Genetic diversity of drug-resistant Vibrio cholerae: a systematic review with exploratory quantitative synthesis

Antimicrobial resistance (AMR) in Vibrio cholerae is shaped by the interaction between pandemic lineages and mobile genetic elements, complicating treatment choices and accelerating regional spread. We synthesised evidence on the genetic diversity of drug-resistant V. cholerae, with emphasis on seventh-pandemic El Tor (7PET) lineages, SXT/R391 family integrative and conjugative elements (ICEs), IncA/C(2)/IncC plasmids, and key quinolone and macrolide determinants. We conducted a systematic review of genomic and molecular epidemiology studies reporting drug-resistant V. cholerae from clinical outbreaks, surveillance datasets, and linked environmental sampling. Data were extracted on lineage or sublineage, resistance determinants, mobile genetic elements, and phenotypic or genotypic AMR profiles. Because comparable quantitative datasets were limited, meta-analysis was restricted to an exploratory pooled estimate for IncA/C(2)/IncC plasmid carriage among clinical isolates. Evidence supports a clonal-expansion plus horizontal-gene-transfer model: outbreaks are often dominated by closely related 7PET clusters, although AMR breadth changes through acquisition, reshuffling, or loss of resistance cassettes carried by SXT/R391 ICEs and IncA/C(2)/IncC plasmids. Yemen showed a rapid transition toward a broader MDR profile after acquisition of an IncC plasmid, whereas Malawi and Kenya demonstrated clonal outbreak expansion with different accessory-genome resistance profiles [5–7]. An exploratory random-effects calculation using two heterogeneous datasets ( n =174) yielded 0.95 (95% CI 0.36–1.00; I 2 =83.8%; tau2 = 5.35; H2 = 6.16) [7, 8]. This calculation is presented solely to illustrate between-study heterogeneity and must not be cited or interpreted as a prevalence estimate. Drug-resistant V. cholerae diversity is best understood as the overlay of pandemic lineage movement, local persistence, and modular exchange of AMR cassettes. The two-dataset quantitative calculation is only an illustration of heterogeneity and is not a prevalence estimate. Routine integration of whole-genome sequencing with phenotypic testing can improve outbreak response and antimicrobial policy. The review protocol was not registered because the work was initiated as a focused synthesis of published genomic and molecular epidemiology studies; this is acknowledged as a limitation.