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Updated: Jan 19, 2026
An Allelotyping PCR for Identifying Salmonella enterica serovars Enteritidis, Hadar, Heidelberg, and Typhimurium
Published on: July 22, 2011
Genome sequence of a clinical Salmonella Enteritidis sequence type 11 strain from South Africa
Roxanne Rule1, Mohamed Said1, Nontombi Mbelle1
1Department of Medical Microbiology, Pathology Building, University of Pretoria, Prinshof Campus, Corner of Steve Biko Road and Dr Savage Road, Pretoria 0084, South Africa; Tshwane Academic Division, National Health Laboratory Service, Corner of Steve Biko Road and Dr Savage Road, Pretoria 0084, South Africa.
Objectives:
The underlying resistance mechanism and phylogenetic relationship of a colistin-resistant Salmonella enterica serovar Enteritidis strain EC20120916 that resulted in fatal meningitis in an immunocompromised patient was investigated by whole-genome sequencing (WGS) analysis.
Methods:
WGS of strain EC20120916 was performed on an Illumina MiSeq platform and annotation of the sequence was performed using the Prokaryotic Genome Annotation Pipeline (PGAP). Antimicrobial resistance genes, plasmid replicons and pathogenicity islands were identified. A phylogenetic tree was constructed using Parsnp and was edited with FigTree.
Results:
The genome size of strain EC20120916 is 4 699 318 bp with a GC content of 55.2% and 4471 protein-coding genes. The aac(6')-laa gene, encoding resistance to aminoglycosides, was identified although this was not expressed phenotypically in the isolate. No colistin resistance-conferring mutations or plasmid-mediated mechanisms were identified to explain the colistin resistance. The strain was phylogenetically related to three international strains, although it was not close enough to suggest importation from outside of South Africa.
Conclusion:
This is the first report of a colistin-resistant Salmonella Enteritidis isolate causing meningitis in an immunocompromised patient in South Africa. The absence of colistin resistance-conferring mutations or plasmid-mediated resistance mechanisms suggest that a novel mechanism is responsible for the colistin resistance in this isolate. The isolate was acquired locally.
