Indian journal of medical microbiology · 2019
An emerging threat of ceftriaxone-resistant non-typhoidal salmonella in South India: Incidence and molecular profile.
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Pragasam Agila Kumari, Anandan Shalini, John James, Neeravi Ayyanraj, Narasimman Vignesh, Muthuirulandi Sethuvel Dhiviya Prabaa, Elangovan Divyaa, Veeraraghavan Balaji
Аннотация
BACKGROUND: Non-typhoidal Salmonella (NTS) infection is a serious public health problem globally. Although NTS infections are self-limited, antimicrobial therapy is recommended for severe infections and immunocompromised patients. Antimicrobial resistance (AMR) in these pathogens further limits its therapeutic options. Here, we report an incidence of ceftriaxone resistance in NTS over the past 9 years in a southern Indian region.
MATERIALS AND METHODS: Molecular mechanisms of resistance in ceftriaxone-resistant NTS have been tested by both phenotypic and molecular methods. Minimum inhibitory concentration was determined by the E-test and broth microdilution method. AMR gene markers of β-lactamases such as AmpCs (blaMOX, blaCMY, blaDHA, blaFOX, blaACC and blaACT) and extended-spectrum β-lactamases (ESBLs) (blaSHV, blaTEM, blaVEB, blaPER, blaCTXM-1like,blaCTXM-2like, blaCTXM-8like, blaCTXM-9like and blaCTXM-25like) were screened. The presence of IncH12 and IncI1 plasmid was also analysed.
RESULTS: The study reports a 5% prevalence of ceftriaxone resistance in NTS. The most common serogroup was Salmonella Group B followed by Salmonella Group E and Salmonella group C1/C2. The occurrence of blaCTX-M-1, blaTEM, blaCMY and blaSHV genes was observed in 54%, 54%, 48% and 3% of the isolates, respectively. Interestingly, few isolates carried dual resistance genes (ESBLs and AmpCs). IncH12 and IncI1 plasmid was identified in isolates carrying ESBL and AmpC genes, respectively.
CONCLUSION: This study shows that ceftriaxone resistance is mainly mediated by β-lactamases such as ESBL and AmpC. As the incidence of ceftriaxone resistance is rising gradually over the years, it is imperative to monitor the AMR in this species.
MATERIALS AND METHODS: Molecular mechanisms of resistance in ceftriaxone-resistant NTS have been tested by both phenotypic and molecular methods. Minimum inhibitory concentration was determined by the E-test and broth microdilution method. AMR gene markers of β-lactamases such as AmpCs (blaMOX, blaCMY, blaDHA, blaFOX, blaACC and blaACT) and extended-spectrum β-lactamases (ESBLs) (blaSHV, blaTEM, blaVEB, blaPER, blaCTXM-1like,blaCTXM-2like, blaCTXM-8like, blaCTXM-9like and blaCTXM-25like) were screened. The presence of IncH12 and IncI1 plasmid was also analysed.
RESULTS: The study reports a 5% prevalence of ceftriaxone resistance in NTS. The most common serogroup was Salmonella Group B followed by Salmonella Group E and Salmonella group C1/C2. The occurrence of blaCTX-M-1, blaTEM, blaCMY and blaSHV genes was observed in 54%, 54%, 48% and 3% of the isolates, respectively. Interestingly, few isolates carried dual resistance genes (ESBLs and AmpCs). IncH12 and IncI1 plasmid was identified in isolates carrying ESBL and AmpC genes, respectively.
CONCLUSION: This study shows that ceftriaxone resistance is mainly mediated by β-lactamases such as ESBL and AmpC. As the incidence of ceftriaxone resistance is rising gradually over the years, it is imperative to monitor the AMR in this species.