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Multi-Drug Resistance (MDR) is a global concern that is having a very bad impact on health care. Microbes are getting resistant to antibiotic therapies due to the constant exposure of antimicrobial drugs. In the past decade, microbial infections have raised enormously and this has led to an increased amount of resistance [1]. Multi drug resistance is the phenomenon in which pathogenic organisms are resistant to multiple chemotherapeutic agents [2]. The emergence of MDR rises the mortality and morbidity rates for which they are known as ‘Superbugs’. It is said that MDR is a very natural process among microorganisms but the increasing amount of this process is due to several reasons like the use of undefined antimicrobial agents, unhygienic sanitary conditions, poor health care facilities. The omnipresent threat of antibiotic-resistant pathogens entails having very few antimicrobial agents for other infections [2, 3].
Many different definitions for multidrug-resistant (MDR), extensively drug-resistant (XDR) and pandrug-resistant (PDR) bacteria are being used to characterize the different patterns of resistance. Was defined as acquired non-susceptibility to at least one agent in three or more antimicrobial categories, XDR was defined as non-susceptibility to at least one agent in all but two or fewer antimicrobial categories (i.e. bacterial isolates remain susceptible to only one or two categories) and PDR was defined as non-susceptibility to all agents in all antimicrobial categories. MDR is a frequently encountered phenomenon in
Classification of MDR.
Before studying the resistance of
Multi drug resistance mechanism.
Drug Efflux Pumps are one of the major ways for the MDR mechanism. ABC transporters (ATP Binding Cassette) are membrane proteins which are commonly defined as drug efflux pumps that specifically helps in the transport of the drugs in the cell. The P-glycoprotein or multi-resistant protein (MRP) damages the permeability and influences the ATP-dependent efflux of the drugs which is responsible for decreasing the intracellular concentrations [7, 8, 9].
The genetic determinants of resistance to many antimicrobial agents are believed to have evolved prior to the era of antibiotic chemotherapy. Processes such as phosphorylation, glycosylation, acetylation whose inactivation or chemical transformation is the major cause of the MDR. The schematic diagram shows the possible ways of causing antimicrobial resistance (Figure 3) [1, 4, 10, 11, 12].
Schematic diagram of antimicrobial resistance.
Methicillin-Resistant
A schematic diagram of SCCmec element. The SCC
Plasmids are capable of carrying the resistant genes and also several toxic genes. In a recent study, it has been observed that when an
There is also support for the notion that some resistance determinants in staphylococci are derived from genes present in antibiotic-producing organisms. The
Due to the high resistance against methicillin and after the failure of the drug, Vancomycin was playing a major role in treating most MRSA infections. Isolates of
In case of Penicillin, R plasmids encode the enzyme called as
Transmission of MRSA infections can take place from person to person who is contaminated with such infections. Proper hygienic condition is required to maintain infection from getting spread. Although the mode of transmission of infections mainly relies upon direct contact but contact with contaminated fomites can also transmit the infection. Several other factors of the host such as immunocompromised patients, defects in neutrophils, or destruction of the skin barriers can also give rise to the infections.
Drugs that are discussed to be used for MRSA infections are Daptomycin and Linezolid. Daptomycin is a synthetic drug that is the class of antibiotics that destroy the cell membrane ability by a calcium-dependent binding phenomenon which leads to bactericidal activity in a concentration-dependent way. So, one of the widely used antibiotics and which shows good efficacy even more than methicillin and vancomycin. Therefore, for any MRSA bacteremia, Daptomycin is considered to be very effective [38, 39, 40]. There were many topical drugs used against the MRSA strains. These anti MRSA drugs were quite effective. Mupirocin, is one of the anti MRSA topical drug which is applied on the skin for curing skin infections caused by
Similarly, Linezolid which belongs to the oxazolidinones class predominantly inhibits the protein synthesis in the 50S ribosome of the cell. Linezolid shows a good amount of efficacy against several toxin-producing strains such as toxic shock syndrome toxin, Panton-Valentine leukocidin, α-hemolysin [38]. But the resistance against Linezolid was also observed. So, the combinatorial theory was taken into account. Combinatorial theory helps to mix multiple compounds to balance the inadequate conditions of other compounds and increase efficacy of drugs. The combinatorial theory started with Vancomycin and it shows synergistic interaction with β-lactams widely. Studies cleared that the capacity of clearing the MRSA infection-causing strains was not high in amount when the patients were only subjected to Vancomycin but in combination with β-lactams the clearance efficiency was much higher in amount. Combination with Vancomycin shows a specific effect named as Sea-Saw Effect where if the susceptibility of the vancomycin is decreased which results in decrease of transcription of the
Few drugs are in development such as Dalbavancin, Oritavancin, Tigecycline. Tigecycline inhibits protein synthesis and it shows broad-spectrum antibiotic activity. These are the possible treatments upon which the work is going on to reduce the resistance against the invasive MRSA. The prospect of the medication for
According to the future perspective, there is an immense need for an alternative strategy for treating the resistance against
The major limitation or failure that rises is intrinsic mechanisms of bacterial resistance and the target-specific antibiotics or drugs have disappointed to come up with any useful product. Another unique novel approach has come forth which combines the genomic information on the drug target and undergo chemical modifications along with efficacy testing [50].
We acknowledge the support of SRM University and C4D of SRM University for the help.
There is no Conflict of Interest in working with this chapter.
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