Pseudomonas aeruginosa and Cystic Fibrosis: A Detailed Research Report

This report provides a detailed overview of Pseudomonas aeruginosa, a bacterium commonly found in the environment and a significant cause of infection, especially in hospitalized individuals and those with weakened immune systems. The report emphasizes the bacterium's role in cystic fibrosis, its mechanisms of infection through biofilm formation and antibiotic resistance, and the challenges in treatment. It explores the complexities of managing cystic fibrosis, including acute pulmonary exacerbations and chronic infections, and highlights the use of antibiotics, particularly inhaled antibiotics, as a standard care. The report also discusses the importance of early intervention strategies and the ongoing research to combat antibiotic resistance and improve patient outcomes. Finally, the report provides a comprehensive list of references for further study and in-depth understanding of Pseudomonas aeruginosa.

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Title: Pseudomonas aeruginosa

Introduction on Pseudomonas aeruginosa
Pseudomonas infection is caused by bacteria strains mostly found in the environment,
with Pseudomonas aeruginosa being the common infection causing microorganism. This
infection is common with hospitalized individuals with weak immune systems. This infection
can lead to severe illness or even death in case the patient gets infected with pneumonia or
blood infection after a surgery. Biggers (2018) stated that this bacteria breeds and lives in
water, damp places and in the soil. Warm and wet areas gives the bacteria a conducive
environment to grow and breed faster. It can also be found in fresh fruits and vegetables. In
humans its colonization starts at the gastrointestinal tract where it moves to cutaneous sites
and forms florescent green groups with a grape like odour at 42 0C making easier to notice
them. Pseudomonas aeruginosa is a bacteria of genus Pseudomonas. It has water pyoverdin
and pyocyanin, which are water soluble pigments and give the bacteria its blue-green
pigment. The bacteria secretes enzyme indophenol oxidase which make them positive in
oxidase test, which is the only distinction between other gram negative bacteria. Below is a
figure showing this bacteria
Pseudomonas aeruginosa
According to Fujitani, Moffett and Yu (2017) Pseudomonas aeruginosa accounts for
17 percent of nosocomial pneumonia, the third leading cause of urinary tract infection and
surgical site infections (accounting for about 11 percent) and the fifth most isolated

microorganism from nosocomial infection sites. Pseudomonas aeruginosa is considered in the
diagnosis of gram negative bacterial infections. Chronic infection of this microorganism leads
to cystic fibrosis and it is well known for its resistance to antibiotics. During the 1960s when
Pseudomonas aeruginosa was first discovered as a cause of gram negative bacteremia, its
mortality rate was 90 percent. With the invention of antipseudomonal antibiotics the
treatment outcomes were improved but still in the 21 century Pseudomonas aeruginosa
causes serious infections, with its mortality and morbidity levels ranging between 18 and 61
percent.
It is not easy to distinguish pseudomonas infection from other gram negative bacterial
disease and patients may be prescribed with imperial antibiotics against pseudomonas
especially before the results of antibiotic susceptibility is attained. There has been cases of
inappropriate antimicrobial therapy but researchers argue that this does not cause much effect
on the outcomes especially when given within the first 72 hours. Torrens et al (2019) claim
that its increasing antibiotic resistance is alarming and therefore the need for more research to
come up with a “therapeutic arsenal” to prevent more effects of this microorganism on
patients. Its resistance to antibiotics has been associated with chromosomal mutations
(Gellatly and Hancock, 2013). The research on Pseudomonas aeruginosa targets on its cell
wall and its metabolism so as to come up with an effective drug for this microorganism.
Some research by Moya et al (2012) and Zamorano et al (2011) have suggested on regulating
the expression of AmpC β-lactam. Pseudomonas aeruginosa gathers adaptive mutations
which increase its persistence in cystitis fibrosis lung niche, where the bacteria uses biofilm
and mucus to prevent diffusion of certain immune elements (phagocytes and antibodies)
(Mulcahy, Isabella and Lewis, 2014).

Pseudomonas aeruginosa and how it causes cystic fibrosis
According to Bassetti et al. (2018) Pseudomonas aeruginosa is an important organism
in the severe and progressive cystic fibrosis with it having the ability to proliferate and grow
in the patient’s system. Pseudomonas aeruginosa uses the biofilms to prevent mucociliary
clearance of microorganisms inhaled in to the system hence crating its habitat. After the
formation of the biofilm, inflammation begins and could result to chronic infections. At the
early stages of this cystic fibrosis the patient experiences complications such as hypoxia,
bronchiectasis, pulmonary hypertension, phlegm production, blood mucus and incessant
coughing. The severity of its effect on the lungs is considered as the determining factor on the
survival of the patient.
According to Waters and Goldberg (2019), the bacteria produces factors such as
protease, hydrogen cyanide, exoenzyme S, flagella, pili and exotoxin A which help it
development and protection of the biofilms. The biofilms and secreted factors act in
coordination and nave a high ability of adapting to their environment. They also have
extracellular DNA as a component of the biofilms in their young stages. The fast growth of
Pseudomonas aeruginosa is associated with their resistance to antibiotics and also their
resistance to the host’s immune system. The infection by this bacteria become chronic, with
the hereditary factors undergoing phenotypic changes characterized by production of
alginate. Pseudomonas aeruginosa phenotype (mucoid phenotype) is linked with the
difficulties faced in eradication of this pathogen, resulting to inflammations and reduced
functioning of the lungs (Juan et al. 2018).
Treatment and management of cystic fibrosis
Silva Filho et al (2013) think that there is no cure for cystic fibrosis but there are
treatments to ease and reduce the symptoms and complications of this disease. Researchers

recommend close, aggressive and early intervention and monitoring of this cystic fibrosis.
They also recommend screening and treatment done by health professionals well trained and
with adequate experience on cystic fibrosis due to its complex nature. According to Ehsan
and Clancy (2015), the treatment of Pseudomonas aeruginosa cystic fibrosis has two goals:
treating the acute pulmonary exacerbations and managing the chronic Pseudomonas
aeruginosa disease during its early stages and during its times of clinical stability. In cystic
fibrosis, acute pulmonary exacerbations includes increased systematic and pulmonary
symptoms and reduced functioning of the lungs. The treatment which includes antibiotics
focuses on clearing the airway while targeting known airway pathogens. For patients with
chronic Pseudomonas aeruginosa infection, anti- Pseudomonas aeruginosa antibiotics are
given orally inhaled and through other intravenous ways (Maiz et al. 2013).
Sanders et al. (2010) claim that 25 percent of patients who use this approach do not
recover completely. Since the decline of the proper functioning of the lungs can take the
patient’s lifespan (as a result of this infection), developing strategies to manage and restore
the lung functioning is crucial. Management of cystic fibrosis especially during its clinical
stability applies use of antibiotics. Aerosolized antibiotics, since they have fewer side effects
on the patient, are mostly used to attain intrapulmonary concentrations. The use of inhaled
antibiotics therapy is a standard care for cystic fibrosis with it showing better outcomes in
reducing inflammations, acute pulmonary exacerbations and also reducing Pseudomonas
aeruginosa density (Flume and van Devanter, 2015).
Clearing the Pseudomonas aeruginosa could be spontaneous or after administering
anti- Pseudomonas aeruginosa antibiotics. Treggiari et al (2011) claim that the Pseudomonas
infections are sensitive to certain antibiotics and the organisms causing them are not
associated with long term decrease in pulmonary activity (Ratjen, Brockhaus and Angyalosi,
2009). Different cystic fibrosis centres in Europe have come up with a strategy to treat

Pseudomonas aeruginosa infections at their early stages. A study by Brodt, Stovold and
Zhang (2014) proved that the approach of treating cystic fibrosis and other Pseudomonas
aeruginosa infections at their early stages is a better strategy to eradicate these infections.

References
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cystic fibrosis patients using inhaled antibiotics with a focus on nebulized liposomal
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