enables it to be motile. On a petri dish, colonies of this species appear small, grayish-white, smooth, and shiny. B. bronchiseptica is gram-negative. The most thoroughly studied of the Bordetella species are B. bronchiseptica, B. pertussis and B. parapertussis, and the pathogenesis of respiratory disease caused by these bacteria has been reviewed. Transmission occurs by direct contact, via respiratory aerosol droplets, or fomites. Bacteria initially adhere to ciliated epithelial cells in the nasopharynx, and this interaction with epithelial cells is mediated by a series of protein adhesins. These include filamentous haemaglutinin, pertactin, fimbriae, and pertussis toxin (though expression of pertussis toxin is unique to B. pertussis). As well as assisting in adherence to epithelial cells, some of these are also involved in attachment to immune effector cells. The initial catarrhal phase of infection produces symptoms similar to those of the common cold, and during this period, large numbers of bacteria can be recovered from the pharynx. Thereafter, the bacteria proliferate and spread further into the respiratory tract, where the secretion of toxins causes ciliostasis and facilitates the entry of bacteria to tracheal/bronchial ciliated cells. One of the first toxins to be expressed is tracheal cytotoxin, which is a disaccharide-tetrapeptide derived from peptidoglycan. Unlike most other Bordetella toxins, tracheal cytotoxin is expressed constitutively, being a normal product of the breakdown of the bacterial cell wall. Other bacteria recycle this molecule back into the cytoplasm, but in Bordetella and Neisseria gonorrhoeae, it is released into the environment. Tracheal cytotoxin itself is able to reproduce paralysis of the ciliary escalator, inhibition of DNA synthesis in epithelial cells and ultimately killing of the same. One of the most important of the regulated toxins is adenylate cyclase toxin, which aids in the evasion of innate immunity. The toxin is delivered to phagocytic immune cells upon contact. Immune cell functions are then inhibited in part by the resulting accumulation of cyclic AMP. Recently discovered activities of adenylate cyclase toxin, including transmembrane pore formation and stimulation of calcium influx, may also contribute to the intoxication of phagocytes. Virulence factors The virulence factors identified in the bordetella are common to all three species. These include adhesins, such as filamentous hemagglutinin (FHA), pertactin, tracheal colonization factor and fimbriae, and toxins, such as adenylate cyclase-hemolysin, dermonecrotic toxin and tracheal cytotoxin. These factors are then expressed and regulated most often by environmental stimuli. Regulation of virulence factor expression The expression of