Introductory Chapter: An Overview of the Genus Staphylococcus and Streptococcus

1. Introduction

We live in a world that inhibits many life forms including microorganisms. Bacteria, an important member of these microorganisms, sometimes become a very tough enemy of the human being with the stimulation of the conditions and environment. Bacterial infections that are sourced from pathogenic bacteria are one of the leading causes of the human death worldwide. For instance, lower respiratory infections killed 3 million people globally in 2016 [1].

Among the most pathogenic bacteria for human, genera of Staphylococcusand Streptococcuscome forward with their pathogenicity. Staphylococci and Streptococci are grouped as Gram-positive cocci. Staphylococci form clumps, whereas Streptococci grow in chains. They can be discriminated by catalase test because Staphylococci have the capability to produce catalase [2].

Staphylococci and Streptococci are together responsible of the pathogenesis of a variety of diseases such as wound infections, mastitis, toxic shock syndrome, scarlet fever, cystic fibrosis, nosocomial and community-acquired infections, periodontitis, and indwelling device-associated infections [3, 4].

2. Virulence factors of Staphylococcusspp. and Streptococcusspp.

3. Antibiotic resistance of Staphylococcusand Streptococcus

Antibiotic resistance becomes a worldwide serious health threat due to the inappropriate prescribing, overuse, and the extensive agricultural use of antibiotics [15]. S. aureus, a well-known pathogenic bacterium, exhibits resistance to the some of the important and widely used antibiotics such as β-lactam antibiotics, tetracycline, and methicillin through its genome and extrachromosomal elements [16].

The genetic elements of S. aureusplay a critical role in antibiotic resistance. S. aureuscan hydrolase the β-lactam ring of penicillin by using the penicillinase which is expressed from the blaZ gene localized in S. aureusplasmid. This emerging feature can be observed more than 80 percent of the S. aureusstrains [17].

Another example of plasmid-originated antibiotic resistance can be observed for tetracycline in S. aureus. Tetgene in conjugative plasmid of S. aureusencodes ribosomal protection protein which prevents the binding of tetracycline to ribosome and thus the inactivation of it [18].

The occurrence of S. aureusisolates that are resistant to β-lactam antibiotics provide the discovery of penicillinase-stable penicillins. One of these molecules, methicillin, is the medication of choice to treat β-lactam-resistant S. aureusinfections. But some of the S. aureusisolates are also resistant to methicillin and different types of antibiotics such as macrolides and cephalosporins. Methicillin-resistant S. aureus(MRSA) isolates demonstrate their characteristics of multi-antibiotic resistance through their chromosomes and extrachromosomal elements. Penicillin binding protein 2a which is encoded by chromosomal mecA gene is the main reason of methicillin resistance of S. aureus[19, 20].

Enterococci are the members of the microflora of the intestinal system. But they are also opportunistic and nosocomial pathogens. Especially, they are accused of sepsis, endocarditis, and urinary tract infections in immunosuppressed patients [21].

These pathogens demonstrate a different feature compared to other Gram-positive cocci: adaptation to different antimicrobials such as vancomycin quickly and exhibition of multidrug resistance [21].

Vancomycin is a member of glycopeptide antibiotics. It targets the precursors of peptidoglycan, while this system is crucial for the enterococcal cell wall biosynthesis. By binding to these precursors and preventing the transglycosylation and transpeptidation, vancomycin prevents the building and growing of bacterial cell wall [22]. But enterococci overcome this destructive problem with different vanoperon systems, for instance, vanA, vanB, vanC, and vanD. The common feature of these systems is to alter the peptidoglycan biosynthesis pathway with different molecules so that vancomycin cannot identify the molecule thus cannot interfere [22].