Table of Contents
- Introduction
- Classification
- Habitat
- Morphology
- Cultural Characteristics
- Biochemical Characteristics
- Virulence Factors
- Pathogenesis
- Clinical Manifestation
- Lab Diagnosis
- Treatment
- Prevention
- Industrial uses/Applications
- References
Introduction to Pseudomonas aeruginosa
- Pseudomonas aeruginosa is an aerobic, motile, Gram-negative, rod-shaped bacterium that is widely distributed across various habitats around the world.
- It possesses an obligate aerobic metabolism, meaning it requires oxygen for growth and gives a positive oxidase reaction.
- Pseudomonas aeruginosa is the most notable and unique species of its genus and is often used as the type species to represent the genus Pseudomonas.
- This species not only displays all the general characteristics of its genus but also exhibits some uncommon properties that distinguish it from other members.
- P. aeruginosa is classified as one of the fluorescent species because it produces pigments that fluoresce under ultraviolet (UV) radiation.
- In recent years, it has gained significant attention in the medical field due to its wide distribution, high resistance to many antibacterial agents, and the presence of numerous virulence or pathogenicity factors.
- The species name 'aeruginosa' is derived from the Latin term 'aeruginosa', meaning 'full of copper rust' or 'verdigris (green)', referring to the characteristic fluorescence and pigmentation of the organism.
- Initially, this organism was named Bacterium aeruginosum by Schroeter in 1872, but it was later renamed Pseudomonas aeruginosa.
- Medically, P. aeruginosa is of great concern as it is a major cause of both community-acquired and hospital-acquired infections, including hospital-acquired pneumonia and urinary tract infections, among others.
- It is a ubiquitous gamma-proteobacterium found in a wide range of environments, including soil, water, and the living surfaces of plants, animals, and humans.
- P. aeruginosa acts as an opportunistic pathogen; although it may exist harmlessly as part of the normal flora in living organisms, it can cause infections, especially when the host is immunocompromised.
- Despite its pathogenic nature, this bacterium also has industrial significance as it is cultivated for the production of various primary and secondary metabolites.
- These metabolites are utilized in different applications, such as the production of biosurfactants used in environmental cleanup, restoration, and bioremediation.
- One of the primary clinical challenges posed by P. aeruginosa is its increasing resistance to multiple antibiotics, which makes infections caused by it highly difficult to treat once the bacterium has invaded the host body.
Classification of Pseudomonas aeruginosa
- Pseudomonas aeruginosa is classified under the order Pseudomonadales, as determined by phylogenetic analysis of 16S rRNA gene sequences.
- The order Pseudomonadales includes two main families: Pseudomonadaceae and Moraxellaceae.
- Species of the genus Pseudomonas are proteobacteria, specifically belonging to the gamma-proteobacteria subgroup, which is considered the most diverse among the proteobacteria.
- According to rRNA/DNA hybridization studies, the genus Pseudomonas can be further categorized into rRNA homology groups, each of which is significant enough to represent at least a separate genus.
- Historically, the name Pseudomonas was originally applied to rRNA group I, which notably included P. aeruginosa.
- There are approximately 65 recognized species within the genus Pseudomonas. However, this number may be underestimated, as some non-pathogenic species might not yet be officially included.
- A significant aspect of classifying Pseudomonas species involves their ability to produce pigments and fluorescence. P. aeruginosa belongs to the fluorescent group within the genus.
- Among fluorescent Pseudomonas species, P. aeruginosa is uniquely distinguished by the presence of a polar flagellum, aiding in its motility.
- The complete taxonomical classification of Pseudomonas aeruginosa is as follows:
- Domain: Bacteria
- Phylum: Proteobacteria
- Class: Gammaproteobacteria
- Order: Pseudomonadales
- Family: Pseudomonadaceae
- Genus: Pseudomonas
- Species: Pseudomonas aeruginosa
Habitat of Pseudomonas aeruginosa
- Pseudomonas aeruginosa is a ubiquitous bacterium with a wide ecological distribution, inhabiting both natural environments and clinical settings.
- In nature, this microorganism is commonly present in soil and aquatic ecosystems, where it often exists in close association with Bacillus species.
- P. aeruginosa plays an essential role in the rhizosphere of plants and is frequently found in various plant-root and soil samples.
- The bacterium is occasionally detected in natural and processed food products, which can act as potential sources of infection under certain conditions.
- In humans, P. aeruginosa is part of the normal flora, colonizing body areas such as the respiratory tract, skin, and digestive system.
- As a member of the normal microbiota, it contributes to the production of primary and secondary metabolites that may be beneficial to the host.
- Despite its role in normal flora, P. aeruginosa is an opportunistic pathogen, capable of causing mild to severe infections when it reaches sterile body sites.
- Its versatile metabolic capabilities enable it to colonize both living (animate) surfaces and diverse environmental habitats.
- Additionally, the organism’s ability to respond to environmental fluctuations and exchange genetic material with other microbes enhances its adaptability, making it a key component of natural microbial communities.
Morphology of Pseudomonas aeruginosa
- The cells of Pseudomonas aeruginosa are rod-shaped, typically measuring 0.5 to 0.8 µm in width and 1.5 to 3.0 µm in length.
- These cells are Gram-negative and usually occur as single cells or in pairs.
- P. aeruginosa produces water-soluble pigments that diffuse through the surrounding media, contributing to its characteristic appearance.
- All strains of P. aeruginosa are motile, possessing a single flagellum located at the tip of the cell.
- The flagella can be either polar or subpolar, depending on the strain.
- These flagella generate heat-labile antigens (H antigens), which function as virulence factors in pathogenic strains.
- In addition to flagella, some strains also possess polar fimbriae or pili, typically 6 nm wide, which serve as receptors for various bacteriophages and can be retractile.
- The cell envelope structure is typical of Gram-negative bacteria and is composed of three distinct layers:
- An outer membrane
- A peptidoglycan layer
- An inner cytoplasmic membrane
- The cell membrane consists of a lipid bilayer that can rapidly adjust its fluidity in response to environmental changes.
- The outer membrane is asymmetrical and contains a special lipopolysaccharide (LPS) that reduces membrane fluidity.
- Different serologic types of P. aeruginosa have been identified based on O-specific antigen analysis.
- The cells often appear pigmented, as they are capable of producing up to six different pigments, with phenazine blue pigment being the most commonly observed among them.
Cultural Characteristics of Pseudomonas aeruginosa
- Pseudomonas aeruginosa can grow on solid agar media within a temperature range of 4°C to 44°C, but growth is more prominent at higher temperatures.
- It has simple nutritional requirements, being able to grow in media where acetate is used as a carbon source and ammonium sulfate as a nitrogen source.
- On solid media, P. aeruginosa produces two main colony types:
- Large, smooth colonies with flat edges and elevated centers, giving a fried-egg appearance.
- Small, rough, convex colonies.
- Clinical isolates of the organism tend to produce large colony types, while environmental or natural source isolates usually produce small colonies.
- Large colonies may exhibit silver-grey metallic sheen patches at their edges.
- A third colony type, the mucoid form, is observed particularly in strains isolated from respiratory or urinary tract infections.
- Colonies on agar often show localized swarming starting from the edge of the colony and produce green, fluorescent pigments.
- Colonies typically emit a distinct fruity odor and display metallic patches, which are characteristic features.
- On sheep blood agar, when incubated at 37°C, colonies are visible after 24 to 48 hours, showing various appearances, from smooth to rough.
- P. aeruginosa strains are frequently β-hemolytic on blood agar, as seen by a clear zone around the colonies under reflected and transmitted light.
- Some colonies exhibit a “beaten-copper” surface with slightly irregular edges.
- Capsulated strains, especially those isolated from pneumonia patients, produce large, mucoid colonies.
- On routine blood agar, colonies appear pigmented, ranging from gray or gray-white with yellowish tint to green, red, or brown, depending on the pigment type.
- Pigment production is more distinct and enhanced on transparent media, such as Mueller-Hinton agar.
On Nutrient Agar (NA):
- Colonies are large, opaque, flat, with irregular margins and emit a fruity or earthy odor.
- Colonies are usually green-pigmented due to the production of pyoverdin pigment.
On Cetrimide Agar:
- Colonies appear yellow-green to blue in color, indicating the presence of P. aeruginosa.
- Colonies are medium-sized with irregular edges.
- Ultraviolet light is used to detect fluorescein pigment for confirmation.
On MacConkey Agar:
- Colonies are round, flat, and colorless, indicating the organism is a lactose non-fermenter.
- Fluorescence is also observed under UV light, similar to cetrimide agar.
On Blood Agar:
- Colonies are of mucoid type with a metallic sheen.
- β-hemolysis is evident by a clear hemolytic zone around the colonies.
Biochemical Characteristics of Pseudomonas aeruginosa
Biochemical Characteristics of Pseudomonas aeruginosa
S.N | Biochemical Characteristic | P. aeruginosa |
---|---|---|
1 | Capsule | Non-Capsulated |
2 | Shape | Rod |
3 | Gram Staining | Gram-Negative |
4 | Catalase | Positive (+) |
5 | Oxidase | Positive (+) |
6 | Citrate | Positive (+) |
7 | Methyl Red (MR) | Negative (-) |
8 | Voges Proskauer (VP) | Negative (-) |
9 | OF (Oxidative-Fermentative) | Oxidative |
10 | Coagulase | Negative (-) |
11 | DNase | Negative (-) |
12 | Urease | Negative (-) |
13 | Gas | Negative (-) |
14 | H2S | Negative (-) |
15 | Hemolysis | β-hemolytic |
16 | Motility | Motile with single flagella |
17 | Nitrate Reduction | Positive (+) |
18 | Gelatin Hydrolysis | Positive (+) |
19 | Pigment Production | Positive (+) |
20 | Indole | Negative (-) |
21 | TSIA | Alkali/Alkali (Red/Red) |
22 | Spore | Non-sporing |
23 | Cetrimide Test | Positive (+) |
Fermentation Profile of P. aeruginosa
S.N | Substrate | Result |
---|---|---|
1 | Adonitol | Negative (-) |
2 | Arabinose | Negative (-) |
3 | Cellobiose | Negative (-) |
4 | Dulcitol | Negative (-) |
5 | Fructose | Positive (+) |
6 | Galactose | Negative (-) |
7 | Glucose | Positive (+) |
8 | Glycerol | Positive (+) |
9 | Glycogen | Negative (-) |
10 | Hippurate | Negative (-) |
11 | Inulin | Negative (-) |
12 | Inositol | Negative (-) |
13 | Lactose | Negative (-) |
14 | Malonate | Positive (+) |
15 | Maltose | Positive (+) |
16 | Mannitol | Negative (-) |
17 | Mannose | Negative (-) |
18 | Pyruvate | Negative (-) |
19 | Raffinose | Negative (-) |
20 | Rhamnose | Negative (-) |
21 | Ribose | Positive (+) |
22 | Salicin | Positive (+) |
23 | Sorbitol | Negative (-) |
24 | Starch | Negative (-) |
25 | Sucrose | Negative (-) |
26 | Trehalose | Negative (-) |
27 | Xylose | Negative (-) |
Enzymatic Reactions of P. aeruginosa
S.N | Enzyme | Result |
---|---|---|
1 | Acetoin | Negative (-) |
2 | Acetate Utilization | Positive (+) |
3 | Arginine Dehydrolase | Positive (+) |
4 | Esculin Hydrolysis | Negative (-) |
5 | Lecithinase | Negative (-) |
6 | Lipase | Positive (+) |
7 | Lysine | Negative (-) |
8 | Ornithine Decarboxylase | Negative (-) |
9 | Phenylalanine Deaminase | Negative (-) |
Virulence Factors of Pseudomonas aeruginosa
Pseudomonas aeruginosa is a highly adaptable opportunistic pathogen, frequently implicated in a range of nosocomial infections, especially among immunocompromised individuals. Its ability to establish infection, survive, and evade host immune responses is largely attributed to an array of virulence factors.
These virulence determinants are classified based on their role during the course of infection and include:
1. Factors involved in entry, attachment, and motility
2. Factors facilitating host colonization
3. Mechanisms promoting chronic infection
1. Factors Involved in Entry, Attachment, and Motility
Flagella
- All P. aeruginosa strains possess a single polar flagellum, enabling swimming motility. The flagellar filament is driven by a basal motor, functioning in a helical motion. This structure facilitates bacterial movement through the respiratory tract and plays a critical role in initial attachment to respiratory epithelial cells.
- Flagella also activate the host immune system by interacting with Toll-like receptors (TLRs) on epithelial surfaces, triggering the release of inflammatory mediators such as interleukin-8 (IL-8), interleukin-6 (IL-6), and mucin.
Pili
- Type IV pili are primary adhesins that promote adherence of P. aeruginosa to host epithelial cells. These pili recognize and bind to glycosylated moieties on glycosphingolipids GM1 and GM2 of the host cell surface.
- Additionally, fimbrial (chaperone/cup)-type pili support attachment to both biotic and abiotic surfaces, facilitating the formation of robust biofilms.
Lipopolysaccharides (LPS)
- The outer membrane of P. aeruginosa contains lipopolysaccharides, which provide protection from host immune components and contribute to endotoxicity.
- LPS is composed of:
- Lipid A: The toxic component responsible for excessive immune activation and potential septic shock.
- Core oligosaccharide
- O-antigen: Shields the bacteria from lysis by the host's complement system.
- LPS is a potent inducer of inflammation due to its interaction with host immune receptors.
2. Factors Involved in Host Colonization
Exotoxin A
- Exotoxin A is among the most significant protein toxins produced by P. aeruginosa. Secreted initially as an inactive precursor, it consists of two functional domains:
- Domain B binds to host cell surface receptors.
- Domain A inhibits protein synthesis within host cells, leading to cell necrosis.
Elastase
- Elastase is a zinc metalloprotease with strong proteolytic activity against elastin, a key component of connective tissue.
- Two key elastases mediate this function:
- LasA: A serine protease
- LasB: A zinc metalloprotease
- These enzymes act synergistically to enhance elastin degradation. Additionally, they target and degrade:
- Immunoglobulins IgA and IgG
- Components of the complement system
- Cytokines including interferon-gamma (IFN-γ) and tumor necrosis factor (TNF)
Pigments
- P. aeruginosa synthesizes characteristic pigments such as pyocyanin and pyoverdin:
- Pyocyanin: Suppresses host immune responses and induces neutrophil apoptosis.
- Pyoverdin: Functions in iron scavenging and also regulates secretion of virulence factors, including exotoxin A.
- These pigments contribute to inflammation by upregulating IL-8 and disrupt cellular functions by inhibiting vacuolar ATPases and mitochondrial transport.
Enzymes
- Enzymatic factors like alkaline protease and protease IV also play important roles in pathogenesis.
- Alkaline protease degrades fibrin, enhancing tissue invasion and colonization by the bacteria.
3. Factors Involved in Chronic Infections
a. Iron Acquisition
- Iron is a vital micronutrient for P. aeruginosa survival and virulence during infection. The bacterium employs various strategies to obtain iron, including:
- Production of chelating agents
- Utilization of iron-loaded pyoverdin
- Secretion of exotoxin A
- These mechanisms ensure bacterial proliferation and persistence in iron-limited environments within the host.
b. Alginates and Biofilm Formation
- Biofilm development is a hallmark of chronic P. aeruginosa infections, particularly in hospital environments. The biofilm consists of microcolonies embedded within an exopolysaccharide matrix, predominantly composed of alginates.
- Benefits of biofilm formation include:
- Enhanced resistance to host immune defenses
- Reduced antibiotic penetration
- Protection from phagocytosis and antibody activity
- These properties contribute significantly to the chronic and recurrent nature of P. aeruginosa infections.
Pathogenesis of Pseudomonas aeruginosa
Pseudomonas aeruginosa is an opportunistic pathogen capable of causing severe infections, particularly in immunocompromised individuals. Its pathogenesis is attributed to a wide array of virulence factors that assist in colonization, tissue invasion, immune evasion, and long-term persistence.
1. Bacterial Attachment and Colonization
- The infection begins with the entry of the bacterium into the host, commonly through damaged or punctured skin and mucosal tissues—especially in hospital-acquired infections.
- Motility structures such as the flagellum allow the bacteria to move through host tissues toward target sites.
- Type IV pili facilitate attachment to host epithelial cells by binding to glycosphingolipids present on their surfaces.
- Proteolytic enzymes, particularly elastase, degrade elastin in tissues, creating a path for bacterial invasion and enhancing colonization.
2. Invasion of Host Tissues
- Once colonization is established, P. aeruginosa utilizes the Type III secretion system (T3SS) to inject toxic effector proteins directly into host cells.
- Key toxins include:
- ExoS and ExoT: Bifunctional cytotoxins with Rho GTPase-activating and ADP-ribosyltransferase activity. These disrupt:
- Cytoskeletal structures
- Focal adhesions
- Host signaling pathways
- ➝ Resulting in impaired phagocytosis.
- ExoU: A potent phospholipase contributing to acute cytotoxicity, especially damaging epithelial cells and macrophages.
- Other effectors affect cAMP levels and cytoskeleton reorganization, further compromising host cell integrity.
3. Biofilm Formation

- Biofilm formation is a major virulence mechanism that protects P. aeruginosa from host immunity and antibiotics.
- Components involved in biofilm structure include:
- Exopolysaccharides
- Rhamnolipids
- Pyoverdine
- Surface proteins and appendages
- In a mature biofilm:
- Cell differentiation occurs.
- Water and oxygen channels form to nourish deep cells.
- Bacteria exhibit up to 1000× more resistance to antimicrobial agents compared to planktonic (free-living) cells.
Clinical Manifestation of Pseudomonas aeruginosa
Pseudomonas aeruginosa is an opportunistic pathogen responsible for a wide range of infections. The clinical severity can vary from mild urinary tract infections to life-threatening conditions such as bacteremia and septic shock. Infections are often associated with immunocompromised patients and those exposed to invasive medical procedures or devices.
a. Pneumonia
- Pneumonia caused by P. aeruginosa is typically nosocomial (hospital-acquired). One of the most common sources is contaminated bronchoscopes or ventilators.
- Symptoms: Fever, chills, shortness of breath, and productive cough with yellow, green, or even bloody mucus.
- The bacteria can colonize both upper and lower respiratory tracts, leading to:
- Extensive bronchopneumonia
- Necrosis of alveolar walls
- Abscess formation across lung lobes
- Ventilator-associated pneumonia (VAP) is a common presentation in ICU settings.
b. Sepsis / Bacteremia
- P. aeruginosa is a significant cause of nosocomial bloodstream infections, especially in immunocompromised or critically ill patients.
- Septicemia occurs when the bacteria enter and spread through the bloodstream.
- Clinical features may include:
- Hypotension
- Irregular cardiac output
- Metabolic acidosis
- Multiorgan dysfunction
- The bacteria may reach heart valves, causing endocarditis, particularly in IV drug users or patients with indwelling catheters.
- Biofilm formation and exotoxins contribute to immune system evasion and septic shock.
c. Urinary Tract Infection (UTI)
- UTIs caused by P. aeruginosa often occur in hospitalized patients using catheters, external medical devices, or undergoing dialysis.
- Entry route: Skin colonization followed by ascent through the urinary tract.
- Site of infection: The bacteria may colonize the bladder, forming biofilms that resist host immune responses and antibiotics.
- Symptoms:
- Dysuria (painful urination)
- Hematuria (bloody urine)
- Cloudy urine
- Lower abdominal or pelvic pain
- Tissue invasion may lead to necrosis and extensive epithelial damage.
Lab Diagnosis of Pseudomonas aeruginosa
Diagnosis is primarily based on the isolation and identification of P. aeruginosa from relevant clinical samples depending on the site of infection.
a. Sample collection
- The type of clinical sample depends on the site of infection:
- Sputum or respiratory aspirates for pneumonia
- Urine for urinary tract infections
- The quality and appropriateness of the sample are crucial for accurate detection.
- If required, suitable transport media should be used to maintain sample integrity during transit to the lab.
b. Morphological, Cultural and Biochemical Characteristics
- P. aeruginosa can be cultured on blood agar or eosin-methylene blue (EMB) agar.
- Optimal growth is observed at 37°C, but it can also grow at temperatures up to 42°C.
- On microscopic examination, it appears as Gram-negative rods, offering preliminary diagnostic clues.
- Colony morphology on various media helps distinguish P. aeruginosa from other organisms.
- A unique feature is the production of fluorescein pigment, which is visible under UV light.
- Confirmation is achieved by performing biochemical tests, which support species-level identification.
c. Immunological tests
- Although not used routinely, tests like crossed immune electrophoresis (CIE), Western blot, and ELISA can be used as confirmatory methods.
- These assays detect specific P. aeruginosa antigens such as elastase, exotoxin A, and alkaline proteases.
- Immunological tests are rapid and support early diagnosis, potentially preventing chronic or systemic infection.
d. Molecular Diagnosis
- Molecular methods are now widely used due to their accuracy and speed.
- Techniques such as Polymerase Chain Reaction (PCR) and DNA hybridization are common.
- RNA sequencing may also be employed for high-precision identification.
- These tests can provide a rapid and definitive diagnosis, improving patient management and treatment outcomes.
Treatment of Pseudomonas aeruginosa
- The choice of treatment depends on the severity of the infection.
- For mild infections, IV antibiotics are often sufficient for effective treatment.
- In more severe or deep infections, surgical debridement may be required to remove infected tissue.
- For patients experiencing respiratory failure, pneumonia, sepsis, or other systemic infections, ICU admission may become necessary.
- Double pseudomonal coverage is sometimes considered in addition to broad-spectrum antibiotics for enhanced efficacy.
- First-line antibiotics commonly used include:
- Carbapenems (e.g., imipenem, meropenem)
- Cephalosporins (e.g., ceftazidime, cefepime)
- Aminoglycosides (e.g., gentamicin, tobramycin)
- Fluoroquinolones (e.g., ciprofloxacin, levofloxacin)
- For systemic infections, a longer duration of antibiotic therapy may be needed for complete eradication.
- If the infection is related to medical devices such as catheters, the removal of the device is recommended to prevent recurrence.
Prevention of Pseudomonas aeruginosa
- Most Pseudomonas aeruginosa infections are nosocomial (hospital-acquired), so specific precautions in clinical settings are essential.
- Health personnel should follow strict infection control precautions.
- Strict adherence to hand hygiene and consistent use of gowns and gloves is recommended.
- Infections can also be triggered by poor sanitary habits of patients, so maintaining patient hygiene is important.
- Respirators, catheters, and other medical instruments must be carefully cleaned and regularly monitored.
- The use of topical antibacterial agents on burns has been shown to dramatically reduce the incidence of P. aeruginosa infections.
Industrial uses / Applications of Pseudomonas aeruginosa
- Various secondary metabolites produced by Pseudomonas aeruginosa play a vital role in controlling multiple drug-resistant bacteria.
- An esterase enzyme from P. aeruginosa can hydrolyze racemic methyl ester of β-acetylthioisobutyrate to form the D-enantiomer, which serves as a precursor for captopril—an essential drug for treating congestive heart failure and hypertension.
- Vanillin produced by P. aeruginosa is used as a natural flavoring agent in food, cosmetic, and pharmaceutical products.
- Rhamnolipids from P. aeruginosa are employed in the food industry to extend shelf life due to their antimicrobial properties.
- Proteases produced by this bacterium have widespread applications in food processing and textile industries.
- Pigments synthesized by P. aeruginosa serve as bio-pigments for coloring and are also used in environmental remediation of harmful pesticides and chemicals.
References
- Whitman, W.B., Garrity, G.M., De Vos, P., Jones, D., & Bergey, D.H. (2009). Bergey’s Manual of Systematic Bacteriology: Volume 2. Springer, New York.
- Alhazmi, A. (2015). Pseudomonas aeruginosa – Pathogenesis and Pathogenic Mechanisms. International Journal of Biology, 7(2). https://doi.org/10.5539/ijb.v7n2p44
- Klockgether, J., & Tümmler, B. (2017). Recent developments in understanding Pseudomonas aeruginosa as a pathogen. F1000Research, 6, 1261. https://doi.org/10.12688/f1000research.10506.1
- Fujitani, S., Sun, H.Y., Yu, V.L., & Weingarten, J.A. (2011). Pneumonia due to Pseudomonas aeruginosa: Part I: Epidemiology, clinical diagnosis, and sources. Chest, 139(4), 909–919. https://doi.org/10.1378/chest.10-0166
- Palleroni, N.J. (2015). Pseudomonas. In Trujillo, M.E. et al. (Eds.), Bergey’s Manual of Systematics of Archaea and Bacteria. https://doi.org/10.1002/9781118960608.gbm01210
- Dropulic, L.K., Leslie, J.M., Eldred, L.J., Zenilman, J., & Sears, C.L. (1995). Clinical Features and Risk Factors of Pseudomonas aeruginosa Infection in AIDS Patients. Journal of Infectious Diseases, 171(4), 930–937. https://doi.org/10.1093/infdis/171.4.930
- Orji, F.A., Ezeanyanso, C.S., Onyemali, C.P., Ukaegbu, G.N., Ajunwa, O., & Lawal, O.M. (2019). The Beneficial Roles of Pseudomonas in Medicine, Industries, and Environment. In Sriramulu, D. (Ed.), Pseudomonas aeruginosa – An Armory Within. IntechOpen. https://doi.org/10.5772/intechopen.85996
- Wilson, M.G., & Pandey, S. (2020). Pseudomonas aeruginosa. In: StatPearls. StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK557831/
- de Bentzmann, S., & Plésiat, P. (2011). Pseudomonas aeruginosa as an Opportunistic Pathogen and Its Role in Human Infections. Environmental Microbiology, 13(7), 1655–1665. https://doi.org/10.1111/j.1462-2920.2011.02469.x
- Hatchette, T.F., Gupta, R., & Marrie, T.J. (2000). Community-acquired Pneumonia Due to Pseudomonas aeruginosa in Healthy Adults: Case Report and Literature Review. Clinical Infectious Diseases, 31(6), 1349–1356. https://doi.org/10.1086/317486
- Iglewski, B.H. (1996). Pseudomonas. In Baron, S. (Ed.), Medical Microbiology (4th ed.). University of Texas Medical Branch at Galveston. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK8326/
- Morales, G. et al. (2004). Genetic Structure of Pseudomonas aeruginosa Populations by SNP and PFGE Genotyping. Journal of Bacteriology, 186(13), 4228–4237. https://doi.org/10.1128/JB.186.13.4228-4237.2004
- Van der Bij, A.K., Mol, M., van Westreenen, M., Goessens, W.H., & Pitout, J.D. (2011). Lab Diagnosis of Metallo-β-lactamase-Producing Pseudomonas aeruginosa in a Dutch Tertiary Care Centre. Scandinavian Journal of Infectious Diseases, 43(8), 596–602. https://doi.org/10.3109/00365548.2011.574148
- Topley, W.W.C. (2007). Topley and Wilson’s Microbiology and Microbial Infections: Bacteriology (10th ed., Vol. 2). John Wiley & Sons.
- Tramper-Stranders, G.A., et al. (2006). Diagnostic Utility of Serological Tests for Pseudomonas aeruginosa in a Large CF Population. Thorax, 61(8), 689–693. https://doi.org/10.1136/thx.2005.054726
- Ben Haj Khalifa, A., Moissenet, D., Vu Thien, H., & Khedher, M. (2011). Virulence Factors of Pseudomonas aeruginosa: Mechanisms and Regulation. Annales de Biologie Clinique, 69(4), 393–403. https://doi.org/10.1684/abc.2011.0589
- Berube, B.J., et al. (2016). Pseudomonas aeruginosa: Breaching Barriers. Current Genetics, 62(1), 109–113. https://doi.org/10.1007/s00294-015-0522-x