Pneumonia pathophysiology: Difference between revisions

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===Mode of Transmission===
===Mode of Transmission===
=====1. Inhalation of Aerosolized Droplets=====
=====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>
* [[Inhalation]] of aerosolized droplets of 0.5 to 1 micrometer is the most common pathway of acquiring [[pneumonia]].
* A few [[Bacteria|bacterial]] and [[Virus|viral]] [[Infection|infections]] are transmitted in this fashion.   
* The [[lung]] can normally filter out particles between 0.5 to 2 micrometer by recruiting the [[Alveolus|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>
 
=====2. 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 pneumonia|Aspiration]] of [[Oropharyngeal airway|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 [[Gastroesophageal reflux disease|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>
 
=====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 [[Lung|pulmonary]] [[Infection|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 [[Lung|pulmonary]] procedure or a penetrating trauma to the [[Lung|lungs]].
* A local spread of a [[hepatic abscess]] can also lead to pneumonia.


===Agent Specific 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 spreading 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 (biology)|cell]] surface and [[Virus|viral]] [[Protein|proteins]], which prevent aggregation and facilitate propagation of [[Virus|viral]] particles.


* ''[[Chlamydophila pneumoniae]]'' induces complete abortion of cilia motions which assists colonization at the [[respiratory epithelium]].<ref name="Shemer-Avni-1995">{{Cite journal  | last1 = Shemer-Avni | first1 = Y. | last2 = Lieberman | first2 = D. | title = Chlamydia pneumoniae-induced ciliostasis in ciliated bronchial epithelial cells. | journal = J Infect Dis | volume = 171 | issue = 5 | pages = 1274-8 | month = May | year = 1995 | doi =  | PMID = 7751703 }}</ref>
* ''[[Chlamydophila pneumoniae]]'' induces complete abortion of cilia motions which assists colonization at the [[respiratory epithelium]].<ref name="Shemer-Avni-1995">{{Cite journal  | last1 = Shemer-Avni | first1 = Y. | last2 = Lieberman | first2 = D. | title = Chlamydia pneumoniae-induced ciliostasis in ciliated bronchial epithelial cells. | journal = J Infect Dis | volume = 171 | issue = 5 | pages = 1274-8 | month = May | year = 1995 | doi =  | PMID = 7751703 }}</ref>
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===Host Factors===
===Host Factors===
* The lungs can normally filter out large droplets of aerosols.  
* The [[Lung|lungs]] can normally filter out large droplets of [[Aerosol|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 [[Macrophage|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.<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 [[Microorganism|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>


======1. Diminished Mucociliary Clearance======
======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.  
*The [[Respiratory epithelium#Ciliary Escalator|cilia]] lining the [[respiratory epithelium]] serve to move secreted [[mucus]] containing trapped foreign particles including [[Pathogen|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 [[Genetics|genetic]] defects affecting [[mucociliary clearance]] such as [[primary ciliary dyskinesia]] suggests its role in the [[pathogenesis]] of community-acquired pneumonia.


======2. Impaired Cough Reflex======
======2. Impaired Cough Reflex======
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*[[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 [[Microorganism|microorganisms]] causing pneumonia.


==Microscopic Pathology==
==Microscopic Pathology==
[[Image:Pneumonia alveolus.jpg|thumb|left|286 px|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.]]
[[Image:Pneumonia alveolus.jpg|thumb|left|286 px|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.]]
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==Community Acquired Pneumonia==
The symptoms of CAP are the result of both, the invasion of the lungs by [[microorganism]]s and the [[immune system]]'s response to the infection. The mechanisms of infection are quite different for [[virus]]es and the other microorganisms.
===Viruses===
*Viruses must invade cells to reproduce. Typically, a virus reaches the lungs by travelling in droplets through the [[mouth]] and [[Human nose|nose]] during [[inhalation]]. There, the virus invades the cells lining the airways and the alveoli.
* This invasion often leads to cell death, either through direct killing by the virus or by self-destruction through [[apoptosis]].
*Further lung damage occurs when the immune system responds to the infection.
*[[White blood cell]]s, in particular [[lymphocyte]]s, activate a variety of chemicals ([[cytokine]]s), which make fluid leak into the alveoli.
*The combination of cellular destruction and fluid-filled alveoli interrupts the transportation of oxygen into the bloodstream.
*In addition to their affect on the lungs, many viruses affect other [[Organ (anatomy)|organ]]s; this can lead to illnesses that affect many different bodily functions.
*Viruses also make the body more susceptible to bacterial infection; for this reason, bacterial pneumonia often complicates viral CAP.
===Bacteria and Fungi===
*Bacteria and fungi also typically enter the lung with inhalation, although they reach the lung through the bloodstream if other parts of the body are infected.
*Often, bacteria live in parts of the [[upper respiratory tract]] and are constantly being inhaled into the alveoli.
*Once inside the alveoli, [[bacteria]] and [[fungus|fungi]] travel into the spaces between the cells and also between adjacent alveoli through connecting pores.
*This invasion triggers the [[immune system]] to respond by sending white blood cells, responsible for attacking microorganisms ([[neutrophil]]s), to the lungs.
* The neutrophils [[phagocytosis|engulf]] and kill the offending organisms, but they also release cytokines; this results in the general activation of the immune system. This causes the fever, chills, and fatigue which are common to CAP.
*The neutrophils, bacteria, and fluid leaked from surrounding blood vessels fill the alveoli and result in impaired oxygen transportation.
* Bacteria often travel from the lungs to the blood stream; this can often result in serious illness, such as [[septic shock]], in which there is low blood pressure leading to damage to multiple parts of the body, including the [[brain]], [[kidney]], and [[heart]].
===Parasites===
*A variety of parasites can affect the lungs.
*In general, parasites enter the body through the skin or by ingestion.
*Once inside the body, these parasites travel to the lungs, most often through the blood.
*There, a similar combination of cellular destruction and immune response causes disruption of oxygen transportation.


==Microbial Pathogenesis==
==Microbial Pathogenesis==
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* ''[[Streptococcus pneumoniae]]'' possesses [[pneumolysin]] that aid the bacteria during colonization, by facilitating adherence to the host,<ref>{{cite journal|last=Rubins|first=JB|coauthors=Paddock, AH, Charboneau, D, Berry, AM, Paton, JC, Janoff, EN|title=Pneumolysin in pneumococcal adherence and colonization.|journal=Microbial pathogenesis|date=December 1998|volume=25|issue=6|pages=337–42|pmid=9895272|doi=10.1006/mpat.1998.0239}}</ref> during invasion by damaging host cells,<ref>{{cite journal|last=Rubins|first=JB|coauthors=Janoff, EN|title=Pneumolysin: a multifunctional pneumococcal virulence factor.|journal=The Journal of laboratory and clinical medicine|date=January 1998|volume=131|issue=1|pages=21–7|pmid=9452123}}</ref> and during infection by interfering with the host immune response.<ref>{{cite journal|last=Cockeran|first=R|coauthors=Anderson, R, Feldman, C|title=The role of pneumolysin in the pathogenesis of Streptococcus pneumoniae infection.|journal=Current Opinion in Infectious Diseases|date=June 2002|volume=15|issue=3|pages=235–9|pmid=12015456}}</ref>
* ''[[Streptococcus pneumoniae]]'' possesses [[pneumolysin]] that aid the bacteria during colonization, by facilitating adherence to the host,<ref>{{cite journal|last=Rubins|first=JB|coauthors=Paddock, AH, Charboneau, D, Berry, AM, Paton, JC, Janoff, EN|title=Pneumolysin in pneumococcal adherence and colonization.|journal=Microbial pathogenesis|date=December 1998|volume=25|issue=6|pages=337–42|pmid=9895272|doi=10.1006/mpat.1998.0239}}</ref> during invasion by damaging host cells,<ref>{{cite journal|last=Rubins|first=JB|coauthors=Janoff, EN|title=Pneumolysin: a multifunctional pneumococcal virulence factor.|journal=The Journal of laboratory and clinical medicine|date=January 1998|volume=131|issue=1|pages=21–7|pmid=9452123}}</ref> and during infection by interfering with the host immune response.<ref>{{cite journal|last=Cockeran|first=R|coauthors=Anderson, R, Feldman, C|title=The role of pneumolysin in the pathogenesis of Streptococcus pneumoniae infection.|journal=Current Opinion in Infectious Diseases|date=June 2002|volume=15|issue=3|pages=235–9|pmid=12015456}}</ref>


==Host Factors==
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The lungs can normally filter out large droplets of aerosols. Smaller droplets 0.5 to 2 micrometer in size are deposited in the terminal [[alveoli]] and then engulfed by alevolar macrophages. These [[macrophages]] release [[cytokines]] and [[chemokines]] such as [[tumor necrosis factor-alpha]], [[interleukin]]-8 and [[leukotriene|LTB4]]. This leads to accelerated recruitment of [[neutrophils]] to the involved area.<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======
 
The [[Respiratory epithelium#Ciliary Escalator|ciliary]] lining of the [[respiratory epithelium]] serves to move secreted [[mucus]] containing trapped foreign particles, including pathogens, towards the [[oropharynx]] for either expectoration or swallowing. The elevated incidence of [[pneumonia]] among patients with genetic defects affecting [[mucociliary clearance]], such as [[primary ciliary dyskinesia]], suggests the important role of ciliary clearance in preventing community-acquired pneumonia.
 
======Impaired Cough Reflex======
 
[[Cough]], together with [[mucociliary clearance]], prevents pathogens from entering the lower [[respiratory tract]]. Cough suppression or [[cough reflex]] inhibition seen in patients with [[cerebrovascular accident]]s and [[overdose|drug overdose]]s is associated with an increased risk for [[aspiration pneumonia]]. The role of [[cough]] in preventing infection of the lower respiratory tract is demonstrated by a higher risk of [[pneumonia]] among patients with lower levels of [[bradykinin]] and [[tachykinins]], such as [[substance P]]. These patients have a diminished cough reflex. <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 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 of the immune system, such as [[complement system]], [[cytokine]]s, and [[collectin]]s, also mediate the defense against microorganisms that cause pneumonia. Any defects in the this immune pathway can cause and increased risk of infections, namely pneumonia.


===Aspiration Pneumonia===
===Aspiration Pneumonia===


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=== Lobar Pneumonia===
=== Lobar Pneumonia===
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=== Aspiration Pneumonia, Infant===
=== Aspiration Pneumonia, Infant===


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===Scanning Electron Micrograph (SEM) Gallery===
{|
|[[File:SEM Klebsiella pneumoniae.jpg |thumb|250px|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.  <br><small>Image obtained from CDC PHIL<ref name=PHIL>http://phil.cdc.gov/phil/home.asp</ref></small>]]
|[[File:SEM S. aureus.jpg |thumb|250px|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. <br><small>Image obtained from CDC PHIL<ref name=PHIL>http://phil.cdc.gov/phil/home.asp</ref></small>]]
|[[File:SEM Legionella pneumophilia.jpg|thumb|300px|Magnified 8000X, this colorized scanning electron micrograph (SEM) depicted a grouping of Gram-negative '''Legionella pneumophila''' bacteria.  <br><small>Image obtained from CDC PHIL<ref name=PHIL>http://phil.cdc.gov/phil/home.asp</ref></small>]]
|[[File:SEM Streptococcus pneumoniae.jpg|thumb|250px|Scanning Electron Micrograph of '''Streptococcus pneumoniae'''. <br><small>Image obtained from CDC PHIL<ref name=PHIL>http://phil.cdc.gov/phil/home.asp</ref></small>]]
|}


==References==
==References==

Latest revision as of 20:48, 11 November 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Priyamvada Singh, M.D. [3]

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
2. Microaspiration of Oropharyngeal Contents
3. Blood-Borne or Systemic Infection
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.

  • 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. Diminished Mucociliary Clearance
2. Impaired Cough Reflex
3. Defective Immune 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.


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. ↑ 2.0 2.1 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. ↑ 3.0 3.1 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. ↑ 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)
  12. ↑ 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)
  13. ↑ 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)

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