**16. Genomics of** *P. aeruginosa*

The genome of a bacterium has two components first is the core genome and second the mobile genome. In a same species the core genome is common for all bacteria which include genes for the bacteria essential for development and the mobile genome can propagate within the whole genome [66, 67]. The mobile genome is varies between strains within a species. The mobile genome consists of a range of genetic elements such as insertion sequences, transposons, prophages, plasmids, and genomic islands. Horizontal gene transfer (HGT) processes such as conjugation, transformation, and transduction acquired the mobile genome. Genomic islands are the Clusters of genes in the mobile genome. Genomic islands encode gene products which enhance the fitness of a bacterium by survivability in new environment, increasing host range, and utilization of new nutrients. Genomic Island can be defined by various features [68].

**23**

explained.

**Figure 3.**

locate it (**Figure 4**).

strains to reference strain that is PAO1 [73].

Psuedomonas aeruginosa*-Associated Acute and Chronic Pulmonary Infections*

In *P. aeruginosa* classical clades, the most of homologous *exlB-exlA* loci are existing in *P. fluorescens, P. putida*, and *P. entomophila*, signifying this locus acquired by horizontal transfer in *Pseudomonas* spp. Strain toxicity data related to neutrophils and macrophages and ability of inflammatory cells to phagocytic *exlA*+ strains are not accessible for recognition the behavior of these strains *in vivo* in detail. Different mechanism for expression are used by bacteria for virulence effect to infect mammals and plants and that *ExlA* is not required for bacterial plants toxicity. It shows unequal level of virulence that could not be aid in one toxin, *Exl A* [70]. All strains have *lasB* gene which have *lasB* PAO1 sequence at same location and with the sequence identity up to 91–98%. Quorum sensing is regulatory for the expression of *LasB* and lacking of Quorum sensing genes affected the*lasB* expression. Quorum sensing genes are *lasR, lasI, vqsM, vqsR*, *rhlR, and rhlI* all existed at same locations in genomes of all the strains of *P. aeruginosa*. The sequences displayed identity of 98%, except for the strain PA39 (92%). Internally a frameshift mutation of *mvfR* gene, coding for an important regulator of the Quorum sensing, observed in PA7 genome [71]. Same mutation is also present in *mvfR* genes and absent in most of strains hence lacking *LasB* activity.It is reported that in the absence of *LasB* activity *lasB* sequences and Quorum sensing cannot

PAO1 **Figure 3** (2001), PA14 (2005), PAS7 (2007) and LES (2008) are four complete sequenced genome available and *P. aeruginosa* is recent strain sequenced*.* Falagas et al. reported PAO1 had 44.2% of predicted ORFs in the class 4 with unknown function [72]. The labeling of pathogenicity islands in the genomic island must have virulence genes with known function other was this would be difficult to

*P. aeruginosa* PAO1 complete genome was available in 2001 and for remaining three strain genome sequences available in 2005–2008. The recent research data are based primarily on subtractive hybridization and microarray, for comparing the

*DOI: http://dx.doi.org/10.5772/intechopen.93504*

*The novel hypervirulent ExlA-ExlB system [69].*

Psuedomonas aeruginosa*-Associated Acute and Chronic Pulmonary Infections DOI: http://dx.doi.org/10.5772/intechopen.93504*

#### **Figure 3.**

*Pathogenic Bacteria*

or eradicate this use of antibiotics.

resistance genes by horizontal gene transfer. Fluoroquinolones, gentamicin and imipenem are restricted antibiotics as effective against *P. aeruginosa* and susceptibility to these antibiotics can vary between different strains. Bacterial infections are cured traditionally with the use of antibiotics and immune system is unable to have

Fluoroquinolones (ciprofloxacin) prevented DNA repair and replication [58]. Aminoglycosides, Beta-lactams (imipenam but not penicillins), 3rd and 4th generation cephalosporins, and fluoroquinolones are anti-pseudomonal drugs [59]. Colistin, is a drug having lesser side-effect profile, and mainly used against multi drug resistant strains (MDR) *P. aeruginosa* strains these days. The pattern or the use of antibiotic treatment now bettered towards the treatment of specific diseases including CF. The transmission of *P. aeruginosa* reduced by separation of

The unavailability of the effective therapeutic option, the treatment of infections with pseudomonas is becoming difficult to deal a very few anti-pseudomonal drugs are being considered good for the treatment of emerging resistance strain, these include aminoglycosides beta-lactams, and fluoroquinolones [61–63].

The bactericidal MoA (mechanism of action) is significant for the survival by selection pressure for the fittest one. Antibiotic resistant bacteria are selected and propagated very well in the absence of the environmental resources competitions. Specific antibiotic resistance can be void of by the use of an alternative group of antibiotic. Bacteria have established active defense mechanisms which lead to MDR species such as methicillin-resistant *Staphylococcus aureus (S. aureus), Escherichia coli (E. coli), Acinetobacter baumannii (A. baumannii),* or *P. aeruginosa* are promoted as MDR strains and are difficult to eradicate this opportunistic pathogens [64].

The mechanisms of resistance in *P. aeruginosa* against antibiotics can be intrinsic, adaptive, or acquired. Innately *P. aeruginosa* is resistant to many antibiotics. Intrinsically it has impermeable cell wall, outer membrane protein (Opr) channels, and multi-drug efflux pumps which give the bacteria resistance to certain antibiotics. Extended treatment and continuous use of higher therapeutic doses resulting in

The genome of a bacterium has two components first is the core genome and second the mobile genome. In a same species the core genome is common for all bacteria which include genes for the bacteria essential for development and the mobile genome can propagate within the whole genome [66, 67]. The mobile genome is varies between strains within a species. The mobile genome consists of a range of genetic elements such as insertion sequences, transposons, prophages, plasmids, and genomic islands. Horizontal gene transfer (HGT) processes such as conjugation, transformation, and transduction acquired the mobile genome. Genomic islands are the Clusters of genes in the mobile genome. Genomic islands encode gene products which enhance the fitness of a bacterium by survivability in new environment, increasing host range, and utilization of new nutrients. Genomic

infected and susceptible one and use of strict hygiene procedures [60].

**15.** *P. aeruginosa* **and mechanisms of resistance**

complete resistance [65].

**16. Genomics of** *P. aeruginosa*

Island can be defined by various features [68].

**22**

*The novel hypervirulent ExlA-ExlB system [69].*

In *P. aeruginosa* classical clades, the most of homologous *exlB-exlA* loci are existing in *P. fluorescens, P. putida*, and *P. entomophila*, signifying this locus acquired by horizontal transfer in *Pseudomonas* spp. Strain toxicity data related to neutrophils and macrophages and ability of inflammatory cells to phagocytic *exlA*+ strains are not accessible for recognition the behavior of these strains *in vivo* in detail. Different mechanism for expression are used by bacteria for virulence effect to infect mammals and plants and that *ExlA* is not required for bacterial plants toxicity. It shows unequal level of virulence that could not be aid in one toxin, *Exl A* [70]. All strains have *lasB* gene which have *lasB* PAO1 sequence at same location and with the sequence identity up to 91–98%. Quorum sensing is regulatory for the expression of *LasB* and lacking of Quorum sensing genes affected the*lasB* expression. Quorum sensing genes are *lasR, lasI, vqsM, vqsR*, *rhlR, and rhlI* all existed at same locations in genomes of all the strains of *P. aeruginosa*. The sequences displayed identity of 98%, except for the strain PA39 (92%). Internally a frameshift mutation of *mvfR* gene, coding for an important regulator of the Quorum sensing, observed in PA7 genome [71]. Same mutation is also present in *mvfR* genes and absent in most of strains hence lacking *LasB* activity.It is reported that in the absence of *LasB* activity *lasB* sequences and Quorum sensing cannot explained.

PAO1 **Figure 3** (2001), PA14 (2005), PAS7 (2007) and LES (2008) are four complete sequenced genome available and *P. aeruginosa* is recent strain sequenced*.* Falagas et al. reported PAO1 had 44.2% of predicted ORFs in the class 4 with unknown function [72]. The labeling of pathogenicity islands in the genomic island must have virulence genes with known function other was this would be difficult to locate it (**Figure 4**).

*P. aeruginosa* PAO1 complete genome was available in 2001 and for remaining three strain genome sequences available in 2005–2008. The recent research data are based primarily on subtractive hybridization and microarray, for comparing the strains to reference strain that is PAO1 [73].

**Figure 4.** *Circular representation of the* P. aeruginosa *genome.*

The differences in the genome targeted for further screening by using mutagenesis and virulence assays in models of *in vivo* infections. The current in vivo models commonly used for *P. aeruginosa* infection are:


Murine used for infection models that imitate the human mood of infection are not common [74].

The results of current studies of pathogenicity island mutant have explained the effectiveness in finding their influence towards virulence. PAI I536–PAI V536 are five pathogenic island of *E. coli* and analyzed for their involvement in infection [75].
