Impetigo natural history, complications and prognosis
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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
If left untreated, most cases of non-bullous impetigo resolve within 1-2 weeks. The complications of impetigo include poststreptococcal glomerulonephritis and rheumatic fever.[1][2][3][4][5]
Natural History
If left untreated, most cases of non-bullous impetigo resolve within 1-2 weeks. All forms of impetigo start as a lesion which then ruptures leading to variable pattern of crusting.[5][6][7][8]
Non-bullous Impetigo
- Non-bullous impetigo begins as a vesicle with erythematous base.
- The lesions are 1-2cm each and distant lesions can be seen because of its contagious nature.
- The vesicle ruptures easily forming a yellow exudate on the surface.
- This exudate dries to form a golden brown crust.
- Lymphadenopathy and fever may be observed.
- This is followed by complete recovery of the lesion.
- If left untreated, most cases of non-bullous impetigo resolve within 1-2 weeks.
Bullous Impetigo
- Bullus impetigo begins as smaller vesicles which form flaccid blisters.
- If left untreated the bullae are filled with clear fluid which turns yellow and less clearer later.
- Rupture of the bullae leaves a ring of golden crust.
- The bullous impetigo lesions are painful and associated with itching.
- The lesions of bullous impetigo are commonly seen on the trunk and the extremities.
- Bullous impetigo when left untreated for long, may lead to cellulitis, poststreptococcal glomerulonephritis or rheumatic fever.
Ecthyma
- Ecthyma starts as pus filled, painful lesions on the extremities.
- The lesions rupture to form a hard crust along with an ulcer that can involve deeper layers.
- The lesions of ecthyma may form a scar after their resolution.
Complications
The complications of impetigo include:[1][2][3][4][5][6]
- Recurrent impetigo
- Poststreptococcal glomerulonephritis
- Rheumatic fever
- Cellulitis
Prognosis
The prognosis of non-bullous impetigo is very good.
References
- ↑ 1.0 1.1 McDonald MI, Towers RJ, Andrews RM, Benger N, Currie BJ, Carapetis JR (2006). "Low rates of streptococcal pharyngitis and high rates of pyoderma in Australian aboriginal communities where acute rheumatic fever is hyperendemic". Clin Infect Dis. 43 (6): 683–9. doi:10.1086/506938. PMID 16912939.
- ↑ 2.0 2.1 Weinstein L, Le Frock J (1971). "Does antimicrobial therapy of streptococcal pharyngitis or pyoderma alter the risk of glomerulonephritis?". J Infect Dis. 124 (2): 229–31. PMID 4942062.
- ↑ 3.0 3.1 Cohen PR (2016). "Bullous impetigo and pregnancy: Case report and review of blistering conditions in pregnancy". Dermatol Online J. 22 (4). PMID 27617460.
- ↑ 4.0 4.1 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.
- ↑ 5.0 5.1 5.2 Eison TM, Ault BH, Jones DP, Chesney RW, Wyatt RJ (2011). "Post-streptococcal acute glomerulonephritis in children: clinical features and pathogenesis". Pediatr Nephrol. 26 (2): 165–80. doi:10.1007/s00467-010-1554-6. PMID 20652330.
- ↑ 6.0 6.1 Hartman-Adams H, Banvard C, Juckett G (2014). "Impetigo: diagnosis and treatment". Am Fam Physician. 90 (4): 229–35. PMID 25250996.
- ↑ 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.
- ↑ Chiller K, Selkin BA, Murakawa GJ (2001). "Skin microflora and bacterial infections of the skin". J Investig Dermatol Symp Proc. 6 (3): 170–4. doi:10.1046/j.0022-202x.2001.00043.x. PMID 11924823.