Published online 21 March 2005
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The genome sequence of Salmonella enterica serovar Choleraesuis, a highly invasive and resistant zoonotic pathogen
1Department of Pediatrics, Chang Gung Children's Hospital Taoyuan, Taiwan 2Chang Gung Genomic Medicine Center, Chang Gung Memorial Hospital Taoyuan, Taiwan 3Department of Internal Medicine, Chang Gung Memorial Hospital Taoyuan, Taiwan 4Department of Obstetrics and Gynecology, Chang Gung Memorial Hospital Taoyuan, Taiwan 5Department of Parasitology, Chang Gung University College of Medicine Taoyuan, Taiwan 6Chang Gung Bioinformatics Center, Chang Gung University Taoyuan, Taiwan 7Beijing Genomics Institute, Center of Bioinformatics and Genomics, Chinese Academy of Sciences Beijing, People's Republic of China 8James D. Watson Institute of Genome Sciences, Zhejiang University Hangzhou, People's Republic of China
*To whom correspondence should be addressed. Tel: +886 3 3281200; Fax: +886 3 3288957; Email: chchiu{at}adm.cgmh.org.tw
Received October 20, 2004. Revised January 5, 2005. Accepted February 22, 2005.
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.
DDBJ/EMBL/GenBank accession nos+
+AE017220, AY509003 and AY509004
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