**1. Introduction**

*P. aeruginosa* contributes its pathogenicity onwards respiratory infections in the hospitalized patients. Dasenbrook et al. has reported two types of airways infection acute and chronic spread by hospital community *P. aeruginosa* is a bacterium that lives in versatile environments [1]. It is Gram negative bacterium, metabolically able to regulate its systems and highly resistance to antibiotic causing it to spread in diverse habitats mainly in hospitals. *P. aeruginosa* is recognized as a human adaptable pathogen causing acute infections (bacteremia, pneumonia and urinary tract infections) in individuals with HIV infections, surgical wounds, cancer, carrying catheters or burns, or an organ transplantations. *P. aeruginosa* is persistence in

#### **Figure 1.**

P. aeruginosa *features relevant to pathogenicity and adaptation [2].*

chronic obstructive pulmonary diseases and chronic infections in individuals with cystic fibrosis (CF) [3, 4]. *P. aeruginosa* strains showed variation in their population as reported by characterization of the phenotypic clones. Four main clade of *P. aeruginosa* population are identified by the phylogenic analysis of single nucleotide polymorphisms (SNPs) which showed most different clade colonized by clonal outliers linked to the PA7 strain (**Figure 1**) [5].

### **2. Virulence factors**

Acute infection usually observed in hospitalized patients having ventilator breathing. It is one of the main causative agents of hospital-acquired pneumonia and causing morbidity and mortality in the infected patients. Chastre and Fagon has reported 70–80% rate of mortality due to infection of *P. aeruginosa* in ventilatorassociated pneumonia (Research has focused on type III secretion system (TTSS) secreting four exotoxins (ExoS, ExoT, ExoU and ExoY) [6]. ExoU is an effective virulence causing effector in TTSS. It is associated with morbidity and mortality in ventilator-associated pneumonia. Hogardt et al. reported that 40% of the isolates from such cases harbor the *exoU* gene [7].

#### **3. Pathogenicity**

The pathogenicity of *P. aeruginosa* makes its able to adhere and colonize in the presence of vast virulence factors and causing disease. Virulence factors used or synthesized by *P. aeruginosa* are enlisted in **Table 1**.


**17**

• Swimming: It is aided by the flagellum

• Twitching: it depends upon type IV pili

[15–20] (**Figure 2**).

• Swarming: it requires both flagellum and type IV pili

**4. Biofilm**

**Table 1.**

Psuedomonas aeruginosa*-Associated Acute and Chronic Pulmonary Infections*

Protease Degrades complement factors, plasmin, IgG, and fibrinogen Pyocyanin Inhibits lymphocyte proliferation; apoptosis of neutrophils

Biofilm Confers protection against biocides and immune system effectors as

Exotoxin A Unknown role—possibly causes apoptosis of cells

Type III secretion Exoenzyme (Exo) S, T and Y, and exotoxin U

Alkaline protease Degrades immune system components Elastase Degrade elastin; disrupt membranes; impair

Lipase A and C Involvement in degradation Phospholipase C Lung surfactant disruption

Hydrogen cyanide Unclear role, may be toxic agent.

Rhamnolipids Dissolve phospholipids

*Virulence factors produced and used by* P. aeruginosa *[8–10].*

The pathogen colonized as planktonic form, and the cells convert to the sessile state to form biofilms. The hydrated structured matrices made up of exopolysaccharides and proteins, having 'slimy' characteristic can form on many surfaces from catheters to prokaryotic cells and eukaryotic. The main cause of persistent chronic infections is biofilm formation is essentially impenetrable inhabitants are protective for the bacterial strains from biocides [11]. The only one treatment to deal this situation is physical removal of the biofilm through surgery. Biofilms have heterogeneous populations of intra-species (phenotype and genotype, growth) and inter-species diversification. *P. aeruginosa* may be as dominant pathogen or with other pathogens such as Gram-negative *Burkholderia cenocepacia* and Gram-positive *S. aureus* [12]. The heterogeneous bacterial population of *P. aeruginosa* show distinct microenvironments for biofilms [13]. Metabolically active cells are at periphery and consume most of the oxygen, causing oxygen gradients in the biofilm [14]. The deeper layers of the biofilm have less metabolically active bacteria and are hypoxic. The actively growing peripheral bacterial cells of biofilms mostly susceptible to antibiotics or to the provided the drug which can penetrate slimy layer of the biofilm. Presence of a single polar flagellum made *P. aeruginosa* as motile. *P. aeruginosa is* exhibiting three distinctive types of motility and all of these types are required for development of biofilm which are;

Monocyte chemotaxis and degrade complement proteins

Impenetrable to antibodies (Ab), antibiotics, and biocides

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

**Virulence factor Action**

**2.Invasion**

**3.Pathogenesis**

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


**Table 1.**

*Pathogenic Bacteria*

chronic obstructive pulmonary diseases and chronic infections in individuals with cystic fibrosis (CF) [3, 4]. *P. aeruginosa* strains showed variation in their population as reported by characterization of the phenotypic clones. Four main clade of *P. aeruginosa* population are identified by the phylogenic analysis of single nucleotide polymorphisms (SNPs) which showed most different clade colonized by clonal

Acute infection usually observed in hospitalized patients having ventilator breathing. It is one of the main causative agents of hospital-acquired pneumonia and causing morbidity and mortality in the infected patients. Chastre and Fagon has reported 70–80% rate of mortality due to infection of *P. aeruginosa* in ventilatorassociated pneumonia (Research has focused on type III secretion system (TTSS) secreting four exotoxins (ExoS, ExoT, ExoU and ExoY) [6]. ExoU is an effective virulence causing effector in TTSS. It is associated with morbidity and mortality in ventilator-associated pneumonia. Hogardt et al. reported that 40% of the isolates

The pathogenicity of *P. aeruginosa* makes its able to adhere and colonize in the presence of vast virulence factors and causing disease. Virulence factors used or

Lipopolysaccharide Endotoxin; inflammatory agent; adherence and biofilm formation

outliers linked to the PA7 strain (**Figure 1**) [5].

P. aeruginosa *features relevant to pathogenicity and adaptation [2].*

from such cases harbor the *exoU* gene [7].

**Virulence factor Action**

synthesized by *P. aeruginosa* are enlisted in **Table 1**.

Flagella Motility and invasion and adherence Pili Adhesion; transfer of secretions Exopolysaccharides Adherence and pathogen persistence

**2. Virulence factors**

**Figure 1.**

**3. Pathogenicity**

**1.Colonization**

**16**

*Virulence factors produced and used by* P. aeruginosa *[8–10].*
