Toxic shock syndrome pathophysiology: Difference between revisions
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In both TSS (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen toxin that allows the non-specific binding of MHC II with T cell receptors, resulting in polyclonal T-cell activation. TSS due to Clostridium sordelli has also been identified in women undergoing medical abortion. | In both TSS (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen toxin that allows the non-specific binding of MHC II with T cell receptors, resulting in polyclonal T-cell activation. TSS due to Clostridium sordelli has also been identified in women undergoing medical abortion. | ||
Toxic shock syndrome is known to be caused by intoxication of one of the various exotoxins produced by Staphylococcus aureus, namely Toxic shock syndrome toxin-1 (TSST-1). It may also be caused by Group A streptococcal (GAS) infection. There have been reports of TSS caused by Clostridium sordelli in women undergoing medical abortion.<ref name="pmid2801850">{{cite journal |vauthors=McGregor JA, Soper DE, Lovell G, Todd JK |title=Maternal deaths associated with Clostridium sordellii infection |journal=Am. J. Obstet. Gynecol. |volume=161 |issue=4 |pages=987–95 |year=1989 |pmid=2801850 |doi= |url=}}</ref><ref name="pmid16049422">{{cite journal |vauthors= |title=Clostridium sordellii toxic shock syndrome after medical abortion with mifepristone and intravaginal misoprostol--United States and Canada, 2001-2005 |journal=MMWR Morb. Mortal. Wkly. Rep. |volume=54 |issue=29 |pages=724 |year=2005 |pmid=16049422 |doi= |url=}}</ref><ref name="pmid16319384">{{cite journal |vauthors=Fischer M, Bhatnagar J, Guarner J, Reagan S, Hacker JK, Van Meter SH, Poukens V, Whiteman DB, Iton A, Cheung M, Dassey DE, Shieh WJ, Zaki SR |title=Fatal toxic shock syndrome associated with Clostridium sordellii after medical abortion |journal=N. Engl. J. Med. |volume=353 |issue=22 |pages=2352–60 |year=2005 |pmid=16319384 |doi=10.1056/NEJMoa051620 |url=}}</ref><ref name="pmid12439811">{{cite journal |vauthors=Sinave C, Le Templier G, Blouin D, Léveillé F, Deland E |title=Toxic shock syndrome due to Clostridium sordellii: a dramatic postpartum and postabortion disease |journal=Clin. Infect. Dis. |volume=35 |issue=11 |pages=1441–3 |year=2002 |pmid=12439811 |doi=10.1086/344464 |url=}}</ref><ref name="pmid19628200">{{cite journal |vauthors=Ho CS, Bhatnagar J, Cohen AL, Hacker JK, Zane SB, Reagan S, Fischer M, Shieh WJ, Guarner J, Ahmad S, Zaki SR, McDonald LC |title=Undiagnosed cases of fatal Clostridium-associated toxic shock in Californian women of childbearing age |journal=Am. J. Obstet. Gynecol. |volume=201 |issue=5 |pages=459.e1–7 |year=2009 |pmid=19628200 |doi=10.1016/j.ajog.2009.05.023 |url=}}</ref> | |||
===TSST-1 associated Toxic shock syndrome=== | ===TSST-1 associated Toxic shock syndrome=== | ||
TSST-1 associated Toxic Shock Syndrome. A protein based exotoxin, called toxic shock syndrome toxin-1 (TSST-1), which acts as a superantigen (SAg) has been identified that is associated with strains of S. aureus isolated from patients with TSS. SAgs bind to certain regions of major histocompatibility complex (MHC) class II molecules of antigen-presenting cells (APCs) outside the traditional antigen-binding site and at the same time bind in their native form to T cells at specific motifs of the variable region of the beta chain (Vbeta) of the T cell receptor (TcR). This interaction triggers the activation (proliferation) of the targeted T lymphocytes and leads to release of high amounts of various cytokines and other effectors by immune cells. <ref name="pmid12635926">{{cite journal |vauthors=Alouf JE, Müller-Alouf H |title=Staphylococcal and streptococcal superantigens: molecular, biological and clinical aspects |journal=Int. J. Med. Microbiol. |volume=292 |issue=7-8 |pages=429–40 |year=2003 |pmid=12635926 |doi=10.1078/1438-4221-00232 |url=}}</ref>The SAg binds through its dodecapeptide region to human epithelial cells, possible CD40 or another unknown receptor, stimulating the production of pro-inflammatory chemokines. Small amounts of cytolysins, particularly α-toxin, are required to facilitate this process through combinations of their cytotoxic and pro-inflammatory properties. The SAg must penetrate the mucosal barrier to cause disease, but it appears likely that submucosal SAg activities, rather than systemic activities, are sufficient for TSS production. <ref name="pmid24838262">{{cite journal |vauthors=Stach CS, Herrera A, Schlievert PM |title=Staphylococcal superantigens interact with multiple host receptors to cause serious diseases |journal=Immunol. Res. |volume=59 |issue=1-3 |pages=177–81 |year=2014 |pmid=24838262 |pmc=4125451 |doi=10.1007/s12026-014-8539-7 |url=}}</ref>. SAgs cause release of IL-1 beta and IL-6 from antigen presenting cells (APC) and have a direct action on the hypothalamic temperature control center. Staphylococcal toxic shock syndrome toxin 1 (TSST-1) is also the cause of menstrual toxic shock syndrome (mTSS) associated with vaginal colonization by Staphylococcus aureus; IL-8 and MIP-3α, may originate from vaginal epithelial cells, which are highly chemotactic.<ref name="pmid20335433">{{cite journal |vauthors=Schlievert PM, Nemeth KA, Davis CC, Peterson ML, Jones BE |title=Staphylococcus aureus exotoxins are present in vivo in tampons |journal=Clin. Vaccine Immunol. |volume=17 |issue=5 |pages=722–7 |year=2010 |pmid=20335433 |pmc=2863369 |doi=10.1128/CVI.00483-09 |url=}}</ref> | TSST-1 associated Toxic Shock Syndrome. A protein based exotoxin, called toxic shock syndrome toxin-1 (TSST-1), which acts as a superantigen (SAg) has been identified that is associated with strains of S. aureus isolated from patients with TSS. SAgs bind to certain regions of major histocompatibility complex (MHC) class II molecules of antigen-presenting cells (APCs) outside the traditional antigen-binding site and at the same time bind in their native form to T cells at specific motifs of the variable region of the beta chain (Vbeta) of the T cell receptor (TcR). This interaction triggers the activation (proliferation) of the targeted T lymphocytes and leads to release of high amounts of various cytokines and other effectors by immune cells. <ref name="pmid12635926">{{cite journal |vauthors=Alouf JE, Müller-Alouf H |title=Staphylococcal and streptococcal superantigens: molecular, biological and clinical aspects |journal=Int. J. Med. Microbiol. |volume=292 |issue=7-8 |pages=429–40 |year=2003 |pmid=12635926 |doi=10.1078/1438-4221-00232 |url=}}</ref>The SAg binds through its dodecapeptide region to human epithelial cells, possible CD40 or another unknown receptor, stimulating the production of pro-inflammatory chemokines. Small amounts of cytolysins, particularly α-toxin, are required to facilitate this process through combinations of their cytotoxic and pro-inflammatory properties. The SAg must penetrate the mucosal barrier to cause disease, but it appears likely that submucosal SAg activities, rather than systemic activities, are sufficient for TSS production. <ref name="pmid24838262">{{cite journal |vauthors=Stach CS, Herrera A, Schlievert PM |title=Staphylococcal superantigens interact with multiple host receptors to cause serious diseases |journal=Immunol. Res. |volume=59 |issue=1-3 |pages=177–81 |year=2014 |pmid=24838262 |pmc=4125451 |doi=10.1007/s12026-014-8539-7 |url=}}</ref>. SAgs cause release of IL-1 beta and IL-6 from antigen presenting cells (APC) and have a direct action on the hypothalamic temperature control center. Staphylococcal toxic shock syndrome toxin 1 (TSST-1) is also the cause of menstrual toxic shock syndrome (mTSS) associated with vaginal colonization by Staphylococcus aureus; IL-8 and MIP-3α, may originate from vaginal epithelial cells, which are highly chemotactic.<ref name="pmid20335433">{{cite journal |vauthors=Schlievert PM, Nemeth KA, Davis CC, Peterson ML, Jones BE |title=Staphylococcus aureus exotoxins are present in vivo in tampons |journal=Clin. Vaccine Immunol. |volume=17 |issue=5 |pages=722–7 |year=2010 |pmid=20335433 |pmc=2863369 |doi=10.1128/CVI.00483-09 |url=}}</ref> | ||
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==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
In both TSS (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen toxin that allows the non-specific binding of MHC II with T cell receptors, resulting in polyclonal T-cell activation. TSS due to Clostridium sordelli has also been identified in women undergoing medical abortion.
Toxic shock syndrome is known to be caused by intoxication of one of the various exotoxins produced by Staphylococcus aureus, namely Toxic shock syndrome toxin-1 (TSST-1). It may also be caused by Group A streptococcal (GAS) infection. There have been reports of TSS caused by Clostridium sordelli in women undergoing medical abortion.[1][2][3][4][5]
TSST-1 associated Toxic shock syndrome
TSST-1 associated Toxic Shock Syndrome. A protein based exotoxin, called toxic shock syndrome toxin-1 (TSST-1), which acts as a superantigen (SAg) has been identified that is associated with strains of S. aureus isolated from patients with TSS. SAgs bind to certain regions of major histocompatibility complex (MHC) class II molecules of antigen-presenting cells (APCs) outside the traditional antigen-binding site and at the same time bind in their native form to T cells at specific motifs of the variable region of the beta chain (Vbeta) of the T cell receptor (TcR). This interaction triggers the activation (proliferation) of the targeted T lymphocytes and leads to release of high amounts of various cytokines and other effectors by immune cells. [6]The SAg binds through its dodecapeptide region to human epithelial cells, possible CD40 or another unknown receptor, stimulating the production of pro-inflammatory chemokines. Small amounts of cytolysins, particularly α-toxin, are required to facilitate this process through combinations of their cytotoxic and pro-inflammatory properties. The SAg must penetrate the mucosal barrier to cause disease, but it appears likely that submucosal SAg activities, rather than systemic activities, are sufficient for TSS production. [7]. SAgs cause release of IL-1 beta and IL-6 from antigen presenting cells (APC) and have a direct action on the hypothalamic temperature control center. Staphylococcal toxic shock syndrome toxin 1 (TSST-1) is also the cause of menstrual toxic shock syndrome (mTSS) associated with vaginal colonization by Staphylococcus aureus; IL-8 and MIP-3α, may originate from vaginal epithelial cells, which are highly chemotactic.[8]
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References
- ↑ McGregor JA, Soper DE, Lovell G, Todd JK (1989). "Maternal deaths associated with Clostridium sordellii infection". Am. J. Obstet. Gynecol. 161 (4): 987–95. PMID 2801850.
- ↑ "Clostridium sordellii toxic shock syndrome after medical abortion with mifepristone and intravaginal misoprostol--United States and Canada, 2001-2005". MMWR Morb. Mortal. Wkly. Rep. 54 (29): 724. 2005. PMID 16049422.
- ↑ Fischer M, Bhatnagar J, Guarner J, Reagan S, Hacker JK, Van Meter SH, Poukens V, Whiteman DB, Iton A, Cheung M, Dassey DE, Shieh WJ, Zaki SR (2005). "Fatal toxic shock syndrome associated with Clostridium sordellii after medical abortion". N. Engl. J. Med. 353 (22): 2352–60. doi:10.1056/NEJMoa051620. PMID 16319384.
- ↑ Sinave C, Le Templier G, Blouin D, Léveillé F, Deland E (2002). "Toxic shock syndrome due to Clostridium sordellii: a dramatic postpartum and postabortion disease". Clin. Infect. Dis. 35 (11): 1441–3. doi:10.1086/344464. PMID 12439811.
- ↑ Ho CS, Bhatnagar J, Cohen AL, Hacker JK, Zane SB, Reagan S, Fischer M, Shieh WJ, Guarner J, Ahmad S, Zaki SR, McDonald LC (2009). "Undiagnosed cases of fatal Clostridium-associated toxic shock in Californian women of childbearing age". Am. J. Obstet. Gynecol. 201 (5): 459.e1–7. doi:10.1016/j.ajog.2009.05.023. PMID 19628200.
- ↑ Alouf JE, Müller-Alouf H (2003). "Staphylococcal and streptococcal superantigens: molecular, biological and clinical aspects". Int. J. Med. Microbiol. 292 (7–8): 429–40. doi:10.1078/1438-4221-00232. PMID 12635926.
- ↑ Stach CS, Herrera A, Schlievert PM (2014). "Staphylococcal superantigens interact with multiple host receptors to cause serious diseases". Immunol. Res. 59 (1–3): 177–81. doi:10.1007/s12026-014-8539-7. PMC 4125451. PMID 24838262.
- ↑ Schlievert PM, Nemeth KA, Davis CC, Peterson ML, Jones BE (2010). "Staphylococcus aureus exotoxins are present in vivo in tampons". Clin. Vaccine Immunol. 17 (5): 722–7. doi:10.1128/CVI.00483-09. PMC 2863369. PMID 20335433.