Pseudomonas aeruginosa

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Pseudomonas aeruginosa
P. aeruginosa on an XLD agar plate.
P. aeruginosa on an XLD agar plate.
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Pseudomonadales
Family: Pseudomonadaceae
Genus: Pseudomonas
Species: P. aeruginosa
Binomial name
Pseudomonas aeruginosa
(Schröter 1872)
Migula 1900
Type strain
ATCC 10145

CCUG 551
CFBP 2466
CIP 100720
DSM 50071
JCM 5962
LMG 1242
NBRC 12689
NCCB 76039
NCIMB 8295
NCTC 10332
NRRL B-771
VKM B-588


Bacterium aeruginosum Schroeter 1872
Bacterium aeruginosum Cohn 1872
Micrococcus pyocyaneus Zopf 1884
Bacillus aeruginosus (Schroeter 1872) Trevisan 1885
Bacillus pyocyaneus (Zopf 1884) Flügge 1886
Pseudomonas pyocyanea (Zopf 1884) Migula 1895
Bacterium pyocyaneum (Zopf 1884) Lehmann and Neumann 1896
Pseudomonas polycolor Clara 1930
Pseudomonas vendrelli nomen nudum 1938

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".

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.


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][16]


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 empirically. 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:

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.


  1. Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9.
  2. Iglewski BH (1996). Pseudomonas. In: Baron's Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
  3. Anzai; et al. (2000, Jul). "Phylogenetic affiliation of the pseudomonads based on 16S rRNA sequence". Int J Syst Evol Microbiol. 50 (Pt 4): 1563–89. PMID 10939664. Check date values in: |year= (help)
  4. King EO, Ward MK, Raney DE (1954). "Two simple media for the demonstration of pyocyanin and fluorescin". J Lab Clin Med. 44 (2): 301–7. PMID 13184240.
  5. Todar's Online Textbook of Bacteriology
  6. Fine MJ, Smith MA, Carson CA; et al. (1996). "Prognosis and outcomes of patients with community-acquired pneumonia. A meta-analysis". JAMA. 275 (2): 134–41. PMID 8531309.
  7. Diekema DJ, Pfaller MA, Jones RN; et al. (1999). "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". Clin. Infect. Dis. 29 (3): 595–607. PMID 10530454.
  8. Prithiviraj B, Bais H, Weir T, Suresh B, Najarro E, Dayakar B, Schweizer H, Vivanco J (2005). "Down regulation of virulence factors of Pseudomonas aeruginosa by salicylic acid attenuates its virulence on Arabidopsis thaliana and Caenorhabditis elegans". Infect Immun. 73 (9): 5319–28. PMID 16113247.
  9. 9.0 9.1 Rahme LG, Stevens EJ, Wolfort SF, Shao J, Tompkins RG, Ausubel FM (1995). "Common virulence factors for bacterial pathogenicity in plants and animals". Science. 268 (5219): 1899–902. PMID 7604262.
  10. Rahme LG, Tan MW, Le L; et al. (1997). "Use of model plant hosts to identify Pseudomonas aeruginosa virulence factors". Proc. Natl. Acad. Sci. U.S.A. 94 (24): 13245–50. PMID 9371831.
  11. Walker TS, Bais HP, Déziel E; et al. (2004). "Pseudomonas aeruginosa-plant root interactions. Pathogenicity, biofilm formation, and root exudation". Plant Physiol. 134 (1): 320–31. doi:10.1104/pp.103.027888. PMID 14701912.
  12. Mahajan-Miklos S, Tan MW, Rahme LG, Ausubel FM (1999). "Molecular mechanisms of bacterial virulence elucidated using a Pseudomonas aeruginosa-Caenorhabditis elegans pathogenesis model". Cell. 96 (1): 47–56. PMID 9989496.
  13. Martínez C, Pons E, Prats G, León J (2004). "Salicylic acid regulates flowering time and links defence responses and reproductive development". Plant J. 37 (2): 209–17. PMID 14690505.
  14. D'Argenio DA, Gallagher LA, Berg CA, Manoil C (2001). "Drosophila as a model host for Pseudomonas aeruginosa infection". J. Bacteriol. 183 (4): 1466–71. doi:10.1128/JB.183.4.1466-1471.2001. PMID 11157963.
  15. Miyata S, Casey M, Frank DW, Ausubel FM, Drenkard E (2003). "Use of the Galleria mellonella caterpillar as a model host to study the role of the type III secretion system in Pseudomonas aeruginosa pathogenesis". Infect. Immun. 71 (5): 2404–13. PMID 12704110.
  16. Rahme LG, Ausubel FM, Cao H; et al. (2000). "Plants and animals share functionally common bacterial virulence factors". Proc. Natl. Acad. Sci. U.S.A. 97 (16): 8815–21. PMID 10922040.
  17. Hachem RY, Chemaly RF, Ahmar CA; et al. (2007). "Colistin is effective in treatment of infections caused by multidrug-resistant Pseudomonas aeruginosa in cancer patients". Antimicrob. Agents Chemother. 51 (6): 1905–11. doi:10.1128/AAC.01015-06. PMID 17387153.

See also

External links

cs:Pseudomonas aeruginosa de:Pseudomonas aeruginosa nl:Pseudomonas aeruginosa