1887

Abstract

In this work it is shown that the majority of serovars most frequently associated with the systemic infection of vertebrate hosts produce a major outer-membrane porin, OmpD. However, OmpD is absent from the outer-membrane protein profiles of strain Ty2 and 26 clinical isolates of . examined by SDS-PAGE. To determine whether the gene is present in , primers internal to the coding sequence were used to amplify the gene by PCR. With the exception of strains, the gene was amplified from the genomes of all serovars tested. Consistently, a specific probe did not hybridize with DNA isolated from the strains. Taken together, these results demonstrate that does not produce OmpD due to the absence of the gene. Furthermore, it was investigated whether the deletion of extended to . This gene is adjacent to in the chromosome and encodes a protein involved in the resistance to methyl viologen, a superoxide-generating agent. Although PCR failed to amplify the gene from the strain Ty2 genome, it was possible to amplify it from the chromosome of the clinical strains. On the other hand, hybridization analyses showed that the gene is present in all the strains tested. In contrast to the other serovars, strain Ty2 and the clinical isolates showed sensitivity to methyl viologen, suggesting that gene is inactive in . In conclusion, the region is variable in structure among serovars. It is hypothesized that the absence of may suggest a role in host specificity.

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2001-07-01
2020-09-25
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