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Infection and Immunity, January 2005, p. 652-656, Vol. 73, No. 1
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.1.652-656.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Atypical cpb2 Genes, Encoding Beta2-Toxin in Clostridium perfringens Isolates of Nonporcine Origin
B. Helen Jost,*
Stephen J. Billington,
Hien T. Trinh,
Dawn M. Bueschel, and
J. Glenn Songer
Department of Veterinary Science and Microbiology, University of Arizona, Tucson, Arizona
Received 25 August 2004/
Accepted 3 September 2004
Beta2-toxin, encoded by cpb2, is implicated in the pathogenesis of Clostridium perfringens enteritis. However, cpb2 genes from nonporcine C. perfringens isolates were not always expressed, at least in vitro. Nucleotide sequencing identified atypical cpb2 genes with 70.2 to 70.7% DNA identity to previously identified (consensus) cpb2. Atypical beta2-toxin displayed 62.3% identity and 80.4% similarity to consensus beta2-toxin. No porcine type C isolates (n = 16) and only 3.3% of porcine type A isolates (n = 60) carried atypical cpb2 genes. However, 88.5% of nonporcine isolates carried atypical cpb2 (n = 78), but beta2-toxin was not expressed. Almost half of the nonporcine consensus cpb2 genes (44.4%) carried a frameshift mutation (n = 9), resulting in an absence of beta2-toxin expression. These findings strengthen the role of beta2-toxin in the pathogenesis of enteritis in neonatal pigs. However, the identification of apparently nonexpressed, atypical cpb2 genes raises the question of whether this protein plays the same role in enteritis in other animal species.
* Corresponding author. Mailing address: Department of Veterinary Science and Microbiology, University of Arizona, 1117 East Lowell St., Tucson, AZ 85721. Phone: (520) 621-5996. Fax: (520) 621-6366. E-mail:
jost{at}u.arizona.edu.
Editor: J. T. Barbieri
Infection and Immunity, January 2005, p. 652-656, Vol. 73, No. 1
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.1.652-656.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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