Bordetella species, with the exception of B. petrii, are obligate aerobes, as well as highly fastidious, or difficult to culture.

[6] B. bronchiseptica causes several diseases in other mammals, including kennel cough in dogs and atrophic rhinitis in pigs.

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.

This species is also typically associated with kennel cough (Canine Respiratory Infectious Disease (CRID)) in dogs.

[7][8] 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.

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.

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.

Recently discovered activities of adenylate cyclase toxin, including transmembrane pore formation and stimulation of calcium influx, may also contribute to the intoxication of phagocytes.

[5] Bordetella pertussis also affects human adults and even with an 85% vaccination coverage over 160,000 related deaths occur each year all around the globe.

BvgS is a plasma membrane-bound sensor kinase which responds to stimulation by phosphorylating a cytoplasmic helix-turn-helix-containing protein, BvgA.

[15] The regulation of Bvg repressed genes is mediated by the product of a 624-bp open reading frame downstream of BvgA, the so-called Bvg-activated repressor protein, BvgR.

[17] It is not known what the physiological signals for BvgS are, but in vitro BvgAS can be inactivated by millimolar concentrations of magnesium sulfate or nicotinic acid, or by reduction of the incubation temperature to ≤ 26 °C.

In these conditions, some, but not all of the virulence factors associated with the Bvg+ phase are expressed, suggesting this two-component regulatory system can give rise to a continuum of phenotypic states in response to the environment.

Therefore, it is possible for a pet to become infected with another Bordetella species or contract kennel cough from another source, such as the parainfluenza virus, even after being vaccinated for B.