Advances in Medical Ethics
Open Access

Drug Resistance Mechanism with Antibiotic Resistance

Marafa Ibiam^{2* *}Correspondence: Marafa Ibiam, Department of Pharmacology, University of Benin, Benin City, Nigeria, Email:

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Description

Ceftazidime, Ceftriaxone, Ertapenem, and Aztreonam were all effective against all strains. 87.5% of the samples had piperacillin resistance. Five carbapenem-resistant Klebsiella pneumoniae were identified by multisite sequence typing as belonging to four distinct kinds. Kpn6099 and Kpn6617 shared the same sequence types. Escherichia coli J53 was shown to be more sensitive to these two antibiotics in the sensitivity comparison, with minimum inhibitory concentration values of 0.5 and 0.25 g/ml, respectively.

Additionally, E. coli J53 had somewhat higher carbapenem sensitivity than kpn6617. The outcomes demonstrated that the manufacture of acrB antibody was successful since the enzymelinked immunosorbent assay titer of the antibody was 1:40,000. The deletion of the IMP-1 metallo-lactamase binding outer memberane protein via plasmid-mediated implies the efficiency of a medicine as a chemotherapeutic is considerably diminished as drug resistance develops as one of the primary causes of the loss in antibiotic sensitivity. According to its root causes, drug resistance can be split into two categories: acquired drug resistance and natural drug resistance. Natural resistance may also exist in pathogens found in nature, such as a particular bacterial strain. Treatment of infectious disorders is severely hampered by the characteristics of bacterial resistance. A particular class of antibiotics or a variety of medicines with various chemical structures may make bacteria resistant. Single drug resistance and multidrug resistance are two categories for bacterial resistance.

For instance, Escherichia coli that produces broad-spectrum polylactase is more resistant to aminoglycosides, sulfonamides, and quinolones. The medication resistance mechanism of E. coli isolated from urinary tract infections is intricate. The majority of drug-resistant genes are found in plasmids, which make it simple for drug resistance to spread. This makes the treatment very challenging. Typically, these harmful genes are shared by various strains and are encoded in mobile protoplasts. The production of inactive enzymes, which results in the loss of drug activity or structural changes, changes in the permeability of bacterial cell membrane, which prevents drugs or disinfectants, detergents, and other chemicals from entering the bacteria, changes in the target structure or quantity of antibacterial drugs, which prevent them from combining with antibacterial drugs effectively, and drug pump out are the main mechanisms for bacterial resistance.

Antibiotics are a group of secondary metabolites created by microbes, higher animals, and plants during the course of life that have anti-pathogen or other properties that may obstruct the functioning of other living cells during development. The simultaneous occurrence of the aforementioned processes typically determines the antibiotic resistance of particular microorganisms. The active jet system can be split into five superfamilies based on their mechanisms of action: the ABC binding box superfamily, the primarily promoting subfamilies, and the drug-resistant nodal cell differentiation family.

The primary components of the bacterial efflux pump system are outer membrane proteins, extra proteins, and transporters. The transporter serves as a pump and is situated on the cytoplasmic membrane. The extra protein serves as a link between the transporter and the outer membrane protein. The outer membrane or cell wall contains proteins called outer membranes that resemble channel proteins. These proteins are crucial for the proper functioning of the bacterial efflux mechanism. Additionally, bacteria have an active pump system that excretes antibiotics in addition to secondary metabolites.

The bacteria in the family Enterobacteriaceae are widespread and have a wide range of hosts. The ability to live in soil or water, as well as having parasitic or symbiotic relationships with other living things, is shared by people, animals, and plants. Additionally, their genetic material (such as plasmids or transposons) can be obtained from the outside world. This results in the horizontal transmission of drug-resistant genes. It accelerates the proliferation of microorganisms with a drug resistance With the widespread use of -lactamases (ESBLs) and AmpC enzymes in recent years, carbapenem has become an important drug in the treatment of clinically important bacterial infections, and carbapenem-resistant Enterobacteriaceae has increased year by year. ESBLs in Enterobacteriaceae can now virtually eliminate all cephalosporins except for carbapenem.

Inferred high-yield enzymes, sustained high-yield enzymes, and sustained low-yield enzymes are the three categories into which ampC enzymes fall. High-yield enzyme production frequently involves -lactam antibiotics. There is a high level of AmpC enzyme, regardless of whether -lactam antibiotics are present. The cause is that one of the faulty ampD proteins and prevent the mutation of the ampD gene.

It results in the activation of ampr protein and the restricted production of the ampC enzyme because it does not form a protein complex with the additional regulatory protein ampr.

With the widespread use of antibiotics, particularly cephalosporins, Gram-negative bacteria are producing more ampC enzymes, particularly with the introduction of ampC enzyme and plasmid-mediated ampC enzyme, which promotes the spread of drug-resistant strains. Three mechanisms, including the production of carbapenemases, the loss or downregulation of high-yield ESBLs or AmpC enzyme binding stomatal proteins, which reduces sensitivity to carbapenems, and the alteration of Penicillin-Binding Protein (PBP), the target of carbapenems, are primarily responsible for Enterobacteriaceae's resistance to carbapenems.

Conclusion

The carbapenemases made by Klebsiella pneumoniae are referred to as Klebsiella pneumoniae carbapenemase (KPC) enzymes. K. pneumoniae is one of the Enterobacteriaceae bacteria. K. pneumoniae st258 is the most prevalent kind worldwide and carries the KPC enzyme, while K. pneumoniae st11 is the predominant strain in China. The primary multisite sequence typing (MLST) classification for K. pneumoniae in China that carries the KPC enzyme is ST131, which is consistent with the international MLST classification, and the mode of transmission is more complex and varied. Drug-resistant genes can be horizontally distributed in the same or different strains through coupling, transformation, transduction, and transposition and are found in the common region of plasmid, integron, transposon, or insertion sequence.

Kpn6617 was sensitive to ciprofloxacin, polymyxin, and tigecycline but resistant to all -lactamases and carbapenems. Compared to kpn6617, E. coli J53 was more sensitive to aztreonam and tigecycline. One of the main causes of the decline in antibiotic sensitivity is the deletion of the IMP-1 metallo— lactamase binding outer membrane protein through plasmidmediated means. One of the typical mechanisms of bacterial resistance is the loss of the protein that lines the pores in the outer membrane. Combination therapy with many antibiotics has a more pronounced effect than single antibiotic therapy and can slow the development of drug resistance.