Bordetella pertussis 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 are free to 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 phagocytes convert too much ATP to cyclic AMP, which can cause disturbances in
Schindler disease of the disease is mostly palliative. However, Type II Schindler disease, with its late onset of symptoms, is not characterized by neurological degeneration. There is no known cure for Schindler disease, but bone marrow transplants have been trialed, as they have been successful in curing other glycoprotein disorders. Schindler disease was named after Detlev Schindler (1946- ) M.D., the first author of a 1988 paper detailing the disease. It also named after the Japanese Biochemist and Physician, Hiro Kanzaki (1949- ), who further studied it and released papers detailing the disease in 2006. Schindler disease Schindler disease, also known as