Pathophysiology
The development of bronchiectasis requires two factors: an initial injury to the lung (such as from infection, auto-immune destruction of lung tissue, or other destruction of lung tissue (as seen in gastroesophageal reflux disease or aspiration syndromes)) which leads to impaired mucociliary clearance, obstruction, or a defect in host defense. This triggers a host immune response from neutrophils (elastases), reactive oxygen species, and inflammatory cytokines that results in progressive destruction of normal lung architecture. In particular, the elastic fibers of bronchi are affected. The result is permanent abnormal dilation and destruction of the major bronchi and bronchiole walls.Disordered neutrophil function is believed to play a role in the pathogenesis of bronchiectasis. Neutrophil extracellular traps(NETs), which are extracellular fibers secreted by neutrophils that are used to trap and destroy pathogens, are hyperactive in bronchiectasis. Increased NET activity is associated with more severe bronchiectasis. Neutrophil elastase, which is an extracellular protein secreted by neutrophils to destroy pathogens as well as host tissue, is also hyperactive in many cases of bronchiectasis. An increased neutrophil elastase activity is also associated with worse outcomes and more severe disease in bronchiectasis. The initial lung injury in bronchiectasis leads to an impaired mucociliary clearance of the lung airways, which leads to mucous stasis. This mucous stasis leads to bacterial colonization in bronchiectasis which leads to neutrophil activation. This neutrophil activation leads to further further tissue destruction and airway distortion by neutrophils in addition to direct tissue destruction by the pathogenic bacteria.
Some evidence has found that it may worsen outcomes in certain cases. Fluid replacement, blood transfusions, and medication for low blood pressure may be required. Intravenous interferon therapy has also been used. Pregnancy
When Lassa fever infects pregnant women late in their third trimester, inducing delivery is necessary for the mother to have a good chance of survival. This is because the virus has an affinity for the placenta and other highly vascular tissues. The fetus has only a one in ten chance of survival no matter what course of action is taken; hence, the focus is always on saving the life of the mother. Following delivery, women should receive the same treatment as other people with Lassa fever. Prognosis
About 15–20% of hospitalized people with Lassa fever will die from the illness. The overall case fatality rate is estimated to be 1%, but during epidemics, mortality can climb as high as 50%. The mortality rate is greater than 80% when it occurs in pregnant women during their third trimester; fetal death also occurs in nearly all those cases. Abortion decreases the risk of death to the mother. Some survivors experience lasting effects of the disease, and can include partial or complete deafness.Because of treatment with ribavirin, fatality rates have declined. Epidemiology
There are about 300,000 to 500,000 cases which result in 5,000 deaths a year.