Impetigo pathophysiology: Difference between revisions
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==Pathogenesis== | ==Pathogenesis== | ||
Impetigo, the infection of epidermis, can either be primary or secondary to scratches, injuries, bites or conditions that lead to a break in the continuity of the skin. The breaks in the continuity are potential sites for the pathogens to enter and infect.<ref name="pmid19331587">{{cite journal| author=Wasserzug O, Valinsky L, Klement E, Bar-Zeev Y, Davidovitch N, Orr N et al.| title=A cluster of ecthyma outbreaks caused by a single clone of invasive and highly infective Streptococcus pyogenes. | journal=Clin Infect Dis | year= 2009 | volume= 48 | issue= 9 | pages= 1213-9 | pmid=19331587 | doi=10.1086/597770 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19331587 }} </ref><ref name="pmid22299710">{{cite journal| author=Bangert S, Levy M, Hebert AA| title=Bacterial resistance and impetigo treatment trends: a review. | journal=Pediatr Dermatol | year= 2012 | volume= 29 | issue= 3 | pages= 243-8 | pmid=22299710 | doi=10.1111/j.1525-1470.2011.01700.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22299710 }} </ref><ref name="pmid21282415">{{cite journal| author=Kato F, Kadomoto N, Iwamoto Y, Bunai K, Komatsuzawa H, Sugai M| title=Regulatory mechanism for exfoliative toxin production in Staphylococcus aureus. | journal=Infect Immun | year= 2011 | volume= 79 | issue= 4 | pages= 1660-70 | pmid=21282415 | doi=10.1128/IAI.00872-10 | pmc=3067547 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21282415 }} </ref><ref name="pmid20728315">{{cite journal| author=Nishifuji K, Shimizu A, Ishiko A, Iwasaki T, Amagai M| title=Removal of amino-terminal extracellular domains of desmoglein 1 by staphylococcal exfoliative toxin is sufficient to initiate epidermal blister formation. | journal=J Dermatol Sci | year= 2010 | volume= 59 | issue= 3 | pages= 184-91 | pmid=20728315 | doi=10.1016/j.jdermsci.2010.07.010 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20728315 }} </ref> | |||
===Streptococcal Impetigo=== | ===Streptococcal Impetigo=== | ||
*The D and E strains of emm protein act as a virulence factor for group A Streptococci.<ref name="pmid19331587">{{cite journal| author=Wasserzug O, Valinsky L, Klement E, Bar-Zeev Y, Davidovitch N, Orr N et al.| title=A cluster of ecthyma outbreaks caused by a single clone of invasive and highly infective Streptococcus pyogenes. | journal=Clin Infect Dis | year= 2009 | volume= 48 | issue= 9 | pages= 1213-9 | pmid=19331587 | doi=10.1086/597770 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19331587 }} </ref><ref name="pmid8603968">{{cite journal| author=Bessen DE, Sotir CM, Readdy TL, Hollingshead SK| title=Genetic correlates of throat and skin isolates of group A streptococci. | journal=J Infect Dis | year= 1996 | volume= 173 | issue= 4 | pages= 896-900 | pmid=8603968 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8603968 }} </ref> | *The D and E strains of emm protein act as a virulence factor for group A Streptococci.<ref name="pmid19331587">{{cite journal| author=Wasserzug O, Valinsky L, Klement E, Bar-Zeev Y, Davidovitch N, Orr N et al.| title=A cluster of ecthyma outbreaks caused by a single clone of invasive and highly infective Streptococcus pyogenes. | journal=Clin Infect Dis | year= 2009 | volume= 48 | issue= 9 | pages= 1213-9 | pmid=19331587 | doi=10.1086/597770 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19331587 }} </ref><ref name="pmid8603968">{{cite journal| author=Bessen DE, Sotir CM, Readdy TL, Hollingshead SK| title=Genetic correlates of throat and skin isolates of group A streptococci. | journal=J Infect Dis | year= 1996 | volume= 173 | issue= 4 | pages= 896-900 | pmid=8603968 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8603968 }} </ref> | ||
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===Bullous Impetigo=== | ===Bullous Impetigo=== | ||
The following are important aspects in the pathogenesis of bullous impetigo:<ref name="pmid27617460">{{cite journal| author=Cohen PR| title=Bullous impetigo and pregnancy: Case report and review of blistering conditions in pregnancy. | journal=Dermatol Online J | year= 2016 | volume= 22 | issue= 4 | pages= | pmid=27617460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27617460 }} </ref><ref name="pmid27458596">{{cite journal| author=Duggal SD, Bharara T, Jena PP, Kumar A, Sharma A, Gur R et al.| title=Staphylococcal bullous impetigo in a neonate. | journal=World J Clin Cases | year= 2016 | volume= 4 | issue= 7 | pages= 191-4 | pmid=27458596 | doi=10.12998/wjcc.v4.i7.191 | pmc=4945591 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27458596 }} </ref> | The following are important aspects in the pathogenesis of bullous impetigo:<ref name="pmid27617460">{{cite journal| author=Cohen PR| title=Bullous impetigo and pregnancy: Case report and review of blistering conditions in pregnancy. | journal=Dermatol Online J | year= 2016 | volume= 22 | issue= 4 | pages= | pmid=27617460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27617460 }} </ref><ref name="pmid27458596">{{cite journal| author=Duggal SD, Bharara T, Jena PP, Kumar A, Sharma A, Gur R et al.| title=Staphylococcal bullous impetigo in a neonate. | journal=World J Clin Cases | year= 2016 | volume= 4 | issue= 7 | pages= 191-4 | pmid=27458596 | doi=10.12998/wjcc.v4.i7.191 | pmc=4945591 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27458596 }} </ref><ref name="pmid21282415">{{cite journal| author=Kato F, Kadomoto N, Iwamoto Y, Bunai K, Komatsuzawa H, Sugai M| title=Regulatory mechanism for exfoliative toxin production in Staphylococcus aureus. | journal=Infect Immun | year= 2011 | volume= 79 | issue= 4 | pages= 1660-70 | pmid=21282415 | doi=10.1128/IAI.00872-10 | pmc=3067547 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21282415 }} </ref> | ||
*Bullous impetigo is caused by exfoliative toxins which are released by ''[[Staphylococcus aureus|Stapphylococcus aureus]]''. | *Bullous impetigo is caused by exfoliative toxins which are released by ''[[Staphylococcus aureus|Stapphylococcus aureus]]''. | ||
*The exfoliative toxins can hydrolyze desmoglein-1 and thus weaken the desmosomes. | *The exfoliative toxins can hydrolyze desmoglein-1 and thus weaken the desmosomes. |
Revision as of 16:00, 18 April 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]
Overview
Impetigo is spread by direct lesion contact. The incubation period is 1–3 days and 4-10 days for for Streptococci and Staphylococci respectively. Bullous impetigo is caused by exfoliative toxins which are released by Stapphylococcus aureus. The toxins are of two types, A and B, and lead to the production of bullae in the superficial layer of epidermis.[1]
Pathogenesis
Impetigo, the infection of epidermis, can either be primary or secondary to scratches, injuries, bites or conditions that lead to a break in the continuity of the skin. The breaks in the continuity are potential sites for the pathogens to enter and infect.[2][3][4][5]
Streptococcal Impetigo
- The D and E strains of emm protein act as a virulence factor for group A Streptococci.[2][6]
- Group A Streptococci have great invasive potential. They can be isolated from the skin 10 days before an infection and from the oropharynx, 2-3 weeks after the appearance on the skin.[7]
Staphylococcal Impetigo
Staphylococci cause toxin mediated impetigo in the following way:[8]
- Staphylococci produce toxins that act as super antigens.
- These super antigens can activate T-lymphocytes.
- The exfoliative toxins produced can hydrolyze desmoglein-1 and thus weaken the desmosomes.
- They can also produce IL-1 and IL-6 and tumor necrosis factor alpha (TNF-a).
- These lymphokines can act on the skin producing bullous impetigo.
Bullous Impetigo
The following are important aspects in the pathogenesis of bullous impetigo:[9][10][4]
- Bullous impetigo is caused by exfoliative toxins which are released by Stapphylococcus aureus.
- The exfoliative toxins can hydrolyze desmoglein-1 and thus weaken the desmosomes.
- The toxins are of two types, A and B, and lead to the production of bullae in the superficial layer of epidermis.
- These bullae are flaccid and can rupture easily.
Genetic
Impetigo associated with group A Streptococci is understood to have genetic basis and is associated with subfamilies of emm gene.'[6]
Associated Conditions
The conditions associated with impetigo include:[11]
- Diabetes
- Immunodeficiency
- Eczema
- Diseases associated with rash
- Cellulitis
- Dermatological disorders of all kinds
- Trauma
Gross Pathology
Face
Trunk/Axillae
Golden Crusting
Microscopic Pathology
References
- ↑ "ISDH: Impetigo".
- ↑ 2.0 2.1 Wasserzug O, Valinsky L, Klement E, Bar-Zeev Y, Davidovitch N, Orr N; et al. (2009). "A cluster of ecthyma outbreaks caused by a single clone of invasive and highly infective Streptococcus pyogenes". Clin Infect Dis. 48 (9): 1213–9. doi:10.1086/597770. PMID 19331587.
- ↑ Bangert S, Levy M, Hebert AA (2012). "Bacterial resistance and impetigo treatment trends: a review". Pediatr Dermatol. 29 (3): 243–8. doi:10.1111/j.1525-1470.2011.01700.x. PMID 22299710.
- ↑ 4.0 4.1 Kato F, Kadomoto N, Iwamoto Y, Bunai K, Komatsuzawa H, Sugai M (2011). "Regulatory mechanism for exfoliative toxin production in Staphylococcus aureus". Infect Immun. 79 (4): 1660–70. doi:10.1128/IAI.00872-10. PMC 3067547. PMID 21282415.
- ↑ Nishifuji K, Shimizu A, Ishiko A, Iwasaki T, Amagai M (2010). "Removal of amino-terminal extracellular domains of desmoglein 1 by staphylococcal exfoliative toxin is sufficient to initiate epidermal blister formation". J Dermatol Sci. 59 (3): 184–91. doi:10.1016/j.jdermsci.2010.07.010. PMID 20728315.
- ↑ 6.0 6.1 Bessen DE, Sotir CM, Readdy TL, Hollingshead SK (1996). "Genetic correlates of throat and skin isolates of group A streptococci". J Infect Dis. 173 (4): 896–900. PMID 8603968.
- ↑ Lin JN, Chang LL, Lai CH, Lin HH, Chen YH (2011). "Clinical and molecular characteristics of invasive and noninvasive skin and soft tissue infections caused by group A Streptococcus". J Clin Microbiol. 49 (10): 3632–7. doi:10.1128/JCM.00531-11. PMC 3187321. PMID 21865425.
- ↑ Manders SM (1998). "Toxin-mediated streptococcal and staphylococcal disease". J Am Acad Dermatol. 39 (3): 383–98, quiz 399-400. PMID 9738772.
- ↑ Cohen PR (2016). "Bullous impetigo and pregnancy: Case report and review of blistering conditions in pregnancy". Dermatol Online J. 22 (4). PMID 27617460.
- ↑ Duggal SD, Bharara T, Jena PP, Kumar A, Sharma A, Gur R; et al. (2016). "Staphylococcal bullous impetigo in a neonate". World J Clin Cases. 4 (7): 191–4. doi:10.12998/wjcc.v4.i7.191. PMC 4945591. PMID 27458596.
- ↑ Hartman-Adams H, Banvard C, Juckett G (2014). "Impetigo: diagnosis and treatment". Am Fam Physician. 90 (4): 229–35. PMID 25250996.