Aspiration pneumonia pathophysiology: Difference between revisions
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{{CMG}}; {{AE}} | {{CMG}}; {{AE}} | ||
==Overview== | ==Overview== | ||
The | 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: | |||
=== Mode of Transmission === | |||
===== 1. 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]]. | |||
[ | ===== 2. Microaspiration of Oropharyngeal Contents[edit | edit source] ===== | ||
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]]. | |||
=== Agent Specific Virulence Factors === | |||
Several strategies are evolved to evade host defence 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. | |||
* ''[[Chlamydophila pneumoniae]]'' induces complete abortion of cilia motions which assists colonization at the [[respiratory epithelium]]. | |||
* ''[[Mycoplasma pneumoniae]]'' produces a virulence factor with [[ADP-ribosylation|ADP-ribosylating]] activity which is responsible for airway cellular damage and mucociliary dysfunction. | |||
* ''[[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. | ||
=== 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 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. | |||
====== 1. Diminished Mucociliary Clearance ====== | |||
* The [[Respiratory epithelium#Ciliary Escalator|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 accident|cerebrovascular accidents]] and [[Overdose|drug overdosages]] is associated with an enhanced risk for [[aspiration pneumonia]]. | |||
* Another relation to [[cough]] is [[Genetic polymorphism|genetic polymorphisms]] in the [[Angiotensin-converting enzyme|angiotensin-converting enzyme (ACE)]] gene. | |||
*[ | * The role of [[cough]] in preventing [[pneumonia]] may be explained by a higher risk for developing [[pneumonia]] in [[Homozygote|homozygotes]] carrying [[Deletion|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 pattern|Pathogen-associated molecular patterns (PAMPs)]] are initially recognized by [[Toll-like receptor|Toll-like receptors (TLRs)]] and other [[Pattern recognition receptor|pattern-recognition receptors (PRRs)]] of the [[innate immune system]]. | |||
* Effectors in the [[Acquired immunity|acquired immune system]] are involved in elimination of microorganisms and generation of immunological memory. | |||
* Other components in the immune system such as [[complement system]], [[Cytokine|cytokines]], and [[Collectin|collectins]], also mediate the defense against microorganisms causing pneumonia. | |||
==Genetics== | ==Genetics== | ||
*[Disease name] is transmitted in [mode of genetic transmission] pattern. | *[Disease name] is transmitted in [mode of genetic transmission] pattern. |
Revision as of 20:26, 20 February 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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:
Mode of Transmission
1. 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.
2. Microaspiration of Oropharyngeal Contents[edit | edit source]
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.
Agent Specific Virulence Factors
Several strategies are evolved to evade host defence 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 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 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.
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
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
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].