Pneumococcal infections pathophysiology: Difference between revisions
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== Pathophysiology == | |||
''S. pneumoniae'' is normally found in the [[nasopharynx]] of 5-10% of healthy adults, and 20-40% of healthy children.<ref name=Sherris>{{cite book | author = Ryan KJ; Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th | publisher = McGraw Hill | year = 2004 | isbn = 0-8385-8529-9 }}</ref> It can be found in higher amounts in certain environments, especially those where people are spending a great deal of time in close proximity to each other (day care centers, military barracks). It attaches to nasopharyngeal cells through interaction of bacterial surface [[adhesin]]s. This normal colonization can become infectious if the organisms are carried into areas such as the [[Eustachian tube]] or [[nasal sinus]]es where it can cause [[otitis media]] and [[sinusitis]], respectively. Pneumonia occurs if the organisms are inhaled into the lungs and not cleared (again, viral infection, or [[Tobacco smoking|smoking]]-induced ciliary paralysis might be contributing factors). The organism's [[polysaccharide]] capsule makes it resistant to [[phagocytosis]], and if there is no pre-existing anticapsular antibody, alveolar [[macrophage]]s cannot adequately kill the pneumococci. The organism spreads to the blood stream (where it can cause [[bacteremia]]) and is carried to the [[meninges]], joint spaces, [[bone]]s, and [[peritoneal cavity]], and may result in [[meningitis]], [[brain abscess]], [[septic arthritis]], or [[osteomyelitis]]. | |||
''S. pneumoniae'' has several [[virulence factor]]s, including the polysaccharide capsule mentioned earlier, that help it evade a host's immune system. It has pneumococcal surface proteins that inhibit complement-mediated opsonization, and it secretes IgA1 protease that will destroy secretory IgA produced by the body and mediates its attachment to respiratory mucosa. | |||
The risk of pneumococcal infection is much increased in persons with impaired IgG synthesis, impaired phagocytosis, or defective clearance of pneumococci. In particular, the absence of a functional [[spleen]], through [[congenital asplenia]], [[splenectomy]], or [[sickle-cell disease]] predisposes one to a more severe course of infection ([[Overwhelming post-splenectomy infection]]) and prevention measures are indicated (see [[asplenia]]). ''S. pneumoniae'' expresses different virulence factors on its cell surface and inside the organism. These virulence factors contribute to some of the clinical manifestations during infection with ''S. pneumoniae''. | |||
===Virulence factors=== | |||
*'''Polysaccharide capsule''' - prevents phagocytosis by host immune cells by inhibiting C3b opsonization of the bacterial cells | |||
*'''[[Pneumolysin]]''' (Ply) - a 53-kDa pore-forming protein that can cause lysis of host cells and activate complement | |||
*'''Autolysin''' (LytA) - activation of this protein lyses the bacteria releasing its internal contents (i.e., pneumolysin) | |||
*'''[[Hydrogen peroxide]]''' - causes damage to host cells (can cause apoptosis in neuronal cells during meningitis) and has bactericidal effects against competing bacteria ([[Haemophilus influenzae]], [[Neisseria meningitidis]], [[Staphylococcus aureus]])<ref>{{cite journal |author=Pericone, Christopher D., Overweg, Karin, Hermans, Peter W. M., Weiser, Jeffrey N. |title=Inhibitory and Bactericidal Effects of Hydrogen Peroxide Production by Streptococcus pneumoniae on Other Inhabitants of the Upper Respiratory Tract |journal=Infect Immun |volume=68 |issue=7 |pages=3990–3997 |year=2000 |pmid=10858213 |doi=10.1128/IAI.68.7.3990-3997.2000 |pmc=101678}}</ref><ref>{{cite journal |author=Regev-Yochay G, Trzcinski K, Thompson CM, Malley R, Lipsitch M. |title=Interference between Streptococcus pneumoniae and Staphylococcus aureus: In vitro hydrogen peroxide-mediated killing by Streptococcus pneumoniae |journal=J Bacteriol |volume=188|issue=13 |pages=4996–5001| year=2006 |pmid=16788209 |doi=10.1128/JB.00317-06 |pmc=1482988}}</ref> | |||
*'''[[Pilus|Pili]]''' - hair-like structures that extend from the surface of many strains of ''S. pneumoniae''. They contribute to colonization of upper respiratory tract and increase the formation of large amounts of [[tumor necrosis factors|TNF]] by the immune system during [[sepsis]], raising the possibility of [[septic shock]]<ref>{{cite journal |author=Barocchi M, Ries J, Zogaj X, Hemsley C, Albiger B, Kanth A, Dahlberg S, Fernebro J, Moschioni M, Masignani V, Hultenby K, Taddei A, Beiter K, Wartha F, von Euler A, Covacci A, Holden D, Normark S, Rappuoli R, Henriques-Normark B |title=A pneumococcal pilus influences virulence and host inflammatory responses |journal=Proc Natl Acad Sci USA |volume=103 |issue=8 |pages=2857–2862 |year=2006 |pmid=16481624 |doi=10.1073/pnas.0511017103 |pmc=1368962}}</ref> | |||
*'''Choline binding protein A/Pneumococcal surface protein A''' (CbpA/PspA) -an adhesin that can interact with carbohydrates on the cell surface of pulmonary epithelial cells and can inhibit complement-mediated opsonization of pneumococci | |||
==References== | ==References== | ||
Revision as of 20:59, 6 December 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
S. pneumoniae is normally found in the nasopharynx of 5-10% of healthy adults, and 20-40% of healthy children.[1] It can be found in higher amounts in certain environments, especially those where people are spending a great deal of time in close proximity to each other (day care centers, military barracks). It attaches to nasopharyngeal cells through interaction of bacterial surface adhesins. This normal colonization can become infectious if the organisms are carried into areas such as the Eustachian tube or nasal sinuses where it can cause otitis media and sinusitis, respectively. Pneumonia occurs if the organisms are inhaled into the lungs and not cleared (again, viral infection, or smoking-induced ciliary paralysis might be contributing factors). The organism's polysaccharide capsule makes it resistant to phagocytosis, and if there is no pre-existing anticapsular antibody, alveolar macrophages cannot adequately kill the pneumococci. The organism spreads to the blood stream (where it can cause bacteremia) and is carried to the meninges, joint spaces, bones, and peritoneal cavity, and may result in meningitis, brain abscess, septic arthritis, or osteomyelitis.
S. pneumoniae has several virulence factors, including the polysaccharide capsule mentioned earlier, that help it evade a host's immune system. It has pneumococcal surface proteins that inhibit complement-mediated opsonization, and it secretes IgA1 protease that will destroy secretory IgA produced by the body and mediates its attachment to respiratory mucosa.
The risk of pneumococcal infection is much increased in persons with impaired IgG synthesis, impaired phagocytosis, or defective clearance of pneumococci. In particular, the absence of a functional spleen, through congenital asplenia, splenectomy, or sickle-cell disease predisposes one to a more severe course of infection (Overwhelming post-splenectomy infection) and prevention measures are indicated (see asplenia). S. pneumoniae expresses different virulence factors on its cell surface and inside the organism. These virulence factors contribute to some of the clinical manifestations during infection with S. pneumoniae.
Virulence factors
- Polysaccharide capsule - prevents phagocytosis by host immune cells by inhibiting C3b opsonization of the bacterial cells
- Pneumolysin (Ply) - a 53-kDa pore-forming protein that can cause lysis of host cells and activate complement
- Autolysin (LytA) - activation of this protein lyses the bacteria releasing its internal contents (i.e., pneumolysin)
- Hydrogen peroxide - causes damage to host cells (can cause apoptosis in neuronal cells during meningitis) and has bactericidal effects against competing bacteria (Haemophilus influenzae, Neisseria meningitidis, Staphylococcus aureus)[2][3]
- Pili - hair-like structures that extend from the surface of many strains of S. pneumoniae. They contribute to colonization of upper respiratory tract and increase the formation of large amounts of TNF by the immune system during sepsis, raising the possibility of septic shock[4]
- Choline binding protein A/Pneumococcal surface protein A (CbpA/PspA) -an adhesin that can interact with carbohydrates on the cell surface of pulmonary epithelial cells and can inhibit complement-mediated opsonization of pneumococci
References
- ↑ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9.
- ↑ Pericone, Christopher D., Overweg, Karin, Hermans, Peter W. M., Weiser, Jeffrey N. (2000). "Inhibitory and Bactericidal Effects of Hydrogen Peroxide Production by Streptococcus pneumoniae on Other Inhabitants of the Upper Respiratory Tract". Infect Immun. 68 (7): 3990&ndash, 3997. doi:10.1128/IAI.68.7.3990-3997.2000. PMC 101678. PMID 10858213.
- ↑ Regev-Yochay G, Trzcinski K, Thompson CM, Malley R, Lipsitch M. (2006). "Interference between Streptococcus pneumoniae and Staphylococcus aureus: In vitro hydrogen peroxide-mediated killing by Streptococcus pneumoniae". J Bacteriol. 188 (13): 4996&ndash, 5001. doi:10.1128/JB.00317-06. PMC 1482988. PMID 16788209.
- ↑ Barocchi M, Ries J, Zogaj X, Hemsley C, Albiger B, Kanth A, Dahlberg S, Fernebro J, Moschioni M, Masignani V, Hultenby K, Taddei A, Beiter K, Wartha F, von Euler A, Covacci A, Holden D, Normark S, Rappuoli R, Henriques-Normark B (2006). "A pneumococcal pilus influences virulence and host inflammatory responses". Proc Natl Acad Sci USA. 103 (8): 2857&ndash, 2862. doi:10.1073/pnas.0511017103. PMC 1368962. PMID 16481624.