Pseudomonas aeruginosa
Pseudomonas aeruginosa | |
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P. aeruginosa colonies on blood agar
| |
Scientific classification | |
Domain: | Bacteria |
Phylum: | Pseudomonadota |
Class: | Gammaproteobacteria |
Order: | Pseudomonadales |
Family: | Pseudomonadaceae |
Genus: | Pseudomonas |
Species: | P. aeruginosa
|
Binomial name | |
Pseudomonas aeruginosa (Schröter 1872)
Migula 1900 | |
Synonyms | |
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Pseudomonas aeruginosa is a common
The organism is considered
It is
Nomenclature
The word Pseudomonas means "false unit", from the Greek pseudēs (
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.[7] Another assertion from 1956 is that aeruginosa may be derived from the Greek prefix ae- meaning "old or aged", and the suffix ruginosa means wrinkled or bumpy.[8]
The names pyocyanin and pyoverdine are from the Greek, with pyo-, meaning "pus",[9] cyanin, meaning "blue",[10] and verdine, meaning "green".[citation needed] Hence, the term "pyocyanic bacteria" refers specifically to the "blue pus" characteristic of a P. aeruginosa infection. Pyoverdine in the absence of pyocyanin is a fluorescent-yellow color.[citation needed]
Biology
Genome
The genome of Pseudomonas aeruginosa consists of a relatively large circular chromosome (5.5–6.8 Mb) that carries between 5,500 and 6,000 open reading frames, and sometimes plasmids of various sizes depending on the strain.[11] 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.[12]
strain: | VRFPA04 | C3719 | PAO1 | PA14 | PACS2 |
---|---|---|---|---|---|
Chromosome size (bp) | 6,818,030 | 6,222,097 | 6,264,404 | 6,537,648 | 6,492,423 |
ORFs | 5,939 | 5,578 | 5,571 | 5,905 | 5,676 |
A comparative genomic study (in 2020) analyzed 494 complete genomes from the Pseudomonas genus, of which 189 were P. aeruginosa strains.
Population structure
The population of P. aeruginosa can be classified in three main lineages, genetically characterised by the model strains PAO1, PA14, and the more divergent PA7.[18]
While P. aeruginosa is generally thought of as an opportunistic pathogen, several widespread clones appear to have become more specialised pathogens, particularly in cystic fibrosis patients, including the Liverpool epidemic strain (LES) which is found mainly in the UK,[19] DK2 in Denmark,[20] and AUST-02 in Australia (also previously known as AES-2 and P2).[21] There is also a clone that is frequently found infecting the reproductive tracts of horses.[22][23]
Metabolism
P. aeruginosa is a
Cellular cooperation
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 environment. Iron is usually found in a largely insoluble ferric form.[31] 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.[32] 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.[33] The magnitude of change in fitness increases with increasing iron limitation.[34] 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.[33]
Enzymes
LigDs form a subfamily of the DNA ligases. These all have a LigDom/ligase domain, but many bacterial LigDs also have separate polymerase domains/PolDoms and nuclease domains/NucDoms. In P. aeruginosa's case the nuclease domains are N-terminus, and the polymerase domains are C-terminus, extensions of the single central ligase domain.[35]
Pathogenesis
This section needs additional citations for verification. (February 2021) |
An
Infections | Details and common associations | High-risk groups |
---|---|---|
Pneumonia | Diffuse bronchopneumonia | Cystic fibrosis, non-CF bronchiectasis patients |
Septic shock | Associated with a purple-black skin lesion ecthyma gangrenosum | Neutropenic patients |
Urinary tract infection | Urinary tract catheterization | |
Gastrointestinal infection | Necrotising enterocolitis
|
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
A comparative genomic analysis of 494 complete Pseudomonas genomes, including 189 complete P. aeruginosa genomes, identified several proteins that are shared by the vast majority of P. aeruginosa strains, but are not observed in other analyzed Pseudomonas genomes.[13] These aeruginosa-specific core proteins, such as CntL, CntM, PlcB, Acp1, MucE, SrfA, Tse1, Tsi2, Tse3, and EsrC are known to play an important role in this species' pathogenicity.[13]
Toxins
P. aeruginosa uses the
Phenazines
When pyocyanin biosynthesis is inhibited, a decrease in P. aeruginosa pathogenicity is observed in vitro. This suggests that pyocyanin is mostly responsible for the initial colonization of P. aeruginosa in vivo.[48]
Triggers
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.[49]
Plants and invertebrates
In higher plants, P. aeruginosa induces
Quorum sensing
P. aeruginosa is an opportunistic pathogen with the ability to coordinate gene expression in order to compete against other species for nutrients or colonization. Regulation of gene expression can occur through cell-cell communication or quorum sensing (QS) via the production of small molecules called autoinducers that 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. aeruginosa employs five interconnected QS systems – las, rhl, pqs, iqs, and pch – that each produce unique signaling molecules.[60] 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.[61] QS in P. aeruginosa is 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.[62] Detection of these molecules indicates P. aeruginosa is growing as biofilm within the lungs of cystic fibrosis patients.[63] The impact of QS and especially las systems on the pathogenicity of P. aeruginosa is unclear, however. Studies have shown that lasR-deficient mutants are associated with more severe outcomes in cystic fibrosis patients[64] and are found in up to 63% of chronically infected cystic fibrosis patients despite impaired QS activity.[65]
QS is known to control expression of a number of
Biofilms formation and cyclic di-GMP
As in most Gram negative bacteria, P. aeruginosa biofilm formation is regulated by one single molecule: cyclic di-GMP. At low cyclic di-GMP concentration, P. aeruginosa has a free-swimming mode of life. But when cyclic di-GMP levels increase, P. aeruginosa start to establish sessile communities on surfaces. The intracellular concentration of cyclic di-GMP increases within seconds when P. aeruginosa touches a surface (e.g.: a rock, plastic, host tissues...).[68] This activates the production of adhesive pili, that serve as "anchors" to stabilize the attachment of P. aeruginosa on 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, preventing P. aeruginosa from swimming. When suppressed, the biofilms are less adherent and easier to treat. The biofilm matrix of P. aeruginosa is composed of nucleic acids, amino acids, carbohydrates, and various ions. It mechanically and chemically protects P. aeruginosa from aggression by the immune system and some toxic compounds.[69] P. aeruginosa biofilm's matrix is composed of up to three types of sugar polymers (or "exopolysacharides") named PSL, PEL, and alginate.[70] Which exopolysacharides are produced varies by strain.[71]
- The polysaccharide synthesis operon and cyclic di-GMP form a positive feedback loop. This 15-gene operon is responsible for the cell-cell and cell-surface interactions required for cell communication.
- PEL is a cationic exopolysaccharide that cross-links extracellular DNA in the P. aeruginosa biofilm matrix.[72]
Upon certain cues or stresses, P. aeruginosa revert the biofilm program and detach. Recent studies have shown that the dispersed cells from P. aeruginosa biofilms have lower cyclic di-GMP levels and different physiologies from those of planktonic and biofilm cells,[73][74] with unique population dynamics and motility.[75] Such dispersed cells are found to be highly virulent against macrophages and C. elegans, but highly sensitive towards iron stress, as compared with planktonic cells.[73]
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 serve to protect these bacteria from adverse environmental factors, including host immune system components in addition to antibiotics. 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.[66]
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.[76]
Diagnosis
Depending on the nature of infection, an appropriate specimen is collected and sent to a
When P. aeruginosa is isolated from a normally sterile site (blood, bone, deep collections), it is generally considered dangerous, and almost always requires treatment.[77][78] 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.[citation needed]
Classification
Morphological, physiological, and biochemical characteristics of Pseudomonas aeruginosa are shown in the Table below.
Test type | Test | Characteristics |
Colony characters | Size | Large |
Type | Smooth | |
Color | ||
Shape | Flat | |
Morphological characters | Shape | Rod |
Physiological characters | Motility | + |
Growth at 6.5% NaCl | - | |
Biochemical characters | Gram staining | - |
Oxidase | + | |
Catalase | + | |
Oxidative-Fermentative | ||
Motility | + | |
Methyl Red | - | |
Voges-Proskauer | - | |
Indole | - | |
H2S Production | - | |
Urease | - | |
Nitrate reductase | + | |
β-Galactosidase | ||
Phenylalanine Deaminase | - | |
DNAse | - | |
Lipase | + | |
Lysine Decarboxylase | - | |
Pigment | + (bluish green pigmentation) | |
Hemolysis | Beta/variable | |
Hydrolysis of | Gelatin | + |
Casein | ||
Utilization of | Glycerol | + |
Galactose | - | |
D-Glucose | + | |
D-Fructose | + | |
D-Mannose | - | |
Mannitol | + | |
Citrate | + | |
Maltose | - | |
Sucrose | - | |
Lactose | - |
Note: + = Positive, - =Negative
P. aeruginosa is a Gram-negative,
Identification of P. aeruginosa can 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.[82] 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.[82] The third, however, is present in biological settings and has been found in respiratory and in the urinary tract.[82] Furthermore, mutations in the gene lasR drastically alter colony morphology and typically lead to failure to hydrolyze gelatin or hemolyze.[citation needed]
In certain conditions, P. aeruginosa can secrete a variety of pigments, including pyocyanin (blue), pyoverdine (yellow and fluorescent), pyorubin (red), and pyomelanin (brown). These can be used to identify the organism.[83]
Clinical identification of P. aeruginosa may include 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.[84] It creates dark, gellish mats sometimes improperly called "algae" because of their appearance.[citation needed]
Treatment
This section needs additional citations for verification. (February 2021) |
Many P. aeruginosa isolates are
Due to widespread resistance to many common first-line antibiotics,
- 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 penicillins.
- carbapenems (meropenem, imipenem, doripenem, but not ertapenem)
- polymyxins (polymyxin B and colistin)[85]
- monobactams (aztreonam)
As fluoroquinolones are one of the few antibiotic classes widely effective against P. 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),
].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.[86]
Antibiotic resistance
One of the most worrisome characteristics of P. aeruginosa is its low antibiotic susceptibility, which is attributable to a concerted action of multidrug
- AmpC: encodes an AmpC-type β-lactamase enzyme, which breaks down penicillins, cephalosporins,[87] and carbapenems;[88]
- PER-1: encodes a PER-1 type extended-spectrum β-lactamase enzyme, which breaks down penicillins and cephalosporins;[89][90][91]
- IMP: encodes active-on-imipenem (IMP) carbapenemase (metallo-β-lactamase) enzyme which breaks down carbapenems;[92][93]
- NDM-1:[94] encodes a New Delhi metallo-β-lactamase 1 enzyme, which breaks down carbapenems;[95][96]
- OXA: encodes an oxacillinase (OCA) β-lactamase enzyme, which breaks down carbapenems;[97]
- AAC(6')-Ib: encodes an aminoglycoside-modifying enzyme called aminoglycoside N6'-acetyltransferase, which alters the structure of aminoglycoside antibiotics such as gentamicin and tobramycin;[98]
- Qnr: encodes a Qnr protein, which protects DNA fluoroquinolone) antibiotics such as ciprofloxacin.[99]
Specific genes and enzymes involved in antibiotic resistance can vary between different strains.[100][101] P. aeruginosa TG523 harbored genes predicted to have antibacterial activity and those which are implicated in virulence.[102]
Another feature that contributes to antibiotic resistance of P. aeruginosa is the low permeability of the bacterial cellular envelopes.
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. 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 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[104]. 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.[105]
Mutations in 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 P. aeruginosa is grown under in vitro conditions designed to mimic a cystic fibrosis patient's lungs, these genes mutate repeatedly.[106]
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, 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.[107] Furthermore, similar to a process found in Salmonella,[108] Sr006 regulation of PagL expression may aid in polymyxin B resistance.[107]
Prevention
Probiotic prophylaxis may prevent colonization and delay onset of Pseudomonas infection in an ICU setting.[109][non-primary source needed] Immunoprophylaxis against Pseudomonas is being investigated.[110] 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.[111]
Experimental therapies
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.[112] Phage therapy against ear infections caused by P. aeruginosa was reported in the journal Clinical Otolaryngology in August 2009.[113] As of 2024,[update] research on the topic is ongoing.[114]
Research
In 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
Research on this bacterium's systems biology led 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.[118][119]
Distribution
Pest risk analysis
As of 2019[update] the
Eyedrops
A small number of infections in the United States in 2022 and 2023 were likely caused by poorly manufactured eyedrops.[121]
See also
References
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Further reading
- Sweere JM, Van Belleghem JD, Ishak H, Bach MS, Popescu M, Sunkari V, et al. (March 2019). "Bacteriophage trigger antiviral immunity and prevent clearance of bacterial infection". Science. 363 (6434). Inoviridae. See also:
External links
- "Pseudomonas aeruginosa DSM 50071". The Bacterial Diversity Metadatabase.