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Antimicrobial Agents and Chemotherapy, June 2009, p. 2319-2326, Vol. 53, No. 6
0066-4804/09/$08.00+0 doi:10.1128/AAC.01532-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Emergence and Evolution of Multiply Antibiotic-Resistant Salmonella enterica Serovar Paratyphi B D-Tartrate-Utilizing Strains Containing SGI1
Steven P. Djordjevic,1,
Amy K. Cain,2
Nick J. Evershed,2
Linda Falconer,1
Renee S. Levings,1
Diane Lightfoot,3 and
Ruth M. Hall2*
New South Wales Department of Primary Industries, Elizabeth Macarthur Agricultural Institute, Microbiology and Immunology Section, Camden, New South Wales 2570, Australia,1 School of Molecular and Microbial Biosciences, The University of Sydney, New South Wales 2006, Australia,2 Microbiological Diagnostic Unit, Public Health Laboratory, Department of Microbiology and Immunology, University of Melbourne, Victoria 3013, Australia3
Received 17 November 2008/ Returned for modification 12 February 2009/ Accepted 23 March 2009
The first Australian isolate of Salmonella enterica serovar Paratyphi B D-tartrate-utilizing (dT+) that is resistant to ampicillin, chloramphenicol, florfenicol, streptomycin, spectinomycin, sulfonamides, and tetracycline (ApCmFlSmSpSuTc) and contains SGI1 was isolated from a patient with gastroenteritis in early 1995. This is the earliest reported isolation globally. The incidence of infections caused by these SGI1-containing multiply antibiotic-resistant S. enterica serovar Paratyphi B dT+ strains increased during the next few years and occurred sporadically in all states of Australia. Several molecular criteria were used to show that the early isolates are very closely related to one another and to strains isolated during the following few years and in 2000 and 2003 from home aquariums and their owners. Early isolates from travelers returning from Indonesia shared the same features. Thus, they appear to represent a true clone arising from a single cell that acquired SGI1. Some minor differences in the resistance profiles and molecular profiles also were observed, indicating the ongoing evolution of the clone, and phage type differences were common, indicating that this is not a useful epidemiological marker over time. Three isolates from 1995, 1998, and 1999 contained a complete sul1 gene but were susceptible to sulfamethoxazole due to a point mutation that creates a premature termination codon. This SGI1 type was designated SGI1-R. The loss of resistance genes also was examined. When strains were grown for many generations in the absence of antibiotic selection, the loss of SGI1 was not detected. However, variants SGI1-C (resistance profile SmSpSu) and SGI1-B (resistant to ApSu), which had lost part of the integron, arose spontaneously, presumably via homologous recombination between duplications in the In104 complex integron.
* Corresponding author. Mailing address: School of Molecular and Microbial Biosciences, Biochemistry and Microbiology Building G08, The University of Sydney, New South Wales 2006, Australia. Phone: 61-2-9351-3465. Fax: 61-2-9351-4571. E-mail: ruth.hall{at}mmb.usyd.edu.au
Published ahead of print on 30 March 2009.
Present address: Institute for the Biotechnology of Infectious Diseases, University of Technology Sydney, Ultimo, NSW2007, Australia.
Antimicrobial Agents and Chemotherapy, June 2009, p. 2319-2326, Vol. 53, No. 6
0066-4804/09/$08.00+0 doi:10.1128/AAC.01532-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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