Bordetella pertussis

Bordetella pertussis is a Gram-negative, aerobic, pathogenic, encapsulated coccobacillus of the genus Bordetella, and the causative agent of pertussis or whooping cough. Like B. bronchiseptica, B. pertussis is motile and expresses a flagellum-like structure. Its virulence factors include pertussis toxin, adenylate cyclase toxin, filamentous hæmagglutinin, pertactin, fimbria, and tracheal cytotoxin. The bacterium is spread by airborne droplets; its incubation period is 7–10 days on average (range 6–20 days). Humans are the only known reservoir for B. pertussis. The complete B. pertussis genome of 4,086,186 base pairs was published in 2003. Compared to its closest relative B. bronchiseptica, the genome size is greatly reduced. This is mainly due to the adaptation to one host species (human) and the loss of capability of survival outside of a host body. The disease pertussis was first described by French physician Guillaume de Baillou after the epidemic of 1578. The causative agent of pertussis was identified and isolated by Jules Bordet and Octave Gengou in 1906. The genus Bordetella contains nine species: B. pertussis, B. parapertussis, B. bronchiseptica, B. avium, B. hinzii, B. holmesii, B. trematum, B. ansorpii and B.petrii. B. pertussis, B. parapertussis and B. bronchiseptica form a closely related phylogenetical group. B. parapertussis causes a disease similar to whooping cough in humans, and B. bronchiseptica infects a range of mammal hosts, including humans, and causes a spectrum of respiratory disorders. Pertussis is an infection of the respiratory system characterized by a “whooping” sound when the person breathes in. In the US, it killed between 10,000 and 20,000 people per year before a vaccine was available. Vaccination has transformed this; between 1985 and 1988, fewer than 100 children died from pertussis. Worldwide in 2000, according to the WHO, around 39 million people were infected annually and about 297,000 died. Since the introduction of vaccination in England in 1957, the rate of pertussis infection has dropped by 97%. B. pertussis infects its host by colonizing lung epithelial cells. The bacterium contains a surface protein, filamentous haemagglutinin adhesin, which binds to the sulfatides found on cilia of epithelial cells. Other adhesins are fimbriae and petractin. Once anchored, the bacterium produces tracheal cytotoxin, which stops the cilia from beating. This prevents the cilia from clearing debris from the lungs, so the body responds by sending the host into a coughing fit. These coughs expel some bacteria into the air, which can then infect other hosts. B. pertussis has the ability to inhibit the function of the host's immune system. The toxin, known as pertussis toxin (or PTx), inhibits G protein coupling that regulates an adenylate cyclase-mediated conversion of ATP to cyclic AMP. The end result is that phagocytes convert too much ATP to cAMP, causing disturbances in cellular signaling mechanisms, and preventing phagocytes from correctly responding to the infection. PTx, formerly known as lymphocytosis-promoting factor, causes a decrease in the entry of lymphocytes into lymph nodes, which can lead to a condition known as lymphocytosis, with a complete lymphocyte count of over 4000/μl in adults or over 8000/μl in children. Beside targeting lymphocytes, it limits neutrophil migration to the lungs. It also decreases the function of tissue-resident macrophages, which are responsible for some bacterial clearance.