Preface

*Pseudomonas aeruginosa* is one bacterium among many that displays fascinating mechanisms of adaptation and evolution. With the mosaic nature of its genome, *P. aeruginosa* is able to thrive on both biotic and abiotic niches, including drinking water, invoking adaptive phenotypes that are well suited for specific microenvironments. The presence of acquired genetic elements, large and small, distributed throughout the genome requires this organism to be able to survive using a wide range of nutrients. The interdisciplinary approach to understanding various strains and isolates of *P. aeruginosa* has unraveled interesting strategies that this organism employs to combat the host defense mechanisms and thrive in unusual niches. The association of *P. aeruginosa* with cystic fibrosis (CF) is by virtue of the bacteria's colonization and formation of biofilms. The CF condition is characterized by abnormal transport of chloride and sodium across the epithelium that leads to thickening of secretions, especially in the lungs, pancreas, liver, and intestine. The complex nature of this disease, involving dysfunction of multiple organs and subsequent secondary infections by microbes, especially *P. aeruginosa*, is the basis for mortality in the CF population. This book is a compilation of chapters that highlight different facets of the capabilities and lifestyle of *P. aeruginosa*.

I would like to thank IntechOpen for appointing me editor of this book and for providing me the opportunity to contribute to the scientific community. I am also grateful to the authors of the chapters for their valuable contributions. Finally, I wish to thank the Helmholtz Centre for Infection Research, Braunschweig, Germany, where I began my research career.

> **Dr. Dinesh Sriramulu** Shres Consultancy, India

**1**

**2. Master in dominating**

**Chapter 1**

Introductory Chapter:

leading to complications in treating cystic fibrosis patients [3].

Cystic fibrosis (CF) is an autosomal recessive genetic condition among Caucasians, with an incidence rate of 1 in 2500 live births. The morbidity and

Omnipresence

*Dinesh Sriramulu*

**1. Master in evolving**

*Pseudomonas aeruginosa* - Toward

Antibiotics are extensively used worldwide for treating predominantly gram-negative bacterial infections and also for treating certain gram-positive infections. While the precise mechanism of their bactericidal action is yet to be unraveled, aminoglycosides, for example, act by binding to the RNA component of ribosomes, leading to both mistranslation and ultimate inhibition of protein synthesis. The widespread use of other major classes of antibiotics has resulted in the emergence of resistant bacteria by expediting the course of its evolution [1, 2]. The emergence of resistance to antibiotics is of special concern in the treatment of infections, particularly of systemic nature, by gram-negative organisms narrowing down the options for antibiotic alternatives. The resistance mechanisms displayed by the bacteria can be classified into the following: (a) reduced uptake, (b) increased efflux, (c) enzymatic modification of drug, and (d) drug target modification. Whereas resistance to streptomycin, the first widely used aminoglycoside, is predominantly through mutations in drug targets (mostly in the ribosomal protein rpsL and also in rRNA), resistance to other aminoglycosides appears to utilize a variety of mechanisms. The question arises, whether antibiotic action facilitates the emergence of resistant mutants. For certain other classes of antibiotics that induce the bacterial SOS response either by direct DNA damage (e.g., ciprofloxacin) or through indirect means (e.g., ampicillin), it has been shown that the action of the antibiotic itself plays a significant role in the emergence of mutations that confer resistance. One such mechanism, mistranslation due to defects in the translation apparatus, can promote hypermutagenesis in a phenomenon called translational stressinduced mutagenesis (TSM) raising the possibility that aminoglycoside exposure, by promoting mistranslation, could also elevate mutagenesis. According to the current understanding, TSM is mediated by a low-level mistranslational corruption of the replicative DNA polymerase leading to episodic hypermutagenesis. Exposure of wildtype bacterial cells to sublethal concentrations of an antibiotic increases mutagenic translesion DNA synthesis in vivo, and exposure of certain mutants also increases spontaneous mutagenesis. Exposure of wild-type *Pseudomonas aeruginosa* PAO1 cells to sublethal concentrations of tobramycin and amikacin, two aminoglycoside antibiotics commonly used to treat *P. aeruginosa* infections, can elevate spontaneous mutagenesis
