Pathophysiology of lower respiratory tract infection
Answers
Acute infection of the lower respiratory tract comprises bronchitis, bronchiolitis, and pneumonia. From a clinical point of view it may be difficult to distinguish these disease entities and one infection may progress into another. The most common pathogens causing these infections are the primary respiratory viruses (respiratory syncytial virus (RSV), influenza virus, adenoviruses, parainfluenza virus, and rhinovirus1 2), Mycoplasma pneumoniae,3 and Chlamydiaspecies.4-6 Legionella may cause pneumonia and non-pneumonic upper respiratory tract infection and approximately 85% of c ases are caused by L pneumophila. Long lasting sequelae such as bronchiectasis, lung fibrosis, and decreased lung function are seen after lower respiratory tract infections7-10 and it has been debated whether respiratory tract infection can cause chronic bronchial asthma.6 11-13
Acute bronchitis and bronchiolitis
Acute bronchitis is an inflammatory condition of the bronchi often caused by infectious agents, although in many cases no aetiology can be established.14 15 It shares many pathological and clinical features with bronchiolitis, and the same agents may induce both conditions. Most cases of acute bronchitis of known aetiology are due to respiratory viruses such as influenza virus, adenovirus, RSV, rhinovirus, and coronavirus,1 2 16 and a few are caused by M pneumoniae, Bordetella pertussis andC pneumoniae.4 5 15 17 Legionella infections limited to the bronchial tree are not described.
ADHERENCE OF PATHOGENS
The pathogenesis has not been studied for all agents, but the transmission of disease is thought to occur through droplet spread from an infected person. After inhalation the infectious agent may adhere to different receptors such as acid containing glycoproteins or the adhesion molecule ICAM-1 on respiratory epithelial cells.18 19 The infectious chlamydial particle is the elementary body that attaches itself to and enters a susceptible cell where it changes to the larger metabolically active reticulate body.20 Viable chlamydiae may be present at the site of infection and induce an inflammatory response.20 M pneumoniae attaches to ciliated epithelial cells by a specialised terminal organelle.18 Metabolic and ultrastructural alterations in the affected cell are seen and these result in epithelial cell damage and ciliostasis. Some epithelial cell lines produce cytokines when stimulated with other bacteria such as Escherichia coli,21 and epithelial cells might therefore play a more active role in the mucosal immune response after extracellular bacterial infection. In acute respiratory viral diseases a number of different inflammatory mediators such as kinins and cytokines have also been demonstrated. In some infections such as influenza extensive infiltrations with polymorphonuclear leucocytes (PMN), oedema, and degeneration of epithelial cells are seen,22 whereas in others such as rhinovirus infection the cytopathic effects are either absent or minor in degree.23
CONCLUSION
Lower respiratory tract infection may be followed by long term sequelae and a direct link between acute respiratory tract infection in early infancy and development of chronic bronchitis and emphysema in adults has been established.9 Interstitial lung fibrosis has been reported after influenza pneumonia8 and Legionnaires’ disease,10 as well as bronchiectasis and abnormal lung function tests after adenovirus pneumonia.7 92 Symptoms recurring and persisting for years have been described in patients with ornithosis.93The occurrence of symptoms was related to a delay in the initiation of antibiotic therapy and to high antibody titres to chlamydial group antigens, which might suggest continued chlamydial infection.32 93 Thus acute pneumonia can lead to chronic pulmonary disease and it is a theoretical possibility that early antimicrobial treatment might prevent this.