Abstract
Glaesserella (Haemophilus) parasuis is a commensal bacterium of the upper respiratory tract in pigs and also the causative agent of Glässer's disease, which causes significant morbidity and mortality in pigs worldwide. Isolates are characterized into 15 serovars by their capsular polysaccharide, which has shown a correlation with isolate pathogenicity. To investigate the role the capsule plays in G. parasuis virulence and host interaction, a capsule mutant of the serovar 5 strain HS069 was generated (HS069Δcap) through allelic exchange following natural transformation. HS069Δcap was unable to cause signs of systemic disease during a pig challenge study and had increased sensitivity to complement killing and phagocytosis by alveolar macrophages. Compared with the parent strain, HS069Δcap produced more robust biofilm and adhered equivalently to 3D4/31 cells; however, it was unable to persistently colonize the nasal cavity of inoculated pigs, with all pigs clearing HS069Δcap by 5 days postchallenge. Our results indicate the importance of the capsular polysaccharide to G. parasuis virulence as well as nasal colonization in pigs.
Highlights
Glaesserella (Haemophilus) parasuis is the etiologic agent of Glӓsser’s disease in pigs, which presents as a fibrinous polyserositis, arthritis and meningitis [1, 2]
To confirm and expand on these findings and better understand how capsule contributes to G. parasuis disease, we generated a capsular mutant of the virulent serovar 5 strain HS069 followed by evaluation of sensitivity to complement killing and macrophage adhesion in vitro as well as virulence, colonization, and immune stimulation in vivo
This investigation of the G. parasuis capsule mutant HS069∆cap confirms the importance of capsule to a fully virulent phenotype in vivo that has been seen previously with
Summary
Glaesserella (Haemophilus) parasuis is the etiologic agent of Glӓsser’s disease in pigs, which presents as a fibrinous polyserositis, arthritis and meningitis [1, 2]. G. parasuis isolates are classified into 15 serovars, based on gene content and diversity at their capsular polysaccharide loci and via the Kielstein-Rapp-Gabrielson typing scheme [3, 4]. SH0165∆cap was highly susceptible to complement mediated killing as compared to the wild type bacteria [10]. This presented evidence for the importance of capsule in causing invasive disease; the characteristics of the capsular mutant were not fully elucidated and the capacity of. Swine were challenged with HS069 and HS069Δcap to evaluate virulence, capacity for nasal colonization, and stimulation of host immunity
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