The three most common species of
Bordetella are
B. pertussis,
B. parapertussis and
B. bronchiseptica. These species are known to accumulate in the respiratory tracts of mammals. This is most commonly seen in human infants as a product of an illness known as whooping cough. The particular species responsible for this illness is
B. pertussis, and can only be found in humans. Even with extensive vaccination research on
B. pertussis, whooping cough is still considered
endemic in many countries. Due to the fact
B. pertussis is only found in humans and shows little genetic variation from the other
Bordetella species, it is thought that it was derived from a common ancestor in recent years.
B. parapertussis can affect both humans and other mammals, primarily sheep. Similar to
B. pertussis, it causes whooping cough in babies. Yet, when strains found in sheep are isolated there is a strong distinction between those found in humans. This suggests that the varying strains of this species evolved independently of one another, the one found in humans and the one found in sheep. With this particular distinction it means that there is little to no transmission between the two reservoirs. The species
B. bronchiseptica (gram-negative, aerobic) however has a broader host range, causing similar symptoms in a wide range of animals, while only occasionally affecting humans. These symptoms often manifest as chronic and
asymptomatic respiratory infections.
B. bronchiseptica is a small,
coccobacillus shape sized at approximately 0.5 μm. It has
peritrichous flagella that enables it to be motile. On a petri dish, colonies of this species appear small, grayish-white, smooth, and shiny. This species is also typically associated with
kennel cough (Canine Respiratory Infectious Disease (CRID)) in dogs. 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==