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, 33 (5), 1690-8

The Genome Sequence of Salmonella Enterica Serovar Choleraesuis, a Highly Invasive and Resistant Zoonotic Pathogen


The Genome Sequence of Salmonella Enterica Serovar Choleraesuis, a Highly Invasive and Resistant Zoonotic Pathogen

Cheng-Hsun Chiu et al. Nucleic Acids Res.

Erratum in

  • Nucleic Acids Res. 2005;33(7):2351


Salmonella enterica serovar Choleraesuis (S. Choleraesuis), a highly invasive serovar among non-typhoidal Salmonella, usually causes sepsis or extra-intestinal focal infections in humans. S. Choleraesuis infections have now become particularly difficult to treat because of the emergence of resistance to multiple antimicrobial agents. The 4.7 Mb genome sequence of a multidrug-resistant S. Choleraesuis strain SC-B67 was determined. Genome wide comparison of three sequenced Salmonella genomes revealed that more deletion events occurred in S. Choleraesuis SC-B67 and S.Typhi CT18 relative to S. Typhimurium LT2. S. Choleraesuis has 151 pseudogenes, which, among the three Salmonella genomes, include the highest percentage of pseudogenes arising from the genes involved in bacterial chemotaxis signal-transduction pathways. Mutations in these genes may increase smooth swimming of the bacteria, potentially allowing more effective interactions with and invasion of host cells to occur. A key regulatory gene of TetR/AcrR family, acrR, was inactivated through the introduction of an internal stop codon resulting in overexpression of AcrAB that appears to be associated with ciprofloxacin resistance. While lateral gene transfer providing basic functions to allow niche expansion in the host and environment is maintained during the evolution of different serovars of Salmonella, genes providing little overall selective benefit may be lost rapidly. Our findings suggest that the formation of pseudogenes may provide a simple evolutionary pathway that complements gene acquisition to enhance virulence and antimicrobial resistance in S. Choleraesuis.


Figure 1
Figure 1
Circular representation of the S.Choleraesuis genome. (A) The chromosome. The outer scale is marked in megabases. Circles range from 1 (outer circle) to 9 (inner circle). Circles 1 and 2, genes on forward and reverse strand; circle 3, transposons, insertion sequences and prophages; circle 4, unique regions (>100 bp in length) in S.Choleraesuis genome, relative to S.Typhi CT18 and S.Typhimurium LT2; circle 5, pseudogenes; circle 6, G+C content, values >52.1% (average) are in red and smaller in blue; circle 7, GC skew (G−C/G+C), values > 0 are in gold and smaller in purple; circle 8, tRNA genes; and circle 9, Salmonella pathogenicity islands 1–6 and 9. (B) Circular representation of pSC138. For the circular diagrams, the outer scale is marked in base pairs. Circles are numbered to the same scheme as in (A). Circles 1 and 2, all genes; circle 3, transposons and insertion sequences (blue) and bacteriophages (red); circle 4, resistance genes on forward (outward orange marks) and reverse (inward orange marks) strand; circle 5, repeat sequences; circle 6, G+C content; and circle 7, GC skew. (C) Circular representation of pSCV50. Circles 1 and 2, all genes; circle 3, G+C content; and circle 4, GC skew. All genes displayed in circles 1 and 2 are color-coded by function: translation/ribosome structure/biogenesis, pink; transcription, olive drab; DNA replication/recombination/repair, forest green; cell division/chromosome partitioning, light blue; posttranslational modification/protein turnover/chaperones, purple; cell envelop biogenesis, red; cell motility/secretion, plum; inorganic ion transport/metabolism, dark sea green; signal transduction mechanisms, medium purple; energy production/conversion, dark olive green; carbohydrate transport/metabolisms, gold; amino acid transport/metabolism, yellow; nucleotide transport/metabolism, orange; coenzyme transport/metabolism, tan; lipid transport/metabolism, salmon; secondary metabolites biosynthesis/transport/catabolism, light green; defense mechanism, black; general function prediction only, dark blue; function unknown, gray.
Figure 2
Figure 2
Distribution of insertions and deletions (indels) among the three sequenced Salmonella genomes. The graph shows the number of the indel events plotted against the size of the inserted or deleted element (shown as number of genes), clearly indicating that most of the events involve a small number of genes. Values above the line represent genes present in one genome relative to the other; values below the line represent genes absent in one genome relative to the other.
Figure 3
Figure 3
Effect of chemotactic attractants on the swarming of S.Choleraesuis SC-B67 and S.Typhimurium LT2 by using tryptone swarm tubes. (A) Swarm distance for S.Choleraesuis SC-B67 and S.Typhimurium LT2 over the time. Control indicates no addition of chemotactic attractants at the bottom of the tube. Each point represents mean ± SD. (B) The swarm rate in the presence of chemotactic attractants of each strain. S.Typhimurium LT2 swarm rate was significantly higher (*P < 0.05 by Student's t-test) in the presence of glucose (with or without PQQ). This situation was not observed in S.Choleraesuis SC-B67.
Figure 4
Figure 4
MICs of Salmonella strains with and without the efflux pump inhibitor (EPI), Phe-Arg-β-naphthylamide and western blotting analysis of AcrA expression by these strains. S.Typhimurium strains BN18, BN18/21, BN18/41, BN18/71 [see (22)], and the ciprofloxacin-susceptible S.Choleraesuis strain SC-B42 were used as controls.

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