Pseudomonas aeruginosa is a common Gram-negative, rod-shaped bacterium
that can cause disease in plants and animals, including humans. A
species of considerable medical importance, P. aeruginosa is a
multidrug resistant pathogen recognized for its ubiquity, its
intrinsically advanced antibiotic resistance mechanisms, and its
association with serious illnesses – hospital-acquired infections
such as ventilator-associated pneumonia and various sepsis syndromes.
The organism is considered opportunistic insofar as serious infection
often occurs during existing diseases or conditions – most notably
cystic fibrosis and traumatic burns. It is also found generally in the
immunocompromised but can infect the immunocompetent as in hot tub
folliculitis. Treatment of P. aeruginosa infections can be difficult
due to its natural resistance to antibiotics. When more advanced
antibiotic drug regimens are needed adverse effects may result.
It is citrate, catalase, and oxidase positive. It is found in soil,
water, skin flora, and most man-made environments throughout the
world. It thrives not only in normal atmospheres, but also in
low-oxygen atmospheres, thus has colonized many natural and artificial
environments. It uses a wide range of organic material for food; in
animals, its versatility enables the organism to infect damaged
tissues or those with reduced immunity. The symptoms of such
infections are generalized inflammation and sepsis. If such
colonizations occur in critical body organs, such as the lungs, the
urinary tract, and kidneys, the results can be fatal. Because it
thrives on moist surfaces, this bacterium is also found on and in
medical equipment, including catheters, causing cross-infections in
hospitals and clinics. It is also able to decompose hydrocarbons and
has been used to break down tarballs and oil from oil spills. P.
aeruginosa is not extremely virulent in comparison with other major
pathogenic bacterial species – for example
Staphylococcus aureus and
Streptococcus pyogenes – though P. aeruginosa is capable of
extensive colonization, and can aggregate into enduring biofilms.
2.3 Cellular cooperation
3.4 Plants and invertebrates
3.5 Quorum sensing
3.6 Biofilms and treatment resistance
5.3 Experimental therapies
7 See also
A culture dish with Pseudomonas
Pseudomonas means "false unit", from the Greek pseudo (Greek:
ψευδο, false) and (Latin: monas, from Greek: μονος, a single
unit). The stem word mon was used early in the history of microbiology
to refer to germs, e.g., kingdom Monera.
The species name aeruginosa is a Latin word meaning verdigris ("copper
rust"), referring to the blue-green color of laboratory cultures of
the species. This blue-green pigment is a combination of two
metabolites of P. aeruginosa, pyocyanin (blue) and pyoverdine (green),
which impart the blue-green characteristic color of cultures. Another
assertion is that the word may be derived from the Greek prefix ae-
meaning "old or aged", and the suffix ruginosa means wrinkled or
The names pyocyanin and pyoverdine are from the Greek, with pyo-,
meaning "pus", cyanin, meaning "blue", and verdine, meaning
Pyoverdine in the absence of pyocyanin is a
Gram-stained P. aeruginosa bacteria (pink-red rods)
The genome of P. aeruginosa is relatively large (5.5–6.8 Mb) and
encodes between 5,500 and 6,000 open reading frames, depending on the
strain; Comparison of 389 genomes from different P. aeruginosa
strains showed that just 17.5% is shared. This part of the genome is
the P. aeruginosa core genome.
genome size (bp)
P. aeruginosa is a facultative anaerobe, as it is well adapted to
proliferate in conditions of partial or total oxygen depletion. This
organism can achieve anaerobic growth with nitrate or nitrite as a
terminal electron acceptor. When oxygen, nitrate, and nitrite are
absent, it is able to ferment arginine and pyruvate by substrate-level
phosphorylation. Adaptation to microaerobic or anaerobic
environments is essential for certain lifestyles of P. aeruginosa, for
example, during lung infection in cystic fibrosis and primary ciliary
dyskinesia, where thick layers of lung mucus and alginate surrounding
mucoid bacterial cells can limit the diffusion of oxygen. P.
aeruginosa growth within the human body can be asymptomatic until the
bacteria form a biofilm, which overwhelms the immune system. These
biofilms are found in the lungs of people with cystic fibrosis and
primary ciliary dyskinesia, and can prove
P. aeruginosa relies on iron as a nutrient source to grow. However,
iron is not easily accessible because it is not commonly found in the
Iron is usually found in a largely insoluble ferric
form. Furthermore, excessively high levels of iron can be toxic to
P. aeruginosa. To overcome this and regulate proper intake of iron, P.
aeruginosa uses siderophores, which are secreted molecules that bind
and transport iron. These iron-siderophore complexes, however, are
not specific. The bacterium that produced the siderophores does not
necessarily receive the direct benefit of iron intake. Rather, all
members of the cellular population are equally likely to access the
iron-siderophore complexes. Members of the cellular population that
can efficiently produce these siderophores are commonly referred to as
cooperators; members that produce little to no siderophores are often
referred to as cheaters. Research has shown when cooperators and
cheaters are grown together, cooperators have a decrease in fitness,
while cheaters have an increase in fitness. The magnitude of
change in fitness increases with increasing iron limitation. With
an increase in fitness, the cheaters can outcompete the cooperators;
this leads to an overall decrease in fitness of the group, due to lack
of sufficient siderophore production. These observations suggest that
having a mix of cooperators and cheaters can reduce the virulent
nature of P. aeruginosa.
Phagocytosis of P. aeruginosa by neutrophil in patient with
bloodstream infection (Gram stain)
An opportunistic, nosocomial pathogen of immunocompromised
individuals, P. aeruginosa typically infects the airway, urinary
tract, burns, and wounds, and also causes other blood infections.
Details and common associations
Cystic fibrosis patients
Associated with a purple-black skin lesion ecthyma gangrenosum
Urinary tract infection
Urinary tract catheterization
Premature infants and neutropenic cancer patients
Skin and soft tissue infections
Hemorrhage and necrosis
People with burns or wound infections
It is the most common cause of infections of burn injuries and of the
outer ear (otitis externa), and is the most frequent colonizer of
medical devices (e.g., catheters).
Pseudomonas can be spread by
equipment that gets contaminated and is not properly cleaned or on the
hands of healthcare workers.
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, salicylic acid can inhibit pyocyanin
production. One in ten hospital-acquired infections is from
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. Since these bacteria like moist
environments, such as hot tubs and swimming pools, they can cause skin
rash or swimmer's ear.
Pseudomonas is also a common cause of
postoperative infection in radial keratotomy surgery patients. The
organism is also associated with the skin lesion ecthyma gangrenosum.
P. aeruginosa is frequently associated with osteomyelitis involving
puncture wounds of the foot, believed to result from direct
inoculation with P. aeruginosa via the foam padding found in tennis
shoes, with diabetic patients at a higher risk.
P. aeruginosa uses the virulence factor exotoxin A to inactivate
eukaryotic elongation factor 2 via
ADP-ribosylation in the host cell,
much as the diphtheria toxin does. Without elongation factor 2,
eukaryotic cells cannot synthesize proteins and necrotise. The release
of intracellular contents induces an immunologic response in
immunocompetent patients. In addition P. aeruginosa uses an exoenzyme,
ExoU, which degrades the plasma membrane of eukaryotic cells, leading
to lysis. Increasingly, it is becoming recognized that the
iron-acquiring siderophore, pyoverdine, also functions as a toxin by
removing iron from mitochondria, inflicting damage on this
Phenazines are redox-active pigments produced by P. aeruginosa. These
pigments are involved in quorum sensing, virulence, and iron
acquisition. P. aeruginosa produces several pigments all produced
by a biosynthetic pathway: pyocyanin, 1-hydroxyphenazine,
phenazine-1-carboxamide, 5-methylphenazine-1-carboxylic acid betaine,
and aeruginosin A. Two operons are involved in phenazine biosynthesis:
phzA1B1C1D1E1F1G1 and phzA2B2C2D2E2F2G2. These operons convert
a chorismic acid to the phenazines mentioned above. Three key genes,
phzH, phzM, and phzS convert phenazine-1-carboxylic acid to the
phenazines mentioned above. Though phenazine biosynthesis is well
studied, questions remain as to the final structure of the brown
When pyocyanin biosynthesis is inhibited, a decrease in P. aeruginosa
pathogenicity is observed in vitro. This suggests that pyocyanin
is most responsible for the initial colonization of P. aeruginosa in
With low phosphate levels, P. aeruginosa has been found to activate
from benign symbiont to express lethal toxins inside the intestinal
tract and severely damage or kill the host, which can be mitigated by
providing excess phosphate instead of antibiotics.
Plants and invertebrates
In higher plants, P. aeruginosa induces soft rot, for example in
Arabidopsis thaliana (Thale cress) and Lactuca sativa
(lettuce). It is also pathogenic to invertebrate animals,
including the nematode Caenorhabditis elegans, the fruit fly
Drosophila and the moth Galleria mellonella. The associations
of virulence factors are the same for plant and animal
Regulation of gene expression can occur through cell-cell
communication or quorum sensing (QS) via the production of small
molecules called autoinducers. The extracellular accumulation of these
molecules signals to bacteria to alter gene expression and coordinate
behavior. P. aeruginosa employs three interconnected QS systems –
lasRl, rhlRl, and PQS – that each produce unique signaling
molecules. Detection of these molecules indicates P. aeruginosa is
growing as biofilm within the lungs of cystic fibrosis patients.
QS is known to control expression of a number of virulence factors,
including the pigment pyocyanin. Another form of gene regulation that
allows the bacteria to rapidly adapt to surrounding changes is through
environmental signaling. Recent studies have discovered anaerobiosis
can significantly impact the major regulatory circuit of QS. This
important link between QS and anaerobiosis has a significant impact on
production of virulence factors of this organism. Garlic
experimentally blocks quorum sensing in P. aeruginosa.
Biofilms and treatment resistance
Biofilms of P. aeruginosa can cause chronic opportunistic infections,
which are a serious problem for medical care in industrialized
societies, especially for immunocompromised patients and the elderly.
They often cannot be treated effectively with traditional antibiotic
therapy. Biofilms seem to protect these bacteria from adverse
environmental factors. P. aeruginosa can cause nosocomial infections
and is considered a model organism for the study of
antibiotic-resistant bacteria. Researchers consider it important to
learn more about the molecular mechanisms that cause the switch from
planktonic growth to a biofilm phenotype and about the role of QS in
treatment-resistant bacteria such as P. aeruginosa. This should
contribute to better clinical management of chronically infected
patients, and should lead to the development of new drugs.
Many genes and factors affect biofilm formation in P. aeruginosa. One
of the main gene operons responsible for the initiation and
maintaining the biofilm is the PSL operon. This 15-gene operon is
responsible for the cell-cell and cell-surface interactions required
for cell communication. It is also responsible for the sequestering of
the extracellular polymeric substance matrix. This matrix is composed
of nucleic acids, amino acids, carbohydrates, and various ions. This
matrix is one of the main resistance mechanisms in the biofilms of P.
Cyclic di-GMP is a major contributor to biofilm adherent properties.
This signalling molecule in high quantities makes superadherent
biofilms. When suppressed, the biofilms are less adherent and easier
to treat. Polysaccharide synthesis locus (PSL) and cdi-GMP form a
positive feedback loop. PSL stimulates cdi-GMP production, while high
cd-GMP turns on the operon and increases activity of the operon.
Recent studies have shown that the dispersed cells from P. aeruginosa
biofilms have lower c-di-GMP levels and different physiologies from
those of planktonic and biofilm cells. Such dispersed cells
are found to be highly virulent against macrophages and C. elegans,
but highly sensitive towards iron stress, as compared with planktonic
Recently, scientists have been examining the possible genetic basis
for P. aeruginosa resistance to antibiotics such as tobramycin. One
locus identified as being an important genetic determinant of the
resistance in this species is ndvB, which encodes periplasmic glucans
that may interact with antibiotics and cause them to become
sequestered into the periplasm. These results suggest a genetic basis
exists behind bacterial antibiotic resistance, rather than the biofilm
simply acting as a diffusion barrier to the antibiotic.
Production of pyocyanin, water-soluble green pigment of P. aeruginosa
Depending on the nature of infection, an appropriate specimen is
collected and sent to a bacteriology laboratory for identification. As
with most bacteriological specimens, a
Gram stain is performed, which
may show Gram-negative rods and/or white blood cells. P. aeruginosa
produces colonies with a characteristic "grape-like" or
"fresh-tortilla" odor on bacteriological media. In mixed cultures, it
can be isolated as clear colonies on
MacConkey agar (as it does not
ferment lactose) which will test positive for oxidase. Confirmatory
tests include production of the blue-green pigment pyocyanin on
cetrimide agar and growth at 42 °C. A
TSI slant is often used to
Pseudomonas species from enteric pathogens
in faecal specimens.
When P. aeruginosa is isolated from a normally sterile site (blood,
bone, deep collections), it is generally considered dangerous, and
almost always requires treatment. However, P.
aeruginosa is frequently isolated from nonsterile sites (mouth swabs,
sputum, etc.), and, under these circumstances, it may represent
colonization and not infection. The isolation of P. aeruginosa from
nonsterile specimens should, therefore, be interpreted cautiously, and
the advice of a microbiologist or infectious diseases
physician/pharmacist should be sought prior to starting treatment.
Often, no treatment is needed.
Hydrogen Sulfide Production
Acid from lactose
acid from glucose
acid from maltose
acid from mannitol
acid from sucrose
+ (bluish green pigmentation)
P. aeruginosa is a Gram-negative, aerobic (and at times
facultatively anaerobic), bacillus with unipolar motility. It has
been identified as an opportunistic pathogen of both humans and
plants. P. aeruginosa is the type species of the genus
In certain conditions, P. aeruginosa can secrete a variety of
pigments, including pyocyanin (blue-green), pyoverdine (yellow-green
and fluorescent), and pyorubin (red-brown). These can be used to
identify the organism.
Pseudomonas aeruginosa fluorescence under UV illumination
P. aeruginosa is often preliminarily identified by its pearlescent
appearance and grape-like or tortilla-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 fuels, where it is known as a hydrocarbon-using
microorganism, causing microbial corrosion. It creates dark,
gellish mats sometimes improperly called "algae" because of their
Many P. aeruginosa isolates are resistant to a large range of
antibiotics and may demonstrate additional resistance after
unsuccessful treatment. 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 (before
administering first dose of antibiotic), and the choice of antibiotic
used should be reviewed when the culture results are available.
The antibiogram of P. aeruginosa on Mueller-Hinton agar
Due to widespread resistance to many common first-line antibiotics,
carbapenems, polymyxins, and more recently tigecycline were considered
to be the drugs of choice; however, resistance to these drugs has also
been reported. Despite this, they are still being used in areas where
resistance has not yet been reported. Use of β-lactamase inhibitors
such as sulbactam has been advised in combination with antibiotics to
enhance antimicrobial action even in the presence of a certain level
of resistance. Combination therapy after rigorous antimicrobial
susceptibility testing has been found to be the best course of action
in the treatment of multidrug-resistant P. aeruginosa. Some
next-generation antibiotics that are reported as being active against
P. aeruginosa include doripenem, ceftobiprole, and ceftaroline.
However, these require more clinical trials for standardization.
Therefore, research for the discovery of new antibiotics and drugs
against P. aeruginosa is very much needed. Antibiotics that may have
activity against P. aeruginosa include:
aminoglycosides (gentamicin, amikacin, tobramycin, but not kanamycin)
quinolones (ciprofloxacin, levofloxacin, but not moxifloxacin)
cephalosporins (ceftazidime, cefepime, cefoperazone, cefpirome,
ceftobiprole, but not cefuroxime, cefotaxime, or ceftriaxone)
antipseudomonal penicillins: carboxypenicillins (carbenicillin and
ticarcillin), and ureidopenicillins (mezlocillin, azlocillin, and
piperacillin). P. aeruginosa is intrinsically resistant to all other
carbapenems (meropenem, imipenem, doripenem, but not ertapenem)
polymyxins (polymyxin B and colistin)
As fluoroquinolone is one of the few antibiotics widely effective
against P. aeruginosa, in some hospitals, its use is severely
restricted to avoid the development of resistant strains. On the rare
occasions where infection is superficial and limited (for example, ear
infections or nail infections), topical gentamicin or colistin may be
For pseudomonal wound infections, acetic acid with concentrations from
0.5% to 5% can be an effective bacteriostatic agent in eliminating the
bacteria from the wound. Usually a sterile gauze soaked with acetic
acid is placed on the wound after irrigation with normal saline.
Dressing would be done once per day.
Pseudomonas is usually eliminated
in 90% of the cases after 10 to 14 days of treatment.
One of the most worrisome characteristics of P. aeruginosa is its low
antibiotic susceptibility, which is attributable to a concerted action
of multidrug efflux pumps with chromosomally encoded antibiotic
resistance genes (e.g., mexAB, mexXY, etc.) and the low permeability
of the bacterial cellular envelopes. In addition to this intrinsic
resistance, P. aeruginosa easily develops acquired resistance either
by mutation in chromosomally encoded genes or by the horizontal gene
transfer of antibiotic resistance determinants. Development of
multidrug resistance by P. aeruginosa isolates requires several
different genetic events, including acquisition of different mutations
and/or horizontal transfer of antibiotic resistance genes.
Hypermutation favours the selection of mutation-driven antibiotic
resistance in P. aeruginosa strains producing chronic infections,
whereas the clustering of several different antibiotic resistance
genes in integrons favors the concerted acquisition of antibiotic
resistance determinants. Some recent studies have shown phenotypic
resistance associated to biofilm formation or to the emergence of
small-colony variants may be important in the response of P.
aeruginosa populations to antibiotics treatment.
Mechanisms underlying antibiotic resistance have been found to include
production of antibiotic-degrading or antibiotic-inactivating enzymes,
outer membrane proteins to evict the antibiotics and mutations to
change antibiotic targets. Presence of antibiotic-degrading enzymes
such as extended-spectrum β-lactamases like PER-1, PER-2, VEB-1, AmpC
cephalosporinases, carbapenemases like serine oxacillinases,
metallo-b-lactamases, OXA-type carbapenemases,
aminoglycoside-modifying enzymes, among others have been reported. P.
aeruginosa can also modify the targets of antibiotic action, for
example methylation of 16S rRNA to prevent aminoglycoside binding and
modification of DNA, or topoisomerase to protect it from the action of
quinolones. P. aeruginosa has also been reported to possess multidrug
efflux pumps like AdeABC and AdeDE efflux systems that confer
resistance against number of antibiotic classes. An important factor
found to be associated with antibiotic resistance is the decrease in
the virulence capabilities of the resistant strain. Such findings have
been reported in the case of rifampicin-resistant and
colistin-resistant strains, in which decrease in infective ability,
quorum sensing and motility have been documented.
DNA gyrase are commonly associated with antibiotic
resistance in P. aeruginosa. These mutations, when combined with
others, confer high resistance without hindering survival.
Additionally, genes involved in cyclic-di-GMP signaling may contribute
to resistance. When grown in vitro conditions designed to mimic a
cystic fibrosis patient's lungs, these genes mutate repeatedly.
Two small RNAs : Sr0161 and ErsA were shown to interact with mRNA
encoding the major porin OprD responsible for the uptake of carbapenem
antibiotics into the periplasm. The sRNAs bind to the 5'UTR of oprD
causing increase in bacterial resistance to meropenem. Another sRNA:
Sr006 was suggested to positively regulate (post-transcriptionally)
the expression of PagL, an enzyme responsible for deacylation of lipid
A. This reduces the pro-inflammatory property of lipid A. 
Furthermore, similarly to study in Salmonella  Sr006 regulation of
PagL expression was suggested to aid in polymyxin B resistance. 
Probiotic prophylaxis may prevent colonization and delay onset of
Pseudomonas infection in an ICU setting. Immunoprophylaxis against
Pseudomonas is being investigated. The risk of contracting P.
aeruginosa can be reduced by avoiding pools, hot tubs, and other
bodies of standing water; regularly disinfecting and/or replacing
equipment that regularly encounters moisture (such as contact lens
equipment and solutions); and washing one's hands often (which is
protective against many other pathogens as well). However, even the
best hygiene practices cannot totally protect an individual against P.
aeruginosa, given how common P. aeruginosa is in the environment.
Phage therapy against P. aeruginosa has been investigated as a
possible effective treatment, which can be combined with antibiotics,
has no contraindications and minimal adverse effects. Phages are
produced as sterile liquid, suitable for intake, applications etc.
Phage therapy against ear infections caused by P. aeruginosa was
reported in the journal Clinical Otolaryngology in August 2009.
Last 2013, João Xavier described an experiment in which P.
aeruginosa, when subjected to repeated rounds of conditions in which
it needed to swarm to acquire food, developed the ability to
"hyperswarm" at speeds 25% faster than baseline organisms, by
developing multiple flagella, whereas the baseline organism has a
single flagellum. This result was notable in the field of
experimental evolution in that it was highly repeatable.
P. aeruginosa has been studied for use in bioremediation and use in
processing polyethylene in municipal solid waste.
Wikimedia Commons has media related to
Bacteriological water analysis
NrsZ small RNA
AsponA antisense RNA
Repression of heat shock gene expression (ROSE) element
Pseudomon-1 RNA motif
Pseudomon-1 RNA motif (ErsA sRNA)
Pseudomonas sRNA P16 (RgsA sRNA)
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Bacterial disease: Proteobacterial G−
primarily A00–A79, 001–041, 080–109
Epidemic typhus, Brill–Zinsser disease, Flying squirrel typhus
Rocky Mountain spotted fever
Japanese spotted fever
North Asian tick typhus
Queensland tick typhus
Flinders Island spotted fever
African tick bite fever
American tick bite fever
Rickettsia aeschlimannii infection
Flea-borne spotted fever
Ehrlichiosis: Anaplasma phagocytophilum
Human granulocytic anaplasmosis, Anaplasmosis
Human monocytotropic ehrlichiosis
Ehrlichiosis ewingii infection
Bartonellosis: Bartonella henselae
Either B. henselae or B. quintana
Carrion's disease, Verruga peruana
Meningococcal disease, Waterhouse–Friderichsen syndrome,
Eikenella corrodens/Kingella kingae
Burkholderia cepacia complex
Bordetella pertussis/Bordetella parapertussis
Rhinoscleroma, Klebsiella pneumonia
Escherichia coli: Enterotoxigenic
Enterobacter aerogenes/Enterobacter cloacae
Citrobacter koseri/Citrobacter freundii
Typhoid fever, Paratyphoid fever, Salmonellosis
Shigellosis, Bacillary dysentery
Proteus mirabilis/Proteus vulgaris
Far East scarlet-like fever
Brazilian purpuric fever
Legionella pneumophila/Legionella longbeachae
Aeromonas hydrophila/Aeromonas veronii
Campylobacteriosis, Guillain–Barré syndrome
Peptic ulcer, MALT lymphoma, Gastric cancer