P. aeruginosa can infect animals, plants and also humans. They cause disease in humans who are already ill, infecting those patients with low
resistance in their bodies. P. aeruginosa are opportunistic pathogens and cause infection in patients who are diagnosed with cystic fibrosis,
have lower respiratory tract infections, surgical wounds, urinary tract infections, skin infections i.e:(dermatitis), and even in patients who
have cancer and are undergoing chemotherapy (Willey). It causes nosocomial infection in patients as this bacterium can grow anywhere where
enough nutrients and enough moisture are found.
An opportunistic pathogen, P. aeruginosa produces a thick biofilm and due to its dense colonization, it is able to resist many antibiotics,
disinfectants, as well as UV light and infected patients can therefore be difficult very to treat. Another factor that contributes to P.aeruginosa
resistance is its Gram-negative cell wall that is composed of three layers; the inner plasma membrane, peptidoglycan, and its outer membrane.
This high level of resistance in P. aeruginosa can be of consequence and dangerous to a patient’s health. Moreover, Pseudomonas maintains
antibiotic resistance plasmids, R-factors and RTFs, and it is able to transfer these genes by horizontal gene transfer (HGT), mainly
transduction and conjugation (Todar).
P. aeruginosa bacterium is naturally resistant to many antibiotics due to the permeabiliity barrier afforded by its Gram-negative outer membrane.
Also, its tendency to colonize surfaces in a biofilm form makes the cells even more resistant to antibiotics. Biofilms form organized and
specialized bacterial communities which mediate bacterial attachment to surfaces and provide protection. Biofilms are made of microcolonies that
are buried in a dense matrix of exopolysaccharides. How exactly does the bacterial colony know to initiate biofilm formation is yet to be
understood.
One of the major factors that makes Pseudomonas aeruginosa infections difficult to treat is their overproduction of a sugar-like substance,
called alginate, an exopolysaccharide. The AlgR protein, which is found to be one factor that regulates alginate production, has recently shown
to be involved with P. aeruginosa's pili function (pili mediate attachment in bacteria). Pili are involved in the initial stages of Pseudomonas
aeruginosa infection of CF lungs. Thus, it is thought that the AlgR protein, might be regulating not only genes controlling alginate production,
but other P. aeruginosa virulence genes involved in the infection process.
As far as symptoms are concerned, cystic fibrosis patients that are infected with P. aeruginosa may not show any at first. However, as the
infection grows and becomes severe, patients may notice symptoms of infection and inflammation as well as decreased tolerance for exercise and
shortness of breath. The inflammation usually leads to blockage of breathing passages and can permanently damage airways in the lungs.
Some more symptoms include salty-tasting skin, persistent coughing with phlegm, poor growth or even weight gain and also difficulty in bowel
movements