**1. Introduction**

Antimicrobials are the substances or agents that kill, inhibit the growth and/or stop the spread of microorganisms. These are named based on the type of microorganism against which they act. Accordingly they are broadly of four different types [1]:


These are suffixed as ~cidal or ~ static antimicrobials depend on whether they kill or inhibit the growth of microorganisms respectively. For instance a bactericidal antibiotic is an antimicrobial that kills the microorganism, e.g., Vancomycin, Rifampin, Pencillins & Cephalosporins, Aminoglycosides (at high doses), Quinolones, Isoniazid, Metronidazole, Polymyxins and Bacitracin;

However, a bacteriostatic antibiotic is an antimicrobial that stops microorganisms from growing and stalls the process of reproduction, without killing them necessarily e.g. Tetracyclines, Clindamycin, Chloramphenicol, Macrolides, Sulfonamides and Timethoprim. The major difference to differentiate between ~cidal or ~ static antimicrobials is that in the former case, upon removal at the decline phase of an antimicrobial having ~cidal effect, the growth curve of target microorganism continues to decline and never resumes while in later case, since the growth of microorganism is stalled and plateaus at stationary phase, removal of such antimicrobials resumes the growth of target microorganisms from stationary to log phase [2]. Though we discussed of antimicrobials above as source agents that kill or inhibit the spread of microorganisms, yet antimicrobial is a broad term that also includes agents applied to non living surfaces e.g. disinfectants like bleach, non pharmaceuticals like essential oils [3, 4], antimicrobial pesticides and pesticide products [5], and ozone [6] among other antimicrobial properties of metal and metal alloys [7, 8]. However here in this chapter we will limit our discussion on antimicrobials in connection with Actinomycetota (formerly called Actinobacteria) - a class of gram positive microorganisms high in Guanine Cytosine (GC) base pair composition in their DNA and evolutionary viewed as rich source of antimicrobials and FDA approved antibiotics among all the microbial taxa [9, 10]. The name change of phylum Actinobacteria to Actinomycetota is very recent and an innumerable number of research articles communicated still retain the word as Actinobacteria and researchers also use the term Actinobacteria very frequently, so here for the sake of brevity, we will use Actinobacteria and Actinomycetota interchangeably.

Although both ~cidal and ~ static antimicrobials display vital possibility to stop the spread of pathogen causing diseases but the antimicrobial crisis to unlock the potential to counter the menace of antimicrobial drug resistance grows continuously. Resistant pathogenic microorganisms employ one or a combination of following anti-bacterial resistance mechanisms to evade killing by approved antimicrobials;


With every new antibiotic discovery, microorganisms opt for one or the other resistance mechanisms to evade killing by an antimicrobial and sometimes execute it successfully-thus add to the already burdened drug resistance pathogenic load [11]. Thoroughly screened and verified efforts need to be searched to subdue antimicrobial drug resistance patterns.

From the **Table 1**, it is clear that different classes of antimicrobials-having different chemical moieties are being produced by varying Actinobacterial strains, majority of which belong to the genus Streptomyces. These antimicrobials range from majorly characterised chemical classes like tetracyclines, β – Lactams, macrolides, aminoglycosides, lactones, alkaloids, glycopeptides to less known drug moieties like peptides-including simple peptides and lipopeptides, esters and nucleosides. Majority of the broadly classified antimicrobials are a product of nonribosomally synthesised bioactive chemicals by mega-enzyme complexes called NRPS Non-ribosomal peptide synthetases (NRPS) and polyketide synthetases (PKS) and hybrid NRPS-PKS complexes.
