Pulmonary viral infection

The exacerbation of asthmatic responses is most frequently caused by a pulmonary viral infection, such as influenza, rhino, or adenovirus infections (81-89). Recent data has indicated that rhinoviral infections are the most common cause of severe asthma exacerbations. In addition to exacerbating asthmatic responses, severe respiratory syncytial virus (RSV) infections early in childhood appears... 

Normal commensals of the upper respiratory tract proliferate in damaged lungs especially following viral infections, pulmonary congestion or pulmonary infarction. Mixed infection is therefore common, and since Haemophilus influenzae and Streptococcus pneumoniae are often the pathogens, amoxicillin or trimethoprim are reasonable choices, but if... 

When designing protocols to measure deposition, a number of clinical factors need to be considered and incorporated into the study design subjects age, sex, smoking history, and current drug regimens, presence of a viral infection, severity of disease, stability of pulmonary function, and other outcome measures that could affect the inhalation of the radioaerosol, the measurement of deposition, and the results. Some of these also apply when using healthy volunteers as subjects for deposition studies. For example, we allow a 4- to 6-week recovery period between repeat studies for subjects who have suffered an exacerbation of their asthma or developed a chest cold or infection after enrollment. 

Thrombophlebitis with pulmonary embolus, systemic viral infection, infectious mononucleosis. 

Wang EEL, Prober CG, Manson B, et al. Association of respiratory viral infections with pulmonary deterioration in patients with cystic fibrosis. N Engl J Med 1984 311 1653-1658. 

In the well infant, bronchiolitis is usually a self-limiting illness, and reassurance and antipyretics are usually all that are necessary while waiting for resolution of the underlying viral infection. In-hospital support is necessary for the child suffering from respiratory failure or dehydration underlying cardiac and pulmonary diseases potentiate these conditions. 

M1P-1q Reduced pulmonary mononuclear infiltrate to challenge with influenza virus resulting in higher titers of influenza virus Less severe autoimmune myocarditis after coxsackie viral infection Knockout has increased MODS mortality and CTL activity Reduced NK-mediated inflammation... 

The mortality rate for street heroin users is very high. Early death comes from involvement in crime to support the habit from uncertainty about the dose, the purity, and even the identity of what is purchased on the street and from serious infections associated with nonsterile drugs and sharing of injection paraphernaha. Heroin users commonly acquire bacterial infections producing skin abscesses endocarditis pulmonary infections, especially tuberculosis and viral infections producing hepatitis C and acquired immune deficiency syndrome (AIDS). 

Infectious Diseases. Recently, AMC487 has been shown to exert several beneficial effects in the pathogenesis of ferrets infected with H5N1 (bird flu). The effects all resulted from blockage of CXCR3-CXCL10 interaction and included reduction of pulmonary viral load, improvement of respiratory function and modest delay in mortality [31]. 

The massive increases in surfactant levels following dust exposure may have important industrial implications, and changes are also noticed in many other diseases (Scarpelli, 1968) such as cystic fibrosis, sudden unexpected death in infants and for adults suffering from multiple trauma, trauma to the lungs, acute pancreatitis and viral infections. In all of these cases the changes noted in pulmonary surfactant would, at the very least, cause an impairment of lung function. 

Introduction - This chapter will review two groups of drugs used for the relief of various manifestations of lung diseases, namely, the bronchodi-lators to terminate or prevent an asthmatic attack, and the pulmonary vasodilators for the treatment of pulmonary hypertension. It should be noted first of all that in the treatment of respiratory diseases the approach is symptomatic rather than etiotropic. The causes of bronchospasm and pulmonary hypertension are difficult to control. Disease processes as such, for example, viral infections of the respiratory system, pulmonary emphysema and pulmonary arteriosclerosis, cannot be treated successfully by drugs, so that one has to resort to treatment of symptoms. 

LIP is part of a spectrum of pulmonary lymphoid proliferations that includes follicular bronchitis/bronchioUtis, NLH, and MALT B-cell lymphoma (4,5). They can be difficult to differentiate from each other (5,6). Indeed, a substantial percentage of the cases that were initially classified by Averill Liebow (3) as LIP were subsequently found to be mucosa-associated lymphoid tissue (MALT) lymphomas. As a result, LIP was excluded from the classification of idiopathic interstitial pneumonias for several decades. Today, it is clear that the majority of patients with LIP have associated immunologic disorders, dysproteinemias or viral infections, so that LIP can be viewed as a morphologic pattern of lung injury that results from multiple causes with varying pathogenetic mechanisms rather than a distinct disease entity (1). However, a few cases of LIP do present as idiopathic disease. LIP therefore is still included in recent classifications of idiopathic interstitial pneumonias (7). 

Environmental triggers such as viral infection may be important (192) and reactivation of Epstein Barr virus (EBV) latent infection has been incriminated in patients with pulmonary involvement (206). 

The in vivo anti-viral activity has partially been demonstrated (Fusco et al. 2010). The in vivo experiment of polysaccharide extract fiom Echinacea purpurea, a widely consumed botanical product, indicated that mice infected with WSN influenza A and treated with E. purpurea polysaccharide extract had less weight loss than untreated mice but similar pulmonary viral titers. Echinacea-treated mice had lower systemic and pulmonary KC and IL-10 levels and lower systemic IFN-y levels following influenza infection. These suggest that E. purpurea alters the clinical course of influenza infection in mice through modulation of cytokines and not direct antiviral activity. 

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