Bordetella 

(/ˌbɔːrdəˈtɛlə/) is a genus of small (0.2 – 0.7 µm), gram-negative coccobacilli of the

phylum Pseudomonadota. Bordetella species, with the exception of B. petrii, are obligate aerobes,
as well as highly fastidious, or difficult to culture. All species can infect humans. The first three
species to be described (B. pertussis, B. parapertussis, B. bronchiseptica); are sometimes referred
to as the 'classical species'. Two of these (B. bronchiseptica and B. pertussis) are also motile.[2][3]
B. pertussis and occasionally B. parapertussis cause pertussis or whooping cough in humans, and
some B. parapertussis strains can colonise sheep. B. bronchiseptica rarely infects healthy humans,
though disease in immunocompromised patients has been reported.[4] B. bronchiseptica causes
several diseases in other mammals, including kennel cough and atrophic rhinitis in dogs and pigs,
respectively. Other members of the genus cause similar diseases in other mammals, and in birds (B.
hinzii, B. avium).
The genus Bordetella is named after Jules Bordet.

he 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 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, coccoid 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. 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.[5][6][7] 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.[8] 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.[9][10]

Virulence Factor[edit]
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.