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. 2020 Oct 7;5(5):e00569-20. doi: 10.1128/mSphere.00569-20

TABLE 1.

Genomic and epidemiological features of S. flexneri versus S. sonnei

Feature Descriptiona
S. flexneri S. sonnei
Geographical distribution(s) Low- and middle-income countries Industrialized countries
 
Multidrug resistance phenotype AMP + SXT + NAL/CIP AMP + SXT + NAL/CIP
 
Genotypic resistance determinant(s)
    Resistance gene(s)
        Trimethoprim/sulfamethoxazole dhfrA1, sulI/sulII dhfrA1, sulI/sulII
        Ampicillin blaOXA-1, blaTEM-1 bla TEM-1
        Ciprofloxacin QRDR mutations (gyrA and parC) QRDR mutations (gyrA and parC)
PMQR—qnrB/S and aac(6′)-Ib-cr Efflux—mdfA, acrA/B, and tolC
Efflux—mdfA, acrA/B, and tolC
        Cefotaxime/cefixime blaCTX-M-15/14, blaCMY2, and blaDHA blaCTX-M-15/14, blaCMY2, and blaDHA
        Azithromycin mphA/ermB mphA/ermB
    Mobile genetic elements
        Plasmid type IncF Col
        Integron class(es) 1 and 2 2
        PAI(s) SHI-1, SHI-2, and SRL SHI-2
    Epidemiological feature(s)
        Existing terms PGs Lineages
        Nature of spread Limited global spread Greater global spread
        Dominant clone in India PG3 Central Asia III lineage
a

AMP, ampicillin; SXT, trimethoprim/sulfamethoxazole; NAL, nalidixic acid; CIP, ciprofloxacin; PAI, pathogenicity island; PGs, phylogenetic groups.