Pseudomonas aeruginosa– Etiology, Pathogenesis, and Treatment

Introduction

There are diverse numbers of Pseudomonas species but P. aerugonisa is considered a clinically significant opportunistic pathogen.
P. aerugonisa are motile, aerobic, gram-negative rods,oxidase-positive, its bacteriologic characterization is the production of water-soluble pigments, few strains appear mucoid in presence of dense polysaccharides capsule.

It can be grown on simple media as it requires simple molecules like ammonia & CO2 for N2 and C requirements.
Can survive on a wide variety of temperatures ranging from 20-42 °C and also in high salt concentration.
In media, confluent growth (merged colonies), has a metallic sheen appearance, also the fruity odor is emitted.
On blood agar, hemolysin is observed.
Pigments are produced that are blue. yellow and rust in color, It helps to differentiate from other gram -ve rods.
- Blue pigment, Pyocyanin
- Yellow pigment, Fluorescin (fluoresces under UV light)
- Yellow-Green pigment, Pyoverdin
- Reddish Brown pigment, Pyorubin

Virulence factors are associated with adhesins, toxins & enzymes which induce pathogenicity for Pseudomonas.

Virulence Factors	Components of Virulence factors	Functions
Adhesins	Flagella Pili Lipopolysaccharide(LPS) Alginate	Flagella & Pili mediate motility LPS induce endotoxin activity Alginate, present in the capsule, protects from phagocytosis & antibiotics
Secreted Toxins and Enzymes	Exotoxin A (ETA) Pyocyanin Pyoverdin LasA (serine protease) and LasB (zinc metalloprotease) Alkaline protease Phospholipase C (heat-labile hemolysin) Exoenzymes S and T	ETA disrupts protein synthesis Pyocyanin produces superoxide and hydrogen peroxide. Stimulates interleukin-8 (IL-8) Pyoverdin, a siderophore that binds iron Secretion of other virulence factors including ETA. Both LasA & LaB act synergistically to degrade elastin Degrade complement components and inhibit neutrophil chemotaxis. Alkaline protease induces tissue destruction. Phospholipase C breaks down lipids and lecithin, initiate tissue destruction Exoenzymes S and T facilitate bacterial spread, tissue invasion, and necrosis when the type III secretion system introduce the protein in the host cell

Pseudomonas is ubiquitous in nature.
It can grow in a diverse range of temperatures (4-42° C) with a minimum requirement.
They are antibiotic-resistant due to porin mutation, which restricts the flow of antibiotic inside the cell; also produce enzymes to inactivates the antibiotics.
They are opportunistic pathogens, usually, cause infection in burn patients.

Infects lower respiratory tract, may cause asymptomatic colonization, tracheobronchitis (benign inflammation of bronchial), and necrotizing bronchopneumonia (severe form).
In cystic fibrosis patients, during Pseudomonas infections, mucoid strains are isolated.
Characteristics of invasive disease caused by P. aeruginosa infections include bilateral bronchopneumonia with the formation of microabscess & tissues necrosis.
- The mortality rate is 70%.

P. aeruginosa causes various types of primary skin infections.
Mostly recognized are burn wounds infections.
- Bacteria colonize the burn wounds, cause localized vascular damage, tissue necrosis, and bacteremia in severe cases of burn patients.
- The moist surface of the burn wound & failure in penetration of the neutrophils causes such infections.
- Only topical antibiotic creams are used for treatment in these cases.
Folliculitis, caused by contaminated water( such as swimming pools, hot tubs) by Pseudomonas.
Also, cause fingernails infections and osteochondritis (Bone & cartilage inflammation) of the foot can occur after penetrating injury (for e.g, stepping on a nail).

Can cause swimmer’s ears infection (external otitis), it is managed by topical antibiotics & drying agents.
In elderly & diabetic patients, P. aeruginosa can cause malignant external otitis, can invade the concealed tissues & damage cranial nerves & bones (fatal disease).
Trauma in the eyes or abrasion from contact lens can cause infection.
A more severe form like corneal ulcers can progress & can be fatal if not treated.

Bacteremia occurs in patients suffering from extensive burns, diabetes mellitus, neutropenia( absence of neutrophils ).
- Originates from lower respiratory tracts, urinary tract, burn wound infections.
- Skin lesions (ecthyma gangrenosum) may develop, it can become ulcerated, hemorrhagic(vascular destruction) & necrotic.
Endocarditis by pseudomonas is uncommon, but this condition is seen in intravenous drug abusers. ( Drug paraphernalia contaminated with waterborne organisms).
- It involves the tricuspid valve of the heart.

Microscopy: Thin, gram-negative rods are observed arranged single or in pairs.
Culture media: Selective isolation media is used, such as Blood Agar & MacConkey agar, it is identified by flat colonies with spreading border, pigmentation, colony size, hemolysis, and by rapid biochemical tests ( especially cytochrome oxidase-positive test).

Antibiotic therapy is not that effective due to antibiotic-resistant.
Effective control practice of infections can be prevented by sterilizing equipment, such as dialysis machines & mechanical ventilation.

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