Emergence of <i>Salmonella enterica</i> Serovar Heidelberg Producing OXA 48 Carbapenemase in Eastern Algeria

<i>Salmonella</i> infections have become increasingly resistant to antibiotics, including fluoroquinolones, third-generation cephalosporins (C3G), and even carbapenems. This report describes the emergence of a strain of <i>Salmonella enterica</i> serovar Heidelberg that produces the carbapenemase OXA 48. The strain was isolated from a stool sample taken from a newborn. Antimicrobial susceptibility testing was carried out following the recommendations of the Clinical and Laboratory Standard Institute. Whole genome sequencing was performed on MiSeq Illumina™. The strain was resistant to ertapenem (minimal inhibitory concentration [MIC] = 12 µg/mL), intermediate to imipenem (MIC = 1.5 µg/mL), resistant to nalidixic acid, and intermediate to fluoroquinolones but was susceptible to C3G, cotrimoxazole, chloramphenicol, and colistin (MIC = 0.064 µg/mL). The strain was identified as ST-15. The strain of <i>Salmonella</i> Heidelberg ST-15 was found to have antimicrobial resistance genes, specifically <i>blaOXA-48</i>, aac(6')-Iaa and <i>fosA7</i>, which mediate resistance to carbapenems, aminoglycosides and fosfomycin, respectively. Additionally, mutations were detected in the <i>gyrA</i>, <i>parC.</i> Three plasmid replicon type IncL, IncX1, and Col156 have been identified. The strain has the potential to cause an epidemic. The genomic analysis of the strain allowed us to understand the mechanisms of resistance. Preventing the spread of <i>Salmonella</i> carbapenemase-producing strains is crucial, particularly in hospital settings. Epidemiological measures are necessary to achieve this goal.