Bordetella pertussis :: Essays Papers

Bordetella whooping coughWhooping CoughEncounter and ColonizationBordetella whooping cough is a highly communicable agent and is transmitted person-to-person via airborne droplets or govern 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 wedge 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 implant on the ciliated cells. Ptx binds to the surface of phagocytes as healthful, causing phagocytosis of the bacteria. Thi s mechanism may lead to enhanced survival as an intracellular parasite. Adding to its many purposes, Ptx deregulates the military cell adenylate cyclase activity. The A subunit of this AB toxin, affects the G protein responsible for inhibiting adenylate cyclase. This leads to an growth in cyclic adenosine monophosphate (cAMP) creating detrimental metabolic changes in the host cells.excess ToxinsAlso 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 deprivation of IL-1, which causes fever. Lastly, lethal toxin causes inflammation and local necrosis at infection sites. Because B. pertussis is a gram-neg ative bacteria, it possesses the endotoxin lipopolysaccharide (LPS). However, its LPS is different from that of the other gram-negative bacteria, in that it is sundry(prenominal) with an alternative form of the Lipid A, called Lipid X. Although not fully soundless at the time, it seems that Lipid X has a greater capacity for virulence.Pathogenesis afterward an incubation period of five to ten days, or as enormous 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 nearly contagious, and it lasts from one to two weeks.