Bacteria can be classified, according to the ability of their cell walls to absorb Gram stain, into Gram positive bacteria possessing thick cell wall and gram negative bacteria possessing thin cell wall and an outer membrane [2]. The commercial production of antibiotics started with the use of penicillin in the late of 1940s and it was great success for many years [3]. Antibiotics can be classified according to their spectrum on bacteria into broad spectrum, works against gram positive and gram negative and narrow spectrum. Also they are classified according to their mechanism of action or the targets. For examples, the main targets for antibiotics are cell wall, cell membrane, protein synthesis and nucleic acid synthesis. Beta lactams and glycoproteins can interfere with the synthesis of cell walls. Major classes of antibiotics that target protein synthesis include the macrolides and aminoglycosides. Antibiotic classes such as quinolones inhibit synthesis of nucleic acid synthesis of bacteria. Other antibiotics, such as the lipopeptides and polymyxins can disrupt the cell membrane of bacteria [4]. Inappropriate antibiotic use was one of the main causes of the evolution of multidrug- resistant pathogens especially in developed and developing countries [5]. The problem is graver in developing nations because of ease availability, inappropriate high doses of antibiotics in and cost constraints to replace older antibiotics with new expensive antibiotics increase the probability of antimicrobialresistant strains [6]. In 2017, the WHO Global Antimicrobial Surveillance System has reported that antibiotic resistance is a worldwide challenge [7].
Development of antimicrobial resistance occurs via various mechanisms. Briefly, the primary mechanisms include inactivation of the antibiotic by the bacterial pathogen, changing of the target site of the antibiotic, alteration of a metabolic pathway to abolish the effect of the antibiotic, and reducing accumulation of the drug by minimizing or inhibiting its entry or maximizing clearance from the cell (efflux effect) as shown in figure 1. It is worth to mention that resistance mechanisms exhibited by bacteria may be intrinsic mechanism such as lacking of oxidative metabolism which prevents drug uptake or the presence of an outer lipid membrane in the Gram-negative bacteria cell wall which prevents entry of glycopeptides [8]. Also, the resistance mechanism may be acquired whereby the resistant bacteria (donator) donate DNA, typically integrated into a plasmid and codes for that resistance mechanism, to susceptible bacteria (recipient). This DNA is retained in the recipient cell, within a plasmid or is transposed into the genome, and expression results in organisms that now harbor resistance to the given antibiotic. Examples of required resistance include the acquisition of code for the production of lactamases that degrade beta-lactam antibiotics [9], or transposable elements such as the transposon Tn1546 which confers VanA type resistance to vancomycin in the Enterococci and in S.aureus.