Location: Ruminant Diseases and Immunology ResearchTitle: Capsular Polysaccharide Interferes With Biofilm Formation by Pasteurella Multocida Serogroup A
|PETRUZZI, BRIANA - Virginia Tech|
|Briggs, Robert - Bob|
|SWORDS, W - Wake Forest University|
|DE CASTRO, CRISTINA - Universita Di Napoli|
|MOLINARO, ANTONIO - Universita Di Napoli|
|INZANA, THOMAS - Virginia Tech|
Submitted to: mBio
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/17/2017
Publication Date: 11/21/2017
Citation: Petruzzi, B., Briggs, R.E., Tatum, F.M., Swords, W.E., De Castro, C., Molinaro, A., Inzana, T.J. 2017. Capsular polysaccharide interferes with biofilm formation by Pasteurella multocida Serogroup A. mBio. 8(6):e01843-17. https://doi.org/10.1128/mBio.01843-17.
Interpretive Summary: Pasteurella multocida is a disease-causing bacteria which can cause a wide variety of acute and chronic diseases in domestic livestock, wildlife, birds, and humans. It is believed that maintenance of this bacteria, and chronic disease, in many of these species is associated with the formation of biofilm, an organized assembly of bacteria generally resistant to killing by host immunity or antibiotics. We've shown in this work that P. multocida does form a biofilm, and that the biofilm is considerably more robust when the P. multocida are not coated in capsular polysaccharide, a viscous coating which the bacteria often makes when causing disease. Understanding of the regulation of this biofilm formation may allow development of new methods to control P. multocida in its various hosts.
Technical Abstract: Pasteurella multocida is an important multihost animal and zoonotic pathogen that is capable of causing respiratory and multisystemic diseases, bacteremia,and bite wound infections. The glycosaminoglycan capsule of P. multocida is an essential virulence factor that protects the bacterium from host defenses. However, chronic infections (such as swine atrophic rhinitis and the carrier state in birds and other animals) may be associated with biofilm formation, which has not been characterized in P. multocida. Biofilm formation by clinical isolates was inversely related to capsule production and was confirmed with capsule-deficient mutants of highly encapsulated strains. Capsule-deficient mutants formed biofilms with a larger biomass that was thicker and smoother than the biofilm of encapsulated strains. Passage of a highly encapsulated, poor-biofilm-forming strain under conditions that favored biofilm formation resulted in the production of less capsular polysaccharide and a more robust biofilm, as did addition of hyaluronidase to the growth medium of all of the strains tested. The matrix material of the biofilm was composed predominately of a glycogen exopolysaccharide (EPS), as determined by gas chromatography-mass spectrometry, nuclear magnetic resonance, and enzymatic digestion. However, a putative glycogen synthesis locus was not differentially regulated when the bacteria were grown as a biofilm or planktonically, as determined by quantitative reverse transcriptase PCR. Therefore, the negatively charged capsule may interfere with biofilm formation by blocking adherence to a surface or by preventing the EPS matrix from encasing large numbers of bacterial cells. This is the first detailed description of biofilm formation and a glycogen EPS by P. multocida.