PSEUDOMONAS AERUGINOSA
'''Pseudomonas aeruginosa''' is a Gram-negative, aerobic, rod-shaped bacterium with unipolar motility.[1] An opportunistic human pathogen, ''P. aeruginosa'' is also an opportunistic pathogen of plants[2]. Based on 16S rRNA analysis, ''P. aeruginosa'' has been placed in the ''P. aeruginosa'' group[3].
''P. aeruginosa'' secretes a variety of pigments, including pyocyanin (blue-green), fluorescein (yellow-green and fluorescent, now also known as pyoverdin), and pyorubin (red-brown). King, Ward, and Raney developed Pseudomonas Agar P (aka King A media) for enhancing pyocyanin and pyorubin production and Pseudomonas Agar F (aka King B media) for enhancing fluorescein production.[4]
''P. aeruginosa'' is often preliminarily identified by its pearlescent appearance and grape-like odor ''in vitro''. Definitive clinical identification of ''P. aeruginosa'' often includes identifying the production of both pyocyanin and fluorescein as well as its ability to grow at 42°C. ''P. aeruginosa'' is capable of growth in diesel and jet fuel, where it is known as a hydrocarbon utilizing microorganism (or "HUM bug"), causing microbial corrosion. It creates dark gellish mats sometimes improperly called "algae".
| Contents |
| The name |
| Pathogenesis |
| Treatment |
| References |
| See also |
| External links |
The name
The word ''Pseudomonas'' means 'false unit', from the Greek ''pseudo'' (Greek: '''ψευδο''' 'false') and ''monas'' (Latin: '''monas''', fr. Greek: '''μονος''' 'a single unit'). The word was used early in the history of microbiology to refer to germs. ''Aeruginosa'' is the Latin word for verdigris or 'copper rust'. This describes the blue-green bacterial pigment seen in laboratory cultures of ''P. aeruginosa''. Pyocyanin biosynthesis is regulated by quorum sensing as in the biofilms associated with ''P. aeruginosa's colonization of the lungs of cystic fibrosis patients.
Pathogenesis
An opportunistic pathogen of immunocompromised individuals, ''P. aeruginosa'' typically infects the pulmonary tract, urinary tract, burns, wounds, and also causes other blood infections.[5] ''Pseudomonas'' can in rare circumstances cause community acquired pneumonias,[6] as well as ventilator-associated pneumonias, being one of the most common agents isolated in several studies.[7] Pyocyanin is a virulence factor of the bacteria and has been known to cause death in ''C. elegans'' by oxidative stress. However, research indicates that salicylic acid can inhibit pyocyanin production[8] One in ten hospital-acquired infections are from ''Pseudomonas''. Cystic fibrosis patients are also predisposed to ''P. aeruginosa'' infection of the lungs. ''P. aeruginosa'' may also be a common cause of "hot-tub rash" (dermatitis), caused by lack of proper, periodic attention to water quality. The most common cause of burn infections is ''P. aeruginosa''.
''P. aeruginosa'' uses the virulence factor exotoxin A to ADP-ribosylate eukaryotic elongation factor 2 in the host cell, much as the diphtheria toxin does. Without elongation factor 2, eukaryotic cells cannot synthesize proteins and necrose. The release of intracellular contents induces an immunologic response in immunocompetent patients.
With plants, ''P. aeruginosa'' induces symptoms of soft rot with ''Arabidopsis thaliana'' (Thale cress) and ''Letuca sativa'' (Lettuce).[9][10] It is a powerful pathogen with ''Arabidopsis''[11] and with some animals: ''Caenorhabditis elegans'',[12][13] ''Drosophila'',[14] and ''Galleria mellonella''.[15] The associations of virulence factors are the same for vegetal and animal infections.[9][17]............
Treatment
''P. aeruginosa'' is frequently isolated from non-sterile sites (mouth swabs, sputum, and so forth) and under these circumstances, it often represents colonisation and not infection. The isolation of ''P. aeruginosa'' from non-sterile specimens should therefore be interpreted cautiously and the advice of a microbiologist or infectious diseases physician should be sought prior to starting treatment. Often no treatment is needed.
When ''P. aeruginosa'' is isolated from a sterile site (blood, bone, deep collections), it should be taken seriously and almost always requires treatment.
''P. aeruginosa'' is naturally resistant to a large range of antibiotics and may demonstrate additional resistance after unsuccessful treatment, particularly through modification of a porin. It should usually be possible to guide treatment according to laboratory sensitivities, rather than choosing an antibiotic . If antibiotics are started empirically, then every effort should be made to obtain cultures and the choice of antibiotic used should be reviewed when the culture results are available.
Antibiotics that have activity against ''P. aeruginosa'' include:
★ aminoglycosides (gentamicin, amikacin, tobramycin);
★ quinolones (ciprofloxacin and levofloxacin but ''not'' moxifloxacin)
★ cephalosporins (ceftazidime, cefepime, cefpirome, but ''not'' cefuroxime, ceftriaxone, cefotaxime)
★ ureidopenicillins (piperacillin, ticarcillin: ''P. aeruginosa'' is intrinsically resistant to all other penicillins)
★ carbapenems (meropenem, imipenem, but ''not'' ertapenem)
★ polymyxins (polymyxin B and colistin)[18]
★ monobactams (aztreonam)
These antibiotics must all be given by injection, with the exception of fluoroquinolones. For this reason, in some hospitals, fluoroquinolone use is severely restricted in order to avoid the development of resistant strains of ''P. aeruginosa''. In the rare occasions where infection is superficial and limited (for example, ear infections or nail infections) topical gentamicin or colistin may be used.
References
1. Sherris Medical Microbiology, Ryan KJ, Ray CG (editors), , , McGraw Hill, 2004,
2. Pseudomonas. ''In:'' Baron's Medical Microbiology (Baron S ''et al'', eds.), Iglewski BH, , , Univ of Texas Medical Branch, 1996,
3. Phylogenetic affiliation of the pseudomonads based on 16S rRNA sequence, Anzai, ''et al.'', , , Int J Syst Evol Microbiol, 2000, Jul
4. Two simple media for the demonstration of pyocyanin and fluorescin., King EO, Ward MK, Raney DE, , , J Lab Clin Med, 1954
5. Todar's Online Textbook of Bacteriology
6. Prognosis and outcomes of patients with community-acquired pneumonia. A meta-analysis, Fine MJ, Smith MA, Carson CA, ''et al'', , , JAMA, 1996
7. Survey of bloodstream infections due to gram-negative bacilli: frequency of occurrence and antimicrobial susceptibility of isolates collected in the United States, Canada, and Latin America for the SENTRY Antimicrobial Surveillance Program, 1997, Diekema DJ, Pfaller MA, Jones RN, ''et al'', , , Clin. Infect. Dis., 1999
8. Down regulation of virulence factors of Pseudomonas aeruginosa by salicylic acid attenuates its virulence on Arabidopsis thaliana and Caenorhabditis elegans., Prithiviraj B, Bais H, Weir T, Suresh B, Najarro E, Dayakar B, Schweizer H, Vivanco J, , , Infect Immun, 2005
9. Common virulence factors for bacterial pathogenicity in plants and animals, Rahme LG, Stevens EJ, Wolfort SF, Shao J, Tompkins RG, Ausubel FM, , , Science, 1995
10. Use of model plant hosts to identify Pseudomonas aeruginosa virulence factors, Rahme LG, Tan MW, Le L, ''et al'', , , Proc. Natl. Acad. Sci. U.S.A., 1997
11. Pseudomonas aeruginosa-plant root interactions. Pathogenicity, biofilm formation, and root exudation, Walker TS, Bais HP, Déziel E, ''et al'', , , Plant Physiol., 2004
12. Molecular mechanisms of bacterial virulence elucidated using a Pseudomonas aeruginosa-Caenorhabditis elegans pathogenesis model, Mahajan-Miklos S, Tan MW, Rahme LG, Ausubel FM, , , Cell, 1999
13. Salicylic acid regulates flowering time and links defence responses and reproductive development, Martínez C, Pons E, Prats G, León J, , , Plant J., 2004
14. Drosophila as a model host for Pseudomonas aeruginosa infection, D'Argenio DA, Gallagher LA, Berg CA, Manoil C, , , J. Bacteriol., 2001
15. Use of the Galleria mellonella caterpillar as a model host to study the role of the type III secretion system in Pseudomonas aeruginosa pathogenesis, Miyata S, Casey M, Frank DW, Ausubel FM, Drenkard E, , , Infect. Immun., 2003
16. Common virulence factors for bacterial pathogenicity in plants and animals, Rahme LG, Stevens EJ, Wolfort SF, Shao J, Tompkins RG, Ausubel FM, , , Science, 1995
17. Plants and animals share functionally common bacterial virulence factors, Rahme LG, Ausubel FM, Cao H, ''et al'', , , Proc. Natl. Acad. Sci. U.S.A., 2000
18. Colistin is effective in treatment of infections caused by multidrug-resistant ''Pseudomonas aeruginosa'' in cancer patients, Hachem RY, Chemaly RF, Ahmar CA, ''et al'', , , Antimicrob. Agents Chemother., 2007
See also
★ Nosocomial infection
External links
★ www.pseudomonas.com, the Pseudomonas genome database
★ Migula's Systematic Bacteriology (in German)
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