Cutaneous abscess: Difference between revisions
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==Overview== | |||
Cutaneous abscess is defined as a collection of pus in skin layers and may occur in any body surface. Although, there is a rare type of sterile skin abscess that is secondary to injection mostly in diabetic patients who use insulin. diagnosis is clinical and consist of a painful, tender, indurated, and usually erythematous nodule or mass that is varying in size. Systemic sign and symptoms are rare except in sever and multiple abscess especially in immunocompromised patients. Treatment is based on incision and drainage associated with antibiotics. | |||
==Historical perspective== | |||
Alexander Ogston, a scottish surgeon first described the pyogenic abscess in the late 19th century.<ref name="pmid6369479">{{cite journal |vauthors= |title=Classics in infectious diseases. "On abscesses". Alexander Ogston (1844-1929) |journal=Rev. Infect. Dis. |volume=6 |issue=1 |pages=122–8 |year=1984 |pmid=6369479 |doi= |url=}}</ref> | |||
==Classification== | |||
Cutaneous abscess may be classified as sterile abscess and infectious abscess. | |||
*Sterile abscesses are mainly seen in diabetic patients secondary to insulin injection. | |||
*Infectious abscesses are mostly secondary to staphylococcus aureus infection. | |||
==Pathophysiology== | |||
[[abscess]] is usually caused by [[staphylococcus aureus]] [[bacterial]] [[infection]] to an injured [[breast]] [[skin]]. [[Staphylococcus aureus]] could form [[abscess]] by secretion of several killing agents like [[enzymes]] and [[toxins]]. In a reaction to these [[bacterial]] substances, assembled [[white blood cells]] in this tissue produces anti-bacterial [[Antibodies|anti-bodies]] that help in killing the [[bacteria]]. However, these cells cause damage to the [[soft tissue]] contributing in the [[abscess]] formation.<ref name="pmid25749135">{{cite journal| author=Kobayashi SD, Malachowa N, DeLeo FR| title=Pathogenesis of Staphylococcus aureus abscesses. | journal=Am J Pathol | year= 2015 | volume= 185 | issue= 6 | pages= 1518-27 | pmid=25749135 | doi=10.1016/j.ajpath.2014.11.030 | pmc=4450319 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25749135 }} </ref> | |||
===Pathogenesis=== | |||
Skin serves as a barrier from pathogen entry. Breech in the skin surface allow the pathogen entry to cause local inflammation. PMNs are the first and the most important responding cells in abscess formation.<ref name="pmid23435331">{{cite journal |vauthors=Kolaczkowska E, Kubes P |title=Neutrophil recruitment and function in health and inflammation |journal=Nat. Rev. Immunol. |volume=13 |issue=3 |pages=159–75 |year=2013 |pmid=23435331 |doi=10.1038/nri3399 |url=}}</ref> Neutrophils, are responsible for phagocytosis. Once the pathogen is opsonized by complement system, it will be recognized by neutrophils and the phagocytosis process will begin. After phagocytosis the bactricidal process will begin by producing superoxide radicals and other reactive oxygen species (ROS).<ref name="pmid15240752">{{cite journal |vauthors=Quinn MT, Gauss KA |title=Structure and regulation of the neutrophil respiratory burst oxidase: comparison with nonphagocyte oxidases |journal=J. Leukoc. Biol. |volume=76 |issue=4 |pages=760–81 |year=2004 |pmid=15240752 |doi=10.1189/jlb.0404216 |url=}}</ref> | |||
===Genetic factors=== | |||
PMNs are the most important cellular defense. Genetic disorders that negatively affect PMN function may predispose persons to recurrent cutaneous abscess formation. For example, chronic granulomatous disease, which is a genetic disorder characterized by the inability of PMNs and other phagocytes to produce superoxide, often presents with severe and recurrent S. aureus infections.<ref name="pmid6872404">{{cite journal |vauthors=Bieluch VM, Tally FP |title=Pathophysiology of abscess formation |journal=Clin Obstet Gynaecol |volume=10 |issue=1 |pages=93–103 |year=1983 |pmid=6872404 |doi= |url=}}</ref> | |||
==Causes== | |||
[[Category:Infectious disease]] | [[Category:Infectious disease]] | ||
[[Category:Dermatology]] | [[Category:Dermatology]] | ||
[[Category:General surgery]] | [[Category:General surgery]] | ||
Revision as of 16:01, 27 March 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
Cutaneous abscess is defined as a collection of pus in skin layers and may occur in any body surface. Although, there is a rare type of sterile skin abscess that is secondary to injection mostly in diabetic patients who use insulin. diagnosis is clinical and consist of a painful, tender, indurated, and usually erythematous nodule or mass that is varying in size. Systemic sign and symptoms are rare except in sever and multiple abscess especially in immunocompromised patients. Treatment is based on incision and drainage associated with antibiotics.
Historical perspective
Alexander Ogston, a scottish surgeon first described the pyogenic abscess in the late 19th century.[1]
Classification
Cutaneous abscess may be classified as sterile abscess and infectious abscess.
- Sterile abscesses are mainly seen in diabetic patients secondary to insulin injection.
- Infectious abscesses are mostly secondary to staphylococcus aureus infection.
Pathophysiology
abscess is usually caused by staphylococcus aureus bacterial infection to an injured breast skin. Staphylococcus aureus could form abscess by secretion of several killing agents like enzymes and toxins. In a reaction to these bacterial substances, assembled white blood cells in this tissue produces anti-bacterial anti-bodies that help in killing the bacteria. However, these cells cause damage to the soft tissue contributing in the abscess formation.[2]
Pathogenesis
Skin serves as a barrier from pathogen entry. Breech in the skin surface allow the pathogen entry to cause local inflammation. PMNs are the first and the most important responding cells in abscess formation.[3] Neutrophils, are responsible for phagocytosis. Once the pathogen is opsonized by complement system, it will be recognized by neutrophils and the phagocytosis process will begin. After phagocytosis the bactricidal process will begin by producing superoxide radicals and other reactive oxygen species (ROS).[4]
Genetic factors
PMNs are the most important cellular defense. Genetic disorders that negatively affect PMN function may predispose persons to recurrent cutaneous abscess formation. For example, chronic granulomatous disease, which is a genetic disorder characterized by the inability of PMNs and other phagocytes to produce superoxide, often presents with severe and recurrent S. aureus infections.[5]
Causes
- ↑ "Classics in infectious diseases. "On abscesses". Alexander Ogston (1844-1929)". Rev. Infect. Dis. 6 (1): 122–8. 1984. PMID 6369479.
- ↑ Kobayashi SD, Malachowa N, DeLeo FR (2015). "Pathogenesis of Staphylococcus aureus abscesses". Am J Pathol. 185 (6): 1518–27. doi:10.1016/j.ajpath.2014.11.030. PMC 4450319. PMID 25749135.
- ↑ Kolaczkowska E, Kubes P (2013). "Neutrophil recruitment and function in health and inflammation". Nat. Rev. Immunol. 13 (3): 159–75. doi:10.1038/nri3399. PMID 23435331.
- ↑ Quinn MT, Gauss KA (2004). "Structure and regulation of the neutrophil respiratory burst oxidase: comparison with nonphagocyte oxidases". J. Leukoc. Biol. 76 (4): 760–81. doi:10.1189/jlb.0404216. PMID 15240752.
- ↑ Bieluch VM, Tally FP (1983). "Pathophysiology of abscess formation". Clin Obstet Gynaecol. 10 (1): 93–103. PMID 6872404.