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Pseudomonas aeruginosa Pathogenesis

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A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Bacterial Pathogens".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 59255

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Special Issue Editors

Dr. Natalia Kirienko

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Guest Editor

BioSciences, Rice University, 77005, Houston, USA
Interests: P. aeruginosa; C. elegans; host–pathogen interactions; small-molecule screening; novel therapeutics

Dr. Carolyn Cannon

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Guest Editor

Microbial Pathogenesis and Immunology, Texas A&M University Health Science Center, 77807, Bryan, USA
Interests: cystic fibrosis; P. aeruginosa; S. aureus; mouse infection models; antimicrobial development; nanoparticle drug delivery devices

Special Issue Information

Dear Colleagues,

Pseudomonas aeruginosa is an important, opportunistic Gram-negative pathogen that causes a wide variety of hospital-acquired infections, including ventilator-associated pneumonia, and infections of surgical sites, medical implants, and various soft tissues [1]. The pathogen is well-known for its diverse armamentarium of virulence determinants, including biofilm formation, production of various toxins, and its characteristic resistance to antimicrobials [2–6].

P. aeruginosa is also a key example of a bacterial species reemerging as a clinical threat with the spread of antimicrobial resistance, as highly lethal, pandrug-resistant strains are beginning to be identified throughout the world [7]. To address these concerns, it is imperative that we gain new insight into the interactions between this pathogen and its hosts, and mechanisms of pathogenesis to guide the development of effective treatments [8,9].

Despite extensive study, new discoveries about P. aeruginosa pathogenesis, and its interactions with its hosts, are made regularly, highlighting how much remains to be discovered. In this Special Issue, we are requesting publications that shine new light on P. aeruginosa virulence determinants, interactions with its host, mechanisms of pathogenesis and immune avoidance or activation, or other aspects of the ability of this pathogen to cause disease, or new ways of preventing these. It is only by understanding these mechanisms and determinants that effective treatments can be discovered, an essential goal as the efficacy of conventional antimicrobials continues to wane.

We encourage the submission of Articles, Communications, or Reviews focused on mechanisms of pathogenesis or novel compounds intended to mitigate it. All submitted papers will undergo a standard independent peer-review process.

References [optional]:

Baron, S. (1996) Medical microbiology. Galveston, Tex.: University of Texas Medical Branch at Galveston. xvii, 1273 p. p.
Wagner, V.E.; Frelinger, J.G.; Barth, R.K.; Iglewski, B.H. (2006) Quorum sensing: dynamic response of Pseudomonas aeruginosa to external signals. Trends Microbiol 14: 55-58.
Hauser, A.R. (2009) The type III secretion system of Pseudomonas aeruginosa: infection by injection. Nat Rev Microbiol 7: 654-665.
Piddock, L.J. (2006) Multidrug-resistance efflux pumps - not just for resistance. Nat Rev Microbiol 4: 629-636.
Rada, B.; Leto, T.L. (2013) Pyocyanin effects on respiratory epithelium: relevance in Pseudomonas aeruginosa airway infections. Trends Microbiol 21: 73-81.
Deng, Q.; Barbieri, J.T. (2008) Molecular mechanisms of the cytotoxicity of ADP-ribosylating toxins. Annu Rev Microbiol 62: 271-288.
Wang, C.Y.; Jerng, J.S.; Chen, K.Y.; Lee, L.N.; Yu, C.J.; et al. (2006) Pandrug-resistant Pseudomonas aeruginosa among hospitalised patients: clinical features, risk-factors and outcomes. Clin Microbiol Infect 12: 63-68.
Martinez, O.F.; Cardoso, M.H.; Ribeiro, S.M.; Franco, O.L. (2019) Recent Advances in Anti-virulence Therapeutic Strategies With a Focus on Dismantling Bacterial Membrane Microdomains, Toxin Neutralization, Quorum-Sensing Interference and Biofilm Inhibition. Front Cell Infect Microbiol 9: 74.
Kirienko, N.V.; Rahme, L.; Cho, Y.-H. (2019) Beyond Antimicrobials: Non-traditional approaches to combating multidrug-resistant bacteria. Front Cell Infect Microbiol. in press

Dr. Natalia Kirienko
Dr. Carolyn Cannon
Guest Editors

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Keywords

Pseudomonas aeruginosa
pathogenesis
virulence determinants
toxins
biofilm
quorum sensing
host–pathogen interactions
antimicrobial resistance
novel therapeutics

Published Papers (11 papers)

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Research

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12 pages, 296 KiB

Open AccessArticle

Pseudomonas aeruginosa Bloodstream Infections in Patients with Cancer: Differences between Patients with Hematological Malignancies and Solid Tumors

by Cristina Royo-Cebrecos, Julia Laporte-Amargós, Marta Peña, Isabel Ruiz-Camps, Pedro Puerta-Alcalde, Edson Abdala, Chiara Oltolini, Murat Akova, Miguel Montejo, Malgorzata Mikulska, Pilar Martín-Dávila, Fabian Herrera, Oriol Gasch, Lubos Drgona, Hugo Manuel Paz Morales, Anne-Sophie Brunel, Estefanía García, Burcu Isler, Winfried V. Kern, Zaira R. Palacios-Baena, Guillermo Maestro de la Calle, Maria Milagro Montero, Souha S. Kanj, Oguz R. Sipahi, Sebnem Calik, Ignacio Márquez-Gómez, Jorge I. Marin, Marisa Z. R. Gomes, Philipp Hemmatti, Rafael Araos, Maddalena Peghin, José Luis del Pozo, Lucrecia Yáñez, Robert Tilley, Adriana Manzur, Andrés Novo, Jordi Carratalà and Carlota Gudiol Show full author list Hide full author list

Pathogens 2022, 11(10), 1132; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11101132 - 30 Sep 2022

Cited by 8 | Viewed by 2518

Abstract

Objectives: To assess the clinical features and outcomes of Pseudomonas aeruginosa bloodstream infection (PA BSI) in neutropenic patients with hematological malignancies (HM) and with solid tumors (ST), and identify the risk factors for 30-day mortality. Methods: We performed a large multicenter, retrospective cohort study including onco-hematological neutropenic patients with PA BSI conducted across 34 centers in 12 countries (January 2006–May 2018). Episodes occurring in hematologic patients were compared to those developing in patients with ST. Risk factors associated with 30-day mortality were investigated in both groups. Results: Of 1217 episodes of PA BSI, 917 occurred in patients with HM and 300 in patients with ST. Hematological patients had more commonly profound neutropenia (0.1 × 10⁹ cells/mm) (67% vs. 44.6%; p < 0.001), and a high risk Multinational Association for Supportive Care in Cancer (MASCC) index score (32.2% vs. 26.7%; p = 0.05). Catheter-infection (10.7% vs. 4.7%; p = 0.001), mucositis (2.4% vs. 0.7%; p = 0.042), and perianal infection (3.6% vs. 0.3%; p = 0.001) predominated as BSI sources in the hematological patients, whereas pneumonia (22.9% vs. 33.7%; p < 0.001) and other abdominal sites (2.8% vs. 6.3%; p = 0.006) were more common in patients with ST. Hematological patients had more frequent BSI due to multidrug-resistant P. aeruginosa (MDRPA) (23.2% vs. 7.7%; p < 0.001), and were more likely to receive inadequate initial antibiotic therapy (IEAT) (20.1% vs. 12%; p < 0.001). Patients with ST presented more frequently with septic shock (45.8% vs. 30%; p < 0.001), and presented worse outcomes, with increased 7-day (38% vs. 24.2%; p < 0.001) and 30-day (49% vs. 37.3%; p < 0.001) case-fatality rates. Risk factors for 30-day mortality in hematologic patients were high risk MASCC index score, IEAT, pneumonia, infection due to MDRPA, and septic shock. Risk factors for 30-day mortality in patients with ST were high risk MASCC index score, IEAT, persistent BSI, and septic shock. Therapy with granulocyte colony-stimulating factor was associated with survival in both groups. Conclusions: The clinical features and outcomes of PA BSI in neutropenic cancer patients showed some differences depending on the underlying malignancy. Considering these differences and the risk factors for mortality may be useful to optimize their therapeutic management. Among the risk factors associated with overall mortality, IEAT and the administration of granulocyte colony-stimulating factor were the only modifiable variables. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

8 pages, 974 KiB

Open AccessCommunication

Host Protease Activity on Bacterial Pathogens Promotes Complement and Antibiotic-Directed Killing

by Shaorong Chen, Dongmei Zhang, Alexandria-Jade Roberts, Hsueh-Chung Lu, Carolyn L. Cannon, Qing-Ming Qin and Paul de Figueiredo

Pathogens 2021, 10(11), 1506; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10111506 - 18 Nov 2021

Cited by 1 | Viewed by 2029

Abstract

Our understanding of how the host immune system thwarts bacterial evasive mechanisms remains incomplete. Here, we show that host protease neutrophil elastase acts on Acinetobacter baumannii and Pseudomonas aeruginosa to destroy factors that prevent serum-associated, complement-directed killing. The protease activity also enhances bacterial susceptibility to antibiotics in sera. These findings implicate a new paradigm where host protease activity on bacteria acts combinatorially with the host complement system and antibiotics to defeat bacterial pathogens. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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16 pages, 3274 KiB

Open AccessArticle

Human Single-Chain Antibodies That Neutralize Elastolytic Activity of Pseudomonas aeruginosa LasB

by Sirijan Santajit, Thida Kong-ngoen, Manas Chongsa-Nguan, Usa Boonyuen, Pornpan Pumirat, Nitat Sookrung, Wanpen Chaicumpa and Nitaya Indrawattana

Pathogens 2021, 10(6), 765; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10060765 - 17 Jun 2021

Cited by 8 | Viewed by 2469

Abstract

LasB (elastase/pseudolysin) is an injurious zinc-metalloprotease secreted by the infecting Pseudomonas aeruginosa. LasB is recognized as the bacterial key virulence factor for establishment of successful infection, acquisition of nutrients, dissemination, tissue invasion, and immune modulation and evasion. LasB digests a variety of the host tissue proteins, extracellular matrices, as well as components of both innate and adaptive immune systems, including immunoglobulins, complement proteins, and cytokines. Thus, this enzyme is an attractive target for disarming the P. aeruginosa. This study generated human single-chain antibodies (HuscFvs) that can neutralize the elastolytic activity of native LasB by using phage display technology. Gene sequences coding HuscFvs (huscfvs) isolated from HuscFv-displaying phage clones that bound to enzymatically active LasB were sub-cloned to expression plasmids for large scale production of the recombinant HuscFvs by the huscfv-plasmid transformed Escherichia coli. HuscFvs of two transformed E. coli clones, i.e., HuscFv-N42 and HuscFv-N45, neutralized the LasB elastolytic activities in vitro. Computer simulation by homology modeling and molecular docking demonstrated that antibodies presumptively formed contact interfaces with the LasB residues critical for the catalytic activity. Although the LasB neutralizing mechanisms await elucidation by laboratory experiments, the HuscFvs should be tested further towards the clinical application as a novel adjunctive therapeutics to mitigate severity of the diseases caused by P. aeruginosa. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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10 pages, 1570 KiB

Open AccessEditor’s ChoiceArticle

A Novel Infection Protocol in Zebrafish Embryo to Assess Pseudomonas aeruginosa Virulence and Validate Efficacy of a Quorum Sensing Inhibitor In Vivo

by Pauline Nogaret, Fatima El Garah and Anne-Béatrice Blanc-Potard

Pathogens 2021, 10(4), 401; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10040401 - 29 Mar 2021

Cited by 15 | Viewed by 3393

Abstract

The opportunistic human pathogen Pseudomonas aeruginosa is responsible for a variety of acute infections and is a major cause of mortality in chronically infected cystic fibrosis patients. Due to increased resistance to antibiotics, new therapeutic strategies against P. aeruginosa are urgently needed. In this context, we aimed to develop a simple vertebrate animal model to rapidly assess in vivo drug efficacy against P. aeruginosa. Zebrafish are increasingly considered for modeling human infections caused by bacterial pathogens, which are commonly microinjected in embryos. In the present study, we established a novel protocol for zebrafish infection by P. aeruginosa based on bath immersion in 96-well plates of tail-injured embryos. The immersion method, followed by a 48-hour survey of embryo viability, was first validated to assess the virulence of P. aeruginosa wild-type PAO1 and a known attenuated mutant. We then validated its relevance for antipseudomonal drug testing by first using a clinically used antibiotic, ciprofloxacin. Secondly, we used a novel quorum sensing (QS) inhibitory molecule, N-(2-pyrimidyl)butanamide (C11), the activity of which had been validated in vitro but not previously tested in any animal model. A significant protective effect of C11 was observed on infected embryos, supporting the ability of C11 to attenuate in vivo P. aeruginosa pathogenicity. In conclusion, we present here a new and reliable method to compare the virulence of P. aeruginosa strains in vivo and to rapidly assess the efficacy of clinically relevant drugs against P. aeruginosa, including new antivirulence compounds. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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14 pages, 3325 KiB

Open AccessArticle

An In Vitro Cell Culture Model for Pyoverdine-Mediated Virulence

by Donghoon Kang and Natalia V. Kirienko

Pathogens 2021, 10(1), 9; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10010009 - 24 Dec 2020

Cited by 12 | Viewed by 3046

Abstract

Pseudomonas aeruginosa is a multidrug-resistant, opportunistic pathogen that utilizes a wide-range of virulence factors to cause acute, life-threatening infections in immunocompromised patients, especially those in intensive care units. It also causes debilitating chronic infections that shorten lives and worsen the quality of life for cystic fibrosis patients. One of the key virulence factors in P. aeruginosa is the siderophore pyoverdine, which provides the pathogen with iron during infection, regulates the production of secreted toxins, and disrupts host iron and mitochondrial homeostasis. These roles have been characterized in model organisms such as Caenorhabditis elegans and mice. However, an intermediary system, using cell culture to investigate the activity of this siderophore has been absent. In this report, we describe such a system, using murine macrophages treated with pyoverdine. We demonstrate that pyoverdine-rich filtrates from P. aeruginosa exhibit substantial cytotoxicity, and that the inhibition of pyoverdine production (genetic or chemical) is sufficient to mitigate virulence. Furthermore, consistent with previous observations made in C. elegans, pyoverdine translocates into cells and disrupts host mitochondrial homeostasis. Most importantly, we observe a strong correlation between pyoverdine production and virulence in P. aeruginosa clinical isolates, confirming pyoverdine’s value as a promising target for therapeutic intervention. This in vitro cell culture model will allow rapid validation of pyoverdine antivirulents in a simple but physiologically relevant manner. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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14 pages, 1558 KiB

Open AccessArticle

Clinical Biofilm Ring Test^® Reveals the Potential Role of β-Lactams in the Induction of Biofilm Formation by P. aeruginosa in Cystic Fibrosis Patients

by Elodie Olivares, Jason Tasse, Stéphanie Badel-Berchoux, Christian Provot, Gilles Prévost and Thierry Bernardi

Pathogens 2020, 9(12), 1065; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens9121065 - 19 Dec 2020

Cited by 5 | Viewed by 2333

Abstract

Biofilms are characterized by high tolerance to antimicrobials. However, conventional antibiograms are performed on planktonic microorganisms. Through the clinical Biofilm Ring Test^® (cBRT), initially aimed to measure the adhesion propensity of bacteria, we discerned a variable distribution of biofilm-producer strains among P. aeruginosa samples isolated from expectorations of cystic fibrosis (CF) patients. Despite a majority of spontaneous adherent isolates, few strains remained planktonic after 5 h of incubation. Their analysis by an adapted protocol of the cBRT revealed an induction of the biofilm early formation by sub-inhibitory doses of β-lactams. Microscopic observations of bacterial cultures stained with Syto 9/Propidium Iodide (PI) confirmed the ability of antimicrobials to increase either the bacterial biomass or the biovolume occupied by induced sessile cells. Finally, the cBRT and its derivatives enabled to highlight in a few hours the potential inducer property of antibiotics on bacterial adhesion. This phenomenon should be considered carefully in the context of CF since patients are constantly under fluctuating antimicrobial treatments. To conclude, assays derived from the Biofilm Ring Test^® (BRT) device, not only define efficient doses preventing biofilm formation, but could be useful for the antimicrobial selection in CF, to avoid inducer molecules of the early biofilm initiation. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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26 pages, 5276 KiB

Open AccessArticle

Mobilization of Iron Stored in Bacterioferritin Is Required for Metabolic Homeostasis in Pseudomonas aeruginosa

by Achala N. D. Punchi Hewage, Leo Fontenot, Jessie Guidry, Thomas Weldeghiorghis, Anil K. Mehta, Fabrizio Donnarumma and Mario Rivera

Pathogens 2020, 9(12), 980; https://doi.org/10.3390/pathogens9120980 - 24 Nov 2020

Cited by 9 | Viewed by 3570

Abstract

Iron homeostasis offers a significant bacterial vulnerability because pathogens obtain essential iron from their mammalian hosts, but host-defenses maintain vanishingly low levels of free iron. Although pathogens have evolved mechanisms to procure host-iron, these depend on well-regulated iron homeostasis. To disrupt iron homeostasis, our work has targeted iron mobilization from the iron storage protein bacterioferritin (BfrB) by blocking a required interaction with its cognate ferredoxin partner (Bfd). The blockade of the BfrB–Bfd complex by deletion of the bfd gene (Δbfd) causes iron to irreversibly accumulate in BfrB. In this study we used mass spectrometry and NMR spectroscopy to compare the proteomic response and the levels of key intracellular metabolites between wild type (wt) and isogenic ΔbfdP. aeruginosa strains. We find that the irreversible accumulation of unusable iron in BfrB leads to acute intracellular iron limitation, even if the culture media is iron-sufficient. Importantly, the iron limitation and concomitant iron metabolism dysregulation trigger a cascade of events that lead to broader metabolic homeostasis disruption, which includes sulfur limitation, phenazine-mediated oxidative stress, suboptimal amino acid synthesis and altered carbon metabolism. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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14 pages, 1770 KiB

Open AccessArticle

Effects of Glycyrrhizin on Multi-Drug Resistant Pseudomonas aeruginosa

by Nicholas J. Carruthers, Sharon A. McClellan, Mallika Somayajulu, Ahalya Pitchaikannu, Denise Bessert, Xudong Peng, Kylie Huitsing, Paul M. Stemmer and Linda D. Hazlett

Pathogens 2020, 9(9), 766; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens9090766 - 18 Sep 2020

Cited by 8 | Viewed by 2718

Abstract

The effects of glycyrrhizin (GLY) on multi-drug resistant (MDR) systemic (MDR9) vs. ocular (B1045) Pseudomonas aeruginosa clinical isolates were determined. Proteomes of each isolate with/without GLY treatment were profiled using liquid chromatography mass spectrometry (LC-MS/MS). The effect of GLY on adherence of MDR isolates to immortalized human (HCET) and mouse (MCEC) corneal epithelial cells, and biofilm and dispersal was tested. Both isolates were treated with GLY (0.25 minimum inhibitory concentration (MIC), 10 mg/mL for MDR9 and 3.75 mg/mL for B1045) and subjected to proteomic analysis. MDR9 had a greater response to GLY (51% of identified proteins affected vs. <1% in B1045). In MDR9 vs. controls, GLY decreased the abundance of proteins for: antibiotic resistance, biofilm formation, and type III secretion. Further, antibiotic resistance and type III secretion proteins had higher control abundances in MDR9 vs. B1045. GLY (5 and 10 mg/mL) significantly reduced binding of both isolates to MCEC, and B1045 to HCET. MDR9 binding to HCET was only reduced at 10 mg/mL GLY. GLY (5 and 10 mg/mL) enhanced dispersal for both isolates, at early (6.5 h) but not later times (24–72 h). This study provides evidence that GLY has a greater effect on the proteome of MDR9 vs. B1045, yet it was equally effective at disrupting adherence and early biofilm dispersal. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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Review

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19 pages, 857 KiB

Open AccessEditor’s ChoiceReview

Pathogenesis of the Pseudomonas aeruginosa Biofilm: A Review

by Felipe Francisco Tuon, Leticia Ramos Dantas, Paula Hansen Suss and Victoria Stadler Tasca Ribeiro

Pathogens 2022, 11(3), 300; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11030300 - 27 Feb 2022

Cited by 99 | Viewed by 24724

Abstract

Pseudomonas aeruginosa is associated with several human infections, mainly related to healthcare services. In the hospital, it is associated with resistance to several antibiotics, which poses a great challenge to therapy. However, one of the biggest challenges in treating P. aeruginosa infections is that related to biofilms. The complex structure of the P. aeruginosa biofilm contributes an additional factor to the pathogenicity of this microorganism, leading to therapeutic failure, in addition to escape from the immune system, and generating chronic infections that are difficult to eradicate. In this review, we address several molecular aspects of the pathogenicity of P. aeruginosa biofilms. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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33 pages, 1596 KiB

Open AccessReview

Oxidative Stress Response in Pseudomonas aeruginosa

by Waleska Stephanie da Cruz Nizer, Vasily Inkovskiy, Zoya Versey, Nikola Strempel, Edana Cassol and Joerg Overhage

Pathogens 2021, 10(9), 1187; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10091187 - 14 Sep 2021

Cited by 28 | Viewed by 7797

Abstract

Pseudomonas aeruginosa is a Gram-negative environmental and human opportunistic pathogen highly adapted to many different environmental conditions. It can cause a wide range of serious infections, including wounds, lungs, the urinary tract, and systemic infections. The high versatility and pathogenicity of this bacterium is attributed to its genomic complexity, the expression of several virulence factors, and its intrinsic resistance to various antimicrobials. However, to thrive and establish infection, P. aeruginosa must overcome several barriers. One of these barriers is the presence of oxidizing agents (e.g., hydrogen peroxide, superoxide, and hypochlorous acid) produced by the host immune system or that are commonly used as disinfectants in a variety of different environments including hospitals. These agents damage several cellular molecules and can cause cell death. Therefore, bacteria adapt to these harsh conditions by altering gene expression and eliciting several stress responses to survive under oxidative stress. Here, we used PubMed to evaluate the current knowledge on the oxidative stress responses adopted by P. aeruginosa. We will describe the genes that are often differently expressed under oxidative stress conditions, the pathways and proteins employed to sense and respond to oxidative stress, and how these changes in gene expression influence pathogenicity and the virulence of P. aeruginosa. Understanding these responses and changes in gene expression is critical to controlling bacterial pathogenicity and developing new therapeutic agents. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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Other

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6 pages, 657 KiB

Open AccessCase Report

Concurrent Pseudomonas Periorbital Necrotizing Fasciitis and Endophthalmitis: A Case Report and Literature Review

by Yu-Kuei Lee and Chun-Chieh Lai

Pathogens 2021, 10(7), 854; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10070854 - 07 Jul 2021

Cited by 3 | Viewed by 2557

Abstract

(1) Background: Necrotizing fasciitis (NF) is an infection involving the superficial fascia and subcutaneous tissue. Endophthalmitis is an infection within the ocular ball. Herein we report a rare case of concurrent periorbital NF and endophthalmitis, caused by Pseudomonas aeruginosa (PA). We also conducted a literature review related to periorbital PA skin and soft-tissue infections. (2) Case presentation: A 62-year-old male had left upper eyelid swelling and redness; orbital cellulitis was diagnosed. During eyelid debridement, NF with the involvement of the upper Müller’s muscle and levator muscle was noted. The infection soon progressed to scleral ulcers and endophthalmitis. The eye developed phthisis bulbi, despite treatment with intravitreal antibiotics. (3) Conclusions: Immunocompromised individuals are more likely than immunocompetent hosts to be infected by PA. Although periorbital NF is uncommon due to the rich blood supply in the area, the possibility of PA infection should be considered in concurrent periorbital soft-tissue infection and endophthalmitis. Full article

(This article belongs to the Special Issue Pseudomonas aeruginosa Pathogenesis)

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