Abstract
The emergence of carbapenem-resistant bacterial pathogens is a significant and mounting health concern across the globe. At present, carbapenem resistance (CR) is considered as one of the most concerning resistance mechanisms and mainly found in gram-negative bacteria of the Enterobacteriaceae family. Although carbapenem resistance has been recognized in Enterobacteriaceae from last 20 years or so, recently it emerged as a global health issue as CR clonal dissemination of various Enterobacteriaceae members especially E. coli, and Klebsiella pneumoniae are reported from across the globe at an alarming rate. Phenotypically, carbapenems resistance is in due to the two key mechanisms, like structural mutation coupled with β-lactamase production and the ability of the pathogen to produce carbapenemases which ultimately hydrolyze the carbapenem. Additionally, penicillin-binding protein modification and efflux pumps are also responsible for the development of carbapenem resistance. Carbapenemases are classified into different classes which include Ambler classes A, B, and D. Several mobile genetic elements (MGEs) have their potential role in carbapenem resistance like Tn4401, Class I integrons, IncFIIK2, IncF1A, and IncI2. Taking together, resistance against carbapenems is continuously evolving and posing a significant health threat to the community. Variable mechanisms that are associated with carbapenem resistance, different MGEs, and supplementary mechanisms of antibiotic resistance in association with virulence factors are expanding day by day. Timely demonstration of this global health concern by using molecular tools, epidemiological investigations, and screening may permit the suitable measures to control this public health menace.
Highlights
In a historical perspective, antibiotic resistance is a mounting and compelling concern
The patients infected with bacterial strains that are resistant to antibiotics must stay in the hospital minimum for 13 days, which adds to 8 million days annually
Carbapenems work by penetrating the cell wall of bacteria, binding with penicillin-binding proteins (PBPs), and result in inactivation of intracellular autolytic inhibitor enzymes, killing the bacterial cell
Summary
The global burden of antibiotic resistance is mounting continuously; preferably it piles up the pressure on veterinary medicine and on human. It has been estimated that yearly about two million people acquire vulnerable infections just because of these antibiotic-resistant pathogens, and as a result of this, about 23,000 people die according to Centers for Disease Control and Prevention (CDC) [2]. Antibiotic resistance is a mounting and compelling concern. It has been reported that annually, in the USA, about 99,000 deaths are caused by antibiotic-resistant pathogen-related hospital-acquired infections [3]. The patients infected with bacterial strains that are resistant to antibiotics must stay in the hospital minimum for 13 days, which adds to 8 million days annually. An annual report of the cost of economy loss with regard to a productivity loss of around $35 billion has been demonstrated within healthcare settings [3]
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