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__NOTOC__
__NOTOC__
{{Pneumonia}}
{{Pneumonia}}
'''Editor(s)-in-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org] Phone:617-632-7753; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh@perfuse.org]
{{CMG}}; {{AE}} {{HQ}}, [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com]


==Overview==
==Overview==
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==Pathophysiology==
==Pathophysiology==
===Microscopic Pathology===
===Mode of Transmission===
===Viruses===
=====1. Inhalation of Aerosolized Droplets=====
* Viruses must invade cells in order to reproduce.
* [[Inhalation]] of aerosolized droplets of 0.5 to 1 micrometer is the most common pathway of acquiring [[pneumonia]].
* Typically, a virus will reach the lungs by traveling in droplets through the [[mouth]] and [[nose]] with [[inhalation]].
* A few [[Bacteria|bacterial]] and [[Virus|viral]] [[Infection|infections]] are transmitted in this fashion.
* There, the virus invades the cells lining the airways and the alveoli.
* 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>
* This invasion often leads to cell death either by directly killing the virus or by self-destruction through [[apoptosis]].
* Further damage to the lungs occurs when the immune system responds to the infection. [[White blood cell]]s, in particular [[lymphocyte]]s, are responsible for activating a variety of chemicals ([[cytokine]]s) which cause leaking of fluid into the alveoli.
* The combination of cellular destruction and fluid-filled alveoli interrupts the transportation of oxygen into the bloodstream.
* In addition to the effects on the lungs, many viruses affect other [[Organ (anatomy)|organ]]s and can lead to illness affecting many different bodily functions.
* Viruses also make the body more susceptible to bacterial infection; for this reason, bacterial pneumonia often complicates viral CAP.
===Bacteria===
* Bacteria and fungi also typically enter the lung with inhalation, though they can 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 also release cytokines which result in a general activation of the immune system.
* Fever, chills, and fatigue are common in 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 lung into the blood stream and can result in serious illness such as [[septic shock]]. Septic shock results in low blood pressure leading to damage in multiple parts of the body including the [[brain]], [[kidney]], and [[heart]].
[[Media:Example.ogg]]


===Fungi===
=====2. Microaspiration of Oropharyngeal Contents=====
Fungi typically enter the lung with inhalation of their spores, though they can reach the lung through the bloodstream if other parts of the body are infected. Also, fungal pneumonia can be caused by reactivation of a latent infection. Once inside the alveoli, 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 (neutrophils) to the lungs. The neutrophils engulf and kill the offending organisms but also release cytokines which result in a general activation of the immune system. This results in the fever, chills, and fatigue that is commonly seen in bacterial and fungal pneumonia. The neutrophils and fluid leaked from surrounding blood vessels fill the alveoli and result in impaired oxygen transportation.
* [[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>


Specific instances of fungal infections that can manifest with pulmonary involvement include:
=====3. Blood-Borne or Systemic Infection=====
* 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.


*[[Pneumocystis jirovecii pneumonia]]
=====4. Trauma or Local Spread=====
*[[Histoplasmosis]], which has primary pulmonary lesions and hematogenous dissemination
* Pneumonia can occur after a [[Lung|pulmonary]] procedure or a penetrating trauma to the [[Lung|lungs]].
*[[Coccidioidomycosis]], which begins with an often self-limited respiratory infection (also called "Valley fever" or "San Joaquin fever")
* A local spread of a [[hepatic abscess]] can also lead to pneumonia.
*[[Pulmonary blastomycosis]]  
*[[Sporotrichosis]] - primarily a lymphocutaneous disease, but can involve the lungs as well
*[[Cryptococcosis]] - contracted through inhalation of soil contaminated with the yeast, it can manifest as a pulmonary infection and as a disseminated one
*[[Aspergillosis]], resulting in invasive pulmonary aspergillosis
*[[Candidiasis]] - rarely has pulmonary manifestations in immunocompromised patients.


===Parasites===
===Agent Specific Virulence Factors===
* In general, these parasites enter the body through the skin or by being swallowed.
Several strategies are evolved to evade host defence mechanisms and facilitate spreading before establishing an [[infection]].
* 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.


==Aspiration Pneumonia Pathophysiology==
* [[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.
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.  


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.
* ''[[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>


===Microscopic Pathology===
* ''[[Mycoplasma pneumoniae]]'' produces a virulence factor with [[ADP-ribosylation|ADP-ribosylating]] activity which is responsible for airway cellular damage and mucociliary dysfunction.<ref name="Kannan-2006">{{Cite journal  | last1 = Kannan | first1 = TR. | last2 = Baseman | first2 = JB. | title = ADP-ribosylating and vacuolating cytotoxin of Mycoplasma pneumoniae represents unique virulence determinant among bacterial pathogens. | journal = Proc Natl Acad Sci U S A | volume = 103 | issue = 17 | pages = 6724-9 | month = Apr | year = 2006 | doi = 10.1073/pnas.0510644103 | PMID = 16617115 }}</ref>


[[Image:Pneumonia alveolus.jpg|thumb|left|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.]]
* ''[[Haemophilus influenzae]]'', ''[[Streptococcus pneumoniae]]'', and ''[[Neisseria meningitidis]]'' produce [[protease]]s that split mucosal [[immunoglobulin A|IgA]].


* ''[[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===
* 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 [[Macrophage|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 [[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======
*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 [[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======
*[[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]].
* Another relation to [[cough]] is [[genetic polymorphism]]s 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]]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>


======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]]s, and [[collectin]]s, also mediate the defense against [[Microorganism|microorganisms]] causing pneumonia.


==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.]]
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==Microbial Pathogenesis==


===Virulence Factors===


Several mechanisms have evolved to evade host defense mechanisms and facilitate microbial spread to establish an infection.


* [[Influenza virus]]es possess [[neuraminidase]] that cleaves sialic acid residues on the cell surface, which prevents viral aggregation and facilitates the propagation of viral particles.


* ''[[Chlamydophila pneumoniae]]'' induces complete paralysis of the respiratory cilia, which assists with the colonization of 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>


* ''[[Mycoplasma pneumoniae]]'' produces a virulence factor with [[ADP-ribosylation|ADP-ribosylating]] activity that is responsible for airway cellular damage and mucociliary dysfunction.<ref name="Kannan-2006">{{Cite journal  | last1 = Kannan | first1 = TR. | last2 = Baseman | first2 = JB. | title = ADP-ribosylating and vacuolating cytotoxin of Mycoplasma pneumoniae represents unique virulence determinant among bacterial pathogens. | journal = Proc Natl Acad Sci U S A | volume = 103 | issue = 17 | pages = 6724-9 | month = Apr | year = 2006 | doi = 10.1073/pnas.0510644103 | PMID = 16617115 }}</ref>


* ''[[Haemophilus influenzae]]'', ''[[Streptococcus pneumoniae]]'', and ''[[Neisseria meningitidis]]'' produce [[protease]]s that cleave mucosal [[immunoglobulin A|IgA]].


* ''[[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>


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===Aspiration 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]].'''
 
== Histopathological Findings in Aspiration Pneumonia==


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==Histopathological Findings==
=== Lobar Pneumonia===
 
=== Lobar pneumonia===


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  {{#ev:youtube|dxXrxYIXbL8}}


=== Pneumocystis pneumonia===
=== Pneumocystis Pneumonia===


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=== Pneumocystis Pneumonia===


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=== Aspiration pneumonia, infant===
=== Aspiration Pneumonia, Infant===


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{{#ev:youtube|RXnnEuEZ0BY}}


=== Desquamative interstitial pneumonia===
=== Desquamative Interstitial Pneumonia===


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{{#ev:youtube|G0TFmAAYjWU}}


=== Legionella pneumonia===
=== Legionella Pneumonia===


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{{#ev:youtube|BDWEnPilfIQ}}


=== Measles pneumonia===
=== Measles Pneumonia===


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{{#ev:youtube|v80kA_dt6EE}}


=== Abscess, bronchopneumonia===
=== Abscess, Bronchopneumonia===


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==References==
==References==
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[[Category:Disease]]
[[Category:Disease]]
[[Category:Pulmonology]]
[[Category:Pulmonology]]
[[Category:Infectious disease]]
 
[[Category:Pneumonia|Pneumonia]]
[[Category:Pneumonia|Pneumonia]]
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]

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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