P. aeruginosa on an XLD agar plate.
|ATCC 10145 |
Bacterium aeruginosum Schroeter 1872
Pseudomonas aeruginosa is a Gram-negative, aerobic, rod-shaped bacterium with unipolar motility. An opportunistic human pathogen, P. aeruginosa is also an opportunistic pathogen of plants. Based on 16S rRNA analysis, P. aeruginosa has been placed in the P. aeruginosa group.
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.
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 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. Pseudomonas can in rare circumstances cause community acquired pneumonias, as well as ventilator-associated pneumonias, being one of the most common agents isolated in several studies. 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 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). It is a powerful pathogen with Arabidopsis and with some animals: Caenorhabditis elegans, Drosophila, and Galleria mellonella. The associations of virulence factors are the same for vegetal and animal infections.
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:
- 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)
- 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.
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