Bordetella pertussis

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Bordetella pertussis

"Whooping Cough"

Encounter and Colonization

Bordetella pertussis is a highly communicable agent and is transmitted person-to-person via airborne droplets or direct contact with discharges from the respiratory mucous membranes of an infected person. This small, gram-negative coccobacillus is non-motile, aerobic and fastidious. B. pertussis colonizes the respiratory tract including the mouth, nose, throat and beginning of the lungs of young children worldwide. The bacteria bind to ciliated cells in the respiratory mucosa by producing adhesions. Filamentous hemagglutinin on the cell surface and pertussis toxin (Ptx) both help the bacteria in binding. Filamentous hemagglutinin binds to the galactose residues on the glycolipid of the ciliated cells. Ptx, in its cell-bound form, binds to the glycolipid lactosylceramide, which is also found on the ciliated cells. Ptx binds to the surface of phagocytes as well, causing phagocytosis of the bacteria. This mechanism may lead to enhanced survival as an intracellular parasite. Adding to its many purposes, Ptx deregulates the host cell adenylate cyclase activity. The A subunit of this AB toxin, affects the G protein responsible for inhibiting adenylate cyclase. This leads to an increase in cyclic adenosine monophosphate (cAMP) creating detrimental metabolic changes in the host cells.

Additional Toxins

Also contributing to the virulence of the bacteria are the exotoxins including invasive adenylate cyclase, tracheal cytotoxin, and lethal toxin. Invasive adenylate cyclase reduces local phagocytic activity as well as acting as a hemolysin. Tracheal toxin affects the ciliated respiratory epithelium by inhibiting the ciliary beating. This kills the cells and causes them to be eliminated from the mucosa. Tracheal toxin also stimulates the release of IL-1, which causes fever. Lastly, lethal toxin causes inflammation and local necrosis at infection sites.

Because B. pertussis is a gram-negative bacteria, it possesses the endotoxin lipopolysaccharide (LPS). However, its LPS is different from that of the other gram-negative bacteria, in that it is heterogeneous with an alternative form of the Lipid A, called Lipid X. Although not fully understood at the time, it seems that Lipid X has a greater capacity for virulence.

Pathogenesis

After an incubation period of five to ten days, or as long as 21 days, numerous symptoms can be observed. The symptoms come in two stages. The first stage consists of common cold symptoms such as sneezing, runny nose, low-grade fever, and a mild cough. It is during this time that the disease is most contagious, and it lasts from one to two weeks.

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