Airway infection

The particle size is the most important factor that contributes to the clearance of particles. For particles deposited in the anterior parts of the nose, wiping and blowing are important mechanisms whereas particles on the other areas of the nose are removed with mucus. The cilia move the mucus toward the glottis where the mucus and the particles are swallowed. In the tracheobronchial area, the mucus covering the tracheobronchial tree is moved upward by the cilia beating under the mucus. This mucociliary escalator transports deposited particles and particle-filled macrophages to the pharynx, where they are also swallowed. Mucociliary clearance is rapid in healthy adults and is complete within one to two days for particles in the lower airways. Infection and inflammation due to irritation or allergic reaction can markedly impair this form of clearance. 

Treatment depends on the symptoms and severity of the exacerbation. Mild exacerbations can often be treated at home with an increase in bronchodilator therapy with or without oral corticosteroids (Fig. 12-3). Antibiotics are indicated only if there are clinical signs of airway infection (e.g., increased volume and change in color of sputum and/or fever). Moderate to severe exacerbations require management in the... 

Pulmonary disease is characterized by thick mucus secretions, impaired mucus clearance, chronic airway infection and colonization, obstruction, and an exaggerated neutrophil-dominated inflammatory response. 

Upper respiratory tract infection (URI) is a term that refers to various upper airway infections, including otitis media, sinusitis, pharyngitis, and rhinitis. Most URIs are viral and often selflimited. Over 1 billion viral URIs occur annually in the United States, resulting in millions of physician office visits each year.1 Excessive antibiotic use for URIs has contributed to the significant development of bacterial resistance. Guidelines have been established to reduce inappropriate antibiotic use for viral URIs.2 This chapter will focus on acute otitis media, sinusitis, and pharyngitis because they are frequently caused by bacteria and require appropriate antibiotic therapy to minimize complications. 

In productive cough mucolytics such as bromhex-ine and acetylcysteine might work although there is no strong evidence for their effectiveness. Inhalation steroids may sometimes be effective even in nonasthmatics in cases of protracted cough in connection with airways infections. 

The major precipitants of exacerbations of COPD are acute airways infections. The role of bacteria in precipitating exacerbations is controversial. Bacteria may have a primary role in the development of an exacerbation or represent a secondary superinfection of an initial viral process. The major bacterial organisms that have been associated with exacerbations are Haemophilus influenzae. Streptococcus pneumoniae, and Moraxella (Branhamella) catarrhalis. Mycoplasma pneumoniae and Chlamydia pneumoniae may play a part. In COPD patients with a FEVi < 35% predicted gram-negative bacteria, especially Enterobacteriaceae and Pseudomonas spp. play an important part in acute exacerbations. 

Direct toxic effects such as irritation, inflammation, or increased permeability will bring about symptoms such as the sneeze reflex, nasal discomfort, and hypersecretion with the possibility of underlying pathological changes such as squamous metaplasia, cilia erosion, plasma exudation, epithelial necrosis, inflammatory remodeling, or neutrophil accumulation. Indirect adverse effects can also occur and any alteration to normal nasal homeostasis should be avoided. For example, a reduction in mucociliary clearance can cause rhinitis, sinusitis, and an increased susceptibility to airway infections, and consequently ciliary movement should not be altered by any nasal medication. In the context of absorption enhancers, the rate and extent of recovery of normal nasal epithelial function after nasal administration is a prime consideration. 

The outer region of the core oligosaccharide affects the innate immune responses in the normal host. For example, patients with cystic fibrosis are hypersusceptible to chronic airway infections, particularly with Pseudomonas aeruginosa [127], It was shown that the outer-core region of the LPS of P. aeruginosa influences a critical step... 

The Role of Pseudomonas Lipopolysaccharide in Cystic Fibrosis Airway Infection... 

Dales RE. Granulocyte inflammatory markers and airway infection during acute exacerbation of chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2001 163 349-355. 33. 

Valproate-induced fatal liver failure developed in a 29-year-old woman with Friedreich s disease (78). The first symptoms (apathy during febrile upper airways infection) occurred after 2 months of therapy at a dosage of 20 mg/kg. The drug was withdrawn 10 days later, when she had hepatic encephalopathy and a severe bleeding diathesis supportive treatment was provided but she died after 4 weeks. 

Antonela Antoniu S (2012) Inhaled ciprofloxacin for chronic airways infections caused by Pseudomonas aeruginosa. Expert Rev Anti Infect Ther 10(12) 1439-1446... 

Young children with CF have an extended period of time, perhaps months or years, when they have no evidence of airway infection. Later, they develop a mild airway infection or early bacterial colonization, often without associated symptoms. However, bronchoalve-olar lavage fluid reveals evidence of infection and inflammation (high neutrophil count with a predominance of proinflammatory cytokines). Eventually, they develop a chronic airway infection that cannot be eradicated fully even with prolonged use of systemic or topical antibiotics. This scenario is best explained by the ability of bacteria such... 

Brandtzaeg P. The role of humoral mucosal immunity in the induction and maintenance of chronic airway infections. Am J Respir Crit Care Med 1995 151 2081-2087. 

Kahl BC, MeUmann A, Deiwick S, Peters G, Harmsen D (2005) Variation of the polymorphic region X of the protein A gene during persistent airway infection of cystic fibrosis patients reflects two independent mechanisms of genetic change in Staphylococcus aureus. J Chn Microbiol 43 502-505... 

A Role for the Anti-Inflammatory Actions of Erythromycin in Chronic Airway Infection... 

Fig. 5. Infection and inflammation of respiratory tract. EM may block the vicious circle of chronic airway infection. PMN, polymolphonucear cells.

We believe that treatment with antibiotics for chronic airway infection is naturally limited, because chronic airway infection is different from acute airway infection in terms of the disease process. First, chronic airway infection exists for certain reasons, i.e., a defect of the defense mechanism of the airway. Second, chronic airway infection is accompanied by an inflammatory process, which results in the vicious circle proposed by Cole [38]. Presently, we think that EM blocks the vicious circle in chronic airway infection as it inhibits the inflammatory process (Fig. 5). 

Furthermore, it has become clear recently that even the subminimum inhibitory concentration of 14-membered ring macrolides has the inhibitory effects of biofilm formation and expression of virulence factors (piocyanin, elastase, proteases) of P. aeruginosa (see following section). Thus, an anti-inflammatory agent such as EM should be used as basic treatment in the therapy of chronic airway infection. 

Sato, K., Suga, M., Nishimura, J., Kushima, Y, Muranaka, H., and Ando, M. (1997). Pyocyanine synthesis by Pseudomonas aeruginosa in chronic airway infection and the effect of erythromycin on its biological activity. Jpn. J. Antibiot. 50 (Suppl.), 89-91. 

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