Impetigo pathophysiology
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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
- 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 superantigens.
- These 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-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.
Non-bullous Impetigo
The pathogenesis of non-bulbous impetigo involves:[11]
- Staphylococcus aureus is involved in almost 80% cases.
- Group A streptococci also contribute in the pathogenesis either alone or in combination with Staphylococcus aureus.
- Toxins are produced by the bacteria which act as superantigens.
- Activation of T-lymphocytes and the production of IL-1, IL-6 and TNF-a is mediated by the toxins.
- These lead to exfoliative skin changes and thus impetigo.
Ecthyma
The pathogenesis of ecthyma involves:[12]
- Infection is usually caused by Streptococcus pyogenes.
- Immunodeficient individuals have a higher risk of ecthyma.
- The deficiency of antibody that opsonizes the 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
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]
- Diabetes
- Immunodeficiency
- Eczema
- Diseases associated with rash
- Cellulitis
- Dermatological disorders of all kinds
- Trauma
- Atopic dermatitis
- Contact dermatitis
- Pediculosis
Gross Pathology
Face
Trunk/Axillae
Golden Crusting
Microscopic Pathology
Microscopic pathology findings are not significant for the diagnosis or treatment of impetigo.
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.
- ↑ 11.0 11.1 Pereira LB (2014). "Impetigo - review". An Bras Dermatol. 89 (2): 293–9. PMC 4008061. PMID 24770507.
- ↑ 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.
- ↑ Hartman-Adams H, Banvard C, Juckett G (2014). "Impetigo: diagnosis and treatment". Am Fam Physician. 90 (4): 229–35. PMID 25250996.
- ↑ 14.0 14.1 14.2 "Dermatology Atlas".