Pseudomonas aeruginosa

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Pseudomonas aeruginosa

Pseudomonas aeruginosa

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Pseudomonas aeruginosa

The microorganism chosen is Pseudomonas aeruginosa.. This is an opportunistic gram-negative bacterium found mainly in soil and water. This pathogen is known for causing a wide range of severe chronic and acute infections, mainly among patients with a compromised immune system. Pseudomonas aeruginosa grows well between 25°C and 37°C, and its capacity to survive 42°C assists in distinguishing it from most Pseudomonas species (Castro et al., 2021). Pseudomonas aeruginosa has been of particular interest since it is the major cause of mortality and morbidity in Cystic Fibrosis (CF) patients. It is also among the main nosocomial infections that affect hospitalized individuals and is resistant to a variety of antibiotics (Moradali et al., 2017). This microorganism profile paper comprehensively describes Pseudomonas aeruginosa, its virulence factors, and the defenses that protect individuals from infections caused by this pathogen. It also outlines the infectious disease information of the microorganism, epidemiology, and prevention mechanism for infections caused by Pseudomonas aeruginosa. Other areas covered include the treatment for infections caused by this microorganism and the clinical relevance of this microorganism.

Description of the Organism

Pseudomonas aeruginosa is a Gram-negative and opportunistic bacterium used to study bacterial social traits and virulence. The bacterium is monoflagellated, asporogenous, slender, and rod-shaped, and it measures approximately 1.5 to 3.0 μm long and 0.5 to 0.8 μm wide (Diggle & Whiteley, 2020). Although Pseudomonas aeruginosa is a non-capsulated bacterium, some strains possess a slime layer. The cell envelop of the Pseudomonas aeruginosa comprises three layers: the outer membrane, peptidoglycan layer, and the inner/cytoplasmic membrane (Tavares et al., 2020). The outer membrane comprises protein, lipopolysaccharide (LPS), and phospholipid. The isolates of Pseudomonas aeruginosa reveal 3 types of colonies. The natural isolates from water or soil are a small and rough colony. On the other hand, clinical isolates are a smooth colony, and sometimes they appear to have a large and smooth fried egg appearance with an elevated appearance and flat edges (Wu & Li, 2015). Pseudomonas aeruginosa has a complete nucleotide sequence of the single-stranded RNA. Pseudomonas aeruginosa comprises relatively large circular chromosomes that carry about 5500-6000 open reading frames and other times plasmids of different sizes depending on the strain. Usually, Confocal Laser Scanning (CLS) microscopy is used to view Pseudomonas aeruginosa.

Virulence Factors

Virulence factors are the molecules that help bacterium to invade the host, avoid host defenses, and cause diseases, thus colonizing the host at the cellular level (Sharma et al., 2017). Pseudomonas aeruginosa secretes several virulence factors that facilitate successful infection and colonization across a broad spectrum of environments. One of the virulence factors is lipopolysaccharide (LPS). Lipopolysaccharide is a crucial surface structural component that poisons host cells and protects the exterior leaflet. The endotoxicity of the lipid A in LPS facilitates attachment, the damage of tissues, as well as identification by the receptors of the host. LPS is also associated with biofilm formation and antibiotic tolerance. These biofilms impede phagocytosis, confer the capacity for long-term persistence, and protect Pseudomonas aeruginosa from the surrounding environmental stresses. Another virulence factor is Out Membrane Proteins (OMPs), which contribute to antibiotic resistance, nutrient exchange, and adhesion. Exopolysaccharides including Pel, alginate, and Psl are other virulence factors of Pseudomonas aeruginosa and facilitate biofilm formation and impair bacterial clearance. Other virulence factors include the different types of secretion systems: pili (T4SS), flagella (T6SS-associated), and multi-toxin components type III secretion system (T3SS). These help in adhesion, host colonization, swimming, and swarming as they respond to chemotactic signaling (Qin et al., 2022). Additional virulence factors include toxins, adhesins, and hydrolytic protease, which cause tissue damage, enhance bacterial attachment, and induce immune responses.

Immunity

Collagen-containing lectins called surfactant proteins (SP), which is primarily used for pulmonary alveolar immunity and homeostasis is also employed for Pseudomonas aeruginosa immune response (Noutsios et al., 2017). By encouraging AM phagocytosis and controlling the lung’s inflammatory reaction, SP-A and SP-D improve pulmonary clearance of Pseudomonas aeruginosa (Ujma et al., 2017). The body’s immune response includes SP-A and SP-D, which control the actions of macrophages and other host defense cells. Engaging with T cells and antigen-presenting cells also regulate adaptive immune response, bridging innate and adaptive immunity. Pseudomonas aeruginosa infection pathogens can erode the host’s countermeasures, then adjust and grow inside the host to survive (Faure et al., 2018). In chronic infections, Pseudomonas aeruginosa’s relations with the host are extraordinarily complicated because they involve a variety of host cell types and bacterial components.

Infectious Disease Formation

Pseudomonas aeruginosa is an opportunistic pathogen that causes severe infections in individuals whose immune systems are compromised or people with cystic fibrosis (Waters & Goldberg, 2019). This bacterium is mostly known for chronically colonizing and infecting the lungs of people in advanced stages of Chronic Obstructive Pulmonary Disease (COPD) and those suffering from cystic fibrosis (CF). Chronic lung infections cause airflow obstructions and persist for many years. Also, Pseudomonas aeruginosa is associated with hospital-acquired infections (HAIs) such as urinary catheter-related infections, ventilator-associated pneumonia, central line-associated bloodstream infection, and transplantation/surgical infections. Pseudomonas aeruginosa also causes acute infection of the soft tissue in open wounds, burns, and post-surgery patients. It also causes diabetic foot ulcers and chronic suppurative otitis externa and media (Morin et al., 2022). If Pseudomonas aeruginosa infection is left untreated, it enters the bloodstream and deteriorates pulmonary function. Eventually, it causes respiratory failure leading to death (Cantin et al., 2015).

-262393216010Patient 1 is infected with Pseudomonas aeruginosa.

00Patient 1 is infected with Pseudomonas aeruginosa.

4381169128546Patient 2 is not infected with Pseudomonas aeruginosa.

0Patient 2 is not infected with Pseudomonas aeruginosa.

Epidemiology

left8255Portals of Exist

Mouth

Airways

Urethra

Anus

Damaged skin

00Portals of Exist

Mouth

Airways

Urethra

Anus

Damaged skin

46674158697Portals of Entry

Skin

Urinary tract

Respiratory system

Open wounds

00Portals of Entry

Skin

Urinary tract

Respiratory system

Open wounds

1407381210848Cross Transmission from P1 to P2

00Cross Transmission from P1 to P2

1386205118800

4500438265651001431235173880Environmental Reservoirs

00Environmental Reservoirs

230588278627004547761463830065995827862700158115095250Infected Medical equipment

Water points (sinks and taps)

Wet surfaces

00Infected Medical equipment

Water points (sinks and taps)

Wet surfaces

4427527250511Cross Transmission

00Cross Transmission

-413468311204Cross Transmission

00Cross Transmission

1033531161207Hands of Nursing staff

0Hands of Nursing staff

-238539216590Figure SEQ Figure * ARABIC 1: Epidemiology of Pseudomonas aeruginosa

00Figure SEQ Figure * ARABIC 1: Epidemiology of Pseudomonas aeruginosa

Since most P. aeruginosa infections are acquired in the hospital, the above diagram presents the transmission of Pseudomonas aeruginosa in a hospital setting. Most Pseudomonas aeruginosa infections are transmitted through cross-transmission from patient to patient through the nursing staff’s hands or through the environmental reservoirs in the hospital setting. The portals of exist of Pseudomonas aeruginosa microorganism include the mouth, airways, urethra, anus, and damaged skin. These microorganisms are then transferred to an healthy person through the nursing staff hands or through environmental reservoirs such as water points (sinks and taps), mops, and infected medical equipment such as respiratory equipment. The transmission process is shown in Figure 1 below.

Prevention

Despite the identification of Pseudomonas aeruginosa as an opportunistic pathogen, no vaccine against this bacterium has come to market (Johansen & Gotzsche, 2015). Since there is no vaccine for the infection, a number of measures are put into place to avoid infection. The main technique is to ensure that hands are clean for both the patient and the caregiver. They should use an alcohol-based hand sanitizer or wash their hands with water and soap after cleaning patients’ wounds. Clean hands will aid in reducing the chances of getting sick or spreading the bacteria. All medical devices should also be sterilized and kept clean after use (Hoang et al., 2018). Medical practitioners and caregivers should ensure that the rooms occupied by the patients are cleaned on a regular basis. Water management policies that assist in guaranteeing water quality and reduce the likelihood of exposure to dangerous microorganisms like Pseudomonas aeruginosa should be implemented in medical centers.

Treatment

In medical care, antimicrobial chemotherapy continues to be the backbone of pseudomonal cure. Being inherently MDR, P. aeruginosa may have been successful in being among the most prevalent nosocomial pathogens. Different antibiotics for instance penicillins and cephalosporins, fluoroquinolones, monobactams, carbapenems, and aminoglycosides can often eradicate environmental Pseudomonas aeruginosa strains (Horcajada et al., 2019). Ever since the 1980s, the quality of care for treating viral illness caused by Pseudomonas aeruginosa has been the intravenous compromising of piperacillin or ceftazidime with an aminoglycoside, but the occurrence of bacterial resistance, specifically in the case of critical care or prolonged perseverance in defenseless sickly demographics, has prompted the need for other solutions (Ibrahim et al., 2020). The use of old medications colistin and polymyxin B, which had been discontinued for several years due to their substantial toxicity and harmful impacts, has been one method for treating MDR Pseudomonas aeruginosa (Horcajada et al., 2019). The creation of compounds that combat -lactam antimicrobial resistance has been a substitute tactic.

Clinical Relevance

Despite having an inherent resistance to many antibiotics, Pseudomonas aeruginosa is responsive to a small number of medications, including certain -lactams like ceftazidime and imipenem and aminoglycosides like amikacin and tobramycin (Benthall et al., 2015). Modern research has revealed that a number of Pseudomonas aeruginosa strains have evolved and are spreading widely despite being immune to these medications. Persons mostly at risk of being exposed to Pseudomonas aeruginosa are mostly in health care settings. Patients who are on breathing machines, medical devices such as catheters, and those with wounds from burns or surgery are at more risk. The medical practitioners or caregivers should ensure hygiene to avoid contracting the infection in case the patient is already affected (Hoang et al., 2018). Four recent antibiotics have good efficacy against MDR strains. They include ceftazidime-avibactam (Avycaz®), imipenem-cilastatin/relebactam, cefiderocol, and ceftolozane-tazobactam (Zerbaxa®) (Yusuf et al., 2021). This is despite the fact that many endorsed and pipeline antibiotics have an action against wild-type P. aeruginosa but were not as effective.

Conclusion

Pseudomonas aeruginosa is an opportunistic bacterium that causes life-threatening acute and chronic infections in hospitalized patients. The bacterium is resistant to antibiotics and has been reported as one of the principal causes of mortality and morbidity among cystic fibrosis (CF) patients. This organism is asporogenous and monoflagellated. It is also non-capsulated, although some of its strains contain a slime layer. It also possesses a complete nucleotide sequence of the single-stranded RNA. The virulence factors of Pseudomonas aeruginosa include LPS, OMPs, pili, flagella, T3SS, toxins, adhesins, and hydrolytic protease. These virulence factors cause tissue damage, enhance bacterial attachment, and facilitate biofilm formation and antibiotic tolerance. Biofilms protect the bacterium from identification by host receptors. Surfactant proteins are employed for Pseudomonas aeruginosa’s immune response. If Pseudomonas aeruginosa infection is left untreated, it deteriorates the pulmonary function, causing respiratory failure. Eventually, this leads to death. So far, a vaccine for Pseudomonas aeruginosa has not been introduced to the market to help prevent the infections caused by this pathogen. However, nurses and other healthcare professionals who attend to hospitalized patients can prevent such infections by maintaining hand hygiene. Also, sterilizing medical equipment and keeping them clean can help prevent infections caused by Pseudomonas aeruginosa. Colistin and polymyxin B medications have been used for treating Pseudomonas aeruginosa infections. However, these medications have been discontinued due to their toxicity and harmful impacts. Since Pseudomonas aeruginosa is increasingly becoming resistant to antibiotics, more treatment methods and prevention efforts such as a vaccine need to be introduced.

References

Benthall, G., Touzel, R. E., Hind, C. K., Titball, R. W., Sutton, J. M., Thomas, R. J., & Wand, M. E. (2015). Evaluation of antibiotic efficacy against infections caused by planktonic or biofilm cultures of Pseudomonas aeruginosa and Klebsiella pneumoniae in Galleria mellonella. International journal of antimicrobial agents, 46(5), 538-545.

Cantin, A. M., Hartl, D., Konstan, M. W., & Chmiel, J. F. (2015). Inflammation in cystic fibrosis lung disease: pathogenesis and therapy. Journal of Cystic Fibrosis, 14(4), 419-430.

Castro, M. S. R., da Silva Fernandes, M., Kabuki, D. Y., & Kuaye, A. Y. (2021). Modelling Pseudomonas fluorescens and Pseudomonas aeruginosa biofilm formation on stainless steel surfaces and controlling through sanitisers. International Dairy Journal, 114, 1-9. https://doi.org/10.1016/j.idairyj.2020.104945Diggle, S. P., & Whiteley, M. (2020). Microbe Profile: Pseudomonas aeruginosa: opportunistic pathogen and lab rat. Microbiology, 166(1), 30-33. https://doi.org/10.1099%2Fmic.0.000860Faure, E., Kwong, K., & Nguyen, D. (2018). Pseudomonas aeruginosa in chronic lung infections: how to adapt within the host?. Frontiers in immunology, 9, 2416.

Hoang, S., Georget, A., Asselineau, J., Venier, A. G., Leroyer, C., Rogues, A. M., & Thiébaut, R. (2018). Risk factors for colonization and infection by Pseudomonas aeruginosa in patients hospitalized in intensive care units in France. PloS one, 13(3), e0193300.

Horcajada, J. P., Montero, M., Oliver, A., Sorlí, L., Luque, S., Gómez-Zorrilla, S., … & Grau, S. (2019). Epidemiology and treatment of multidrug-resistant and extensively drug-resistant Pseudomonas aeruginosa infections. Clinical microbiology reviews, 32(4), e00031-19.

Ibrahim, D., Jabbour, J. F., & Kanj, S. S. (2020). Current choices of antibiotic treatment for Pseudomonas aeruginosa infections. Current Opinion in Infectious Diseases, 33(6), 464-473.

Johansen, H. K., & Gøtzsche, P. C. (2015). Vaccines for preventing infection with Pseudomonas aeruginosa in cystic fibrosis. Cochrane database of systematic reviews, (8).

Moradali, M. F., Ghods, S., & Rehm, B. H. (2017). Pseudomonas aeruginosa lifestyle: a paradigm for adaptation, survival, and persistence. Frontiers in cellular and infection microbiology, 7 (39). 1-29. https://doi.org/10.3389%2Ffcimb.2017.00039Morin, C. D., Déziel, E., Gauthier, J., Levesque, R. C., & Lau, G. W. (2021). An organ system-based synopsis of Pseudomonas aeruginosa virulence. Virulence, 12(1), 1469-1507. https://doi.org/10.1080%2F21505594.2021.1926408Noutsios, G. T., Willis, A. L., Ledford, J. G., & Chang, E. H. (2017, September). Novel role of surfactant protein A in bacterial sinusitis. In International forum of allergy & rhinology (Vol. 7, No. 9, pp. 897-903).

Qin, S., Xiao, W., Zhou, C., Pu, Q., Deng, X., Lan, L., … & Wu, M. (2022). Pseudomonas aeruginosa: pathogenesis, virulence factors, antibiotic resistance, interaction with host, technology advances and emerging therapeutics. Signal Transduction and Targeted Therapy, 7(1), 1-27. https://doi.org/10.1038/s41392-022-01056-1Sharma, A. K., Dhasmana, N., Dubey, N., Kumar, N., Gangwal, A., Gupta, M., & Singh, Y. (2017). Bacterial virulence factors: secreted for survival. Indian journal of microbiology, 57(1), 1-10. https://doi.org/10.1007%2Fs12088-016-0625-1Tavares, T. D., Antunes, J. C., Padrão, J., Ribeiro, A. I., Zille, A., Amorim, M. T. P., … & Felgueiras, H. P. (2020). Activity of specialized biomolecules against gram-positive and gram-negative bacteria. Antibiotics, 9(6), 1-16. https://doi.org/10.3390/antibiotics9060314Ujma, S., Horsnell, W. G., Katz, A. A., Clark, H. W., & Schäfer, G. (2017). Non-pulmonary immune functions of surfactant proteins A and D. Journal of Innate Immunity, 9(1), 3-11.

Waters, C. M., & Goldberg, J. B. (2019). Pseudomonas aeruginosa in cystic fibrosis: A chronic cheater. Proceedings of the National Academy of Sciences, 116(14), 6525-6527. https://doi.org/10.1073/pnas.1902734116Wu, M., & Li, X. (2015). Klebsiella pneumoniae and Pseudomonas aeruginosa. In Molecular medical microbiology (pp. 1547-1564). Academic Press. https://doi.org/10.1016/B978-0-12-397169-2.00087-1Yusuf, E., Bax, H. I., Verkaik, N. J., & van Westreenen, M. (2021). An update on eight “new” antibiotics against multidrug-resistant gram-negative bacteria. Journal of clinical medicine, 10(5), 1068.

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