Community-acquired pneumonia pathophysiology: Difference between revisions
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=====1. Microaspiration of Oropharyngeal Contents===== | =====1. Microaspiration of Oropharyngeal Contents===== | ||
Aspiration of oropharyngeal contents containing pathogenic microorganisms is one of the mechanism of acquiring [[pneumonia]]. It most commonly occurs in normal persons during sleep, in unconscious persons due to gastroesopahegeal reflux or impaired [[gag reflex]] and [[cough reflex]].<ref name="Wunderink-2004">{{Cite journal | last1 = Wunderink | first1 = RG. | last2 = Waterer | first2 = GW. | title = Community-acquired pneumonia: pathophysiology and host factors with focus on possible new approaches to management of lower respiratory tract infections. | journal = Infect Dis Clin North Am | volume = 18 | issue = 4 | pages = 743-59, vii | month = Dec | year = 2004 | doi = 10.1016/j.idc.2004.07.004 | PMID = 15555822 }}</ref> | |||
=====2. Inhalation of Aerosolized Droplets===== | =====2. Inhalation of Aerosolized Droplets===== | ||
Revision as of 19:50, 17 February 2014
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Community-Acquired Pneumonia Microchapters |
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Differentiating Community-acquired pneumonia from other Diseases |
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Risk calculators and risk factors for Community-acquired pneumonia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chetan Lokhande, M.B.B.S [2]
Overview
Pneumonia can be transmitted by various methods. The etiology depends upon various factors like age, immune status, geographical area, and comorbid conditions. The transmission can be systemic , local , trauma or iatrogenic. It could also be due to decreased immunity or inability to filter out pathogen.
Modes of Transmission
1. Microaspiration of Oropharyngeal Contents
Aspiration of oropharyngeal contents containing pathogenic microorganisms is one of the mechanism of acquiring pneumonia. It most commonly occurs in normal persons during sleep, in unconscious persons due to gastroesopahegeal reflux or impaired gag reflex and cough reflex.[1]
2. Inhalation of Aerosolized Droplets
Inhalation of aerosolized droplets of 0.5 to 1 micrometer is the most common pathway of acquiring pneumonia. A few bacterial and viral infections are transmitted in this fashion. The lung can normally filter out particles between 0.5 to 2 micrometer by recruiting the alveolar macrophages.[1]
3. Blood-Borne or Sytemic Infection
Another way of acquiring pneumonia systematically is through blood. Blood-borne pneumonia is more common in intravenous drug users . Staphylococcal aureus causes pneumonia in this way. Gram negative bacteria are found to cause pneumonia in immunocompromised individuals.
4. Trauma or Local Spread
Pneumonia can be caused iatrogenically by a surgeon during an operative procedure or by a penetrating trauma to the lung. A local spread of a hepatic abscess and amoebic abscess can also lead to pneumonia.
Pathogenesis
The lungs can normally filter out large droplets of aerosols. Smaller droplets of the size of 0.5 to 2 micrometer are deposited on the alveoli and then engulfed by alevolar macrophages. These macrophages release cytokines and chemokines , which also includes Tumor necrosis factor-alpha, interleukin-8 and leukotrieneB4 . The neutrophils are recruited by these cells and they kill these micro-organisms.[2][3]
Diminished Mucociliary Clearance
The cilia lining the respiratory epithelium serve to move secreted mucus containing trapped foreign particles including pathogens towards the oropharynx for either expectoration or swallowing. Elevated incidence of pneumonia in patients with genetic defects affecting mucociliary clearance such as primary ciliary dyskinesia suggests its role in the pathogenesis of community-acquired pneumonia.
Impaired Cough Reflex
Cough, together with mucociliary clearance, prevent pathogens from entering the lower respiratory tract. Cough suppression or cough reflex inhibition seen in patients with cerebrovascular accidents and drug overdosages is associated with an enhanced risk for aspiration pneumonia. Another relation to cough is genetic polymorphisms in the angiotensin-converting enzyme (ACE) gene. The role of cough in preventing pneumonia may be explained by a higher risk for developing pneumonia in homozygotes carrying deletion/deletion (DD) genotype who are found to have lower levels of bradykinin and tachykinins such as substance P.[4][5]
Defective Immnue System
Pathogen-associated molecular patterns (PAMPs) are initially recognized by Toll-like receptors (TLRs) and other pattern-recognition receptors (PRRs) of the innate immune system. Effectors in the acquired immune system are involved in elimination of microorganisms and generation of immunological memory. Other components in the immune system such as complement system, cytokines, and collectins, also mediate the defense against microorganisms causing pneumonia.
References
- ↑ 1.0 1.1 Wunderink, RG.; Waterer, GW. (2004). "Community-acquired pneumonia: pathophysiology and host factors with focus on possible new approaches to management of lower respiratory tract infections". Infect Dis Clin North Am. 18 (4): 743–59, vii. doi:10.1016/j.idc.2004.07.004. PMID 15555822. Unknown parameter
|month=ignored (help) - ↑ Strieter, RM.; Belperio, JA.; Keane, MP. (2003). "Host innate defenses in the lung: the role of cytokines". Curr Opin Infect Dis. 16 (3): 193–8. doi:10.1097/01.qco.0000073766.11390.0e. PMID 12821807. Unknown parameter
|month=ignored (help) - ↑ Mason, CM.; Nelson, S. (2005). "Pulmonary host defenses and factors predisposing to lung infection". Clin Chest Med. 26 (1): 11–7. doi:10.1016/j.ccm.2004.10.018. PMID 15802161. Unknown parameter
|month=ignored (help) - ↑ Morimoto, S.; Okaishi, K.; Onishi, M.; Katsuya, T.; Yang, J.; Okuro, M.; Sakurai, S.; Onishi, T.; Ogihara, T. (2002). "Deletion allele of the angiotensin-converting enzyme gene as a risk factor for pneumonia in elderly patients". Am J Med. 112 (2): 89–94. PMID 11835945. Unknown parameter
|month=ignored (help) - ↑ Rigat, B.; Hubert, C.; Alhenc-Gelas, F.; Cambien, F.; Corvol, P.; Soubrier, F. (1990). "An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels". J Clin Invest. 86 (4): 1343–6. doi:10.1172/JCI114844. PMID 1976655. Unknown parameter
|month=ignored (help)