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.

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.

Significant differences in type IV pilin allele distribution among Pseudomonas aeruginosa isolates from cystic fibrosis (CF) versus non-CF patients

Microbiology ◽  
2004 ◽  
Vol 150 (5) ◽  
pp. 1315-1326 ◽  
Author(s):  
Julianne V. Kus ◽  
Elizabeth Tullis ◽  
Dennis G. Cvitkovitch ◽  
Lori L. Burrows
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Opportunistic Pathogen ◽  
Host Cells ◽  
Phylogenetic Groups ◽  
Allele Distribution ◽  
Specific Pcr ◽  
Type Iv ◽  
Accessory Genes ◽  
Group I

Type IV pili (TFP) are important colonization factors of the opportunistic pathogen Pseudomonas aeruginosa, involved in biofilm formation and attachment to host cells. This study undertook a comprehensive analysis of TFP alleles in more than 290 environmental, clinical, rectal and cystic fibrosis (CF) isolates of P. aeruginosa. Based on the results, a new system of nomenclature is proposed, in which P. aeruginosa TFP are divided into five distinct phylogenetic groups. Each pilin allele is stringently associated with characteristic, distinct accessory genes that allow the identification of the allele by specific PCR. The invariant association of the pilin and accessory genes implies horizontal transfer of the entire locus. Analysis of pilin allele distribution among isolates from various sources revealed a striking bias in the prevalence of isolates with group I pilin genes from CF compared with non-CF human sources (P<0·0001), suggesting this particular pilin type, which can be post-translationally modified by glycosylation via the action of TfpO (PilO), may confer a colonization or persistence advantage in the CF host. This allele was also predominant in paediatric CF isolates (29 of 43; 67·4 %), showing that this bias is apparent early in colonization. Group I pilins were also the most common type found in environmental isolates tested. To the authors' knowledge, this is the first example of a P. aeruginosa virulence factor allele that is strongly associated with CF isolates.

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 Molecular Cloning, Expression and FPLC Purification of Lectin A from Pseudomonas aeruginosa

2014 ◽  
Vol 2 (4) ◽  
pp. 529-536
Author(s):  
Peyman Ghoraishizadeh ◽  
Shraddha Raikar ◽  
Mahsa Takhtechian
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Molecular Cloning ◽  
Opportunistic Pathogen ◽  
Host Cells ◽  
Related Protein ◽  
Burn Victims ◽  
Gene Coding ◽  
Lectin Protein

Pseudomonas aeruginosa (PA) as an opportunistic pathogen infects the pulmonary tract, bladder, cystic fibrosis patients and burn victims. PA infections treatment is challenging because of its ability to rapidly develop resistance to multiple classes of antibiotics. Lectin is protein that isexpressed in cell of PA and cause of infection by attaching to the host cells. Lectin A gene coding lectin protein so we cloned and expressedthis gene then purified of related protein, that can be used in preparation of vaccine to treat PA infections.DOI: http://dx.doi.org/10.3126/ijasbt.v2i4.11559 Int J Appl Sci Biotechnol, Vol. 2(4): 529-536 

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 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.

scholarly journals Role of an Alginate Lyase for Alginate Transport in Mucoid Pseudomonas aeruginosa

2005 ◽  
Vol 73 (10) ◽  
pp. 6429-6436 ◽  
Author(s):  
Sumita Jain ◽  
Dennis E. Ohman
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Alginate Lyase ◽  
Opportunistic Pathogen ◽  
Chronic Pulmonary Disease ◽  
Host Defenses ◽  
Alginate Production ◽  
Mutant Cells ◽  
Alginate Biosynthesis

ABSTRACT The opportunistic pathogen Pseudomonas aeruginosa secretes a capsule-like polysaccharide called alginate that is important for evasion of host defenses, especially during chronic pulmonary disease of patients with cystic fibrosis (CF). Most proteins for alginate biosynthesis are encoded by the 12-gene algD operon. Interestingly, this operon also encodes AlgL, a lyase that degrades alginate. Mutants lacking AlgG, AlgK, or AlgX, also encoded by the operon, synthesize alginate polymers that are digested by the coregulated protein AlgL. We examined the phenotype of an ΔalgL mutation in the highly mucoid CF isolate FRD1. Generating a true ΔalgL mutant was possible only when the algD operon was under the control of a LacIq-repressed trc promoter. Upon induction of alginate production with isopropyl-β-d-thiogalactopyranoside, the ΔalgL mutant cells were lysed within a few hours. Electron micrographs of the ΔalgL mutant showed that alginate polymers accumulated in the periplasm, which ultimately burst the bacterial cell wall. The requirement of AlgL in an alginate-overproducing strain led to a new model for alginate secretion in which a multiprotein secretion complex (or scaffold, that includes AlgG, AlgK, AlgX, and AlgL) guides new polymers through the periplasm for secretion across the outer membrane. In this model, AlgL is bifunctional with a structural role in the scaffold and a role in degrading free alginate polymers in the periplasm.

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