Toxin Plasmids of Clostridium perfringens

Author:

Li Jihong1,Adams Vicki2,Bannam Trudi L.2,Miyamoto Kazuaki3,Garcia Jorge P.4,Uzal Francisco A.4,Rood Julian I.2,McClane Bruce A.12

Affiliation:

1. Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

2. Australian Research Council Centre of Excellence in Structural and Functional Microbial Genomics, Department of Microbiology, Monash University, Clayton, Victoria, Australia

3. Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan

4. California Animal Health and Food Safety Laboratory, San Bernadino Branch, School of Veterinary Medicine, University of California—Davis, San Bernadino, California, USA

Abstract

SUMMARY In both humans and animals, Clostridium perfringens is an important cause of histotoxic infections and diseases originating in the intestines, such as enteritis and enterotoxemia. The virulence of this Gram-positive, anaerobic bacterium is heavily dependent upon its prolific toxin-producing ability. Many of the ∼16 toxins produced by C. perfringens are encoded by large plasmids that range in size from ∼45 kb to ∼140 kb. These plasmid-encoded toxins are often closely associated with mobile elements. A C. perfringens strain can carry up to three different toxin plasmids, with a single plasmid carrying up to three distinct toxin genes. Molecular Koch's postulate analyses have established the importance of several plasmid-encoded toxins when C. perfringens disease strains cause enteritis or enterotoxemias. Many toxin plasmids are closely related, suggesting a common evolutionary origin. In particular, most toxin plasmids and some antibiotic resistance plasmids of C. perfringens share an ∼35-kb region containing a Tn 916 -related conjugation locus named tcp (transfer of clostridial plasmids). This tcp locus can mediate highly efficient conjugative transfer of these toxin or resistance plasmids. For example, conjugative transfer of a toxin plasmid from an infecting strain to C. perfringens normal intestinal flora strains may help to amplify and prolong an infection. Therefore, the presence of toxin genes on conjugative plasmids, particularly in association with insertion sequences that may mobilize these toxin genes, likely provides C. perfringens with considerable virulence plasticity and adaptability when it causes diseases originating in the gastrointestinal tract.

Publisher

American Society for Microbiology

Subject

Molecular Biology,Microbiology,Infectious Diseases

Reference260 articles.

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3. McClaneBA UzalFA MiyakawaMF LyerlyD WilkinsTD. 2006. The enterotoxic clostridia, p 688–752. In DworkinM FalkowS RosenburgE SchleiferH StackebrandtE (ed), The prokaryotes: a handbook on the biology of bacteria, 3rd ed. Springer, New York, NY.

4. RoodJI. 2006. Clostridium perfringens and histotoxic disease, p 753–770. In DworkinM FalkowS RosenburgE SchleiferH StackebrandtE (ed), The prokaryotes: a handbook on the biology of bacteria, 3rd ed. Springer, New York, NY.

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