scholarly journals BIOFILMS OF PATHOGENIC BURKHOLDERIA AND THEIR ROLE IN RESISTANCE TO ANTIBIOTICS

Author(s):  
E. V. Shubnikova ◽  
L. K. Merinova ◽  
T. V. Senina ◽  
E. V. Korol ◽  
O. A. Merinova

The review contains the current knowledge on the main issues of Burkholderia pseudomallei and Burkholderia mallei biofilm formation. The role ofknown structural elements of Burkholderia cells (flagella, type IV pili, LPS), as well as autotransporter adhesin proteins in the attachment of bacteria to surfaces, the formation of microcolonies and biofilm is described. The review also includes information of genetic regulatory mechanisms (QS-systems, RpoE-sigma factor, c-di-GMP, two-component signal transduction system), differentially expressed genes related to the formation of B. pseudomallei biofilm, role ofbiofilms in the virulence and resistance to antibiotics of pathogenic Burkholderia and their significance for the chronic processes and recurrent course of melioidosis and glanders.

2004 ◽  
Vol 186 (17) ◽  
pp. 5692-5698 ◽  
Author(s):  
Yasuhiko Irie ◽  
Seema Mattoo ◽  
Ming H. Yuk

ABSTRACT Bordetella species utilize the BvgAS (Bordetella virulence gene) two-component signal transduction system to sense the environment and regulate gene expression among at least three phases: a virulent Bvg+ phase, a nonvirulent Bvg− phase, and an intermediate Bvgi phase. Genes expressed in the Bvg+ phase encode known virulence factors, including adhesins such as filamentous hemagglutinin (FHA) and fimbriae, as well as toxins such as the bifunctional adenylate cyclase/hemolysin (ACY). Previous studies showed that in the Bvgi phase, FHA and fimbriae continue to be expressed, but ACY expression is significantly downregulated. In this report, we determine that Bordetella bronchiseptica can form biofilms in vitro and that the generation of biofilm is maximal in the Bvgi phase. We show that FHA is required for maximal biofilm formation and that fimbriae may also contribute to this phenotype. However, expression of ACY inhibits biofilm formation, most likely via interactions with FHA. Therefore, the coordinated regulation of adhesins and ACY expression leads to maximal biofilm formation in the Bvgi phase in B. bronchiseptica.


2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Olga L. Voronina ◽  
Marina S. Kunda ◽  
Natalia N. Ryzhova ◽  
Ekaterina I. Aksenova ◽  
Andrey N. Semenov ◽  
...  

Biofilm formation byBurkholderiaspp. is a principal cause of lung chronic infections in cystic fibrosis patients. A “lacking biofilm production” (LBP) strainB. contaminansGIMC4587:Bct370-19 has been obtained by insertion modification of clinical strain with plasposon mutagenesis. It has an interrupted transcriptional response regulator (RR) gene. The focus of our investigation was a two-component signal transduction system determination, including this RR.B. contaminansclinical and LBP strains were analyzed by whole genome sequencing and bioinformatics resources. A four-component operon (BiofilmReg) has a key role in biofilm formation. The relative location (i.e., by being separated by another gene) of RR and histidine kinase genes is unique in BiofilmReg. Orthologs were found in other members of the Burkholderiales order. Phylogenetic analysis of strains containing BiofilmReg operons demonstrated evidence for earlier inheritance of a three-component operon. During further evolution one lineage acquired a fourth gene, whereas others lost the third component of the operon. Mutations in sensor domains have created biodiversity which is advantageous for adaptation to various ecological niches. Different speciesBurkholderiaandAchromobacterstrains all demonstrated similar BiofilmReg operon structure. Therefore, there may be an opportunity to develop a common drug which is effective for treating all these causative agents.


2003 ◽  
Vol 48 (6) ◽  
pp. 1511-1524 ◽  
Author(s):  
Mikkel Klausen ◽  
Arne Heydorn ◽  
Paula Ragas ◽  
Lotte Lambertsen ◽  
Anders Aaes-Jørgensen ◽  
...  

2007 ◽  
Vol 56 (8) ◽  
pp. 1005-1010 ◽  
Author(s):  
M. Sarkar-Tyson ◽  
J. E. Thwaite ◽  
S. V. Harding ◽  
S. J. Smither ◽  
P. C. F. Oyston ◽  
...  

Burkholderia pseudomallei is the causative agent of melioidosis, an infectious disease of humans and animals. Gene clusters which encode capsular polysaccharide (type I O-PS) and LPS (type II O-PS), both of which play roles in virulence, have previously been identified. Here, the identification of two further putative clusters, type III O-PS and type IV O-PS, is reported. Mice challenged with type III O-PS or type IV O-PS mutants showed increased mean times to death (7.8 and 11.6 days) compared to those challenged with wild-type B. pseudomallei (3 days). To investigate the possible roles of polysaccharides in protection, mice were immunized with killed cells of wild-type B. pseudomallei or killed cells of B. pseudomallei with mutations in the O antigen, capsular polysaccharide, type III O-PS or type IV O-PS gene clusters. Immunization with all polysaccharide mutant strains resulted in delayed time to death compared to the naïve controls, following challenge with wild-type B. pseudomallei strain K96243. However, immunization with killed polysaccharide mutant strains conferred different degrees of protection, demonstrating the immunological importance of the polysaccharide clusters on the surface of B. pseudomallei.


2018 ◽  
Vol 11 (525) ◽  
pp. eaaq0825 ◽  
Author(s):  
Gareth S. A. Wright ◽  
Akane Saeki ◽  
Takaaki Hikima ◽  
Yoko Nishizono ◽  
Tamao Hisano ◽  
...  

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