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Clostridium perfringens type E animal enteritis isolates with highly conserved, silent enterotoxin gene sequences
S J Billington1, E U Wieckowski, M R Sarker
1Department of Veterinary Science and Microbiology, University of Arizona, Tucson, Arizona 85721, USA.
Infection and Immunity
|August 26, 1998
Summary
Clostridium perfringens type E isolates cause calf enteritis but cannot produce enterotoxin (CPE) due to silent cpe genes. These silent genes, near iota toxin genes on episomes, suggest recent horizontal gene transfer.
Area of Science:
- Veterinary Microbiology
- Bacterial Genetics
Background:
- Clostridium perfringens is a significant cause of enteritis in animals.
- Neonatal calf hemorrhagic enteritis is often associated with specific C. perfringens types.
Purpose of the Study:
- To investigate the genetic basis of C. perfringens type E isolates associated with calf enteritis.
- To characterize the C. perfringens enterotoxin (cpe) gene in type E isolates.
Main Methods:
- Multiplex PCR was used to identify C. perfringens genotype E isolates.
- Genetic analysis was performed to examine the cpe gene sequences and their regulatory elements.
Main Results:
- Type E isolates expressed alpha and iota toxins but not CPE, despite possessing cpe gene sequences.
- The cpe sequences in type E isolates contained multiple mutations (nonsense, frameshift) and lacked essential regulatory elements, rendering them silent.
- These silent cpe sequences were conserved, located near iota toxin genes on episomal DNA, and not clonally related among isolates.
Conclusions:
- The silent cpe sequences in C. perfringens type E isolates are non-functional due to significant genetic defects.
- The findings suggest horizontal gene transfer of an episome carrying iota toxin and silent cpe genes to different C. perfringens type A strains, leading to type E emergence.