Complete genome sequence of a multiple drug resistant Salmonella enterica serovar Typhi CT18

J. Parkhill (), G. Dougan (), K. D. James, N. R. Thomson, D. Pickard, J. Wain, C. Churcher, K. L. Mungall, S. D. Bentley, M. T. G. Holden, M. Sebaihia, S. Baker, D. Basham, K. Brooks, T. Chillingworth, P. Connerton, A. Cronin, P. Davis, R. M. Davies, L. Dowd, N. White, J. Farrar, T. Feltwell, N. Hamlin, A. Haque, T. T. Hien, S. Holroyd, K. Jagels, A. Krogh, T. S. Larsen, S. Leather, S. Moule, P. Ó'Gaora, C. Parry, M. Quail, K. Rutherford, M. Simmonds, J. Skelton, K. Stevens, S. Whitehead and B. G. Barrell
Additional contact information
J. Parkhill: The Sanger Centre, Wellcome Trust Genome Campus
G. Dougan: Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine
K. D. James: The Sanger Centre, Wellcome Trust Genome Campus
N. R. Thomson: The Sanger Centre, Wellcome Trust Genome Campus
D. Pickard: Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine
J. Wain: Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine
C. Churcher: The Sanger Centre, Wellcome Trust Genome Campus
K. L. Mungall: The Sanger Centre, Wellcome Trust Genome Campus
S. D. Bentley: The Sanger Centre, Wellcome Trust Genome Campus
M. T. G. Holden: The Sanger Centre, Wellcome Trust Genome Campus
M. Sebaihia: The Sanger Centre, Wellcome Trust Genome Campus
S. Baker: The Sanger Centre, Wellcome Trust Genome Campus
D. Basham: The Sanger Centre, Wellcome Trust Genome Campus
K. Brooks: The Sanger Centre, Wellcome Trust Genome Campus
T. Chillingworth: The Sanger Centre, Wellcome Trust Genome Campus
P. Connerton: Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine
A. Cronin: The Sanger Centre, Wellcome Trust Genome Campus
P. Davis: The Sanger Centre, Wellcome Trust Genome Campus
R. M. Davies: The Sanger Centre, Wellcome Trust Genome Campus
L. Dowd: The Sanger Centre, Wellcome Trust Genome Campus
N. White: University of Oxford-Wellcome Trust Clinical Research Unit, Centre for Tropical Diseases
J. Farrar: University of Oxford-Wellcome Trust Clinical Research Unit, Centre for Tropical Diseases
T. Feltwell: The Sanger Centre, Wellcome Trust Genome Campus
N. Hamlin: The Sanger Centre, Wellcome Trust Genome Campus
A. Haque: Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine
T. T. Hien: The Centre for Tropical Diseases
S. Holroyd: The Sanger Centre, Wellcome Trust Genome Campus
K. Jagels: The Sanger Centre, Wellcome Trust Genome Campus
A. Krogh: Centre for Biological Sequence Analysis, BioCentrum-DTU, The Technical University of Denmark, Building 208
T. S. Larsen: Centre for Biological Sequence Analysis, BioCentrum-DTU, The Technical University of Denmark, Building 208
S. Leather: The Sanger Centre, Wellcome Trust Genome Campus
S. Moule: The Sanger Centre, Wellcome Trust Genome Campus
P. Ó'Gaora: Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine
C. Parry: The Centre for Tropical Diseases
M. Quail: The Sanger Centre, Wellcome Trust Genome Campus
K. Rutherford: The Sanger Centre, Wellcome Trust Genome Campus
M. Simmonds: The Sanger Centre, Wellcome Trust Genome Campus
J. Skelton: The Sanger Centre, Wellcome Trust Genome Campus
K. Stevens: The Sanger Centre, Wellcome Trust Genome Campus
S. Whitehead: The Sanger Centre, Wellcome Trust Genome Campus
B. G. Barrell: The Sanger Centre, Wellcome Trust Genome Campus

Nature, 2001, vol. 413, issue 6858, 848-852

Abstract: Abstract Salmonella enterica serovar Typhi (S. typhi) is the aetiological agent of typhoid fever, a serious invasive bacterial disease of humans with an annual global burden of approximately 16 million cases, leading to 600,000 fatalities1. Many S. enterica serovars actively invade the mucosal surface of the intestine but are normally contained in healthy individuals by the local immune defence mechanisms. However, S. typhi has evolved the ability to spread to the deeper tissues of humans, including liver, spleen and bone marrow. Here we have sequenced the 4,809,037-base pair (bp) genome of a S. typhi (CT18) that is resistant to multiple drugs, revealing the presence of hundreds of insertions and deletions compared with the Escherichia coli genome, ranging in size from single genes to large islands. Notably, the genome sequence identifies over two hundred pseudogenes, several corresponding to genes that are known to contribute to virulence in Salmonella typhimurium. This genetic degradation may contribute to the human-restricted host range for S. typhi. CT18 harbours a 218,150-bp multiple-drug-resistance incH1 plasmid (pHCM1), and a 106,516-bp cryptic plasmid (pHCM2), which shows recent common ancestry with a virulence plasmid of Yersinia pestis.

Date: 2001
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DOI: 10.1038/35101607

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