Pseudomonas aeruginosa - an overview (2022)

Pseudomonas aeruginosa (P. aeruginosa) is most frequently encountered in keratitis cases associated with extended contact lens wear and constitute 19–42% of bacterial keratitis cases.

From: Encyclopedia of the Eye, 2010

Pseudomonas aeruginosa and Other Pseudomonas Species

John E. Bennett MD, in Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 2020

Transmission Dynamics ofPseudomonas aeruginosa and Reservoirs

Acquisition ofP. aeruginosa can occur both exogenously and endogenously. Exogenous acquisition occurs through contaminated hands of health care workers and environmental surfaces. An in-depth epidemiologic study characterized the exogenous transmission of multidrug-resistant (MDR)P. aeruginosa in six ICUs.26 The investigators obtained cultures from hands, gloves, and gowns of health care workers during routine patient care activities, surveillance cultures from patients, and environmental samples from sinks, bedrails, vital sign monitors, supply carts, door handles, intravenous pumps, ventilators, and floors. Molecular typing, using pulsed-field gel electrophoresis, was performed to determine clonal relatedness among strains. In that study, MDRAcinetobacter species were the most common pathogens to contaminate health care workers’ gloves and hands, occurring among 33% of interactions between health care workers and patients.P. aeruginosa was the second most common MDR pathogen to contaminate health care workers, which occurred during 17.4% of health care worker–patient interactions. Independent risk factors associated with health care worker contamination were presence of environmental contamination, duration in patients’ room greater than 5 minutes, performing a physical examination, and contact with the mechanical ventilator. Environmental contamination was also very common:P. aeruginosa was recovered from 22% of rooms.26 This study and many others emphasize that exogenous transmission plays a major role in the nosocomial acquisition ofP. aeruginosa and that environmental contamination is central to its transmission to patients and health care workers.

Endogenous acquisition of a resistant strain ofP. aeruginosa is defined as colonization with an antimicrobial-susceptible strain that subsequently becomes resistant primarily through antimicrobial selective pressure within the host. A study of imipenem-resistantP. aeruginosa transmission demonstrated that, among events that could be determined, endogenous acquisition accounted for 19% of identified acquisition events and that exogenous acquisition accounted for 31% of events.27

As outlined earlier, environmental reservoirs contribute substantially to the spread ofP. aeruginosa. The most common sites either have high moisture or humidity or are water related (Table 219.2). In the hospital setting, outbreaks ofP. aeruginosa have been linked predominantly to water sources, including potable water, showerheads, and sinks (seeTable 219.2).28,29 Other sources have included health care workers’ artificial or long nails, intraocular lens solution, ultrasound transmission gel during transesophageal echocardiography, retained tissue in surgical instruments,30 and soap dispensers. The ability ofP. aeruginosa to form biofilms on surfaces increases its ability to survive on inanimate surfaces and makes it difficult to eradicate. Biofilms are microbial communities held together by structural polysaccharides (slime), which attach strongly to surfaces. Biofilms produced byP. aeruginosa lead to antimicrobial tolerance and impede eradication by environmental cleaning agents.19,28

Klebsiella pneumoniae and Pseudomonas aeruginosa

Min Wu, Xuefeng Li, in Molecular Medical Microbiology (Second Edition), 2015

Introduction

Pseudomonas aeruginosa is a Gram-negative, aerobic rod bacterium of the Pseudomonadaceae family (a member of the Gammaproteobacteria) [142]. P. aeruginosa contains 12 other members in its family. Similar to other members of the genus, P. aeruginosa is commonly found in soil and water as well as in plants and humans. Pseudomonas bacteria are believed to be one of only a few true pathogens for plants. Importantly, P. aeruginosa has become an emerging opportunistic pathogen in the clinics. Recent epidemiological studies demonstrate its nosocomial pathogen status, particularly those strains with increased antibiotic resistance.

P. aeruginosa exploits weaknesses in host defence to mount an infection. Indeed, P. aeruginosa is the epitome of an opportunistic pathogen of humans. The bacterium hardly infects uncompromised tissues, but it can invade any tissue beleaguered by immunodeficiency. P. aeruginosa causes infection in the urinary tract, respiratory system, dermis, soft tissue, bacteraemia, bone and joint, gastrointestine and blood, particularly in patients with severe burns, tuberculosis, cancer and AIDS. Importantly, P. aeruginosa causes a significant problem in patients hospitalized with cancer, cystic fibrosis and burns, with 50% fatality [143]. According to the Centers for Disease Control and Prevention (CDC), the overall incidence of P. aeruginosa infections in US hospitals averages about 0.4% (4 per 1000 discharges), and the bacterium is the fourth most common isolated nosocomial pathogen, accounting for 10% of all hospital-acquired infections. P. aeruginosa shows a rod shape of 0.5–0.8µm by 1.5–3.0µm. The bacterial strains are motile with a single polar flagellum. The metabolism is oxygen-based respiratory, but this ubiquitous bacterium will grow in the absence of O2 but in the presence of NO3 [144].

The typical Pseudomonas in nature can exist in biofilm formats, attached to some surface or substrate, or in a planktonic form, as a unicellular organism, actively swimming using its flagellum. Indeed, Pseudomonas is a vigorous, fast-swimming bacterium as seen in samples from the wild or from patients [145].

P. aeruginosa may not be a typical pseudomonad in natural environments. P. aeruginosa needs a simple nutrition supply, and can even grow in distilled water. P. aeruginosa can also grow well in a medium containing acetate (carbon source) and ammonium sulphate (nitrogen source). The optimum temperature for growth is 37°C, but P. aeruginosa also grows at temperatures as high as 42°C [146]. P. aeruginosa is resistant to high concentrations of salts and dyes, weak antiseptics, and many commonly used antibiotics. These properties of P. aeruginosa are critical factors for its ecological success, which also help explain the ubiquitous nature of the organism and its prominence as a nosocomial pathogen.

P. aeruginosa isolates demonstrate three types of colonies. Natural isolates from soil or water typically are a small, rough colony, while clinical isolates are likely smooth colony types, occasionally with a fried-egg appearance that is large, smooth, with flat edges and an elevated appearance. Respiratory and urinary tract secretions may show a mucoid-type (alginate slime). P. aeruginosa has two different soluble pigments, the fluorescent pigment pyoverdin and blue pyocyanin. Pyocyanin refers to blue pus, a typical feature of suppurative infections caused by P. aeruginosa. Pyochelin (a derivative of pyocyanin) is a siderophore and can acquire iron from the host or in low-iron environments to maintain the pathogen growth. Pyocyanin can disrupt the normal function of human nasal cilia and the respiratory epithelium, thereby igniting pro-inflammatory responses [147]. No virulence evidence is described for the fluorescent pigments.

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(Video) Pseudomonas aeruginosa - an Osmosis Preview

Pseudomonas and Related Gram-Negative Bacillary Infections

Lee Goldman MD, in Goldman-Cecil Medicine, 2020

Treatment ofP. aeruginosa Bacteremia

Guidelines from the Surviving Sepsis Campaign for patients with severe infections associated with respiratory failure and septic shock suggest combination therapy.10 For the case ofP. aeruginosa bacteremia this would include, for example, an antipseudomonal β-lactam and either an aminoglycoside or a fluoroquinolone. Nevertheless, combination therapy should not be routinely used for ongoing treatment of most other serious infections, including bacteremia and sepsis without shock or routinely for neutropenic sepsis/bacteremia. Time is of utmost importance and antibiotics should be commenced within an hour in the treatment of sepsis and septic shock. Current guidelines advise de-escalation in response to clinical improvement or infection resolution within the first few days (not specified currently but this was determined as 3 to 5 days in previous guidelines). De-escalation to the most appropriate single-agent therapy should be performed as soon as the susceptibility profile is known or clinical improvement is noted. Indeed, evidence-based data from meta-analyses suggest that a combination may not provide an advantage in terms of clinical outcomes, such as cure of the infection, or less emergence of resistance. Furthermore, a combination of a β-lactam and an aminoglycoside carries a higher rate of nephrotoxicity. There is therefore currently a trend that a β-lactam/β-lactamase inhibitor (piperacillin-tazobactam) or an antipseudomonal carbapenem (meropenem or imipenem-cilastatin) may be used alone as monotherapy without compromising patient outcomes. Nevertheless, monotherapy with an aminoglycoside or a quinolone is not suggested for the treatment of bacteremia because it is associated with poor clinical outcomes. Local invitro antimicrobial susceptibility data regarding the level of resistance of local clinical isolates ofP. aeruginosa to various antibiotics have to be taken into consideration.11 The total duration of treatment of bacteremia was usually considered to be approximately 14 days in the non-neutropenic patient. However, the current guidelines for most serious infections associated with sepsis and septic shock recommend that 7 to 10 days are adequate in addition to source control for most infections (not applicable for endocarditis, osteomyelitis, abscesses of the brain or kidney), whereas longer courses are appropriate for patients with undrainable foci of infection, immunologic deficiencies including neutropenia, and patients with slow clinical resolution. Bacteremia in the non-neutropenic patient may be secondary to the presence of a central venous catheter or the presence of infection elsewhere (e.g., in the lungs, urinary tract, or cardiac valves). Removal of an infected central venous catheter may be necessary in addition to the systemic antibiotics provided for the treatment of bacteremia, while the duration of treatment of endocarditis should be protracted to reach 6 weeks in addition to potential cardiothoracic surgery. In the neutropenic patient at least 14 days are necessary and antibiotics are to be continued until the absolute neutrophil count is equal to or greater than 500 cells/μL. Bacteremia in the neutropenic patient may necessitate prolonged treatment of 4 to 6 weeks in the presence of endocarditis, deep-seated infection, septic thrombosis, or persistent bacteremia occurring more than 72 hours after catheter removal on appropriate antibiotics.

Pseudomonas aeruginosa

Weihui Wu, ... Shouguang Jin, in Molecular Medical Microbiology (Second Edition), 2015

Introduction

Pseudomonas aeruginosa is a Gram-negative, rod-shaped, asporogenous, and monoflagellated bacterium. It has a pearlescent appearance and grape-like or tortilla-like odour. P. aeruginosa grows well at 25°C to 37°C, and its ability to grow at 42°C helps distinguish it from many other Pseudomonas species. P. aeruginosa is a ubiquitous microorganism which has the ability to survive under a variety of environmental conditions. It not only causes disease in plants and animals, but also in humans, causing serious infections in immunocompromised patients with cancer and patients suffering from severe burns and cystic fibrosis (CF).

Most strains of P. aeruginosa produce one or more pigments, including pyocyanin (blue-green), pyoverdine (yellow-green and fluorescent), and pyorubin (red-brown). Previous investigations have suggested that pyocyanin not only contributes to the persistence of P. aeruginosa in the lungs of CF patients, but also interferes with many mammalian cell functions, including cell respiration, ciliary beating, epidermal cell growth, calcium homeostasis and prostacyclin release from lung endothelial cells [1]. However, the precise molecular mechanism mediated by pyocyanin pathology is unknown.

P. aeruginosa strains produce two distinct types of O antigen (O-Ag): a common polysaccharide antigen (A-band) composed of a homopolymer of d-rhamnose, and an O-specific antigen (B-band) composed of a heteropolymer of three to five distinct sugars in its repeat units. So far, P. aeruginosa isolates have been classified into 20 serotypes by the International Antigenic Typing Scheme (IATS) [2]. The lipopolysaccharide (LPS) of P. aeruginosa is less toxic than that of other Gram-negative rods, facilitating its establishment of chronic infections by eliciting a low inflammatory response [3].

The genome of P. aeruginosa consists of a single circular chromosome. P. aeruginosa has a relatively large genome (5.5–7Mb) and high G+C content (65–67%). Because of the large genome, P. aeruginosa encodes a large number of enzymes for various metabolic pathways, conferring high nutritional versatility. In addition, about 8% of the genome encodes regulatory genes, which enables the bacterium to adapt to complex growth environments.

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(Video) Pseudomonas aeruginosa: An Overview of Treatment Options

Cystic Fibrosis

John E. Bennett MD, in Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 2020

Pseudomonas aeruginosa

In prospectively collected oropharyngeal cultures obtained at least every 6 months from patients diagnosed through neonatal screening,101 PA has been recognized to be quite adaptable to inhabiting the CF respiratory tract. Since the first description of CF, PA has become the second most prevalent pathogen found in the respiratory tract of CF patients.57a The establishment of CF centers and cohorting of patients in hospitals is somewhat responsible for the emergence of this organism.102 This observation has led to adoption of strict infection control and practice guidelines.103–106 The neonatal screening program underway since 1985 was a collaboration involving two CF centers in Wisconsin, and its inception had implications for the prevalence of PA infection.7 Observation of screened and control groups were similar overall, but one center, which was located in an urban setting, showed significantly younger age for acquisition of PA. This clinic did not segregate patients by age, and perhaps allowed more opportunity for social interaction outside of the clinic. Although the overall study did not indicate a significantly increased risk for PA acquisition, it suggested risk factors associated with an urban center clinic. Patients identified with CF through neonatal screening had a median of 52 PA-free weeks in the urban CF center, while PA-free survival was 289 weeks at the nonurban center. The acquisition of PA impacts survival and is strongly associated with a decrease in FEV1 and life expectancy.107–109 Kerem and coworkers showed significant association of decreased lung function at age 7 in patients with PA infection compared to those uninfected with PA.109 Also, a decrease in PA-positive cultures at a Danish center occurred when PA-infected and noninfected patients were segregated.109a

Despite the impaired but robust host inflammatory response and treatments directed toward PA, this organism comprises 60% to 70% of all CF respiratory infections by age 18,57a and chronic infection eventually leads to respiratory failure and death. Initial strains are usually unique and begin with strains from an environmental source.110 This is followed by repeated airway infection and eventually chronic airway infection, as well as parenchymal infection, chronic bronchopneumonia, and necrotizing pneumonia.49 The aggressive use of antipseudomonal antibiotics can substantially delay chronic infection.38 The Early Pseudomonal Infection Control (EPIC) study was designed to determine the impact of the acquisition of PA and of four separate antibiotic regimens to eradicate the first positive PA culture: cycled therapy or culture-based therapy with inhaled tobramycin (300 mg twice daily) and ciprofloxacin or placebo.112–114 No one therapy was superior to the others, but each led to decrease rates of PA recurrence.115

PSEUDOMONAS | Pseudomonas aeruginosa

P.R. Neves, ... N. Lincopan, in Encyclopedia of Food Microbiology (Second Edition), 2014

Introduction

Pseudomonas aeruginosa is a ubiquitously distributed opportunistic pathogen that inhabits soil and water as well as animal-, human-, and plant-host-associated environments. It can be recovered, often in high numbers, in common food, especially vegetables. Moreover, it can be recovered in low numbers in drinking water. This ubiquity would be attributed to its versatile energy metabolism. Like other bacterial species found in the environment, P. aeruginosa colonizes a wide variety of surfaces (i.e., food packaging, water tap, medical devices) in a biofilm form, which makes the cells impervious to antibacterial agents – including antiseptic cleaning compounds, disinfectants, and clinically relevant antibiotics – and to host defenses mediated by macrophages and neutrophils. Biofilms in drinking water systems can serve as an environmental reservoir for P. aeruginosa, representing a possible source of water contamination, resulting in a potential health risk for humans (Mena and Gerba, 2009). Alginate slime forms the matrix of the P. aeruginosa biofilm, which anchors the cells to a variety of surfaces. Cell–cell communication by chemical signals is prevalent in the biofilm matrix. Pseudomonas aeruginosa use this form of signaling, termed quorum sensing (QS), to coordinate other behaviors that generally involve population-level benefits, such as biofilm formation or secretion of extracellular factors. The QS uses N-acyl homoserine lactone signals to synchronize gene expression during the production of polysaccharides, rhamnolipid (RL), and other virulence factors. As promising biotechnological products, RLs produced by P. aeruginosa have been the most investigated biosurfactant due to their potential applications in a wide variety of industries and for wastewater bioremediation. Other bioremediation properties of P. aeruginosa have been described from isolates recovered from industrial polluted effluents. Since P. aeruginosa habitat is the soil and water, in association with Bacillus spp., Streptomyces spp., and molds, it has developed resistance to a variety of naturally occurring antibiotics. Moreover, P. aeruginosa can acquire plasmids containing resistance genes, and it is able to transfer these genes by transduction and conjugation. So, P. aeruginosa is intrinsically resistant to many of the antibiotics used in clinical practice. In the last years, the emergence of multidrug-resistant (MDR) P. aeruginosa has been a major public health issue worldwide. On the other hand, metallo-beta-lactamase (MBL)–producing P. aeruginosa isolates have been identified in environmental water samples, a fact that emphasizes the importance of surveying environmental strains that might act as a source or reservoir of resistance genes with clinical relevance and that can be transmitted through food or water.

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Pseudomonas aeruginosa

Paul J. Planet, in Principles and Practice of Pediatric Infectious Diseases (Fifth Edition), 2018

(Video) Pseudomonas aeruginosa introduction

Microbiology

Pseudomonas aeruginosa is a gram-negative bacillus found widely in nature, in soil and water. Classified as an opportunistic pathogen, P. aeruginosa causes disease infrequently in normal hosts but is a major cause of infection in patients with underlying or immunocompromising conditions. The genome of P. aeruginosa, which is especially large for a prokaryote, has provided an understanding of the metabolic and pathogenic mechanisms that underlie the success of this versatile pathogen, and it has become a model for understanding microbial genomic variation and evolution in chronic disease. P. aeruginosa has few nutritional requirements and can adapt to conditions not tolerated by other organisms. It does not ferment lactose or other carbohydrates but oxidizes glucose and xylose. Organisms grow aerobically or anaerobically if nitrate is available as an inorganic electron acceptor, as is the case in the lungs of patients with cystic fibrosis (CF).1 P. aeruginosa gene expression responds to environmental conditions with discrete patterns typical of environmental isolates: motility, piliation, and expression of numerous exoproducts. In subacute and chronic infections, the accumulation of intracellular dinucleotides (cyclic diguanidine monophosphate) favors a biofilm mode of growth with the formation of an extracellular polysaccharide matrix,2 thus enabling the organisms to avoid innate immune clearance mechanisms and persist in human airways.3

The organism produces the fluorescent siderophores pyoverdin and pyochelin, which function to scavenge iron. Redox-active phenazines such as pyocyanin, the pigment that gives P. aeruginosa its characteristic blue color, play an important role in electron transport especially under microaerophilic conditions, increase the bioavailability of iron, and enhance virulence through oxidative stress.4,5 P. aeruginosa can be identified biochemically as having indophenol oxidase-positive, citrate-positive, and l-arginine dehydrolase-positive activity. Differentiation of P. aeruginosa from other pseudomonads or organisms such as Burkholderia species, Stenotrophomonas maltophilia, and Achromobacter spp. occasionally can require testing for DNAse activity, growth at 42°C, and differential carbohydrate metabolism or using molecular methods.

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Etiologic Agents of Infectious Diseases

Alice S. Prince, in Principles and Practice of Pediatric Infectious Diseases (Fourth Edition), 2012

Microbiology

Pseudomonas aeruginosa is a gram-negative bacillus found widely in nature, in soil and water. Classified as an opportunistic pathogen, P. aeruginosa causes disease infrequently in normal hosts but is a major cause of infection in patients with underlying conditions. The sequencing of the genome of several strains including the prototypic laboratory strain PAO1 (www.pseudomonas.com), which is especially large for a prokaryote, has provided an understanding of the metabolic and pathogenic mechanisms that underlie the success of this versatile pathogen. This large genome endows the organism with tremendous genetic flexibility. P. aeruginosa has few nutritional requirements and can adapt to conditions not tolerated by other organisms. It does not ferment lactose or other carbohydrates but oxidizes glucose and xylose. Organisms grow aerobically or anaerobically if nitrate is available as an inorganic electron acceptor, as is the case in the lungs of individuals with cystic fibrosis (CF).1 P. aeruginosa gene expression responds to environmental conditions – with discrete patterns typical of environmental isolates, which are motility, piliation, and expression of numerous exoproducts. In subacute and chronic infections, the accumulation of intracellular dinucleotides (c-di-GMP) favors a biofilm mode of growth, with the formation of an extracellular polysaccharide matrix2 enabling the organisms to avoid innate immune clearance mechanisms and persist in human airways.3

The organism produces fluorescent siderophores pyoverdin and pyochelin, which function to scavenge iron, and pyocyanin, a pigment with oxidant activity that gives P. aeruginosa its characteristic blue color.4 P. aeruginosa can be identified biochemically as having indophenol oxidase-positive, citrate-positive, and L-arginine dehydrolase-positive activity. Differentiation of P. aeruginosa from the non-aeruginosa pseudomonads or organisms such as Burkholderia species, Stenotrophomonas maltophilia, and Achromobacter spp. occasionally can require testing for DNAse activity, growth at 42°C, and differential carbohydrate metabolism or molecular methods.

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Bacteriophages of Pseudomonas aeruginosa

Victor N. Krylov, in Advances in Virus Research, 2014

(Video) Pseudomonas aeruginosa

Abstract

Bacteria Pseudomonas aeruginosa, being opportunistic pathogens, are the major cause of nosocomial infections and, in some cases, the primary cause of death. They are virtually untreatable with currently known antibiotics. Phage therapy is considered as one of the possible approaches to the treatment of P. aeruginosa infections. Difficulties in the implementation of phage therapy in medical practice are related, for example, to the insufficient number and diversity of virulent phages that are active against P. aeruginosa. Results of interaction of therapeutic phages with bacteria in different conditions and environments are studied insufficiently. A little is known about possible interactions of therapeutic phages with resident prophages and plasmids in clinical strains in the foci of infections. This chapter highlights the different approaches to solving these problems and possible ways to expand the diversity of therapeutic P. aeruginosa phages and organizational arrangements (as banks of phages) to ensure long-term use of phages in the treatment of P. aeruginosa infections.

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PSEUDOMONAS | Pseudomonas aeruginosa

Marjon H.J. Bennik, in Encyclopedia of Food Microbiology, 1999

Characteristics of the Species

Pseudomonas aeruginosa is a Gram-negative rod (0.5–0.8 × 1.5–8μm), which is mobile by polar flagella, and occurs singly, in pairs, or in short chains. This organism has a strictly respiratory type of metabolism with oxygen as the terminal electron acceptor, although nitrate can be used as an alternate electron acceptor. The optimum growth temperature of P. aeruginosa is 37°C. Growth occurs at temperatures as high as 42°C, but not at 4°C. It does not require organic growth factors, and is able to multiply on a wide range of substrates (≥ 82 organic compounds). In addition to its nutritional versatility, this organism is able to produce a wide variety of extracellular enzymes and an extensive slime layer, which can confer resistance to various antimicrobial agents. P. aeruginosa has a relatively large chromosome (5.9Mb; mol% G + C 67%), and it is known to harbour plasmids that can readily be exchanged.

P. aeruginosa is generally considered to be an ubiquitous bacterium that is common in moist environments with low nutrient availability and low ionic strength. It can be isolated from surface water, soil and vegetation, including vegetables and salads. Despite the presence of this bacterium in drinking water and on vegetables, it has rarely been associated with food-borne diseases. However, P. aeruginosa is a typical example of an opportunistic pathogen for humans; it does not attack normal healthy tissue, but can cause serious infection when tissue is damaged prior to exposure to virulent clones. Such clones, which constitute only a small percentage (1–2%) of environmental isolates, can synthesize extracellular products that are thought to play a role in its complex pathogenesis. These include a potent endotoxin or lipopolysaccharide, ADP-ribosyltransferase toxins (exotoxin A and exoenzyme S), haemolysins, phospholipase C (a haemolysin), cytotoxins, proteases, including two with elastase activity, and adherence factors (pili) (Table 1). In addition, the production of an alginate slime layer is a significant adaptation that protects P. aeruginosa against a wide range of challenges.

Table 1. Extracellular products of Pseudomonas aeruginosa

Extracellular productFunction
ProteasesMetalloproteases EBreakdown of proteins; release of substrates
Metalloprotease AP
ElastaseCleavage of transferrin: iron release
PhospholipasePhospholipase CDisruption of phospholipids in membranes and surfactants; haemolytic activity
SiderophoresPyochelinGrowth in iron-limiting conditions
Pyoverdin
ADP-ribosyl transferase toxinsExotoxin AInhibition of protein synthesis
Exoenzyme S
Mucoid exopolysaccharideAlginateAdhesion, protection of cells from antibiotics, disinfectants, biofilm formation
EndotoxinLipopolysaccharide (LPS)Major component of bacterial cell wall
Phenazine pigment pyocyaninStrong reducing potential
RhamnolipidBiosurfactant: non-enzymatic haemolysin and cytolysin; strong reducing potential

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FAQs

What is Pseudomonas aeruginosa known for? ›

Pseudomonas aeruginosa is a Gram-negative and ubiquitous environmental bacterium. It is an opportunistic human pathogen capable of causing a wide array of life-threatening acute and chronic infections, particularly in patients with compromised immune defense.

What is unique about Pseudomonas aeruginosa? ›

Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen of humans that provokes acute and chronic infections. Due to its resistance to a majority of clinically employed antibiotics, P. aeruginosa is considered one of the most concerning infectious agents frequently associated with nosocomial infections.

What is Pseudomonas and what causes it? ›

Pseudomonas is a common type of bacteria usually found in soil and water. It rarely causes problems in people with healthy lungs. Pseudomonas can be difficult to treat, as it doesn't respond to commonly-used antibiotics, like penicillin, doxycycline and erythromycin.

Videos

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4. Pseudomonas Aeruginosa Infection, And Treatment (Antibiotic)
(USMLE pass)
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