Whooping cough is a highly contagious and acute respiratory disease caused by an aerobic Gram negative non-sporulating encapsulated coco-bacillus bacterium, Bordetella pertussis. It is a strict human pathogen with no known animal or environmental reservoirs (Cotter and Miller, 2009) and transmitted through inhalation of bacteria-infected droplets. Consequently colonizing the ciliated cells of the bronchio-epithelium causing disease (Relman, D.A, 1995). Bordetella pertussis disease is characterised by mucus hyper-secretion, epithelial damage and pulmonary edema, with paroxysmal coughing that last for close for a month and post-tussive vomiting. In addition, it is often accompanied by pneumonia, otitis edema, seizures and encephalopathy.
For successful infection to occur, the bacterium should disseminate itself in the lower respiratory tract and evade the host's immune responses. Therefore, the inhaled bacteria droplets attach to the ciliated epithelial cells in the nasal-pharynx and trachea. It is at this point that Bordetella pertussis produces virulent factors to enable its survival in the host. These virulent factors are classified basically into adhesins mediate bacterial attachment to the epithelial cells and toxins that mediate the host immune system. Adhesins include; filamentous haemagglutinin, fimbriae and pertactin while toxins include; pertussis toxin, tracheal cytotoxin, adenylate cyclase toxin and lipo-oligosaccharide (Armirthalingam, 2013). To clearly understand the importance of these virulence factors in Bordetella pertussis pathogenesis and immune evasion, a mouse model system has been used (Carbonetti, 2010). The system suggest that the virulence factors not only alter the host's local environment but also modulate innate and adaptive immune responses thereby causing pro and anti-inflammatory responses.
Filamentous haemagglutinin confers infection by attaching onto the host cells in the lower respiratory tract. It is about 2nm wide, and 50nm long and it has been linked to bio-film formation thereby facilitating dissemination of the disease (Serra et al. 2011). Furthermore, studies have shown pertactin, a 69kDa non fimbrial outer membrane protein, facilitates attachment of the bacteria onto ciliated respiratory cells. Experiments conducted on humans to test the role of pertactin have shown no significant effect except with the results from (Bassinet et al. 2000). Fimbriae (pili or agglutinogen) are believed to cause persistent infection by mimicking the natural ligand-receptor interactions. They protrude from the cell surface of B. Pertussis and are composed of major and minor subunits. The major subunit binds to sulphated sugars, heparan sulphate, an abundant component of the respiratory tract while the minor subunit binds to intergrin V1a-5 located on the monocytes. The binding onto the monocytes causes CR3 activation thereby modulating the immune system. (Geuijen et al., 1996).
After the bacteria has attached to the...