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==Pathophysiology==
==Pathophysiology==
===Aspiration Pneumonia Pathophysiology===
===Mode of Transmission===
The location is often gravity dependent, and depends on the patient position. Generally the right middle and lower lung lobes are the most common sites of infiltrate formation due to the larger caliber and more vertical orientation of the right mainstem bronchus.  
=====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]].<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>


Patients who aspirate while standing can have bilateral lower lung lobe infiltrates. The right upper lobe is a common area of consolidation in alcoholics who aspirate in the prone position. Depending on the acidity of the aspirate, a chemical pneumonitis can develop, and bacterial pathogens (particularly [[anaerobic bacteria]]) may add to the inflammation.
==Mode of Transmission==
=====1. Microaspiration of Oropharyngeal Contents=====


=====2. 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>
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=====
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 Systemic Infection=====
=====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. [[Staphylococcus aureus]] causes pneumonia in this way. [[Gram negative bacteria]] typically account for pneumonia in immunocompromised individuals.
Microbial entered through circulation may also result in pulmonary infections. Blood-borne pneumonia is seen more commonly in intravenous drug users. [[Staphylococcus 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 occur after a pulmonary procedure or a penetrating trauma to the lungs. A local spread of a [[hepatic abscess]] can also lead to pneumonia.
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==


===Virulence Factors===
===Agent Specific Virulence Factors===
 
Several strategies are evolved to evade host defence mechanisms and facilitate spreading before establishing an infection.
Several strategies are evolved to evade host defence mechanisms and facilitate speading before establishing an infection.


* [[Influenza virus]] possesses [[neuraminidase]]s 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]]s for cleavage of sialic acid residues on the cell surface and viral proteins, which prevent aggregation and facilitate propagation of viral particles.
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===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 alevolar macrophages.  
* Smaller droplets of the size of 0.5 to 2 micrometer are deposited on the [[alveoli]] and then engulfed by alevolar macrophages.  
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* 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>
* 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======
======1. iminished 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.  
*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.
*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======
======2. mpaired Cough Reflex======
 
*[[Cough]], together with [[mucociliary clearance]], prevent pathogens from entering the lower [[respiratory tract]].  
*[[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]]s and [[overdose|drug overdosage]]s is associated with an enhanced risk for [[aspiration pneumonia]].  
*Cough suppression or [[cough reflex]] inhibition seen in patients with [[cerebrovascular accident]]s and [[overdose|drug overdosage]]s is associated with an enhanced risk for [[aspiration pneumonia]].  
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*The role of [[cough]] in preventing [[pneumonia]] may be explained by a higher risk for developing [[pneumonia]] in [[homozygote]]s carrying [[deletion|deletion/deletion (DD)]] [[genotype]] who are found to have lower levels of [[bradykinin]] and [[tachykinins]] such as [[substance P]].<ref name="Morimoto-2002">{{Cite journal  | last1 = Morimoto | first1 = S. | last2 = Okaishi | first2 = K. | last3 = Onishi | first3 = M. | last4 = Katsuya | first4 = T. | last5 = Yang | first5 = J. | last6 = Okuro | first6 = M. | last7 = Sakurai | first7 = S. | last8 = Onishi | first8 = T. | last9 = Ogihara | first9 = T. | title = Deletion allele of the angiotensin-converting enzyme gene as a risk factor for pneumonia in elderly patients. | journal = Am J Med | volume = 112 | issue = 2 | pages = 89-94 | month = Feb | year = 2002 | doi =  | PMID = 11835945 }}</ref><ref>{{Cite journal  | last1 = Rigat | first1 = B. | last2 = Hubert | first2 = C. | last3 = Alhenc-Gelas | first3 = F. | last4 = Cambien | first4 = F. | last5 = Corvol | first5 = P. | last6 = Soubrier | first6 = F. | title = An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. | journal = J Clin Invest | volume = 86 | issue = 4 | pages = 1343-6 | month = Oct | year = 1990 | doi = 10.1172/JCI114844 | PMID = 1976655 }}</ref>
*The role of [[cough]] in preventing [[pneumonia]] may be explained by a higher risk for developing [[pneumonia]] in [[homozygote]]s carrying [[deletion|deletion/deletion (DD)]] [[genotype]] who are found to have lower levels of [[bradykinin]] and [[tachykinins]] such as [[substance P]].<ref name="Morimoto-2002">{{Cite journal  | last1 = Morimoto | first1 = S. | last2 = Okaishi | first2 = K. | last3 = Onishi | first3 = M. | last4 = Katsuya | first4 = T. | last5 = Yang | first5 = J. | last6 = Okuro | first6 = M. | last7 = Sakurai | first7 = S. | last8 = Onishi | first8 = T. | last9 = Ogihara | first9 = T. | title = Deletion allele of the angiotensin-converting enzyme gene as a risk factor for pneumonia in elderly patients. | journal = Am J Med | volume = 112 | issue = 2 | pages = 89-94 | month = Feb | year = 2002 | doi =  | PMID = 11835945 }}</ref><ref>{{Cite journal  | last1 = Rigat | first1 = B. | last2 = Hubert | first2 = C. | last3 = Alhenc-Gelas | first3 = F. | last4 = Cambien | first4 = F. | last5 = Corvol | first5 = P. | last6 = Soubrier | first6 = F. | title = An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. | journal = J Clin Invest | volume = 86 | issue = 4 | pages = 1343-6 | month = Oct | year = 1990 | doi = 10.1172/JCI114844 | PMID = 1976655 }}</ref>


======Defective Immnue System======
======3. Defective Immnue 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]].  
*[[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.
*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]]s, and [[collectin]]s, also mediate the defense against microorganisms causing pneumonia.
*Other components in the immune system such as [[complement system]], [[cytokine]]s, and [[collectin]]s, also mediate the defense against microorganisms causing pneumonia.


==Major Points for Pathogenesis of Adults with Hospital-acquired, Ventilator-associated, and Healthcare-associated Pneumonia (DONOT EDIT) <ref name="pmid15699079">{{cite journal |author= |title=Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia |journal=[[American Journal of Respiratory and Critical Care Medicine]] |volume=171 |issue=4 |pages=388–416 |year=2005 |month=February |pmid=15699079 |doi=10.1164/rccm.200405-644ST |url=http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=15699079 |accessdate=2012-09-13}}</ref>==
{{cquote|
===Major Points for Pathogenesis===
'''1''' Sources of pathogens for [[HAP]] include healthcare devices, the environment (air, water, equipment, and fomites), and commonly the transfer of microorganisms between the patient and staff or other patients (Level II) .
'''2''' A number of host- and treatment-related colonization factors, such as the severity of the patient's underlying disease, prior surgery, exposure to antibiotics, other medications, and exposure to invasive respiratory devices and equipment, are important in the pathogenesis of HAP and VAP (Level II).
'''3''' [[Aspiration]] of oropharyngeal pathogens, or leakage of secretions containing bacteria around the endotracheal tube cuff, are the primary routes of bacterial entry into the lower respiratory tract (Level II).
'''4''' Inhalation or direct inoculation of pathogens into the lower airway, hematogenous spread from infected intravenous catheters, and bacterial translocation from the gastrointestinal tract lumen are uncommon pathogenic mechanisms (Level II).
'''5''' Infected biofilm in the endotracheal tube, with subsequent embolization to distal airways, may be important in the pathogenesis of VAP (Level III)
'''6''' The stomach and sinuses may be potential reservoirs of nosocomial pathogens that contribute to bacterial colonization of the oropharynx, but their contribution is controversial, may vary by the population at risk, and may be decreasing with the changing natural history and management of HAP (Level II)}}
'''For Level of evidence and classes click [[ACC AHA Guidelines Classification Scheme|here]].'''


==Microscopic Pathology==
==Microscopic Pathology==

Revision as of 19:34, 29 December 2014

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Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.D. [2]

Overview

Bacteria and fungi typically enter the lung with inhalation. Once inside the alveoli, these microbes travel into the spaces between the cells and also between adjacent alveoli through connecting pores. This invasion triggers the immune system response by sending white blood cells responsible for attacking microorganisms (neutrophils) to the lungs resulting in manifestations of pneumonia.

Pathophysiology

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.[1]


2. 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]


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. Staphylococcus 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.


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.
  • Streptococcus pneumoniae possesses pneumolysin that aid the bacteria during colonization, by facilitating adherence to the host,[4] during invasion by damaging host cells,[5] and during infection by interfering with the host immune response.[6]

Host Factors

1. iminished Mucociliary Clearance
2. mpaired Cough Reflex
3. Defective Immnue System


Microscopic Pathology

The upper panel shows a normal lung under a microscope. The white spaces are alveoli that contain air.Lower panel shows a lung with pneumonia under a microscope. The alveoli are filled with inflammation and debris.


Scanning Electron Micrograph (SEM) Gallery

Produced by the National Institute of Allergy and Infectious Diseases (NIAID), this digitally-colorized scanning electron micrograph (SEM) depicts a blue-colored, human white blood cell (WBC) known specifically as a neutrophil, interacting with two pink-colored, rod-shaped, multidrug-resistant (MDR) Klebsiella pneumoniae bacteria, which are known to cause severe hospital-acquired, nosocomial pneumonia.
Image obtained from CDC PHIL[11]
Produced by the National Institute of Allergy and Infectious Diseases (NIAID), this digitally-colorized scanning electron micrograph (SEM) depicts two yellow-colored, spherical methicillin-resistant Staphylococcus aureus (MRSA) bacteria that were in the process of being phagocytized by a blue-colored human white blood cell (WBC) known specifically as a neutrophil.
Image obtained from CDC PHIL[11]
Magnified 8000X, this colorized scanning electron micrograph (SEM) depicted a grouping of Gram-negative Legionella pneumophila bacteria.
Image obtained from CDC PHIL[11]
Scanning Electron Micrograph of Streptococcus pneumoniae.
Image obtained from CDC PHIL[11]

References

  1. ↑ 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)
  2. ↑ Shemer-Avni, Y.; Lieberman, D. (1995). "Chlamydia pneumoniae-induced ciliostasis in ciliated bronchial epithelial cells". J Infect Dis. 171 (5): 1274–8. PMID 7751703. Unknown parameter |month= ignored (help)
  3. ↑ Kannan, TR.; Baseman, JB. (2006). "ADP-ribosylating and vacuolating cytotoxin of Mycoplasma pneumoniae represents unique virulence determinant among bacterial pathogens". Proc Natl Acad Sci U S A. 103 (17): 6724–9. doi:10.1073/pnas.0510644103. PMID 16617115. Unknown parameter |month= ignored (help)
  4. ↑ Rubins, JB (December 1998). "Pneumolysin in pneumococcal adherence and colonization". Microbial pathogenesis. 25 (6): 337–42. doi:10.1006/mpat.1998.0239. PMID 9895272. Unknown parameter |coauthors= ignored (help)
  5. ↑ Rubins, JB (January 1998). "Pneumolysin: a multifunctional pneumococcal virulence factor". The Journal of laboratory and clinical medicine. 131 (1): 21–7. PMID 9452123. Unknown parameter |coauthors= ignored (help)
  6. ↑ Cockeran, R (June 2002). "The role of pneumolysin in the pathogenesis of Streptococcus pneumoniae infection". Current Opinion in Infectious Diseases. 15 (3): 235–9. PMID 12015456. Unknown parameter |coauthors= ignored (help)
  7. ↑ 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)
  8. ↑ 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)
  9. ↑ 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)
  10. ↑ 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)
  11. ↑ 11.0 11.1 11.2 11.3 http://phil.cdc.gov/phil/home.asp

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