TpeL-producing strains of Clostridium perfringens type A are highly virulent for broiler chicks

Coursodon, Christine F.; Glock, Robert D.; Moore, Katherine L.; Cooper, Kerry K.; Songer, J. Glenn

doi:10.1016/j.anaerobe.2011.10.001

Cited by 105 publications

(66 citation statements)

References 11 publications

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“…TpeL modifies the regulatory GTPase Ras at Thr35, which disrupts cell signaling, including RasRaf interactions and ERK activation (136). The role, if any, of TpeL in disease is still unclear, but it has been suggested that TpeL production might enhance virulence of avian necrotic enteritis strains (138).…”

Section: Plasmid-encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

226

282

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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.

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Section: Plasmid-encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

226

282

View full text Add to dashboard Cite

show abstract

“…29) A previous study reported that the production of TpeL may enhance the virulence of poultry necrotizing enterocolitis strains. 9) In the present study, we speculated that C. perfringens may use TpeL to disrupt actin homeostasis in intestinal epithelial cells during the infection, which suggests enterotoxic effects in the intestine. Hence, TpeL provides a newly pathogenic mechanism and is also a valuable tool for studying infectious processes involving the organization of actin.…”

Section: )mentioning

confidence: 65%

<i>Clostridium perfringens</i> TpeL Induces Formation of Stress Fibers <i>via</i> Activation of RhoA-ROCK Signaling Pathway

Nagahama

Ohkubo

Kinouchi

et al. 2015

Biological & Pharmaceutical Bulletin

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“…Wild-type C. perfringens type A to E isolates used in this study are listed and described in Table 1. The toxin genotypes (A to E) and some phenotypic characteristics of these isolates were determined previously (23,24,(26)(27)(28)(29)(30)(31)(32)(33)(34). All C. perfringens isolates used in this study were maintained as stock cultures in cooked meat medium (Oxoid) and stored at Ϫ20°C.…”

Section: Methodsmentioning

confidence: 99%

“…CPB, produced by C. perfringens type B and type C strains, is very sensitive to endogenous trypsin degradation in the intestines of natural host animals (18,19). In contrast, a major toxin of both type B and D strains, i.e., ETX, is produced as an inactive prototoxin that must be proteolytically activated by intestinal proteases (such as trypsin, chymotrypsin, and carboxypeptidases) or, perhaps, proteases produced by C. perfringens (20)(21)(22)(23)(24)(25). Until now, no information has been available regarding whether TpeL, which can be encoded by strains causing diseases originating in the intestines (26,27), is trypsin sensitive.…”

mentioning

confidence: 99%

Characterization of Clostridium perfringens TpeL Toxin Gene Carriage, Production, Cytotoxic Contributions, and Trypsin Sensitivity

Chen

McClane

2015

Infect Immun

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Large clostridial toxins (LCTs) are produced by at least four pathogenic clostridial species, and several LCTs are proven pivotal virulence factors for both human and veterinary diseases. TpeL is a recently identified LCT produced by Clostridium perfringens that has received relatively limited study. In response, the current study surveyed carriage of the tpeL gene among different C. perfringens strains, detecting this toxin gene in some type A, B, and C strains but not in any type D or E strains. This study also determined that all tested strains maximally produce, and extracellularly release, TpeL at the late-log or early-stationary growth stage during in vitro culture, which is different from the maximal late-stationary-phase production reported previously for other LCTs and for TpeL production by C. perfringens strain JIR12688. In addition, the present study found that TpeL levels in culture supernatants can be repressed by either glucose or sucrose. It was also shown that, at natural production levels, TpeL is a significant contributor to the cytotoxic activity of supernatants from cultures of tpeL-positive strain CN3685. Lastly, this study identified TpeL, which presumably is produced in the intestines during diseases caused by TpeL-positive type B and C strains, as a toxin whose cytotoxicity decreases after treatment with trypsin; this finding may have pathophysiologic relevance by suggesting that, like beta toxin, TpeL contributes to type B and C infections in hosts with decreased trypsin levels due to disease, diet, or age.

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TpeL-producing strains of Clostridium perfringens type A are highly virulent for broiler chicks

Cited by 105 publications

References 11 publications

Toxin Plasmids of Clostridium perfringens

Toxin Plasmids of Clostridium perfringens

<i>Clostridium perfringens</i> TpeL Induces Formation of Stress Fibers <i>via</i> Activation of RhoA-ROCK Signaling Pathway

Characterization of Clostridium perfringens TpeL Toxin Gene Carriage, Production, Cytotoxic Contributions, and Trypsin Sensitivity

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