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
(Schroeter 1872)
Migula 1900

Pseudomonas aeruginosa (also known as Pseudomonas pyocyanea) 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] The type strain is ATCC 10145.

Like other Pseudomonads, 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.[3]

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

[edit] The name

The word Pseudomonas means 'false unit', from the Greek pseudo, meaning 'false', and monas, meaning 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.

[edit] Pathogenesis

An opportunistic pathogen of immunocompromised individuals, P. aeruginosa typically infects the pulmonary tract, urinary tract, burns, wounds, and also causes other blood infections.[4] Pseudomonas can cause community acquired pneumonias albeit it is uncommon[5], as well as ventilator-associated pneumonias, being one of the most common agents isolated in several studies [6]. 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[7] One in ten hospital-acquired infections are from Pseudomonas. Cystic fibrosis patients are also predisposed to P. aeruginosa infection of the lungs. P. aeruginosa is also the typical 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.

With plants, P. aeruginosa induces symptoms of soft rot with Arabidopsis thaliana (Thale cress) and Letuca sativa (Lettuce) [8],[9]. It is a powerful pathogen with Arabidopsis[10] and with some animals: Caenorhabditis elegans[11],[12], Drosophila[13] and Galleria mellonella[14]. The associations of virulence factors are the same for vegetal and animal infections[8],[15].

Walker et al have demonstrated in 2001 that upon root colonization, P. aeruginosa forms a biofilm that confers resistance against root-secreted antibiotics. Pathogenic P. aeruginosa strains PAO1 and PA14 cause plant mortality 7 d postinoculation in Arabidopsis and sweet basil (Ocimum basilicum). P. aeruginosa forms the biofilm before mortality around the roots. Upon infection, sweet basil roots secrete rosmarinic acid, a multifunctional caffeic acid ester that exhibits in vitro antibacterial activity against planktonic cells of both P. aeruginosa strains with a minimum inhibitory concentration of 3 µg mL-1. However, in our studies rosmarinic acid did not attain minimum inhibitory concentration levels in sweet basil's root exudates before P. aeruginosa formed a biofilm that resisted the microbicidal effects of rosmarinic acid and ultimately caused plant mortality. Induction of rosmarinic acid secretion by supplying sweet basil roots and exogenous supplementation of Arabidopsis root exudates with rosmarinic acid before infection, conferred resistance to P. aeruginosa. Under the latter conditions and with a confocal scanning laser microscopy, large clusters of dead P. aeruginosa were seen on the root surface of Arabidopsis and sweet basil, and biofilm formation was not observed. Studies with quorum-sensing mutants PAO210 (rhlI), PAO214 (lasI), and PAO216 (lasI rhlI) demonstrated that all of the strains were pathogenic to Arabidopsis, which does not naturally secrete rosmarinic acid as a root exudate. However, PAO214 was the only pathogenic strain toward sweet basil, and PAO214 biofilm appeared comparable with biofilms formed by wild-type strains of P. aeruginosa.[10]

[edit] 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. 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.

[edit] References

  1. ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 0-8385-8529-9. 
  2. ^ Iglewski BH (1996). Pseudomonas. In: Baron's Medical Microbiology (Barron S et al, eds.), 4th ed., Univ of Texas Medical Branch. (via NCBI Bookshelf) ISBN 0-9631172-1-1. 
  3. ^ 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. 
  4. ^ Todar's Online Textbook of Bacteriology
  5. ^ Fine et al, JAMA 1996: 275: 134
  6. ^ Diekema DJ et al. Clin Infect Dis 1999;29:595
  7. ^ 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. 
  8. ^ a b Rahme, L., E. Stevens, S. Wolfort, J. Shao, R. Tompkins, and F. M. Ausubel. 1995. Common virulence factors for bacterial pathogenicity in plants and animals. Science 268:1899-1902
  9. ^ Rahme, L. G., M-W. Tan, L. Le, S. M. Wong, R. G. Tompkins, S. B. Calderwood, and F. M. Ausubel, 1997, Use of model plant hosts to identify Pseudomonas aeruginosa virulence factors. Proc. Natl. Acad. Sci. USA 94:13245-13250
  10. ^ a b Walker, T. S., H. P. Bais, E. Déziel, H. P. Schweizer, L. G. Rahme, R. Fall, and J. M. Vivanco. 2004. Pseudomonas aeruginosa-plant root interactions. Pathogenicity, biofilm formation, and root exudation. Plant Physiol. 134:320-331
  11. ^ Mahajan-Miklos, S., M. W. Tan, L. G. Rahme, and F. M. Ausubel. 1999. Molecular mechanisms of bacterial virulence elucidated using a Pseudomonas aeruginosa-Caenorhabdititis elegans pathogenesis model. Cell 96:47-56
  12. ^ Martinez, C., E. Pons, G. Prats, and J. Leon. 2004. Salicylic acid regulates flowering time and links defense responses and reproductive development. Plant J. 37:209-217
  13. ^ D'Argenio, D. A., L. A. Gallagher, C. A. Berg, and C. Manoil. 2001. Drosophila as a model host for Pseudomonas aeruginosa infection. J. Bacteriol. 183:1466-1471
  14. ^ Miyata, S., M. Casey, D. W. Frank, F. M. Ausubel, and E. Drenkard.,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. 71:2404-2413
  15. ^ Rahme, L. G., F. M. Ausubel, H. Cao, E. Drenkard, B. C. Goumnerov, G. W. Lau, S. Mahajan-Miklos, J. Plotnikova, M. W. Tan, J. Tsongalis, C. L. Walendziewicz, and R. G. Tompkins, 2000, Plants and animals share functionally common bacterial virulence factors. Proc. Natl. Acad. Sci. USA 97:8815-8821
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