Community-acquired pneumonia pathophysiology: Difference between revisions
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==Overview== | ==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. | [[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. | ||
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=====2. Inhalation of Aerosolized Droplets===== | =====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 | 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]].<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> | ||
=====3. Blood-Borne or | =====3. Blood-Borne or Systemic Infection===== | ||
Microbial entered through circulation may also result in pulmonary infections. Blood-borne pneumonia is seen more commonly in intravenous drug users. [[Staphylococcal aureus]] causes pneumonia in this way. [[Gram negative bacteria]] typically account for pneumonia in immunocompromised individuals. | |||
=====4. Trauma or Local Spread===== | =====4. Trauma or Local Spread===== | ||
Pneumonia can | Pneumonia can occur after a pulmonary procedure or a penetrating trauma to the lungs. A local spread of a [[hepatic abscess]] can also lead to pneumonia. | ||
==Pathogenesis== | ==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 | 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 [[leukotriene|LTB4]]. The [[neutrophils]] are recruited by these cells to eliminate these microorganisms.<ref name="Strieter-2003">{{Cite journal | last1 = Strieter | first1 = RM. | last2 = Belperio | first2 = JA. | last3 = Keane | first3 = MP. | title = Host innate defenses in the lung: the role of cytokines. | journal = Curr Opin Infect Dis | volume = 16 | issue = 3 | pages = 193-8 | month = Jun | year = 2003 | doi = 10.1097/01.qco.0000073766.11390.0e | PMID = 12821807 }}</ref><ref name="Mason-2005">{{Cite journal | last1 = Mason | first1 = CM. | last2 = Nelson | first2 = S. | title = Pulmonary host defenses and factors predisposing to lung infection. | journal = Clin Chest Med | volume = 26 | issue = 1 | pages = 11-7 | month = Mar | year = 2005 | doi = 10.1016/j.ccm.2004.10.018 | PMID = 15802161 }}</ref> | ||
====Diminished Mucociliary Clearance==== | ====Diminished Mucociliary Clearance==== | ||
Revision as of 20:01, 17 February 2014
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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 Systemic Infection
Microbial entered through circulation may also result in pulmonary infections. Blood-borne pneumonia is seen more commonly in intravenous drug users. Staphylococcal aureus causes pneumonia in this way. Gram negative bacteria typically account for pneumonia in immunocompromised individuals.
4. Trauma or Local Spread
Pneumonia can occur after a pulmonary procedure or a penetrating trauma to the lungs. A local spread of a hepatic 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 LTB4. The neutrophils are recruited by these cells to eliminate these microorganisms.[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)