Impetigo pathophysiology: Difference between revisions

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==Overview==
==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.<ref name="urlISDH: Impetigo">{{cite web |url=http://www.in.gov/isdh/25463.htm |title=ISDH: Impetigo |format= |work= |accessdate=}}</ref>
Impetigo is spread by direct contact with the lesion. 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 ''[[Staphylococcus aureus]]''. The [[toxins]] are of two types, A and B, and lead to the production of bullae in the superficial layer of [[epidermis]].<ref name="urlISDH: Impetigo">{{cite web |url=http://www.in.gov/isdh/25463.htm |title=ISDH: Impetigo |format= |work= |accessdate=}}</ref>


==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>
Impetigo, the [[infection]] of [[epidermis]], can either be primary or secondary to [[Scratch|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>
*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>
===Streptococcal Impetigo===
*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.<ref name="pmid21865425">{{cite journal| author=Lin JN, Chang LL, Lai CH, Lin HH, Chen YH| title=Clinical and molecular characteristics of invasive and noninvasive skin and soft tissue infections caused by group A Streptococcus. | journal=J Clin Microbiol | year= 2011 | volume= 49 | issue= 10 | pages= 3632-7 | pmid=21865425 | doi=10.1128/JCM.00531-11 | pmc=3187321 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21865425  }} </ref>
*The D and E [[strains]] of emm protein act as a [[virulence factor]] for [[Group A beta-hemolytic streptococci|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>
*[[Group A streptococci|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.<ref name="pmid21865425">{{cite journal| author=Lin JN, Chang LL, Lai CH, Lin HH, Chen YH| title=Clinical and molecular characteristics of invasive and noninvasive skin and soft tissue infections caused by group A Streptococcus. | journal=J Clin Microbiol | year= 2011 | volume= 49 | issue= 10 | pages= 3632-7 | pmid=21865425 | doi=10.1128/JCM.00531-11 | pmc=3187321 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21865425  }} </ref>
===Staphylococcal Impetigo===
[[Staphylococci]] cause toxin mediated impetigo in the following way:<ref name="pmid9738772">{{cite journal| author=Manders SM| title=Toxin-mediated streptococcal and staphylococcal disease. | journal=J Am Acad Dermatol | year= 1998 | volume= 39 | issue= 3 | pages= 383-98; quiz 399-400 | pmid=9738772 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9738772  }} </ref>
*[[Staphylococci]] produce [[toxins]] that act as [[Superantigen|superantigens]].
*These [[Superantigen|superantigens]] 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-alpha|TNF-a]]).
*These lymphokines can act on the skin producing bullous impetigo.
 
===Bullous Impetigo===
===Bullous Impetigo===
The following are important aspects in the pathophysiology 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 toxins are of two types, A and B, and lead to the production of bullae in the superficial layer of epidermis.  
*The exfoliative [[toxins]] can [[hydrolyze]] [[desmoglein 1]] and thus weaken the [[desmosomes]].
*These bullae are flaccid and can rupture easily.
*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.
 
===Non-bullous Impetigo===
The [[pathogenesis]] of non-bulbous impetigo involves:<ref name="pmid24770507">{{cite journal| author=Pereira LB| title=Impetigo - review. | journal=An Bras Dermatol | year= 2014 | volume= 89 | issue= 2 | pages= 293-9 | pmid=24770507 | doi= | pmc=4008061 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24770507  }} </ref>
*[[Staphylococcus aureus|''Staphylococcus aureus'']] is involved in almost 80% cases.
*[[Group A streptococci]] also contribute in the [[pathogenesis]] either alone or in combination with [[Staphylococcus aureus|''Staphylococcus aureus'']].
*[[Toxins]] are produced by the bacteria which act as [[Superantigen|superantigens]].
*Activation of [[T-lymphocytes]] and the production of [[IL-1]], [[IL-6]] and [[TNF-alpha|TNF-a]] is mediated by the toxins.
*These lead to exfoliative [[skin changes]] and thus impetigo.
 
===Ecthyma===
The [[pathogenesis]] of ecthyma involves:<ref name="pmid3276190">{{cite journal| author=Hewitt WD, Farrar WE| title=Bacteremia and ecthyma caused by Streptococcus pyogenes in a patient with acquired immunodeficiency syndrome. | journal=Am J Med Sci | year= 1988 | volume= 295 | issue= 1 | pages= 52-4 | pmid=3276190 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3276190  }} </ref>
*Infection is usually caused by [[Streptococcus pyogenes|''Streptococcus pyogenes'']].
*[[Immunodeficiency|Immunodeficient]] individuals have a higher risk of ecthyma.
*The [[deficiency]] of [[antibody]] that [[Opsonized|opsonizes]] the [[S. pyogenes|''S. pyogenes'']] [[M protein]] is main step in [[pathogenesis]].
*The [[lesions]] are painful and filled with [[pus]].
*The [[lesions]] extend into the epidermis and thus an ulcer is formed after the rupture of the [[lesion]].
*The surface of the [[ulcer]] is covered with a brown [[scab]].


==Genetic==
==Genetic==
Impetigo associated with group A Streptococci is understood to have genetic basis and is associated with subfamilies of ''emm gene.'''<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>
Impetigo associated with [[group A streptococci]] is understood to have a [[genetic]] basis and is associated with subfamilies of ''emm gene.''<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>


==Associated Conditions==
==Associated Conditions==
The conditions associated with impetigo include:<ref name="pmid25250996">{{cite journal| author=Hartman-Adams H, Banvard C, Juckett G| title=Impetigo: diagnosis and treatment. | journal=Am Fam Physician | year= 2014 | volume= 90 | issue= 4 | pages= 229-35 | pmid=25250996 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25250996  }} </ref>
The conditions associated with impetigo include:<ref name="pmid25250996">{{cite journal| author=Hartman-Adams H, Banvard C, Juckett G| title=Impetigo: diagnosis and treatment. | journal=Am Fam Physician | year= 2014 | volume= 90 | issue= 4 | pages= 229-35 | pmid=25250996 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25250996 }} </ref><ref name="pmid24770507">{{cite journal| author=Pereira LB| title=Impetigo - review. | journal=An Bras Dermatol | year= 2014 | volume= 89 | issue= 2 | pages= 293-9 | pmid=24770507 | doi= | pmc=4008061 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24770507 }} </ref>
*Diabetes
*[[Diabetes]]
*Immunodeficiency
*[[Immunodeficiency]]
*Eczema
*[[Eczema]]
*Diseases associated with rash
*Diseases associated with [[rash]]
*Cellulitis
*[[Cellulitis]]
*Dermatological disorders of all kinds
*[[Dermatological lesions|Dermatological disorders]] of all kinds
*Trauma
*[[Trauma]]
*[[Atopic dermatitis]]
*[[Contact dermatitis]]
*[[Pediculosis]]


==Gross Pathology==
==Gross Pathology==
===Face===
===Face===


[[File:Impetigo face 1.jpg|Impetigo crusting lesions on face|left|500px]]
[[File:Impetigo face 1.jpg|thumb|Impetigo crusting lesions on face. Adapted from atlasdermatologico.com<ref name="urlDermatology
Atlas">{{cite web |url=http://www.atlasdermatologico.com.br/ |title=Dermatology Atlas |format= |work= |accessdate=}}</ref>|left|500px]]
<br style="clear:left" />
<br style="clear:left" />


===Trunk/Axillae===
===Trunk/Axillae===
[[File:Impetigo Axillae 1.jpg|Impetigo lesions around axillae|left|500px]]
[[File:Impetigo Axillae 1.jpg|thumb|Impetigo lesions around axillae. Adapted from atlasdermatologico.com<ref name="urlDermatology
Atlas">{{cite web |url=http://www.atlasdermatologico.com.br/ |title=Dermatology Atlas |format= |work= |accessdate=}}</ref>|left|500px]]
<br style="clear:left" />
<br style="clear:left" />


===Golden Crusting===
===Golden Crusting===
[[File:Impetigo crusting 1.jpg|Impetigo lesions with crusting|left|500px]]
[[File:Impetigo crusting 1.jpg|thumb|Impetigo lesions with crusting. Adapted from atlasdermatologico.com<ref name="urlDermatology
Atlas">{{cite web |url=http://www.atlasdermatologico.com.br/ |title=Dermatology Atlas |format= |work= |accessdate=}}</ref>|left|500px]]


<br style="clear:left" />
<br style="clear:left" />


==Microscopic Pathology==
==Microscopic Pathology==
Microscopic pathology findings are not significant for the diagnosis or treatment of impetigo.


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}


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Latest revision as of 22:21, 29 July 2020

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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 contact with the lesion. 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 Staphylococcus 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

Staphylococcal Impetigo

Staphylococci cause toxin mediated impetigo in the following way:[8]

Bullous Impetigo

The following are important aspects in the pathogenesis of bullous impetigo:[9][10][4]

Non-bullous Impetigo

The pathogenesis of non-bulbous impetigo involves:[11]

Ecthyma

The pathogenesis of ecthyma involves:[12]

Genetic

Impetigo associated with group A streptococci is understood to have a genetic basis and is associated with subfamilies of emm gene.[6]

Associated Conditions

The conditions associated with impetigo include:[13][11]

Gross Pathology

Face

Impetigo crusting lesions on face. Adapted from atlasdermatologico.com[14]


Trunk/Axillae

Impetigo lesions around axillae. Adapted from atlasdermatologico.com[14]


Golden Crusting

Impetigo lesions with crusting. Adapted from atlasdermatologico.com[14]


Microscopic Pathology

Microscopic pathology findings are not significant for the diagnosis or treatment of impetigo.

References

  1. ↑ "ISDH: Impetigo".
  2. ↑ 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.
  3. ↑ 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. ↑ 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.
  5. ↑ 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. ↑ 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.
  7. ↑ 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.
  8. ↑ Manders SM (1998). "Toxin-mediated streptococcal and staphylococcal disease". J Am Acad Dermatol. 39 (3): 383–98, quiz 399-400. PMID 9738772.
  9. ↑ Cohen PR (2016). "Bullous impetigo and pregnancy: Case report and review of blistering conditions in pregnancy". Dermatol Online J. 22 (4). PMID 27617460.
  10. ↑ 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.
  11. ↑ 11.0 11.1 Pereira LB (2014). "Impetigo - review". An Bras Dermatol. 89 (2): 293–9. PMC 4008061. PMID 24770507.
  12. ↑ Hewitt WD, Farrar WE (1988). "Bacteremia and ecthyma caused by Streptococcus pyogenes in a patient with acquired immunodeficiency syndrome". Am J Med Sci. 295 (1): 52–4. PMID 3276190.
  13. ↑ Hartman-Adams H, Banvard C, Juckett G (2014). "Impetigo: diagnosis and treatment". Am Fam Physician. 90 (4): 229–35. PMID 25250996.
  14. ↑ 14.0 14.1 14.2 "Dermatology Atlas".


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