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Review
. 2021 Jan 20:7:616490.
doi: 10.3389/fmed.2020.616490. eCollection 2020.

Genetic Diversity, Biochemical Properties, and Detection Methods of Minor Carbapenemases in Enterobacterales

Affiliations
Review

Genetic Diversity, Biochemical Properties, and Detection Methods of Minor Carbapenemases in Enterobacterales

Rémy A Bonnin et al. Front Med (Lausanne). .

Abstract

Gram-negative bacteria, especially Enterobacterales, have emerged as major players in antimicrobial resistance worldwide. Resistance may affect all major classes of anti-gram-negative agents, becoming multidrug resistant or even pan-drug resistant. Currently, β-lactamase-mediated resistance does not spare even the most powerful β-lactams (carbapenems), whose activity is challenged by carbapenemases. The dissemination of carbapenemases-encoding genes among Enterobacterales is a matter of concern, given the importance of carbapenems to treat nosocomial infections. Based on their amino acid sequences, carbapenemases are grouped into three major classes. Classes A and D use an active-site serine to catalyze hydrolysis, while class B (MBLs) require one or two zinc ions for their activity. The most important and clinically relevant carbapenemases are KPC, IMP/VIM/NDM, and OXA-48. However, several carbapenemases belonging to the different classes are less frequently detected. They correspond to class A (SME-, Nmc-A/IMI-, SFC-, GES-, BIC-like…), to class B (GIM, TMB, LMB…), class C (CMY-10 and ACT-28), and to class D (OXA-372). This review will address the genetic diversity, biochemical properties, and detection methods of minor acquired carbapenemases in Enterobacterales.

Keywords: CHDL; antibiotic resistance; carbapenem; detection; insertion sequence; transposon.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Antibiograms of representative class A carbapenemases. (A) IMI-1-producing E. cloacae complex clinical isolate. (B) GES-5 producing K. pneumoniae clinical isolate. (C) SME-3-producing S. marcescens. (D) FRI-1-producing E. coli transformant. AMX, Amoxicillin; AMC, Amoxicillin/clavulanate; ATM, aztreonam; CAZ, ceftazidime; CTX, Cefotaxime; CZA, Ceftazidime/avibactam; ETP, Ertapenem; FEP, Cefepime; FOX, Cefoxitine; IPM, Imipenem; MEM, Meropenem; PIP, Piperacillin; TCC, Ticarcillin/Clavulanate; TEM, Temocillin; TIC, Ticarcillin; TZP, Piperacillin/Tazobactam.
Figure 2
Figure 2
Antibiograms of representative class B carbapenemases. (A) GIM-1-producing E. cloacae complex clinical isolate. (B) TMB-1 producing E. coli transconjugant. (C) SFH-1-producing S. marcescens clinical isolate. (D) LMB-1-producing C. freundii clinical isolates. AMX, Amoxicillin; AMC, Amoxicillin/clavulanate; ATM, aztreonam; CAZ, ceftazidime; CTX, Cefotaxime; CZA, Ceftazidime/avibactam; ETP, Ertapenem; FEP, Cefepime; FOX, Cefoxitine; IPM, Imipenem; MEM, Meropenem; PIP, Piperacillin; TCC, Ticarcillin/Clavulanate; TEM, Temocillin; TIC, Ticarcillin; TZP, Piperacillin/Tazobactam.
Figure 3
Figure 3
Antibiograms of representative class C & D carbapenemases. (A) ACT-28-producing E. kobei clinical isolate. (B) OXA-23 producing P. mirabilis clinical isolate. (C) OXA-372-producing C. freundii clinical isolates. AMX, Amoxicillin; AMC, Amoxicillin/clavulanate; ATM, aztreonam; CAZ, ceftazidime; CTX, Cefotaxime; CZA, Ceftazidime/avibactam; ETP, Ertapenem; FEP, Cefepime; FOX, Cefoxitine; IPM, Imipenem; MEM, Meropenem; PIP, Piperacillin; TCC, Ticarcillin/Clavulanate; TEM, Temocillin; TIC, Ticarcillin; TZP, Piperacillin/Tazobactam.

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