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Pseudomonas aeruginosa is a gram negative bacteria that can cause disease in plants and animals. It is naturally resistant to antibiotics and forms biofilms.

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Pseudomonas aeruginosa is a common encapsulated, 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 generally affects the immunocompromised but can also 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.

The word Pseudomonas means "false unit", from the Greek pseudēs ( Greek: ψευδής, false) and ( Latin: monas, from Greek: μονάς, 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 bumpy.

The names pyocyanin and pyoverdine are from the Greek, with pyo-, meaning "pus", cyanin, meaning "blue", and verdine, meaning "green".[citation needed ] Pyoverdine in the absence of pyocyanin is a fluorescent-yellow color.

The genome of P. 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. 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.

The population of P. aeruginosa forms three main lineages, characterised by the finished genomes PAO1, PA14, and the highly divergent PA7.

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, 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. 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 bacterially-produced 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 fatal.

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. 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.

An opportunistic, nosocomial pathogen of immunocompromised individuals, P. aeruginosa typically infects the airway, urinary tract, burns, and wounds, and also causes other blood 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 by oxidative stress. However, salicylic acid can inhibit pyocyanin production. One in ten hospital-acquired infections is from Pseudomonas. Cystic fibrosis patients are also predisposed to P. aeruginosa infection of the lungs due to a functional loss in chloride ion movement across cell membranes as a result of a mutation. 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 thrive in 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 organelle.

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 phenazine pyomelanin.

When pyocyanin biosynthesis is inhibited, a decrease in P. aeruginosa pathogenicity is observed . This suggests that pyocyanin is most responsible for the initial colonization of P. aeruginosa in vivo.

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.

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 infections.

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 five interconnected QS systems - lasRl, rhlRl, PQS, iqs and pch - 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.

As in most Gram negative bacteria, P. aeruginosa biofilm formation is regulated by one single molecule: cyclic-di-GMP. At low c-di-GMP concentration, P. aeruginosa has a free-swimming mode of life. But when c-di-GMP levels increase, P. aeruginosa start to establish sessile communities on surfaces. The intracellular concentration of c-di-GMP increases within seconds when P. aeruginosa touches a surface ( e.g.: a rock, plastic, host tissues...). 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, c-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. P. aeruginosa biofilm's matrix is composed of 2 types of sugars (or "exopolysacharides") named PSL and PEL:

Polysaccharide synthesis locus (PSL) and c-di-GMP form a positive feedback loop. PSL stimulates c-di-GMP production, while high c-di-GMP turns on the operon and increases activity of the 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.

PEL is a cationic exopolysaccharide that cross-links extracellular DNA in the P. aeruginosa biofilm matrix.

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 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 cells.

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.

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.

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 distinguish nonfermenting 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.[citation needed ] 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 ]P. aeruginosa is a Gram-negative, aerobic (and at times facultatively anaerobic), rod-shaped bacterium 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 Pseudomonas.

Identification of P. aeruginosa can be complicated by the fact individual isolates often lack motility. 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.

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. It creates dark, gellish mats sometimes improperly called " algae" because of their appearance.[citation needed ]

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.

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:

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)

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), topical gentamicin or colistin may 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 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 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 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 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.

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 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.

1. ^ Balcht A, Smith R (1994). Pseudomonas aeruginosa: Infections and Treatment. Informa Health Care. pp. 83-84. ISBN 978-0-8247-9210-7.

2. ^ Roy, Paul H.; Tetu, Sasha G.; Larouche, André; Elbourne, Liam; Tremblay, Simon; Ren, Qinghu; Dodson, Robert; Harkins, Derek; Shay, Ryan (2010-01-22). "Complete Genome Sequence of the Multiresistant Taxonomic Outlier Pseudomonas aeruginosa PA7". PLoS ONE. 5 (1): e8842. Bibcode:2010PLoSO...5.8842R. doi:10.1371/journal.pone.0008842. ISSN 1932-6203. PMC . PMID 20107499.

3. ^ Todar's Online Textbook of Bacteriology. Textbookofbacteriology.net (2004-06-04). Retrieved on 2011-10-09.

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7. ^ Anzai Y, Kim H, Park JY, Wakabayashi H, Oyaizu H (July 2000). "Phylogenetic affiliation of the pseudomonads based on 16S rRNA sequence". International Journal of Systematic and Evolutionary Microbiology. 50 Pt 4 (4): 1563-89. doi:10.1099/00207713-50-4-1563. PMID 10939664.

8. ^ http://www.childrenshospitalofillinois.org/pdfs/specialty-services/cf/germs-infection-control/Pseudomonas-Aeurigonsa-Information-Sheet.pdf

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Pseudomonas aeruginosa is a common encapsulated, 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.

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Lifestyle Facts - Pseudomonas aeruginosa

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Lifestyle Facts - Pseudomonas aeruginosa

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P. aeruginosa is an opportunistic pathogen that causes disease in the body (usually the blood or lungs). This pathogen primarily spread through contaminated water, soil, or surfaces. Most infections occur in hospitals or in people that are immunocompromised (e.g. cystic fibrosis patients).

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P. aeruginosa has displayed increased antibiotic resistance and new treatments are currently in early trials. One of these ideas includes phage therapy which utilizes bacteriophages, a type of virus, to kill bacteria.

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Affiliations

¹ Department of Pathology, Dalhousie University, Halifax, NS B3H 4R2, Canada.

² Department of Microbiology and Immunology, Dalhousie University, Halifax, NS B3H 4R2, Canada.

³ Department of Biology, University of Waterloo, Waterloo, ON N2L 3G1, Canada.

⁴ Department of Pathology, Dalhousie University, Halifax, NS B3H 4R2, Canada; Department of Microbiology and Immunology, Dalhousie University, Halifax, NS B3H 4R2, Canada; Department of Pediatrics, IWK Health Centre, Halifax, NS B3K 6R8, Canada.

⁵ Department of Pathology, Dalhousie University, Halifax, NS B3H 4R2, Canada; Department of Microbiology and Immunology, Dalhousie University, Halifax, NS B3H 4R2, Canada. Electronic address: zhenyu.cheng@dal.ca.

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Free article

Affiliations

¹ Department of Pathology, Dalhousie University, Halifax, NS B3H 4R2, Canada.

² Department of Microbiology and Immunology, Dalhousie University, Halifax, NS B3H 4R2, Canada.

³ Department of Biology, University of Waterloo, Waterloo, ON N2L 3G1, Canada.

⁴ Department of Pathology, Dalhousie University, Halifax, NS B3H 4R2, Canada; Department of Microbiology and Immunology, Dalhousie University, Halifax, NS B3H 4R2, Canada; Department of Pediatrics, IWK Health Centre, Halifax, NS B3K 6R8, Canada.

⁵ Department of Pathology, Dalhousie University, Halifax, NS B3H 4R2, Canada; Department of Microbiology and Immunology, Dalhousie University, Halifax, NS B3H 4R2, Canada. Electronic address: zhenyu.cheng@dal.ca.

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen that is a leading cause of morbidity and mortality in cystic fibrosis patients and immunocompromised individuals. Eradication of P. aeruginosa has become increasingly difficult due to its remarkable capacity to resist antibiotics. Strains of Pseudomonas aeruginosa are known to utilize their high levels of intrinsic and acquired resistance mechanisms to counter most antibiotics. In addition, adaptive antibiotic resistance of P. aeruginosa is a recently characterized mechanism, which includes biofilm-mediated resistance and formation of multidrug-tolerant persister cells, and is responsible for recalcitrance and relapse of infections. The discovery and development of alternative therapeutic strategies that present novel avenues against P. aeruginosa infections are increasingly demanded and gaining more and more attention. Although mostly at the preclinical stages, many recent studies have reported several innovative therapeutic technologies that have demonstrated pronounced effectiveness in fighting against drug-resistant P. aeruginosa strains. This review highlights the mechanisms of antibiotic resistance in P. aeruginosa and discusses the current state of some novel therapeutic approaches for treatment of P. aeruginosa infections that can be further explored in clinical practice.

Keywords: Pseudomonas aeruginosa; alternative therapeutics; antibiotic resistance; new antibiotics; resistance mechanisms.

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pseudomonas aeruginosa / growth & development

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national center for biotechnology information

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Antibiotic resistance in Pseudomonas aeruginosa: mechanisms and alternative therapeutic strategies - PubMed

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Pseudomonas aeruginosa is an opportunistic pathogen that is a leading cause of morbidity and mortality in cystic fibrosis patients and immunocompromised individuals. Eradication of P. aeruginosa has become increasingly difficult due to its remarkable capacity to resist antibiotics. Strains of Pseudo ...

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Lactobacillus rhamnosus is a gram positive rod usually found in the intestines. It produces lactase, which helps digest lactose.

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Lactobacillus rhamnosus is a bacterium that originally was considered to be a subspecies of , but genetic research found it to be a species of its own. It is a short Gram-positive heterofermentative facultative anaerobic non-spore-forming rod that often appears in chains. Some strains of L. rhamnosus bacteria are being used as probiotics, and are particularly useful in treating female-related infections, most particularly very difficult to treat cases of bacterial vaginosis (or "BV"). The Lactobacillus rhamnosus and species are most commonly found in the healthy female genito-urinary tract and are most helpful to supplement in order to regain control over dysbiotic bacterial overgrowth during an active infection. L. rhamnosus sometimes is used in yogurt and dairy products such as fermented and unpasteurized milk and semi-hard cheese. While frequently considered a beneficial organism, L. rhamnosus may not be as beneficial to certain subsets of the population; in rare circumstances, especially those primarily involving weakened immune system or infants, it may cause endocarditis.

Lactobacillus rhamnosus has a wide variety of strains that have been isolated from many different environments including the vagina and gastrointestinal tract. L. rhamnosus strains have the capacity for strain-specific gene functions that are required to adapt to a large range of environments. Its core genome contains 2,164 genes, out of 4,711 genes in total (the pan-genome). The accessory genome is overtaken by genes encoding carbohydrate transport and metabolism, extracellular polysaccharides, biosynthesis, bacteriocin production, pili production, the CRISPR-cas system, the clustered regularly interspaced short palindromic repeat ( CRISPR) loci, and more than 100 transporter functions and mobile genetic elements such as phages, plasmid genes, and transposons.

The genome of the specific strain L. rhamnosus LRB, in this case, taken from a human baby tooth, consists of a circular chromosome of 2,934,954 bp with 46.78% GC content. This genome contains 2,749 total genes with 2,672 that are total protein-coding sequences. This sample did not contain any plasmids. The most extensively studied strain, L. rhamnosus GG, a gut isolate, consists of a genome of 3,010,111 bp. Therefore, the LRB genome is shorter than GG's genome. LRB lacks the spaCBA gene cluster of GG and is not expected to produce functional pili (6). This difference may help explain why each strain lives in a different habitat.

Lactobacillus rhamnosus GG (ATCC 53103)

Lactobacillus rhamnosus GG (ATCC 53103) is a strain of L. rhamnosus that was isolated in 1983 from the intestinal tract of a healthy human being; filed for a patent on 17 April 1985, by Sherwood Gorbach and Barry Goldin, the 'GG' derives from the first letters of their surnames. The patent refers to a strain of " L. acidophilus GG" with American Type Culture Collection (ATCC) accession number 53103; later reclassified as a strain of L. rhamnosus. The patent claims the L. rhamnosus GG (ATCC 53103) strain is acid- and bile-stable, has a great avidity for human intestinal mucosal cells, and produces lactic acid. Since the discovery of the L. rhamnosus GG (ATCC 53103) strain, it has been studied extensively on its various health benefits and currently L. rhamnosus GG (ATCC 53103) strain is the world's most studied probiotic bacterium with more than 800 scientific studies.

The genome sequence of Lactobacillus rhamnosus GG (ATCC 53103) has been decoded in 2009.

In 1983, Lactobacillus rhamnosus GG was isolated from the intestinal tract of a healthy human by Sherwood Gorbach and Barry Goldin.

Medical research and use

While Lactobacillus rhamnosus GG (ATCC 53103) is able to survive the acid and bile of the stomach and intestine, is claimed to colonize the digestive tract, and to balance intestinal microflora, evidence suggests that Lactobacillus rhamnosus is likely a transient inhabitant, and not autochthonous. Regardless, it is considered a probiotic useful for the treatment of various maladies, as it works on many levels. Lactobacillus rhamnosus GG binds to the gut mucosa.

L. rhamnosus GG is beneficial in the prevention of rotavirus diarrhea in children. Prevention and treatment of various types of diarrhea have been shown in children and in adults. L. rhamnosus GG can be beneficial in the prevention of antibiotic-associated diarrhea and nosocomial diarrhea and this has been recently supported by European guidelines. Lactobacillus rhamnosus GG may reduce the risk of traveler's diarrhea.

Acute gastroenteritis

A position paper published by ESPGHAN Working Group for Probiotics and Prebiotics based on a systematic review and randomized controlled trials (RCTs) suggested that L. rhamnosus GG (low quality of evidence, strong recommendation) may be considered in the management of children with acute gastroenteritis in addition to rehydration therapy.

Atopic dermatitis, eczema

Lactobacillus rhamnosus GG has been found to be ineffective for treating eczema.

The use of L. rhamnosus GG for probiotic therapy has been linked with rare cases of sepsis in certain risk groups, primarily those with a weakened immune system and infants. Ingestion of GG is considered to be safe and data show a significant growth in the consumption of L. rhamnosus GG at the population level did not lead to an increase in Lactobacillus bacteraemia cases.

References

Further reading

Salminen MK, Rautelin H, Tynkkynen S, Poussa T, Saxelin M, Valtonen V, Järvinen A (January 2004). "Lactobacillus bacteremia, clinical significance, and patient outcome, with special focus on probiotic L. rhamnosus GG". Clinical Infectious Diseases. 38 (1): 62-9. doi:10.1086/380455. PMID 14679449.

External links

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Lactobacillus rhamnosus is a bacterium that originally was considered to be a subspecies of , but genetic research found it to be a species of its own. It is a short Gram-positive heterofermentative facultative anaerobic non-spore-forming rod that often appears in chains. Some strains of L.

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Lifestyle Facts - Lactobacillus rhamnosus

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Lifestyle Facts - Lactobacillus rhamnosus

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L. rhamnosus is able to survive in the acidic stomach and bile of the intestines. Related strains have been commercialized and marketed as probiotics to prevent or treat various gastrointestinal problems.

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A combination of Lactobacillus strands, including rhamnosus, were combined and given to patients with Irritable Bowel Syndrome (IBS). Most patients had lessened abdominal pain along with improved distention, stool consistency, and quality of life.

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Affiliations

¹ 1 Westlake Medical Research, 550 St. Charles St., Ste. 208, Thousand Oaks, CA 91360, USA.

² 2 Sprim Americas, 254 Front St. Ph, New York, NY 10038, USA.

³ 3 Bio-K Plus International, Inc., 495 Blvd. Armand-Frappier, Laval, H7V 4B3, Canada.

⁴ 4 Digestive and Liver Disease Specialists, 11922 Seacrest Dr., Ste. A, Garden Grove, CA 92840, USA.

Randomized Controlled Trial

Affiliations

¹ 1 Westlake Medical Research, 550 St. Charles St., Ste. 208, Thousand Oaks, CA 91360, USA.

² 2 Sprim Americas, 254 Front St. Ph, New York, NY 10038, USA.

³ 3 Bio-K Plus International, Inc., 495 Blvd. Armand-Frappier, Laval, H7V 4B3, Canada.

⁴ 4 Digestive and Liver Disease Specialists, 11922 Seacrest Dr., Ste. A, Garden Grove, CA 92840, USA.

Abstract

A combination of Lactobacillus acidophilus CL1285, Lactobacillus casei LBC80R and Lactobacillus rhamnosus CLR2 was compared to placebo for relief of symptoms of irritable bowel syndrome (IBS). A total of 113 subjects at 3 clinical sites were randomised in a 2:1 ratio and followed for 12 weeks. Subjects ingested either 2 capsules of active study product, containing 50×10 ⁹ cfu of live organisms, or 2 placebo capsules daily. Endpoints included improvement in abdominal pain, days of pain, distention, stool consistency and frequency, quality of life (QOL), and adequate relief (AR) of IBS symptoms. IBS subtypes constipation (IBS-C), diarrhoea (IBS-D), and mixed (IBS-M) were evaluated separately; the effect of gender was also examined. For all efficacy endpoints improvement of 30% or more vs placebo was considered clinically significant. With the exception of pain intensity and AR, the endpoints demonstrated a therapeutic advantage of active over placebo for IBS symptoms in at least some subject subgroups. The IBS-D and female subgroups showed the largest and most consistent effects. Stool frequency and consistency were evaluated in the IBS-C and IBS-D subgroups, and improvement of active vs placebo was noted in both. QOL improvement was seen overall and in specific domains. Adverse events (AEs) were limited to 7 subjects; all were of mild or moderate intensity except one, severe cramping. Four AEs in the same subject in the placebo group were judged to be related to study product; these resolved by the end of study. There were no serious AEs.

Keywords: constipation; diarrhoea; irritable bowel syndrome; probiotics; quality of life.

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irritable bowel syndrome / drug therapy*

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national center for biotechnology information

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Lactobacillus acidophilus CL1285, Lactobacillus casei LBC80R and Lactobacillus rhamnosus CLR2 improve quality-of-life and IBS symptoms: a double-blind, randomised, placebo-controlled study - PubMed

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A combination of Lactobacillus acidophilus CL1285, Lactobacillus casei LBC80R and Lactobacillus rhamnosus CLR2 was compared to placebo for relief of symptoms of irritable bowel syndrome (IBS). A total of 113 subjects at 3 clinical sites were randomised in a 2:1 ratio and followed for 12 weeks. Subje ...

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Lactobacillus is not closely related to the pseudomonas genus. Rather, it is shares a common ancestor with streptococcus and granulicatella. The two bacteria in this project belong to different phylums, which is why they are far apart on the phylogenetic tree.

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Anytime we examine DNA or RNA sequences, I am humbled by how much information is encoded in just a few letters. My 2 particular strands of bacteria weren't closely related but they still contained very similar properties such as 16S RNA. The research process of these bacteria resulted in a vast amount of information; the phylogenetic tree was particularly helpful in understanding the relationship between them, along with other bacteria of the oral cavity. Bacteria, especially those that make up the human microbiome, are vital for life and function. New research has indicated the human microbiome may be responsible for human metabolism, immunity, and possibly behavior. There is a misconception that all bacteria are bad and that we must decontaminate and sterilize everything around us. At the same time, there have been increasing rates of autoimmune disease, diabetes, and more illnesses. This increase in disease could be linked to an absence of certain bacteria. Microbiome research an important step in science that will hopefully be the answer to current medical mysteries.