Bordetella pertussis clinical strains from Argentina and USA display enhanced biofilm formation and other pathogenic phenotypes

JENNINGS-GEE, J; YANTORNO, OM; CATTELAN, N; DEORA, R

CABA

Simposio; 11th International Bordetella Symposium; 2016

TRABAJO SELECCIONADO COMO PRESENTACIÓN ORALObjective: Bordetella pertussis is a strict human pathogen and the primary etiological agent of whooping cough or pertussis. Whilst, the physiological and pathogenic features of B. pertussis have been extensively studied utilizing the planktonic mode of growth, very few studies have considered the biofilm lifestyle. We hypothesized that recent clinical isolates of B. pertussis will display an increased ability to form biofilms.Materials and methodsSixteen clinical isolates recovered in Argentina and USA, from 2001 to 2012, the reference strains Tohama I and Bp536, and an avirulent strain (Bp369) were used in this study. Biofilm forming capacity was evaluated by the tube method, the microtiter dish assay, and by confocal microscopy. In addition, autoaggregation index and production of FHA were determined. Adhesion to respiratory epithelial cells A549 and colonization of the mouse respiratory tract were also analysed.ResultsWe found that many of the clinical isolates exhibited a hyper-biofilm phenotype. Additionally, a higher autoaggregation rate and enhanced production of FHA (a protein previously shown by us to promote biofilm formation in B. pertussis), were observed. Comparative microscopic analyses of the biofilms of six clinical strains with the reference strain Bp536 showed differences in substrate colonization and in structural features. Consistent with higher production of FHA, an increased capacity to adhere to A549 cells was also observed. Using a mouse intranasal infection model, we compared the respiratory tract colonization profile of one clinical isolate from each Argentina and the USA. Both clinical strains colonized the nasal septum, trachea and lungs at higher levels than the reference strain.ConclusionTaken together, our data provide support for a model in which altered pathogenic phenotypes including enhanced biofilm formation could help recent clinical isolates to colonize the host and lead to re-emergence of pertussis.