Aspiration pneumonia pathophysiology: Difference between revisions
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{{Aspiration pneumonia}} | {{Aspiration pneumonia}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}} {{SKA}}, {{SSH}} | ||
==Overview== | ==Overview== | ||
The mechanism behind damage of lung due to aspiration of depends on the content of aspirate. In case of oropharyngeal secretions the damage is due to bacteria infecting and inducing inflammation in lung tissues. The reason of aspiration is also important to understand as there are many conditions which induce aspiration. | The mechanism behind damage of lung due to aspiration of depends on the content of aspirate. In case of oropharyngeal secretions the damage is due to bacteria infecting and inducing inflammation in lung tissues. The reason of aspiration is also important to understand as there are many conditions which induce aspiration. | ||
==Pathophysiology== | ==Pathophysiology== | ||
To understand the pathogenesis we have to review following physiological facts regarding aspiration pneumonia: | To understand the pathogenesis we have to review following physiological facts regarding aspiration pneumonia:<ref name="pmid19857224">{{cite journal| author=Japanese Respiratory Society| title=Aspiration pneumonia. | journal=Respirology | year= 2009 | volume= 14 Suppl 2 | issue= | pages= S59-64 | pmid=19857224 | doi=10.1111/j.1440-1843.2009.01578.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19857224 }}</ref><ref name="pmid23052002">{{cite journal| author=Almirall J, Cabré M, Clavé P| title=Complications of oropharyngeal dysphagia: aspiration pneumonia. | journal=Nestle Nutr Inst Workshop Ser | year= 2012 | volume= 72 | issue= | pages= 67-76 | pmid=23052002 | doi=10.1159/000339989 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23052002 }}</ref><ref name="pmid9925081">{{cite journal| author=Marik PE, Careau P| title=The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: a prospective study. | journal=Chest | year= 1999 | volume= 115 | issue= 1 | pages= 178-83 | pmid=9925081 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9925081 }}</ref><ref name="pmid23598958">{{cite journal| author=Cordier JF, Cottin V| title=Neglected evidence in idiopathic pulmonary fibrosis: from history to earlier diagnosis. | journal=Eur Respir J | year= 2013 | volume= 42 | issue= 4 | pages= 916-23 | pmid=23598958 | doi=10.1183/09031936.00027913 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23598958 }}</ref><ref name="pmid29500665">{{cite journal| author=Shi X, Zheng J, Yan T| title=Computational redesign of human respiratory syncytial virus epitope as therapeutic peptide vaccines against pediatric pneumonia. | journal=J Mol Model | year= 2018 | volume= 24 | issue= 4 | pages= 79 | pmid=29500665 | doi=10.1007/s00894-018-3613-z | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29500665 }}</ref><ref name="pmid28270104">{{cite journal| author=Shen CF, Wang SM, Ho TS, Liu CC| title=Clinical features of community acquired adenovirus pneumonia during the 2011 community outbreak in Southern Taiwan: role of host immune response. | journal=BMC Infect Dis | year= 2017 | volume= 17 | issue= 1 | pages= 196 | pmid=28270104 | doi=10.1186/s12879-017-2272-5 | pmc=5341368 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28270104 }}</ref><ref name="pmid21311332">{{cite journal| author=Marik PE| title=Pulmonary aspiration syndromes. | journal=Curr Opin Pulm Med | year= 2011 | volume= 17 | issue= 3 | pages= 148-54 | pmid=21311332 | doi=10.1097/MCP.0b013e32834397d6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21311332 }}</ref><ref name="pmid25732447">{{cite journal| author=Hu X, Lee JS, Pianosi PT, Ryu JH| title=Aspiration-related pulmonary syndromes. | journal=Chest | year= 2015 | volume= 147 | issue= 3 | pages= 815-823 | pmid=25732447 | doi=10.1378/chest.14-1049 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25732447 }}</ref> | ||
=== Mode of Transmission === | === Mode of Transmission === | ||
===== | ===== 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]]. | 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]]. | ||
===== | ===== Microaspiration of Oropharyngeal Contents ===== | ||
Aspiration of oropharyngeal contents containing pathogenic microorganisms is one of the | Aspiration of oropharyngeal contents containing pathogenic microorganisms is one of the mechanisms of acquiring [[pneumonia]]. It most commonly occurs in normal persons during sleep, in unconscious persons due to gastroesophageal reflux or impaired [[gag reflex]] and [[cough reflex]]. | ||
=== Agent Specific Virulence Factors === | === Agent Specific Virulence Factors === | ||
Several strategies are evolved to evade host | Several strategies are evolved to evade host defense mechanisms and facilitate spreading before establishing an infection. | ||
* [[Influenza virus]] possesses [[Neuraminidase|neuraminidases]] for cleavage of sialic acid residues on the cell surface and viral proteins, which prevent aggregation and facilitate propagation of viral particles. | * [[Influenza virus]] possesses [[Neuraminidase|neuraminidases]] for cleavage of sialic acid residues on the cell surface and viral proteins, which prevent aggregation and facilitate propagation of viral particles. | ||
| Line 27: | Line 27: | ||
* ''[[Haemophilus influenzae]]'', ''[[Streptococcus pneumoniae]]'', and ''[[Neisseria meningitidis]]'' produce [[Protease|proteases]] that split mucosal [[Immunoglobulin A|IgA]]. | * ''[[Haemophilus influenzae]]'', ''[[Streptococcus pneumoniae]]'', and ''[[Neisseria meningitidis]]'' produce [[Protease|proteases]] that split mucosal [[Immunoglobulin A|IgA]]. | ||
* ''[[Streptococcus pneumoniae]]'' possesses [[pneumolysin]] that aid the bacteria during colonization, by facilitating adherence to the host, during invasion by damaging host cells, and during infection by interfering with the host immune response. | * ''[[Streptococcus pneumoniae]]'' possesses [[pneumolysin]] that aid the bacteria during colonization, by facilitating adherence to the host, during an invasion by damaging host cells, and during infection by interfering with the host immune response. | ||
=== Host Factors === | === Host Factors === | ||
* The lungs can normally filter out large droplets of aerosols. | * 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 | * Smaller droplets of the size of 0.5 to 2 micrometer are deposited on the [[alveoli]] and then engulfed by alveolar macrophages. | ||
* These [[macrophages]] release [[cytokines]] and [[chemokines]], which also includes [[tumor necrosis factor-alpha]], [[interleukin]]-8 and [[Leukotriene|LTB4]]. | * 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. | * The [[neutrophils]] are recruited by these cells to eliminate these microorganisms. | ||
Revision as of 17:46, 21 March 2018
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Aspiration pneumonia Microchapters | |
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Aspiration pneumonia pathophysiology On the Web | |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunny Kumar MD [2], Sadaf Sharfaei M.D.[3]
Overview
The mechanism behind damage of lung due to aspiration of depends on the content of aspirate. In case of oropharyngeal secretions the damage is due to bacteria infecting and inducing inflammation in lung tissues. The reason of aspiration is also important to understand as there are many conditions which induce aspiration.
Pathophysiology
To understand the pathogenesis we have to review following physiological facts regarding aspiration pneumonia:[1][2][3][4][5][6][7][8]
Mode of Transmission
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.
Microaspiration of Oropharyngeal Contents
Aspiration of oropharyngeal contents containing pathogenic microorganisms is one of the mechanisms of acquiring pneumonia. It most commonly occurs in normal persons during sleep, in unconscious persons due to gastroesophageal reflux or impaired gag reflex and cough reflex.
Agent Specific Virulence Factors
Several strategies are evolved to evade host defense mechanisms and facilitate spreading before establishing an infection.
- Influenza virus possesses neuraminidases for cleavage of sialic acid residues on the cell surface and viral proteins, which prevent aggregation and facilitate propagation of viral particles.
- Chlamydophila pneumoniae induces complete abortion of cilia motions which assists colonization at the respiratory epithelium.
- Mycoplasma pneumoniae produces a virulence factor with ADP-ribosylating activity which is responsible for airway cellular damage and mucociliary dysfunction.
- Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis produce proteases that split mucosal IgA.
- Streptococcus pneumoniae possesses pneumolysin that aid the bacteria during colonization, by facilitating adherence to the host, during an invasion by damaging host cells, and during infection by interfering with the host immune response.
Host Factors
- 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 alveolar 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.
1. 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.
2. 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.
3. Defective Immune 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.
Genetics
- There are no genetic causes of aspiration pneumonia.
- However, patients with genetic syndromes and paralysis of following lower cranial nerves might be prone to aspiration pneumonia.
- Cranial nerve 9 (glossopharyngeal)
- Cranial nerve 10 (vagal)
- Cranial nerve 11 (accessory)
- Cranial nerve 12 (hypoglossal)
- Associated genetic syndromes are as follow:
- Cerebral palsy
- Amyotrophic lateral sclerosis (ALS)
- Spinal muscular atrophy
- Bulbospinal muscular atrophy (BSMA)
- Unclassified motor neuron diseases such as:
- Sandhoff disease
- Triple-A syndrome
- Brown-Vialetto-Van Lare-syndrome
- Hereditary neuropathy
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Japanese Respiratory Society (2009). "Aspiration pneumonia". Respirology. 14 Suppl 2: S59–64. doi:10.1111/j.1440-1843.2009.01578.x. PMID 19857224.
- ↑ Almirall J, Cabré M, Clavé P (2012). "Complications of oropharyngeal dysphagia: aspiration pneumonia". Nestle Nutr Inst Workshop Ser. 72: 67–76. doi:10.1159/000339989. PMID 23052002.
- ↑ Marik PE, Careau P (1999). "The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: a prospective study". Chest. 115 (1): 178–83. PMID 9925081.
- ↑ Cordier JF, Cottin V (2013). "Neglected evidence in idiopathic pulmonary fibrosis: from history to earlier diagnosis". Eur Respir J. 42 (4): 916–23. doi:10.1183/09031936.00027913. PMID 23598958.
- ↑ Shi X, Zheng J, Yan T (2018). "Computational redesign of human respiratory syncytial virus epitope as therapeutic peptide vaccines against pediatric pneumonia". J Mol Model. 24 (4): 79. doi:10.1007/s00894-018-3613-z. PMID 29500665.
- ↑ Shen CF, Wang SM, Ho TS, Liu CC (2017). "Clinical features of community acquired adenovirus pneumonia during the 2011 community outbreak in Southern Taiwan: role of host immune response". BMC Infect Dis. 17 (1): 196. doi:10.1186/s12879-017-2272-5. PMC 5341368. PMID 28270104.
- ↑ Marik PE (2011). "Pulmonary aspiration syndromes". Curr Opin Pulm Med. 17 (3): 148–54. doi:10.1097/MCP.0b013e32834397d6. PMID 21311332.
- ↑ Hu X, Lee JS, Pianosi PT, Ryu JH (2015). "Aspiration-related pulmonary syndromes". Chest. 147 (3): 815–823. doi:10.1378/chest.14-1049. PMID 25732447.