Despite major recent advances in the study ofthe virulence of the human opportunistic pathogen Pseudomonas aeruginosa, our understanding of the pathogenesis of P. Aeruginosa infections remains limited.
- Download Virulence Factors Of Pseudomonas Aeruginosa Pdf Chart
- Download Virulence Factors Of Pseudomonas Aeruginosa Pdf Presentation
- Isolation Precautions For Pseudomonas Aeruginosa
By Adam Classen and Jennifer Huxham
Introduction
Pseudomonas aeruginosa is a rod shaped gram-negative bacteria (see figure 1) that is often found in wet areas or bodily fluids. The bacterium was first identified by Carle Gessard in 1882. It is an opportunistic pathogen that is one of the leading causes of infections in hospitals. This bacteria can cause a variety of symptoms but it is most commonly associated with pneumonia in immunocompromised or mechanically ventilated individuals. The microbe’s success can be attributed to its extraordinary adaptability and virulence factors.
Figure 1. Computer generated image of P. aeruginosa with its pili and flagella. Source: Archer USCfDCaP-MIj. 2013. Multidrug-resistant pseudomona aeruginosa. CDC.
Loss of virulence factors and social traits through genetic mutations is commonly observed in P. Aeruginosa isolates collected from chronic CF infections 51–53; however, the genetic adaptations of P. Aeruginosa to chronic wounds are less well described. We conducted whole-genome sequencing on each of the representative morphotypes to. Pseudomonas aeruginosa infection can be disastrous in chronic lung diseases such as cystic fibrosis and chronic obstructive pulmonary disease. Its toxic effects are largely mediated by secreted virulence factors including pyocyanin, elastase and alkaline protease (AprA). Efficient functioning of the. The virulence factors play an important pathological role in the colonization, the survival of the bacteria and the invasion of tissues. There are two types of virulence factors: (1) factors involved in the acute infection: these factors are either on the surface of P. Aeruginosa, either secreted. The pili allow adherence to the epithelium. Jun 17, 2015 Author Summary Pseudomonas aeruginosa causes a devastating infection when it affects patients with cystic fibrosis or other chronic lung diseases. It often causes chronic infection due to its resistance to antibiotic treatment and its ability to form biofilms in these patients. The toxic effects of P. Aeruginosa are largely mediated by secreted virulence factors. Efficient functioning of the.
Disease
Depending on the site of infection P. aeruginosa can cause a variety of different types of symptoms. Bloodstream infections have symptoms such as; fever/chills, aches, light-headedness, vomiting. Pneumonia is often caused by the microbe and can cause difficulty breathing and coughing with yellow, green or even bloody mucus. P. aeruginosa can also cause urinary tract infection (UTI), leading to painful urination.
Infection of severe burns can also occur. This is attributed to the fact that severe burns cause immunosuppression, making affected individuals more at risk of developing infections by P. aeruginosa.
Cystic fibrosis (CF) is a genetic condition that causes buildup of mucus in the lungs among other things. These individuals are immunocompromised and are at particular risk of lung infection by P. aeruginosa because of their inability to effectively clear mucus from their lungs. Normally, the mucus in the lungs captures microorganisms and is swept out, thus helping to prevent pathogens from infecting the lungs. However, because CF patients are unable to clear lung mucus, the microbes get trapped and remain in the lungs allowing for infection. This infection causes inflammation which can restrict breathing and result in death.
Epidemiology
P. aeruginosa affects mostly immunocompromised individuals and is therefore often caught in hospitals. In the United States of America, it is the number 1 cause of intensive care unit pneumonia, accounts for 10% of all infections contracted in hospitals, and is the 3rd most common way of contracting a UTI in a hospital. It can be spread by people, food and medical equipment. P. aeruginosa is one of the most common forms of burn wound infection. Burn victims that become infected with P.aeruginosa have a 40-50% mortality rate, making this type of infection very dangerous. CF patients have a 40% chance of being infected with P. aeruginosa. Chronic infection of this type is one of the leading causes of death in individuals affected by CF, carrying a 40-60% mortality rate.
Virulence factors
P. aeruginosa is a successful pathogen because of its adaptability and variety of virulence factors. One of which is its ability to form biofilms, which are colonies of bacteria that are clustered together. Biofilms are important for protection against the host immune system. Specifically, these biofilms protect against antibodies (tag foreign particles for destruction), the complement system (forms pores in their membrane and tags the bacteria for destruction), phagocytes (eliminates foreign particles, broken cellular components or bacteria). They also protect against antibiotics and antimicrobial peptides (AMPs). Where AMPs are compounds produced by the host to kill microbes. Biofilms also cause massive inflammation at the site of infection causing damage to the host. This impressive virulence factor allows the bacteria to survive for a prolonged amount of time in the host.Other virulence factors that contribute to its pathogenicity are pili, which are surface proteins that help them attach to the host. As well as flagella, which acts as a tail to help the bacteria propel itself and move around.
P. aeruginosa can cause damage to the host by secreting toxins. Specifically, it uses an exotoxin, which are proteins or lipids that are secreted into the external environment from the bacterial pathogen. This exotoxin inactivates eukaryotic elongation factor 2, a protein that is crucial for protein synthesis. Inhibition of this protein stops the host eukaryotic cells from synthesizing proteins necessary for functioning, resulting in death. It also produces the enzyme ExoU which is secreted extracellularly where it functions, causing lysis (cutting) of host cell plasma membranes. Allowing it to steal iron from the host’s mitochondria, inflicting damage.
P. aeruginosa has an outer membrane that has low permeability to antibiotics, thus helping protect it. On top of that it has multidrug efflux pumps (see figure 2). These pumps can take antibiotics that do manage to enter the cell and quickly excrete them back out of the cell into the surrounding environment. Stopping them from affecting the bacterial cell.
Figure 2. Efflux pump in the bacterial membrane pumps antibiotics out of the bacteria, passing through the inner, peptidoglycan and outer membranes in an anti-port manner (protons goes in, antibiotics goes out).
Treatment
Wild type P. aeruginosa strains are sensitive to a variety of antibiotics including aminoglycosides and cephalosporins. However, the strains found in hospitals have developed resistance to many types of antibiotics, making them more difficult to treat. In hopes of clearing these infections a combination of 2 drugs is often used. More than one drug is given intravenously to prevent the development of antibiotic resistance and to enhance their effectiveness. However, despite treatment with antibiotics, P. aeruginosa is often able to adapt and survive in the lungs of CF patient for decades. If infection of burn wounds occur surgical removal of infected skin is often needed to help clear infection. As resistance to all commercially available antibiotics is now commonplace with P. aeruginosa.
References
Bennington-Castro J. Forthcoming 2015. What is pseudomonas aeruginosa? : Everyday Health.
Church D, Elsayed S, Reid O, Winston B, Lindsay R. 2006. Burn wound infections. Clinical microbiology reviews. 19(2):403-434.
Cohen TS, Parker D, Prince A. 2015. Pseudomonas aeruginosa host immune evasion. In:Ramos J-L, Goldberg JB, Filloux A, editors. Pseudomonas: Volume 7: New aspects of pseudomonas biology. Dordrecht: Springer Netherlands. p. 3-23.
EHA consulting group I. Forthcoming 2017. What is pseudomonas aeruginosa? : Environmental & public health consultants
Download Virulence Factors Of Pseudomonas Aeruginosa Pdf Chart
Estahbanati HK, Kashani PP, Ghanaatpisheh F. 2002. Frequency of pseudomonas aeruginosa serotypes in burn wound infections and their resistance to antibiotics. Burns. 28(4):340-348.
Faucher S. 2017. Mechanisms of Pathogenicity. Mcgill University.
Freidreich M. Pseudomonas aeruginosa infections treatment & management. 2016. MedScape; [accessed 2017]. https://emedicine.medscape.com/article/226748-treatment#d5.
Goldberg JB. 2010. Emergence of pseudomonas aeruginosa in cystic fibrosis lung infections. In:Ramos JL, Filloux A, editors. Pseudomonas: Volume 6: Molecular microbiology, infection and biodiversity. Dordrecht: Springer Netherlands. p. 141-175.
Høiby N, Johansen HK, Moser C, Ciofu O. 2008. Clinical relevance of pseudomonas aeruginosa: A master of adaptation and survival strategies. Pseudomonas. Wiley-VCH Verlag GmbH & Co. KGaA. p. 25-44.
Download Virulence Factors Of Pseudomonas Aeruginosa Pdf Presentation
Lister PD, Wolter DJ, Hanson ND. 2009. Antibacterial-resistant pseudomonas aeruginosa: Clinical impact and complex regulation of chromosomally encoded resistance mechanisms. Clinical microbiology reviews. 22(4):582-610.
Pan J, Zha Z, Zhang P, Chen R, Ye C, Ye T. 2017. Serine/threonine protein kinase ppka contributes to the adaptation and virulence in pseudomonas aeruginosa. Microbial Pathogenesis. 113(Supplement C):5-10.
Pirnay J-P, Bilocq F, Pot B, Cornelis P, Zizi M, Van Eldere J, Deschaght P, Vaneechoutte M, Jennes S, Pitt T et al. 2009. Pseudomonas aeruginosa population structure revisited. PLOS ONE. 4(11):e7740.
Saenz-Méndez P, Eriksson M, Eriksson LA. 2017. Ligand selectivity between the adp-ribosylating toxins: An inverse-docking study for multitarget drug discovery. ACS Omega. 2(4):1710-1719.
Shigeki Fujitani, Kathryn Moffett, Victor Yu. 2017. Pseudomonas aeruginosa. Antimicrobe; [accessed]. http://www.antimicrobe.org/b112.asp
Back to Journals » Infection and Drug Resistance » Volume 12
AuthorsEl-Mahdy R, El-Kannishy G
Received8 July 2019
Accepted for publication 24 October 2019
Published 7 November 2019 Volume 2019:12 Pages 3455—3461
DOIhttps://doi.org/10.2147/IDR.S222329
Checked for plagiarism Yes
Review bySingle anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Joachim Wink
Rasha El-Mahdy,1 Ghada El-Kannishy2
1Department of Medical Microbiology And Immunology, Faculty of Medicine, Mansoura University, Mansoura, Egypt; 2Department of Internal Medicine, Faculty of Medicine, Mansoura University, Mansoura, Egypt
Correspondence: Rasha El-Mahdy
Faculty of Medicine, Mansoura University, Mansoura 35516, Egypt
Tel +20 5010 0532 9819
Email rashaamr@mans.edu.eg
Purpose: The problem of carbapenem-resistant Pseudomonas aeruginosa in health-care settings is growing worse. This study was conducted to investigate the rate of carbapenemase genes, antibiotic resistance, and virulence factors in carbapenem-resistant P. aeruginosa associated with hospital-acquired infections.
Patients and methods: Isolates of P. aeruginosa were collected from patients with hospital-acquired infections at Mansoura University Hospital in Mansoura. Carbapenem susceptibility was done by broth dilution. The presence of carbapenemase genes and quorum-sensing genes was assessed by PCR. Production of protease, pyocyanin, twitching motility, hemolytic activity and biofilm formation was evaluated.
Results: Out of 80 P. aeruginosa isolates, 34 (42.5%) were resistant to carbapenem. Among carbapenem-resistant P. aeruginosa isolates, 21 (61.8%) were carbapenemase producers. The most prevalent gene detected was blaVIM. The frequency of protease, pyocyanin, twitching motility, hemolytic activity and biofilm formation was 76.2%, 58.8%, 83.8%, 93.8% and 77.5%, respectively. Biofilm formation was significantly associated with carbapenem-resistant P. aeruginosa. On the other hand, pyocyanin production was significantly lower in carbapenem-resistant isolates. No correlation existed between carbapenem resistance and any other studied virulence factors or quorum-sensing genes.
Conclusion: Association of carbapenem-resistant P. aeruginosa with other antibiotic resistance or the presence of virulence factors in hospital-acquired infection may represent a warning that enhances the need for a stringent surveillance program.
Keywords:Pseudomonas aeruginosa, carbapenem, virulence factor, resistance
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.
Download Article [PDF]View Full Text [HTML]