Antimicrobial resistance and genetic diversity of Shigella sonnei isolates from western Ireland, an area of low incidence of infection

Abstract

Shigella sonnei is a significant cause of gastroenteritis in both developing and industrialized countries. Definition of the diversity and antimicrobial susceptibility of S. sonnei isolates may be helpful in the management of individual cases and outbreaks. Antimicrobial susceptibility testing and pulsed-field gel electrophoresis (PFGE) were performed with 67 isolates of S. sonnei predominantly (n = 59) from three counties in the west of Ireland. Phage typing (n = 17), plasmid profiling (n = 28), and integron analysis (n = 24) were performed with subsets of strains. PFGE typing permitted recognition of two major clusters: PFGE type A (n = 53) and PFGE type B (n = 14). PFGE type A was associated with resistance to ampicillin, streptomycin, and sulfonamides (51 of 53 isolates), and those that were phage typed (n = 6) were phage type 3. PFGE type B was associated with resistance to streptomycin, sulfonamides, tetracycline, and trimethoprim (11 of 14 isolates) and phage type 6 (9 of 11 isolates). Fifteen different plasmid profiles were identified among the 28 isolates analyzed. A class 2 integron was present in all 14 PFGE type B isolates. One of these isolates also contained a class 1 integron and showed a unique variant of the PFGE type B pattern. Sequence analysis of the gene cassette structures contained within these integrons identified distinct open reading frames that encoded determinants of resistance to trimethoprim, streptomycin, and streptothricin. Our data demonstrate two predominant PFGE types among S. sonnei isolates circulating in this region. The limited diversity of the S. sonnei isolates in this region means that detection of isolates indistinguishable by PFGE and according to their antibiograms in two or more patients is not persuasive evidence of a common-source food- or waterborne outbreak. Indistinguishable plasmid profiles in addition to indistinguishable PFGE and antibiogram types may be more suggestive of an epidemiologically relevant link between cases.

FIG. 1.

PFGE patterns generated with XbaI of representative S. sonnei isolates from Ireland. Lane 1, strain F2353 (S. sonnei control); lane 2, isolate 3331 (PFGE type A); lane 3, isolate 3367 (type A); lane 4, isolate 3219 (type A); lane 5, F2353 control; lane 6, isolate Dublin 1 (type A1); lane 7, isolate CK1 (type B); lane 8, isolate Dublin 4 (type B1); lane 9, isolate 510 (type B); lane 10, F2353 control; lane 11, isolate Dublin 2 (type B4); lane 12, isolate 3601 (type B1); lane 13, isolate Dublin 3 (type B3); lane 14, F2353 control.

FIG. 2.

Plasmid profiles of selected S. sonnei isolates along with their respective E. coli J-53 transconjugants. Lane 1, isolate 3331; lane 2, 3331 transconjugant resistant to ampicillin, streptomycin, and sulfonamides; lane 3, 3331 transconjugant A; lane 4, isolate 3599; lane 5, 3599 transconjugant A; lane 6, isolate Dublin 3; lane 7, Dublin 3 transconjugant resistant to streptomycin, sulfonamides, and tetracycline; lane 8, E. coli J-53 recipient; lane 9, controls Rts1 (84 kb), R1 (41 kb), and R6K (17 kb); lane 10, 2- to 10-kb ladder; lane 11, isolate CK2; lane 12, CK2 transconjugant resistant to ampicillin, sulfonamides, and tetracycline; lane 13, isolate 3219; lane 14, 3219 transconjugant A; lane 15, 3219 transconjugant resistant to ampicillin, sulfonamides, and trimethoprim.