scholarly journals Cellulase Inhibits Burkholderia cepacia Biofilms on Diverse Prosthetic Materials

2013 ◽  
Vol 62 (3) ◽  
pp. 327-330 ◽  
Author(s):  
SATISH KUMAR RAJASEKHARAN ◽  
SAMIRAJ RAMESH
Keyword(s):  
Cystic Fibrosis ◽  
Burkholderia Cepacia ◽  
Selection Pressure ◽  
Subsequent Development ◽  
Opportunistic Pathogen ◽  
Antibiofilm Activity ◽  
Prosthetic Materials ◽  
Antibiofilm Agents ◽  
Implanted Devices

Burkholderia cepacia is an opportunistic pathogen causing infections in patients with cystic fibrosis. Patients with implanted devices are prone to B. cepacia infections due to its ability to grow as biofilms. Knowing the importance of polysaccharides in a biofilm, enzymes that degrade them were targeted as a possible candidate for antibiofilm agents. In this study, the antibiofilm potential of cellulase against B. cepacia biofilms formed on various prosthetic materials was tested. Cellulase exhibited significant antibiofilm activity against B. cepacia without having much action on its growth, thus ruling out the chance of selection pressure and subsequent development resistance.

Burkholderia cepacia. [Descriptions of Fungi and Bacteria].

1994 ◽  
Author(s):  
G. S. Saddler
Keyword(s):  
Cystic Fibrosis ◽  
Lycopersicon Esculentum ◽  
Geographical Distribution ◽  
Allium Cepa ◽  
Leaf Spot ◽  
Burkholderia Cepacia ◽  
Allium Sativum ◽  
Opportunistic Pathogen ◽  
Agaricus Bitorquis ◽  
Cultivated Mushroom

Abstract A description is provided for Burkholderia cepacia. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Common host is Allium cepa, but can also cause disease in Allium sativum. Also identified as causing disease in Lycopersicon esculentum (63, 3168), a cavity disease of a cultivated mushroom (Agaricus bitorquis) (72, 5605) and a leaf spot on the a number of orchids including Cymbidium spp., Dendrobium sp. and Paphiopedilum spp. (66, 4326). The bacterium can also be found in soil, in clinical material, in disinfectant solutions and as an opportunistic pathogen of man and animals. It is gaining in significance as a major pathogen for sufferers of cystic fibrosis (Isles et al., 1984; McKevitt & Woods, 1984; Thomassen et al., 1985). DISEASE: Onion slippery skin; this is a rot of bulb scales, usually occurring at or near maturity, sometimes in storage. The bacterium does not appear to be strongly invasive, attacking plants that are damaged or weakened. Bacteria are thought to gain entry through the neck or leaf blades as the foliage falls over and the epidermis breaks, at maturity (64, 5550). GEOGRAPHICAL DISTRIBUTION: Worldwide. TRANSMISSION: Appears to be a soilborne wound pathogen.

scholarly journals Complete Genome Sequence of Burkholderia cenocepacia K56-2, an Opportunistic Pathogen

2020 ◽  
Vol 9 (43) ◽  
Author(s):  
Inmaculada García-Romero ◽  
Miguel A. Valvano
Keyword(s):  
Cystic Fibrosis ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Complete Genome ◽  
Burkholderia Cepacia ◽  
Opportunistic Pathogen ◽  
Burkholderia Cenocepacia ◽  
Content Type ◽  
Advance Research

ABSTRACT Burkholderia cenocepacia K56-2, an opportunistic bacterium for people with cystic fibrosis (CF), belongs to the Burkholderia cepacia complex (Bcc) and is consistently used as a model pathogen. We describe here the closed genome sequence for this strain, which will help advance research in B. cenocepacia biology and omics studies.

scholarly journals Burkholderia cepacia Produces a Hemolysin That Is Capable of Inducing Apoptosis and Degranulation of Mammalian Phagocytes

1998 ◽  
Vol 66 (5) ◽  
pp. 2033-2039 ◽  
Author(s):  
Michael L. Hutchison ◽  
Ian R. Poxton ◽  
John R. W. Govan
Keyword(s):  
Cystic Fibrosis ◽  
Burkholderia Cepacia ◽  
Opportunistic Pathogen ◽  
Cathepsin G ◽  
Human Neutrophils ◽  
Purification Method ◽  
Major Threat ◽  
Low Concentrations ◽  
Neutrophil Degranulation ◽  
Surface Active

ABSTRACT Burkholderia cepacia is an opportunistic pathogen that has become a major threat to individuals with cystic fibrosis (CF). In approximately 20% of patients, pulmonary colonization with B. cepacia leads to cepacia syndrome, a fatal fulminating pneumonia sometimes associated with septicemia. It has been reported that culture filtrates of clinically derived strains of B. cepacia are hemolytic. In this study, we have characterized a factor which contributes to this hemolytic activity and is secreted from B. cepacia J2315, a representative of the virulent and highly transmissible strain belonging to the recently described genomovar III grouping. Biochemical data from the described purification method for this hemolysin allows us to hypothesize that the toxin is a lipopeptide. As demonstrated for other lipopeptide toxins, the hemolysin from B. cepacia was surface active and lowered the surface tension of high-pressure liquid chromatography-grade water from 72.96 to 29.8 mN m−1. Similar to reports for other pore-forming cytotoxins, low concentrations of the hemolysin were able to induce nucleosomal degradation consistent with apoptosis in human neutrophils and the mouse-derived macrophage-type cell line J774.2. Exposure of human neutrophils to higher concentrations of toxin resulted in increased activities of the neutrophil degranulation markers cathepsin G and elastase. Based on the results obtained in this study, we suggest a role that allows B. cepacia to thwart the immune response and a model of the events that may contribute to the severe inflammatory response in the lungs of CF patients.

scholarly journals A Murine Model for Infection withBurkholderia cepacia with Sustained Persistence in the Spleen

1999 ◽  
Vol 67 (8) ◽  
pp. 4027-4032 ◽  
Author(s):  
David P. Speert ◽  
Barbara Steen ◽  
Keith Halsey ◽  
Eddie Kwan
Keyword(s):  
Cystic Fibrosis ◽  
Host Defense ◽  
Murine Model ◽  
Burkholderia Cepacia ◽  
Systemic Infection ◽  
Opportunistic Pathogen ◽  
Granulomatous Disease ◽  
Wild Type ◽  
Murine Spleen ◽  
Systemic Infections

ABSTRACT Burkholderia cepacia is an opportunistic pathogen that causes severe systemic infections in patients with chronic granulomatous disease (CGD) or with cystic fibrosis (CF), but its mechanisms of virulence are poorly understood. We developed a murine model of systemic infection in wild-type (WT) and gamma interferon knockout (GKO) BALB/c mice to facilitate dissection of components of pathogenicity and host defense. Both WT and GKO mice were susceptible to chronic splenic infection with B. cepacia, but not withPseudomonas aeruginosa. B. cepacia strains from patients with CGD persisted longer than those from CF patients. C57BL/6 mice were the most susceptible murine strain; bacteria persisted in the spleen for 2 months. DBA/2, BALB/c, and A/J strains of mice were relatively resistant to infection. Certain strains of B. cepacia complex can persist in the murine spleen after systemic infection; this may provide clues to its virulence in compromised hosts, such as those with CGD and CF.

scholarly journals Suppurative Mediastinitis Secondary toBurkholderia Cepaciain a Patient with Cystic Fibrosis

2006 ◽  
Vol 13 (4) ◽  
pp. 215-218 ◽  
Author(s):  
Ronald B George ◽  
Yannick Cartier ◽  
Alan G Casson ◽  
Paul Hernandez
Keyword(s):  
Cystic Fibrosis ◽  
Weight Loss ◽  
Case Report ◽  
Lung Function ◽  
Blood Cell ◽  
Burkholderia Cepacia ◽  
Clinical Course ◽  
Opportunistic Pathogen ◽  
Blood Cell Count ◽  
Present Case Report

Burkholderia cepaciais an important opportunistic pathogen among patients with cystic fibrosis (CF); it is associated with deterioration of lung function, poor outcome following lung transplantation and increased mortality. Fever, an elevated white blood cell count, weight loss and an often fatal deterioration in pulmonary function characterize a particular clinical course, termed ‘Cepacia syndrome’. The present case report describes a 40-year-old man with CF who developed Cepacia syndrome complicated by suppurative mediastinitis, from whichB cepaciawas isolated. Despite optimal medical and surgical therapy, this patient succumbed to his illness. Those caring for patients with CF should be aware of this potentially catastrophic complication ofB cepaciainfection, especially in the setting of Cepacia syndrome.

scholarly journals Competition in Biofilms between Cystic Fibrosis Isolates ofPseudomonas aeruginosaIs Shaped by R-Pyocins

mBio ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. e01828-18 ◽  
Author(s):  
Olubukola Oluyombo ◽  
Christopher N. Penfold ◽  
Stephen P. Diggle
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Clinical Problem ◽  
Opportunistic Pathogen ◽  
Resistance Mechanisms ◽  
Content Type ◽  
Global Concern ◽  
Antibiofilm Agents ◽  
Major Clinical Problem

ABSTRACTPseudomonas aeruginosais an opportunistic pathogen and the leading cause of morbidity and mortality in cystic fibrosis (CF) patients.P. aeruginosainfections are difficult to treat due to a number of antibiotic resistance mechanisms and the organism’s propensity to form multicellular biofilms. Epidemic strains ofP. aeruginosaoften dominate within the lungs of individual CF patients, but how they achieve this is poorly understood. One way that strains ofP. aeruginosacan compete is by producing chromosomally encoded bacteriocins, called pyocins. Three major classes of pyocin have been identified inP. aeruginosa: soluble pyocins (S types) and tailocins (R and F types). In this study, we investigated the distribution of S- and R-type pyocins in 24 clinical strains isolated from individual CF patients and then focused on understanding their roles in interstrain competition. We found that (i) each strain produced only one R-pyocin type, but the number of S-pyocins varied between strains, (ii) R-pyocins were generally important for strain dominance during competition assays in planktonic cultures and biofilm communities in strains with both disparate R- and S-pyocin subtypes, and (iii) purified R-pyocins demonstrated significant antimicrobial activity against established biofilms. Our work provides support for a role played by R-pyocins in the competition betweenP. aeruginosastrains and helps explain why certain strains and lineages ofP. aeruginosadominate and displace others during CF infection. Furthermore, we demonstrate the potential of exploiting R-pyocins for therapeutic gains in an era when antibiotic resistance is a global concern.IMPORTANCEA major clinical problem caused byPseudomonas aeruginosa, is chronic biofilm infection of the lungs in individuals with cystic fibrosis (CF). EpidemicP. aeruginosastrains dominate and displace others during CF infection, but these intraspecies interactions remain poorly understood. Here we demonstrate that R-pyocins (bacteriocins) are important factors in driving competitive interactions in biofilms betweenP. aeruginosastrains isolated from different CF patients. In addition, we found that these phage-like pyocins are inhibitory against mature biofilms of susceptible strains. This highlights the potential of R-pyocins as antimicrobial and antibiofilm agents at a time when new antimicrobial therapies are desperately needed.

scholarly journals Competition in biofilms between cystic fibrosis isolates ofPseudomonas aeruginosais shaped by R-pyocins

2018 ◽  
Author(s):  
Olubukola Oluyombo ◽  
Christopher N. Penfold ◽  
Stephen P. Diggle
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Species Interactions ◽  
Clinical Problem ◽  
Opportunistic Pathogen ◽  
Resistance Mechanisms ◽  
Global Concern ◽  
Human Infections ◽  
Antibiofilm Agents

ABSTRACTPseudomonas aeruginosais an opportunistic pathogen responsible for a number of different human infections and is the leading cause of morbidity and mortality in cystic fibrosis (CF) patients.P. aeruginosainfections are difficult to treat due to a number of antibiotic resistance mechanisms and the organisms propensity to form multicellular biofilms. Epidemic strains ofP. aeruginosaoften dominate within the lungs of individual CF patients, but how they achieve this is poorly understood. One of the ways strains ofP. aeruginosacan compete, is by producing chromosomally encoded bacteriocins, called pyocins. Three major classes of pyocin have been identified inP. aeruginosa:soluble pyocins (S-types) and tailocins (R- and F-types). In this study, we investigated the distribution of S- and R-type pyocins in 24 clinical strains isolated from individual CF patients and then focused on understanding their roles on inter-strain competition. We found that (i) each strain produced only one R-pyocin type, but the number of S-pyocins varied between strains; (ii) R-pyocins were generally important for strain dominance during competition assays in planktonic cultures and biofilm communities in strains with both disparate R and S pyocin sub-types. (iii) purified R-pyocins demonstrated significant antimicrobial activity against established biofilms. Our work provides support for a key role played by R-pyocins in the competition betweenP. aeruginosastrains, and may help explain why certain strains and lineages ofP. aeruginosadominate and displace others during CF lung infection. Furthermore, we demonstrate the potential of exploiting R-pyocins for therapeutic gains in an era when antibiotic resistance is a global concern.IMPORTANCEA major clinical problem caused byPseudomonas aeruginosa, is chronic biofilm infection of the lungs in individuals with cystic fibrosis (CF). EpidemicP. aeruginosastrains dominate and displace others during CF infection, but these intra-species interactions remain poorly understood. Here we demonstrate that R-pyocins (bacterocins) are important factors in driving competitive interactions in biofilms betweenP. aeruginosastrains isolated from different CF patients. In addition, we found that these phage-like pyocins are inhibitory against mature biofilms of susceptible strains. This highlights the potential of R-pyocins as antimicrobial and antibiofilm agents, at a time when new antimicrobial therapies are desperately needed.

scholarly journals Western Faculty Profile: Dr. Miguel Valvano

2012 ◽  
Vol 3 (1) ◽  
Author(s):  
Suzy Kim
Keyword(s):  
Cystic Fibrosis ◽  
Cell Surface ◽  
Burkholderia Cepacia ◽  
Research Team ◽  
Opportunistic Pathogen ◽  
Host Cells ◽  
Professor Emeritus ◽  
Host Defenses ◽  
Major Health ◽  
Virulence Properties

Dr. Miguel Valvano is a Professor Emeritus in the Department of Microbiology and Immunology at Western University. He also holds an academic Chair of Microbiology and Infectious Diseases at the Centre for Infection and Immunity, Queen’s University Belfast, United Kingdom. His laboratory has become an international leader in molecular research aimed at dissecting key bacterial components that directly interact with host cells to cause infections. His research team focuses on two areas: how lipopolylsaccharide (LPS) assembles on the bacterial cell surface and protects bacteria from host defenses, and characterizing the virulence properties of Burkholderia cepacia, an opportunistic pathogen that causes major health problems in patients suffering from cystic fibrosis. Suzy Kim, a member of WURJ, had the opportunity to interview Dr. Valvano to learn more about his research, his path to Western and his career.

The In Vitro Antibiofilm Activity of Water Leaf Extract of Papaya (Carica papaya L.) against Pseudomonas aeruginosa

2017 ◽  
Vol 2 (3) ◽  
pp. 150-163
Author(s):  
Ekajayanti Kining ◽  
Syamsul Falah ◽  
Novik Nurhidayat
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Contact Time ◽  
Cell Attachment ◽  
Water Extract ◽  
Opportunistic Pathogen ◽  
Bacterial Biofilm ◽  
Antibiofilm Activity ◽  
Bacterial Survival ◽  
Optimum Conditions

Pseudomonas aeruginosa is one of opportunistic pathogen forming bacterial biofilm. The biofilm sustains the bacterial survival and infections. This study aimed to assess the activity of water extract of papaya leaves on inhibition of cells attachment, growth and degradation of the biofilm using crystal violet (CV) biofilm assay. Research results showed that water extract of papaya leaves contains alkaloids, tanins, flavonoids, and steroids/terpenoids and showed antibacterial activity and antibiofilm against P. aeruginosa. Addition of extract can inhibit the cell attachment and was able to degrade the biofilm of 40.92% and 48.058% respectively at optimum conditions: extract concentration of 25% (v/v), temperature 37.5 °C and contact time 45 minutes. With a concentration of 25% (v/v), temperature of 50 °C and the contact time of 3 days, extract of papaya leaves can inhibit the growth of biofilms of 39.837% v/v.

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