From Susceptible to Resistant: The Emergence of Carbapenemase-Producing Escherichia coli

Carbapenemase-producing Escherichia coli (E. coli) has emerged as a critical contributor to antimicrobial resistance (AMR), significantly compromising the efficacy of last-resort carbapenem antibiotics. Carbapenemase-producing E. coli has significantly reduced the effectiveness of carbapenems, which were previously considered last-resort antibiotics for treating severe infections caused by extended-spectrum β-lactamase (ESBL)-producing organisms. Numerous β-lactam antibiotics, including carbapenems, are hydrolyzed by these enzymes, which results in fewer therapy choices, greater rates of treatment failure, and higher rates of morbidity and death. Travel, medical tourism, globalization, and poor infection control practices contribute to the development of resistant strains. AMR spreads more quickly in nations such as India due to factors such as over-the-counter antibiotic usage, inadequate antimicrobial stewardship, and a shortage of diagnostic infrastructure. The high frequency of E. coli in clinical infections and its notable resistance to commonly utilized antibiotics are highlighted by surveillance data from national programs like the ICMR-AMRSN. Both intrinsic and acquired mechanisms contribute to resistance in E. coli. ESBLs, AmpC, and carbapenemases are clinically relevant families of β-lactamases. Carbapenemases fall into three categories: Class A (KPC, for example), Class B (metallo-β-lactamases, such as New Delhi metallo-β-lactamase (NDM), Verona integron-borne metallo-β-lactamase (VIM), and Imipenemase (IMP), and Class D (OXA-type enzymes). Many of these enzymes are plasmid-mediated and capable of rapid horizontal gene transfer.