2018
Elsevier Masson
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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β-toxin, ε-toxin and ι-toxin – to divide C. perfringens strains into toxinotypes A to E. However, this scheme is now outdated since it does not take into account the discovery of other toxins that have been shown to be required for specific C. perfringens-mediated diseases.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. [Display omitted] •An expanded C. perfringens toxinotyping scheme is presented.•Two new toxinotypes are proposed.•C. perfringens type F strains produce CPE, but not β, ε or ι toxins.•C. perfringens type G strains produce NetB.•A mechanism for the introduction of new toxinotypes is presented.
AbstractList 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.
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. [Display omitted] •An expanded C. perfringens toxinotyping scheme is presented.•Two new toxinotypes are proposed.•C. perfringens type F strains produce CPE, but not β, ε or ι toxins.•C. perfringens type G strains produce NetB.•A mechanism for the introduction of new toxinotypes is presented.
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.
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.
Author Moore, Robert J.
Lyras, Dena
Songer, J. Glenn
Lacey, Jake
Uzal, Francisco A.
Rood, Julian I.
Melville, Stephen B.
Popoff, Michel R.
Van Immerseel, Filip
McClane, Bruce A.
Adams, Vicki
Sarker, Mahfuzur R.
AuthorAffiliation 8 California Animal Health and Food Safety Laboratory, San Bernardino Branch, School of Veterinary Medicine, University of California-Davis, San Bernardino, CA 92408, USA
6 Unité Des Bactéries Anaérobies et Toxines, Institut Pasteur, 25 Rue Du Dr Roux, 75724, Paris Cedex 15, France
2 CSIRO Biosecurity Flagship, Australian Animal Health Laboratory, Geelong, Victoria 3220, Australia
3 Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
5 School of Science, RMIT University, Bundoora, Victoria 3083, Australia
9 Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium
7 Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA
1 Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia
4 Department of B
AuthorAffiliation_xml – name: 3 Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
– name: 8 California Animal Health and Food Safety Laboratory, San Bernardino Branch, School of Veterinary Medicine, University of California-Davis, San Bernardino, CA 92408, USA
– name: 5 School of Science, RMIT University, Bundoora, Victoria 3083, Australia
– name: 7 Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA
– name: 9 Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium
– name: 4 Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia, USA
– name: 1 Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia
– name: 2 CSIRO Biosecurity Flagship, Australian Animal Health Laboratory, Geelong, Victoria 3220, Australia
– name: 6 Unité Des Bactéries Anaérobies et Toxines, Institut Pasteur, 25 Rue Du Dr Roux, 75724, Paris Cedex 15, France
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  givenname: Julian I.
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  fullname: Rood, Julian I.
  email: julian.rood@monash.edu
  organization: Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia
– sequence: 2
  givenname: Vicki
  surname: Adams
  fullname: Adams, Vicki
  organization: Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia
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  givenname: Jake
  surname: Lacey
  fullname: Lacey, Jake
  organization: Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia
– sequence: 4
  givenname: Dena
  surname: Lyras
  fullname: Lyras, Dena
  organization: Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia
– sequence: 5
  givenname: Bruce A.
  surname: McClane
  fullname: McClane, Bruce A.
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  surname: Melville
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  organization: Department of Biological Sciences, Virginia Tech, Blacksburg, VA, USA
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  surname: Moore
  fullname: Moore, Robert J.
  organization: Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia
– sequence: 8
  givenname: Michel R.
  surname: Popoff
  fullname: Popoff, Michel R.
  organization: Unité Des Bactéries Anaérobies et Toxines, Institut Pasteur, 25 Rue Du Dr Roux, 75724, Paris Cedex 15, France
– sequence: 9
  givenname: Mahfuzur R.
  surname: Sarker
  fullname: Sarker, Mahfuzur R.
  organization: Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA
– sequence: 10
  givenname: J. Glenn
  surname: Songer
  fullname: Songer, J. Glenn
– sequence: 11
  givenname: Francisco A.
  surname: Uzal
  fullname: Uzal, Francisco A.
  organization: California Animal Health and Food Safety Laboratory, San Bernardino Branch, School of Veterinary Medicine, University of California-Davis, San Bernardino, CA 92408, USA
– sequence: 12
  givenname: Filip
  surname: Van Immerseel
  fullname: Van Immerseel, Filip
  organization: Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29866424$$D View this record in MEDLINE/PubMed
https://pasteur.hal.science/pasteur-02453858$$DView record in HAL
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Snippet Clostridium perfringens causes many different histotoxic and enterotoxic diseases in humans and animals as a result of its ability to produce potent protein...
Clostridium perfringens causes many different histotoxic and enterotoxic diseases in humans and animals as a result of its ability to produce potent protein...
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SubjectTerms Animals
Bacterial Toxins/analysis
Bacterial Typing Techniques/methods
Bacteriology
Cell Behavior
Cellular Biology
Clostridium Infections/microbiology
Clostridium Infections/veterinary
Clostridium perfringens
Clostridium perfringens/classification
Clostridium perfringens/isolation & purification
Disease
Humans
Life Sciences
Microbiology and Parasitology
Pathogenesis
Subcellular Processes
Terminology
Toxinotyping
Toxins
Title Expansion of the Clostridium perfringens toxin-based typing scheme
URI https://dx.doi.org/10.1016/j.anaerobe.2018.04.011
https://www.ncbi.nlm.nih.gov/pubmed/29866424
https://pasteur.hal.science/pasteur-02453858
https://pubmed.ncbi.nlm.nih.gov/PMC6195859
Volume 53
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