Pseudomonas aeruginosa

Pseudomonas aeruginosais a commonencapsulated,Gram-negative,aerobic–facultatively anaerobic,rod-shapedbacteriumthat can causediseasein plants and animals, including humans.Aspeciesof considerable medical importance,P. aeruginosais amultidrug resistantpathogen recognized for its ubiquity, itsintrinsicallyadvancedantibiotic resistancemechanisms, and its association with serious illnesses –hospital-acquired infectionssuch asventilator-associated pneumoniaand varioussepsissyndromes.P. aeruginosais able to selectively inhibit various antibiotics from penetrating its outer membrane - and has high resistance to several antibiotics. According to theWorld Health OrganizationP. aeruginosaposes one of the greatest threats to humans in terms of antibiotic resistance.
The organism is consideredopportunisticinsofar as serious infection often occurs during existingdiseasesor conditions– most notablycystic fibrosisand traumatic burns. It generally affects theimmunocompromisedbut can also infect theimmunocompetentas inhot tub folliculitis. Treatment ofP. aeruginosainfections can be difficult due to its natural resistance to antibiotics. When more advanced antibiotic drug regimens are neededadverse effectsmay result.
It iscitrate,catalase, andoxidase positive. It is found in soil, water,skin flora, and most human-made environments throughout the world. As afacultative anaerobe,P. aeruginosathrives in diverse habitats. 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 generalizedinflammationandsepsis. If such colonizations occur in critical body organs, such as thelungs, theurinary tract, andkidneys, the results can be fatal.Because it thrives on moist surfaces, this bacterium is also found on and inmedical equipment, includingcatheters, causing cross-infectionsinhospitalsandclinics. It is also able to decompose hydrocarbons and has been used to break downtarballsand oil fromoil spills.P. aeruginosais not extremelyvirulentin comparison with other major species ofpathogenic bacteriasuch asGram-positiveStaphylococcus aureusandStreptococcus pyogenes– thoughP. aeruginosais capable of extensive colonization, and can aggregate into enduringbiofilms.
The wordPseudomonasmeans "false unit", from the Greekpseudēs(Greek: ψευδής, false) and (Latin:monas, fromGreek: μονάς, a single unit). The stem wordmonwas used early in the history ofmicrobiologyto refer tomicroorganismsandgerms, e.g., kingdomMonera.
The species nameaeruginosais a Latin word meaningverdigris("copper rust"), referring to the blue-green color of laboratory cultures of the species. This blue-green pigment is a combination of twosecondary metabolitesofP. aeruginosa,pyocyanin(blue) andpyoverdine(green), which impart the blue-green characteristic color of cultures.Another assertion from 1956 is thataeruginosamay be derived from the Greek prefixae-meaning "old or aged", and the suffixruginosameans wrinkled or bumpy.
The names pyocyanin and pyoverdine are from the Greek, withpyo-, meaning "pus",cyanin, meaning "blue",andverdine, meaning "green".Hence, the term "pyocyanic bacteria" refers specifically to the "blue pus" characteristic of aP. aeruginosainfection. Pyoverdine in the absence of pyocyanin is a fluorescent-yellow color.
ThegenomeofPseudomonas aeruginosaconsists of a relatively large circular chromosome (5.5–6.8Mb) that carries between 5,500 and 6,000open reading frames, and sometimesplasmidsof various sizes depending on the strain.Comparison of 389 genomes from differentP. aeruginosastrains showed that just 17.5% is shared. This part of the genome is theP. aeruginosacore genome.
A comparative genomic study (in 2020) analyzed 494 complete genomes from thePseudomonasgenus, of which 189 wereP. aeruginosastrains.The study observed that their protein count andGC contentranged between 5500 and 7352 (average: 6192) and between 65.6 and 66.9% (average: 66.1%), respectively.This comparative analysis further identified 1811 aeruginosa-core proteins, which accounts for more than 30% of the proteome. The higher percentage of aeruginosa-core proteins in this latter analysis could partly be attributed to the use of complete genomes. AlthoughP. aeruginosais a very well-defined monophyletic species, phylogenomically and in terms of ANIm values, it is surprisingly diverse in terms of protein content, thus revealing a very dynamic accessory proteome, in accordance with several analyses.It appears that, on average, industrial strains have the largest genomes, followed by environmental strains, and then clinical isolates.The same comparative study (494Pseudomonasstrains, of which 189 areP. aeruginosa) identified that 41 of the 1811P. aeruginosacore proteins were present only in this species and not in any other member of the genus, with 26 (of the 41) being annotated as hypothetical. Furthermore, another 19 orthologous protein groups are present in at least 188/189P. aeruginosastrains and absent in all the other strains of the genus.
The population ofP. aeruginosacan be classified in three main lineages, genetically characterised by the model strains PAO1, PA14, and the more divergent PA7.
WhileP. aeruginosais generally thought of as an opportunistic pathogen, several widespread clones appear to have become more specialised pathogens, particularly incystic fibrosispatients, including the Liverpool epidemic strain (LES) which is found mainly in the UK,DK2 in Denmark,and AUST-02 in Australia (also previously known as AES-2 and P2).There is also a clone that is frequently found infecting the reproductive tracts of horses.
P. aeruginosais afacultative anaerobe, as it is well adapted to proliferate in conditions of partial or total oxygen depletion. This organism can achieveanaerobicgrowth withnitrateornitriteas aterminal electron acceptor. When oxygen, nitrate, and nitrite are absent, it is able to fermentarginineandpyruvatebysubstrate-level phosphorylation.Additionally, phenazines produced byP. aeruginosacan act as electron shuttles to facilitate survival of cells at depth in biofilms.Adaptation tomicroaerobicor anaerobic environments is essential for certain lifestyles ofP. aeruginosa, for example, during lung infection incystic fibrosisandprimary ciliary dyskinesia, where thick layers of lungmucusand bacterially-producedalginatesurrounding mucoid bacterial cells can limit the diffusion of oxygen.P. aeruginosagrowth 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 fatal.
P. aeruginosarelies onironas anutrient sourceto grow. However, iron is not easily accessible because it is not commonly found in the environment. Iron is usually found in a largely insoluble ferric form.Furthermore, excessively high levels of iron can be toxic toP. aeruginosa. To overcome this and regulate proper intake of iron,P. aeruginosausessiderophores, 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 ofP. aeruginosa.
LigDsform a subfamily of theDNA ligases. These all have a LigDom/ligase domain, but many bacterial LigDs also have separatepolymerasedomains/PolDoms andnucleasedomains/NucDoms. InP. aeruginosa's case the nuclease domains areN-terminus, and the polymerase domains areC-terminus, extensions of the single central ligase domain.
Frequently acting as anopportunistic,nosocomialpathogen ofimmunocompromisedindividuals, but capable of infecting the immunocompetent,P. aeruginosatypically infects the airway,urinary tract,burns, andwounds, and also causes otherblood infections.
It is the most common cause of infections of burn injuries and of theouter ear(otitis externa), and is the most frequent colonizer of medical devices (e.g.,catheters).Pseudomonascan be spread by equipment that gets contaminated and is not properly cleaned or on the hands of healthcare workers.Pseudomonascan, in rare circumstances, causecommunity-acquired pneumonias,as well asventilator-associated pneumonias, being one of the most common agents isolated in several studies.Pyocyaninis avirulence factorof the bacteria and has been known to cause death inC. elegansbyoxidative stress. However,salicylic acidcan inhibit pyocyanin production.One in ten hospital-acquired infections is fromPseudomonas.Cystic fibrosispatients are also predisposed toP. aeruginosainfection of the lungs due to a functional loss in chloride ion movement across cell membranes as a result of amutation.P. aeruginosamay also be a common cause of "hot-tub rash" (dermatitis), caused by lack of proper, periodic attention to water quality. Since these bacteria thrive in moist environments, such as hot tubs and swimming pools, they can cause skin rash or swimmer's ear.Pseudomonasis also a common cause of postoperative infection inradial keratotomysurgery patients. The organism is also associated with the skin lesionecthyma gangrenosum.P. aeruginosais frequently associated withosteomyelitisinvolving puncture wounds of the foot, believed to result from direct inoculation withP. aeruginosavia the foam padding found in tennis shoes, with diabetic patients at a higher risk.
A comparative genomic analysis of 494 completePseudomonasgenomes, including 189 completeP. aeruginosagenomes, identified several proteins that are shared by the vast majority ofP. aeruginosastrains, but are not observed in other analyzedPseudomonasgenomes.These aeruginosa-specific core proteins, such asCntL, CntM, PlcB, Acp1, MucE, SrfA, Tse1, Tsi2, Tse3,andEsrCare known to play an important role in this species' pathogenicity.
P. aeruginosauses thevirulence factorexotoxin Ato inactivateeukaryotic elongation factor 2viaADP-ribosylationin the host cell, much as thediphtheria toxindoes. Without elongation factor2,eukaryotic cellscannot synthesizeproteinsand necrotise. The release of intracellular contents induces animmunologic responseinimmunocompetentpatients.
In additionP. aeruginosauses an exoenzyme, ExoU, which degrades the plasma membrane of eukaryotic cells, leading tolysis. Increasingly, it is becoming recognized that the iron-acquiringsiderophore,pyoverdine, also functions as a toxin by removingironfrommitochondria, inflicting damage on this organelle.Since pyoverdine is secreted into the environment, it can be easily detected by the host or predator, resulting the host/predator migration towards the bacteria.
Phenazinesare redox-active pigments produced byP. aeruginosa. These pigments are involved inquorum sensing,virulence, and iron acquisition.P. aeruginosaproduces several pigments all produced by a biosynthetic pathway: phenazine-1-carboxamide (PCA), 1-hydroxyphenazine, 5-methylphenazine-1-carboxylic acid betaine,pyocyaninand aeruginosin A. Two nearly identical operons are involved in phenazine biosynthesis:phzA1B1C1D1E1F1G1andphzA2B2C2D2E2F2G2.The enzymes encoded by these operons convertchorismic acidto PCA. The products of three key genes,phzH,phzM, andphzSthen convert PCA to the other phenazines mentioned above. Though phenazine biosynthesis is well studied, questions remain as to the final structure of the brownphenazinepyomelanin.
When pyocyanin biosynthesis is inhibited, a decrease inP. aeruginosapathogenicity is observedin vitro. This suggests that pyocyanin is mostly responsible for the initial colonization ofP. aeruginosain vivo.
With lowphosphatelevels,P. aeruginosahas 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.
In higher plants,P. aeruginosainducessoft rot, for example inArabidopsis thaliana(Thale cress)andLactuca sativa(lettuce).It is also pathogenic to invertebrate animals, including the nematodeCaenorhabditis elegans,the fruit flyDrosophila,and the mothGalleria mellonella.The associations of virulence factors are the same for plant and animal infections.In both insects and plants,P. aeruginosavirulenceis highlyquorum sensing(QS) dependent.Its QS is in turn highly dependent upon such genes asacyl-homoserine-lactone synthase, andlasI.
P. aeruginosais an opportunistic pathogen with the ability to coordinate gene expression in order to compete against other species for nutrients or colonization. Regulation ofgene expressioncan occur through cell-cell communication orquorum sensing(QS) via the production of small molecules calledautoinducersthat are released into the external environment. These signals, when reaching specific concentrations correlated with specific population cell densities, activate their respective regulators thus altering gene expression and coordinating behavior.P. aeruginosaemploys five interconnected QS systems– las, rhl, pqs, iqs, and pch– that each produce unique signaling molecules.The las and rhl systems are responsible for the activation of numerous QS-controlled genes, the pqs system is involved in quinolone signaling, and the iqs system plays an important role in intercellular communication.QS inP. aeruginosais organized in a hierarchical manner. At the top of the signaling hierarchy is the las system, since the las regulator initiates the QS regulatory system by activating the transcription of a number of other regulators, such as rhl. So, the las system defines a hierarchical QS cascade from the las to the rhl regulons.Detection of these molecules indicatesP. aeruginosais growing as biofilm within the lungs of cystic fibrosis patients.The impact of QS and especially las systems on the pathogenicity ofP. aeruginosais unclear, however. Studies have shown that lasR-deficient mutants are associated with more severe outcomes in cystic fibrosis patientsand are found in up to 63% of chronically infected cystic fibrosis patients despite impaired QS activity.
QS is known to control expression of a number ofvirulence factorsin a hierarchical manner, including the pigment pyocyanin. However, although the las system initiates the regulation of gene expression, its absence does not lead to loss of virulence factors. Recently, it has been demonstrated that the rhl system partially controls las-specific factors, such as proteolytic enzymes responsible for elastolytic and staphylolytic activities, but in a delayed manner. So, las is a direct and indirect regulator of QS-controlled genes.Another form ofgene regulationthat allows the bacteria to rapidly adapt to surrounding changes is through environmental signaling. Recent studies have discoveredanaerobiosiscan 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.Garlicexperimentally blocks quorum sensing inP. aeruginosa.
As in most Gram negative bacteria,P. aeruginosabiofilmformation is regulated by one single molecule:cyclic di-GMP. At low cyclic di-GMP concentration,P. aeruginosahas a free-swimming mode of life. But when cyclic di-GMP levels increase,P. aeruginosastart to establish sessile communities on surfaces. The intracellular concentration of cyclic di-GMP increases within seconds whenP. aeruginosatouches a surface (e.g.: a rock, plastic, host tissues...).This activates the production ofadhesive pili, that serve as "anchors" to stabilize the attachment ofP. aeruginosaon the surface. At later stages, bacteria will start attaching irreversibly by producing a strongly adhesive matrix. At the same time, cyclic di-GMP represses the synthesis of the flagellar machinery, preventingP. aeruginosafrom swimming. When suppressed, the biofilms are less adherent and easier to treat.
Thebiofilmmatrix ofP. aeruginosais composed of nucleic acids, amino acids, carbohydrates, and various ions. It mechanically and chemically protectsP. aeruginosafrom aggression by the immune system and some toxic compounds.P. aeruginosabiofilm's matrix is composed of up to three types of sugar polymers (or "exopolysacharides") named PSL, PEL, and alginate.Which exopolysacharides are produced varies by strain.
Upon certain cues or stresses,P. aeruginosarevert the biofilm program and detach. Recent studies have shown that the dispersed cells fromP. aeruginosabiofilms have lower cyclic di-GMP levels and different physiologies from those of planktonic and biofilm cells,with unique population dynamics and motility.Such dispersed cells are found to be highly virulent against macrophages andC. elegans, but highly sensitive towards iron stress, as compared with planktonic cells.
BiofilmsofP. aeruginosacan cause chronicopportunistic 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 traditionalantibiotictherapy. Biofilms serve to protect these bacteria from adverse environmental factors, including host immune system components in addition to antibiotics.P. aeruginosacan cause nosocomial infections and is considered amodel organismfor 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 asP. aeruginosa. This should contribute to better clinical management of chronically infected patients, and should lead to the development of new drugs.
Scientists have been examining the possible genetic basis forP. aeruginosaresistance to antibiotics such astobramycin. Onelocusidentified as being an important genetic determinant of the resistance in this species isndvB, which encodesperiplasmicglucansthat 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.
Depending on the nature of infection, an appropriate specimen is collected and sent to abacteriologylaboratory for identification. As with most bacteriological specimens, aGram stainis performed, which may show Gram-negative rods and/orwhite blood cells.P. aeruginosaproduces colonies with a characteristic "grape-like" or "fresh-tortilla" odor on bacteriological media. In mixed cultures, it can be isolated as clear colonies onMacConkey agar(as it does not fermentlactose) which will test positive foroxidase. Confirmatory tests include production of the blue-green pigment pyocyanin oncetrimide agarand growth at 42 °C. ATSI slantis often used to distinguish nonfermentingPseudomonasspecies from enteric pathogens in faecal specimens.
WhenP. aeruginosais isolated from a normally sterile site (blood, bone, deep collections), it is generally considered dangerous, and almost always requires treatment.However,P. aeruginosais frequently isolated from nonsterile sites (mouth swabs,sputum, etc.), and, under these circumstances, it may represent colonization and not infection. The isolation ofP. aeruginosafrom nonsterile specimens should, therefore, be interpreted cautiously, and the advice of amicrobiologistor infectious diseases physician/pharmacist should be sought prior to starting treatment. Often, no treatment is needed.
Morphological, physiological, and biochemical characteristics ofPseudomonas aeruginosaare shown in the Table below.
Note: + = Positive, - =Negative
P. aeruginosais a Gram-negative,aerobic(and at timesfacultatively anaerobic), rod-shaped bacterium withunipolar motility.It has been identified as anopportunistic pathogenof both humans and plants.P. aeruginosais thetype speciesof the genusPseudomonas.
Identification ofP. aeruginosacan be complicated by the fact individual isolates often lack motility. The colony morphology itself also displays several varieties. The main two types are large, smooth, with a flat edge and elevated center and small, rough, and convex.A third type, mucoid, can also be found. The large colony can typically be found in clinal settings while the small is found in nature.The third, however, is present in biological settings and has been found in respiratory and in the urinary tract.Furthermore, mutations in the gene lasR drastically alter colony morphology and typically lead to failure to hydrolyze gelatin or hemolyze.
In certain conditions,P. aeruginosacan secrete a variety of pigments, includingpyocyanin(blue),pyoverdine(yellow andfluorescent), pyorubin (red), and pyomelanin (brown). These can be used to identify the organism.
Clinical identification ofP. aeruginosamay include identifying the production of both pyocyanin and fluorescein, as well as its ability to grow at 42 °C.P. aeruginosais capable of growth indieselandjet fuels, where it is known as ahydrocarbon-usingmicroorganism, causingmicrobial corrosion.It creates dark, gellish mats sometimes improperly called "algae" because of their appearance.
ManyP. aeruginosaisolates areresistantto 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 antibioticempirically. If antibiotics are started empirically, then every effort should be made to obtain cultures (before administering the first dose of antibiotic), and the choice of antibiotic used should be reviewed when the culture results are available.
Due to widespread resistance to many common first-line antibiotics,carbapenems,polymyxins, and more recentlytigecyclinewere 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-resistantP. aeruginosa. Some next-generation antibiotics that are reported as being active againstP. aeruginosainclude doripenem, ceftobiprole, and ceftaroline. However, these require more clinical trials for standardization. Therefore, research for the discovery of new antibiotics and drugs againstP. aeruginosais very much needed.
Antibiotics that may have activity againstP. aeruginosainclude:
As fluoroquinolones are one of the few antibiotic classes widely effective againstP. aeruginosa, in some hospitals, their 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),topicalgentamicinorcolistinmay be used.
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 ofP. aeruginosais its low antibiotic susceptibility, which is attributable to a concerted action of multidrugefflux pumpswith chromosomally encoded antibiotic resistance genes, i.e., the genes that encode proteins that serve asenzymesto break down antibiotics. Examples of such genes are:
Specific genes and enzymes involved in antibiotic resistance can vary between different strains.P.aeruginosaTG523 harbored genes predicted to have antibacterial activity and those which are implicated in virulence.
Another feature that contributes to antibiotic resistance ofP. aeruginosais the low permeability of the bacterial cellular envelopes.In addition to this intrinsic resistance,P. aeruginosaeasily develops acquired resistance either bymutationin chromosomally encoded genes or by thehorizontal gene transferof antibiotic resistance determinants. Development ofmultidrug resistancebyP. aeruginosaisolates 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 inP. aeruginosastrains producing chronic infections, whereas the clustering of several different antibiotic resistance genes inintegronsfavors the concerted acquisition of antibiotic resistance determinants. Some recent studies have shown phenotypic resistance associated tobiofilmformation or to the emergence of small-colony variants may be important in the response ofP. aeruginosapopulations to antibiotic 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, and VEB-1, AmpC cephalosporinases, carbapenemases like serine oxacillinases, metallo-b-lactamases, OXA-type carbapenemases, and aminoglycoside-modifying enzymes, among others, have been reported.P. aeruginosacan 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. aeruginosahas also been reported to possess multidrug efflux pumps systems that confer resistance against a number of antibiotic classes, and the MexAB-OprM (Resistance-nodulation-division(RND) family)is considered as the most important.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.
Mutations inDNA gyraseare commonly associated with antibiotic resistance inP. 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. WhenP. aeruginosais grown underin vitroconditions designed to mimic a cystic fibrosis patient's lungs, these genes mutate repeatedly.
Twosmall RNAs,Sr0161andErsA, were shown to interact with mRNA encoding the major porin OprD responsible for the uptake ofcarbapenem antibioticsinto theperiplasm. The sRNAs bind to the 5'UTR ofoprD, causing increase in bacterial resistance tomeropenem. Another sRNA,Sr006, may 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, similar to a process found inSalmonella,Sr006 regulation of PagL expression may aid inpolymyxin Bresistance.
Probiotic prophylaxis may prevent colonization and delay onset ofPseudomonasinfection in an ICU setting.Immunoprophylaxis againstPseudomonasis being investigated.The risk of contractingP. aeruginosacan 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 againstP. aeruginosa,given how common the organism is in the environment.
Phage therapyagainstP. aeruginosahas 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 byP. aeruginosawas reported in the journalClinical Otolaryngologyin August 2009.As of 2024,research on the topic is ongoing.
In 2013, João Xavier described an experiment in whichP. 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 multipleflagella, whereas the baseline organism has a single flagellum.This result was notable in the field ofexperimental evolutionin that it was highly repeatable.P. aeruginosahas been studied for use inbioremediationand use in processingpolyethyleneinmunicipal solid waste.
Research on this bacterium'ssystems biologyled to the development of genome-scale metabolic models that enable computer simulation and prediction of bacterial growth rates under varying conditions, including its virulence properties.
As of 2019theEast African CommunityconsidersP. aeruginosato be aquarantine concernbecause of the presence ofPhaseolus vulgaris–pathogenic strains ofP. aeruginosainKenyafor the rest of the area. Apest risk analysisby the EAC was based on this bacterium'sCABI's Crop Protection Compendium listing, following Kaaya & Darji 1989's initial detection in Kenya.
A small number of infections in the United States in 2022 and 2023 were likely caused by poorly manufactured eyedrops.