Cutaneous abscess: Difference between revisions

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{{CMG}};{{AE}}{{MehdiP}}
{{CMG}};{{AE}}{{MehdiP}}
==Overview==
==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.
Cutaneous abscess is defined as a collection of [[pus]] in the [[dermis]] or [[subcutaneous tissue]] and appears as a [[Swelling|swollen]], [[Erythema|red]], [[Tenderness (medicine)|tender]], and fluctuant [[mass]], often with surrounding [[cellulitis]] 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 [[Antibiotic|antibiotics]].
==Historical perspective==
==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>
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==
==Classification==
Cutaneous abscess may be classified as sterile abscess and infectious abscess.
Cutaneous abscess may be classified as sterile abscess and infectious abscess.
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*Infectious abscesses are mostly secondary to staphylococcus aureus infection.
*Infectious abscesses are mostly secondary to staphylococcus aureus infection.
==Pathophysiology==
==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>  
[[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===  
===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>
Skin serves as a barrier from [[pathogen]] entry. Breech in the skin surface allow the pathogen entry to cause local [[inflammation]]. Polymorpho nuclear cells ([[PMNs|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> [[Neutrophil|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===
===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>
[[Neutrophil|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 [[Neutrophil|PMNs]] and other [[Phagocyte|phagocytes]] to produce [[superoxide]], often presents with severe and recurrent [[Staphylococcus aureus|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==
==Causes==
===Common causes===
===Common causes===
*S. aureus (either methicillin-susceptible or methicillin-resistant S. aureus) is counting for 75% of cases.<ref name="pmid24947530">{{cite journal |vauthors=Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC |title=Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America |journal=Clin. Infect. Dis. |volume=59 |issue=2 |pages=147–59 |year=2014 |pmid=24947530 |doi=10.1093/cid/ciu296 |url=}}</ref>
*[[Staphylococcus aureus|S. aureus]] (either [[S. aureus|methicillin-susceptible]] or [[Methicillin-resistant staphylococcus aureus|methicillin-resistant S. aureus]]) is counting for 75% of cases.<ref name="pmid24947530">{{cite journal |vauthors=Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC |title=Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America |journal=Clin. Infect. Dis. |volume=59 |issue=2 |pages=147–59 |year=2014 |pmid=24947530 |doi=10.1093/cid/ciu296 |url=}}</ref>
*Mixed flora (including S. aureus together with S. pyogenes and gram-negative bacilli with anaerobes)<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref><ref name="pmid16914702">{{cite journal |vauthors=Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, Talan DA |title=Methicillin-resistant S. aureus infections among patients in the emergency department |journal=N. Engl. J. Med. |volume=355 |issue=7 |pages=666–74 |year=2006 |pmid=16914702 |doi=10.1056/NEJMoa055356 |url=}}</ref>
*Mixed flora (including [[Staphylococcus aureus|S. aureus]] together with [[Streptococcus pyogenes|S. pyogenes]] and [[gram-negative bacilli]] with [[anaerobes]])<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref><ref name="pmid16914702">{{cite journal |vauthors=Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, Talan DA |title=Methicillin-resistant S. aureus infections among patients in the emergency department |journal=N. Engl. J. Med. |volume=355 |issue=7 |pages=666–74 |year=2006 |pmid=16914702 |doi=10.1056/NEJMoa055356 |url=}}</ref>
*Anaerobes, mostly seen in injecting drug users.<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref>
*[[Anaerobes]], mostly seen in [[injecting drug users]].<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref>
===Less common causes===
===Less common causes===
Nontuberculous mycobacteria, blastomycosis, nocardiosis, and cryptococcosis.<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref>
[[Nontuberculous mycobacteria]], [[blastomycosis]], [[nocardiosis]], and [[cryptococcosis]].<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref>
==Differentiating cutaneous abscess from other Diseases==
==Differentiating cutaneous abscess from other Diseases==
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
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|align="left" style="background:#DCDCDC;"|[[Folliculitis]]
|align="left" style="background:#DCDCDC;"|[[Folliculitis]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hair follicle inflammation, presents as pruritic rash or pustule.<ref name="pmid15554731">{{cite journal |vauthors=Luelmo-Aguilar J, Santandreu MS |title=Folliculitis: recognition and management |journal=Am J Clin Dermatol |volume=5 |issue=5 |pages=301–10 |year=2004 |pmid=15554731 |doi= |url=}}</ref><ref name="pmid25441463">{{cite journal |vauthors=Laureano AC, Schwartz RA, Cohen PJ |title=Facial bacterial infections: folliculitis |journal=Clin. Dermatol. |volume=32 |issue=6 |pages=711–4 |year=2014 |pmid=25441463 |doi=10.1016/j.clindermatol.2014.02.009 |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hair follicle [[inflammation]], presents as pruritic [[rash]] or [[Pustules|pustule]].<ref name="pmid15554731">{{cite journal |vauthors=Luelmo-Aguilar J, Santandreu MS |title=Folliculitis: recognition and management |journal=Am J Clin Dermatol |volume=5 |issue=5 |pages=301–10 |year=2004 |pmid=15554731 |doi= |url=}}</ref><ref name="pmid25441463">{{cite journal |vauthors=Laureano AC, Schwartz RA, Cohen PJ |title=Facial bacterial infections: folliculitis |journal=Clin. Dermatol. |volume=32 |issue=6 |pages=711–4 |year=2014 |pmid=25441463 |doi=10.1016/j.clindermatol.2014.02.009 |url=}}</ref>
|-
|-
|align="left" style="background:#DCDCDC;"|[[Hidradenitis suppurativa|Suppurative hydradenitis]]  
|align="left" style="background:#DCDCDC;"|[[Hidradenitis suppurativa|Suppurative hydradenitis]]  
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Inflammation in intertriginous areas (axillae, inguinal area, inner thighs, perianal and perineal areas, mammary,..)
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Inflammation]] in intertriginous areas ([[axillae]], [[Inguinal region|inguinal area]], inner [[thighs]], [[Perianal abscess|perianal]] and [[perineal]] areas, [[mammary]],..)
Presents as painful inflamed nodule, sinus tract and commedons. Associated with systemic symptoms. Needs surgical debridement and  systemic antibiotic.<ref name="pmid19682181">{{cite journal |vauthors=Revuz J |title=Hidradenitis suppurativa |journal=J Eur Acad Dermatol Venereol |volume=23 |issue=9 |pages=985–98 |year=2009 |pmid=19682181 |doi=10.1111/j.1468-3083.2009.03356.x |url=}}</ref>
Presents as painful inflamed [[nodule]], sinus tract and commedons. Associated with systemic symptoms. Needs surgical debridement and  systemic antibiotic.<ref name="pmid19682181">{{cite journal |vauthors=Revuz J |title=Hidradenitis suppurativa |journal=J Eur Acad Dermatol Venereol |volume=23 |issue=9 |pages=985–98 |year=2009 |pmid=19682181 |doi=10.1111/j.1468-3083.2009.03356.x |url=}}</ref>
|-
|-
|align="left" style="background:#DCDCDC;"|[[Epidermoid cyst]]
|align="left" style="background:#DCDCDC;"|[[Epidermoid cyst]]
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|align="left" style="background:#DCDCDC;"|Nodular [[lymphangitis]]
|align="left" style="background:#DCDCDC;"|Nodular [[lymphangitis]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Subcutaneous swelling along with lymphatics. mostly due to Sporothrix schenckii.<ref name="pmid8480962">{{cite journal |vauthors=Kostman JR, DiNubile MJ |title=Nodular lymphangitis: a distinctive but often unrecognized syndrome |journal=Ann. Intern. Med. |volume=118 |issue=11 |pages=883–8 |year=1993 |pmid=8480962 |doi= |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Subcutaneous]] swelling along with [[lymphatics]]. mostly due to [[Sporothrix schenckii]].<ref name="pmid8480962">{{cite journal |vauthors=Kostman JR, DiNubile MJ |title=Nodular lymphangitis: a distinctive but often unrecognized syndrome |journal=Ann. Intern. Med. |volume=118 |issue=11 |pages=883–8 |year=1993 |pmid=8480962 |doi= |url=}}</ref>
|-
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|align="left" style="background:#DCDCDC;"|[[Myiasis]]
|align="left" style="background:#DCDCDC;"|[[Myiasis]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Enlarging nodule secondary to insect bite and due to penetration of fly larvae into subdermal tissue. caused by Dermatobia hominis, the botfly and Cordylobia anthropophaga, the tumbu fly.<ref name="pmid8432924">{{cite journal |vauthors=Arosemena R, Booth SA, Su WP |title=Cutaneous myiasis |journal=J. Am. Acad. Dermatol. |volume=28 |issue=2 Pt 1 |pages=254–6 |year=1993 |pmid=8432924 |doi= |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Enlarging nodule secondary to [[insect bite]] and due to penetration of fly larvae into subdermal tissue. caused by [[Dermatobia hominis]], the [[botfly]] and [[Cordylobia anthropophaga]], the tumbu fly.<ref name="pmid8432924">{{cite journal |vauthors=Arosemena R, Booth SA, Su WP |title=Cutaneous myiasis |journal=J. Am. Acad. Dermatol. |volume=28 |issue=2 Pt 1 |pages=254–6 |year=1993 |pmid=8432924 |doi= |url=}}</ref>
|}
|}
==Epidemiology and Demographics==
==Epidemiology and Demographics==
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==Risk Factors==
==Risk Factors==
Risk factors for developing cutaneous abscess include:<ref name="pmid17420430">{{cite journal |vauthors=McNamara DR, Tleyjeh IM, Berbari EF, Lahr BD, Martinez J, Mirzoyev SA, Baddour LM |title=A predictive model of recurrent lower extremity cellulitis in a population-based cohort |journal=Arch. Intern. Med. |volume=167 |issue=7 |pages=709–15 |year=2007 |pmid=17420430 |doi=10.1001/archinte.167.7.709 |url=}}</ref><ref name="pmid16267325">{{cite journal |vauthors=Gordon RJ, Lowy FD |title=Bacterial infections in drug users |journal=N. Engl. J. Med. |volume=353 |issue=18 |pages=1945–54 |year=2005 |pmid=16267325 |doi=10.1056/NEJMra042823 |url=}}</ref>
Risk factors for developing cutaneous abscess include:<ref name="pmid17420430">{{cite journal |vauthors=McNamara DR, Tleyjeh IM, Berbari EF, Lahr BD, Martinez J, Mirzoyev SA, Baddour LM |title=A predictive model of recurrent lower extremity cellulitis in a population-based cohort |journal=Arch. Intern. Med. |volume=167 |issue=7 |pages=709–15 |year=2007 |pmid=17420430 |doi=10.1001/archinte.167.7.709 |url=}}</ref><ref name="pmid16267325">{{cite journal |vauthors=Gordon RJ, Lowy FD |title=Bacterial infections in drug users |journal=N. Engl. J. Med. |volume=353 |issue=18 |pages=1945–54 |year=2005 |pmid=16267325 |doi=10.1056/NEJMra042823 |url=}}</ref>
*Skin barrier disruption due to trauma (such as abrasion, penetrating wound, pressure ulcer, venous leg ulcer, insect bite, injection drug use)
*Skin barrier disruption due to [[trauma]] (such as [[abrasion]], [[penetrating wound]], [[Pressure ulcers|pressure ulcer]], [[Venous ulcer|venous leg ulcer]], [[insect bite]], [[Intravenous drug use (recreational)|injection drug use]])
*Skin inflammation (such as eczema, radiation therapy)
*Skin inflammation (such as [[eczema]], [[radiation therapy]])
*Edema due to impaired lymphatic drainage
*[[Edema]] due to impaired [[lymphatic drainage]]
*Edema due to venous insufficiency
*[[Edema]] due to [[venous insufficiency]]
*Obesity
*[[Obesity]]
*Immunosuppression (such as diabetes or HIV infection)
*[[Immunosuppression]] (such as [[diabetes]] or [[HIV AIDS|HIV infection]])
*Breaks in the skin between the toes ("toe web intertrigo"); these may be clinically inapparent
*Breaks in the skin between the toes (toe web intertrigo); these may be clinically inapparent
*Preexisting skin infection (such as tinea pedis, impetigo, varicella)
*Preexisting skin infection (such as [[tinea pedis]], [[impetigo]], [[varicella]])
*Hemodialysis
*[[Hemodialysis]]
==Natural History, Complications and Prognosis==
==Natural History, Complications and Prognosis==
===Natural History===
===Natural History===
If cutaneous abscess left untreated it may drain spontaneously or in severe cases may cause systemic spread and result in sepsis.<ref name="pmid6444142">{{cite journal |vauthors=Llera JL, Levy RC, Staneck JL |title=Cutaneous abscesses: natural history and management in an outpatient facility |journal=J Emerg Med |volume=1 |issue=6 |pages=489–93 |year=1984 |pmid=6444142 |doi= |url=}}</ref>
If cutaneous abscess left untreated it may drain spontaneously or in severe cases may cause systemic spread and result in sepsis.<ref name="pmid6444142">{{cite journal |vauthors=Llera JL, Levy RC, Staneck JL |title=Cutaneous abscesses: natural history and management in an outpatient facility |journal=J Emerg Med |volume=1 |issue=6 |pages=489–93 |year=1984 |pmid=6444142 |doi= |url=}}</ref>
===Complications===
===Complications===
A wide range of complications are possible in the course of skin abscess including: bacteremia, endocarditis, osteomyelitis, metastatic infection, sepsis, and toxic shock syndrome.<ref name="pmid27434444">{{cite journal |vauthors=Raff AB, Kroshinsky D |title=Cellulitis: A Review |journal=JAMA |volume=316 |issue=3 |pages=325–37 |year=2016 |pmid=27434444 |doi=10.1001/jama.2016.8825 |url=}}</ref>
A wide range of complications are possible in the course of skin abscess including: [[Bacteremia]], [[endocarditis]], [[osteomyelitis]], metastatic infection, [[sepsis]], and [[toxic shock syndrome]].<ref name="pmid27434444">{{cite journal |vauthors=Raff AB, Kroshinsky D |title=Cellulitis: A Review |journal=JAMA |volume=316 |issue=3 |pages=325–37 |year=2016 |pmid=27434444 |doi=10.1001/jama.2016.8825 |url=}}</ref>
===Prognosis===
===Prognosis===
Depending on the extent of the disease, the prognosis may vary. However, the prognosis is generally regarded as good.
Depending on the extent of the disease, the prognosis may vary. However, the prognosis is generally regarded as good.
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====History====
====History====
A detailed history must be taken from all patients. Specific area of focus when obtaining a history from the patient include:
A detailed history must be taken from all patients. Specific area of focus when obtaining a history from the patient include:
*Recent trauma
*Recent [[trauma]]
*Recent weight change
*Recent [[weight change]]
*Recent immunosuppresive drugs
*Recent immunosuppresive drugs
*Underlying comorbidities (lymphedema, malignancy, neutropenia, immunodeficiency, splenectomy, diabetes)
*Underlying comorbidities ([[lymphedema]], [[malignancy]], [[neutropenia]], [[immunodeficiency]], [[splenectomy]], [[diabetes]])
====Symptoms====
====Symptoms====
The hallmark of the cutaneous abscess is painful, tender, indurated, and usually erythematous nodule.
The hallmark of the cutaneous abscess is painful, tender, indurated, and usually [[erythematous]] [[nodule]].
==Physical examination==
==Physical examination==
===Appearance of the Patient===
===Appearance of the Patient===
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Vital signs are within normal limits unless there is complication.
Vital signs are within normal limits unless there is complication.
===Skin===
===Skin===
Indurated, tender and erythematous nodule with signs of local inflammation is the presenting feature.
Indurated, tender and [[erythematous]] [[nodule]] with signs of local inflammation is the presenting feature.
==Laboratory findings==
==Laboratory findings==
Leukocytosis and increased level of acute phase reactants are the most common laboratory findings.
[[Leukocytosis]] and increased level of [[Acute phase reactant|acute phase reactants]] ([[ESR]], [[CRP]]) are the most common laboratory findings.
==Treatment==
==Treatment==
Treatment is based on incision and drainage and sometimes antibiotic therapy is required. Cure rates with drainage alone are about 85% or higher.<ref name="pmid17846141">{{cite journal |vauthors=Rajendran PM, Young D, Maurer T, Chambers H, Perdreau-Remington F, Ro P, Harris H |title=Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection |journal=Antimicrob. Agents Chemother. |volume=51 |issue=11 |pages=4044–8 |year=2007 |pmid=17846141 |pmc=2151464 |doi=10.1128/AAC.00377-07 |url=}}</ref><ref name="pmid20346539">{{cite journal |vauthors=Schmitz GR, Bruner D, Pitotti R, Olderog C, Livengood T, Williams J, Huebner K, Lightfoot J, Ritz B, Bates C, Schmitz M, Mete M, Deye G |title=Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection |journal=Ann Emerg Med |volume=56 |issue=3 |pages=283–7 |year=2010 |pmid=20346539 |doi=10.1016/j.annemergmed.2010.03.002 |url=}}</ref>
Treatment is based on [[incision and drainage]] and sometimes antibiotic therapy is required. Cure rates with drainage alone are about 85% or higher.<ref name="pmid17846141">{{cite journal |vauthors=Rajendran PM, Young D, Maurer T, Chambers H, Perdreau-Remington F, Ro P, Harris H |title=Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection |journal=Antimicrob. Agents Chemother. |volume=51 |issue=11 |pages=4044–8 |year=2007 |pmid=17846141 |pmc=2151464 |doi=10.1128/AAC.00377-07 |url=}}</ref><ref name="pmid20346539">{{cite journal |vauthors=Schmitz GR, Bruner D, Pitotti R, Olderog C, Livengood T, Williams J, Huebner K, Lightfoot J, Ritz B, Bates C, Schmitz M, Mete M, Deye G |title=Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection |journal=Ann Emerg Med |volume=56 |issue=3 |pages=283–7 |year=2010 |pmid=20346539 |doi=10.1016/j.annemergmed.2010.03.002 |url=}}</ref>
===Medical therapy===
===Medical therapy===
Antibiotic therapy is indicated in some circumstances that include:<ref name="pmid21208910">{{cite journal |vauthors=Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, J Rybak M, Talan DA, Chambers HF |title=Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children |journal=Clin. Infect. Dis. |volume=52 |issue=3 |pages=e18–55 |year=2011 |pmid=21208910 |doi=10.1093/cid/ciq146 |url=}}</ref><ref name="pmid24973422">{{cite journal |vauthors=Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC |title=Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America |journal=Clin. Infect. Dis. |volume=59 |issue=2 |pages=e10–52 |year=2014 |pmid=24973422 |doi=10.1093/cid/ciu444 |url=}}</ref><ref name="pmid26962903">{{cite journal |vauthors=Talan DA, Mower WR, Krishnadasan A, Abrahamian FM, Lovecchio F, Karras DJ, Steele MT, Rothman RE, Hoagland R, Moran GJ |title=Trimethoprim-Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess |journal=N. Engl. J. Med. |volume=374 |issue=9 |pages=823–32 |year=2016 |pmid=26962903 |pmc=4851110 |doi=10.1056/NEJMoa1507476 |url=}}</ref>
Antibiotic therapy is indicated in some circumstances that include and the duration based on severity and clinical response varies between 3 to 7 days:<ref name="pmid21208910">{{cite journal |vauthors=Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, J Rybak M, Talan DA, Chambers HF |title=Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children |journal=Clin. Infect. Dis. |volume=52 |issue=3 |pages=e18–55 |year=2011 |pmid=21208910 |doi=10.1093/cid/ciq146 |url=}}</ref><ref name="pmid24973422">{{cite journal |vauthors=Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC |title=Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America |journal=Clin. Infect. Dis. |volume=59 |issue=2 |pages=e10–52 |year=2014 |pmid=24973422 |doi=10.1093/cid/ciu444 |url=}}</ref><ref name="pmid26962903">{{cite journal |vauthors=Talan DA, Mower WR, Krishnadasan A, Abrahamian FM, Lovecchio F, Karras DJ, Steele MT, Rothman RE, Hoagland R, Moran GJ |title=Trimethoprim-Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess |journal=N. Engl. J. Med. |volume=374 |issue=9 |pages=823–32 |year=2016 |pmid=26962903 |pmc=4851110 |doi=10.1056/NEJMoa1507476 |url=}}</ref>
*Single abscess ≥2 cm
*Single abscess ≥2 cm
*Multiple lesions
*Multiple lesions
*Extensive surrounding cellulitis
*Extensive surrounding [[cellulitis]]
*Associated immunosuppression or other comorbidities
*Associated [[immunosuppression]] or other comorbidities
*Systemic signs of toxicity (fever >100.5°F/38°C, hypotension, or sustained tachycardia)
*Systemic signs of toxicity ([[fever]] >100.5°F/38°C, [[hypotension]], or sustained [[tachycardia]])
*Inadequate clinical response to incision and drainage alone
*Inadequate clinical response to [[incision and drainage]] alone
*Presence of an indwelling medical device (such as prosthetic joint, vascular graft, or pacemaker)
*Presence of an indwelling medical device (such as prosthetic joint, vascular [[graft]], or [[pacemaker]])
*High risk for transmission of S. aureus to others (such as in athletes, military personnel)
*High risk for transmission of [[S. aureus]] to others (such as in athletes, military personnel)
====Antibiotic therapy<ref name="pmid21690621">{{cite journal |vauthors=Talan DA, Krishnadasan A, Gorwitz RJ, Fosheim GE, Limbago B, Albrecht V, Moran GJ |title=Comparison of Staphylococcus aureus from skin and soft-tissue infections in US emergency department patients, 2004 and 2008 |journal=Clin. Infect. Dis. |volume=53 |issue=2 |pages=144–9 |year=2011 |pmid=21690621 |doi=10.1093/cid/cir308 |url=}}</ref><ref name="pmid20346539">{{cite journal |vauthors=Schmitz GR, Bruner D, Pitotti R, Olderog C, Livengood T, Williams J, Huebner K, Lightfoot J, Ritz B, Bates C, Schmitz M, Mete M, Deye G |title=Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection |journal=Ann Emerg Med |volume=56 |issue=3 |pages=283–7 |year=2010 |pmid=20346539 |doi=10.1016/j.annemergmed.2010.03.002 |url=}}</ref>====
====Antibiotic therapy<ref name="pmid21690621">{{cite journal |vauthors=Talan DA, Krishnadasan A, Gorwitz RJ, Fosheim GE, Limbago B, Albrecht V, Moran GJ |title=Comparison of Staphylococcus aureus from skin and soft-tissue infections in US emergency department patients, 2004 and 2008 |journal=Clin. Infect. Dis. |volume=53 |issue=2 |pages=144–9 |year=2011 |pmid=21690621 |doi=10.1093/cid/cir308 |url=}}</ref><ref name="pmid20346539">{{cite journal |vauthors=Schmitz GR, Bruner D, Pitotti R, Olderog C, Livengood T, Williams J, Huebner K, Lightfoot J, Ritz B, Bates C, Schmitz M, Mete M, Deye G |title=Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection |journal=Ann Emerg Med |volume=56 |issue=3 |pages=283–7 |year=2010 |pmid=20346539 |doi=10.1016/j.annemergmed.2010.03.002 |url=}}</ref>====
:*Preferred regimen: [[Trimethoprim-sulfamethoxazole]] one or two double strength doses (160 mg of trimethoprim and 800 mg of sulfamethoxazole) PO twice daily
:*Preferred regimen: [[Trimethoprim-sulfamethoxazole]] one or two double strength doses (160 mg of trimethoprim and 800 mg of sulfamethoxazole) PO twice daily

Revision as of 18:32, 28 March 2017

Cutaneous abscess
Abscess

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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 the dermis or subcutaneous tissue and appears as a swollen, red, tender, and fluctuant mass, often with surrounding cellulitis 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. Polymorpho nuclear cells (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

Common causes

Less common causes

Nontuberculous mycobacteria, blastomycosis, nocardiosis, and cryptococcosis.[7]

Differentiating cutaneous abscess from other Diseases

Disease Clinical features
Folliculitis Hair follicle inflammation, presents as pruritic rash or pustule.[9][10]
Suppurative hydradenitis Inflammation in intertriginous areas (axillae, inguinal area, inner thighs, perianal and perineal areas, mammary,..)

Presents as painful inflamed nodule, sinus tract and commedons. Associated with systemic symptoms. Needs surgical debridement and systemic antibiotic.[11]

Epidermoid cyst Cyst or nodule presents with central punctum. May be secondarily infected.[12]
Nodular lymphangitis Subcutaneous swelling along with lymphatics. mostly due to Sporothrix schenckii.[13]
Myiasis Enlarging nodule secondary to insect bite and due to penetration of fly larvae into subdermal tissue. caused by Dermatobia hominis, the botfly and Cordylobia anthropophaga, the tumbu fly.[14]

Epidemiology and Demographics

  • It is estimated that 4% of children experience the cutaneous abscess.[15]

A national emergency department visit survey from 1996 to 2005 showed:

  • Emergency department visits for abscesses more than doubled over the 10-year study period (1.2 million in 1996 to 3.28 million in 2005).

Gender

Men and women are affected equally.

Age

It is more common among adults age 19 to 45 years.

Risk Factors

Risk factors for developing cutaneous abscess include:[16][17]

Natural History, Complications and Prognosis

Natural History

If cutaneous abscess left untreated it may drain spontaneously or in severe cases may cause systemic spread and result in sepsis.[18]

Complications

A wide range of complications are possible in the course of skin abscess including: Bacteremia, endocarditis, osteomyelitis, metastatic infection, sepsis, and toxic shock syndrome.[19]

Prognosis

Depending on the extent of the disease, the prognosis may vary. However, the prognosis is generally regarded as good.

Diagnosis

History and symptoms

History

A detailed history must be taken from all patients. Specific area of focus when obtaining a history from the patient include:

Symptoms

The hallmark of the cutaneous abscess is painful, tender, indurated, and usually erythematous nodule.

Physical examination

Appearance of the Patient

Patients are usually well appearing.

Vital signs

Vital signs are within normal limits unless there is complication.

Skin

Indurated, tender and erythematous nodule with signs of local inflammation is the presenting feature.

Laboratory findings

Leukocytosis and increased level of acute phase reactants (ESR, CRP) are the most common laboratory findings.

Treatment

Treatment is based on incision and drainage and sometimes antibiotic therapy is required. Cure rates with drainage alone are about 85% or higher.[20][21]

Medical therapy

Antibiotic therapy is indicated in some circumstances that include and the duration based on severity and clinical response varies between 3 to 7 days:[22][23][24]

Antibiotic therapy[25][21]

  • Preferred regimen: Trimethoprim-sulfamethoxazole one or two double strength doses (160 mg of trimethoprim and 800 mg of sulfamethoxazole) PO twice daily
  • Alternative regimen (1): Clindamycin 300-450 mg PO three to four times daily
  • Alternative regimen (2): Doxycycline 100 mg PO twice daily
  • Alternative regimen (3): Minocycline 200 mg PO once, then 100 mg PO twice daily
  • Alternative regimen (4): Linezolid 600 mg PO twice daily
  • Alternative regimen (5): Tedizolid 200 mg PO once daily

Surgery

Incision and drainage is the preferred method of treatment for cutaneous abscesses.[26] The following video, shows this procedure.{{#ev:youtube|MwgNdrA18fM}}

References

  1. "Classics in infectious diseases. "On abscesses". Alexander Ogston (1844-1929)". Rev. Infect. Dis. 6 (1): 122–8. 1984. PMID 6369479.
  2. 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.
  3. 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.
  4. 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.
  5. Bieluch VM, Tally FP (1983). "Pathophysiology of abscess formation". Clin Obstet Gynaecol. 10 (1): 93–103. PMID 6872404.
  6. Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC (2014). "Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America". Clin. Infect. Dis. 59 (2): 147–59. doi:10.1093/cid/ciu296. PMID 24947530.
  7. 7.0 7.1 7.2 Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM (1995). "Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use". Clin. Infect. Dis. 20 Suppl 2: S279–82. PMID 7548575.
  8. Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, Talan DA (2006). "Methicillin-resistant S. aureus infections among patients in the emergency department". N. Engl. J. Med. 355 (7): 666–74. doi:10.1056/NEJMoa055356. PMID 16914702.
  9. Luelmo-Aguilar J, Santandreu MS (2004). "Folliculitis: recognition and management". Am J Clin Dermatol. 5 (5): 301–10. PMID 15554731.
  10. Laureano AC, Schwartz RA, Cohen PJ (2014). "Facial bacterial infections: folliculitis". Clin. Dermatol. 32 (6): 711–4. doi:10.1016/j.clindermatol.2014.02.009. PMID 25441463.
  11. Revuz J (2009). "Hidradenitis suppurativa". J Eur Acad Dermatol Venereol. 23 (9): 985–98. doi:10.1111/j.1468-3083.2009.03356.x. PMID 19682181.
  12. Zuber TJ (2002). "Minimal excision technique for epidermoid (sebaceous) cysts". Am Fam Physician. 65 (7): 1409–12, 1417–8, 1420. PMID 11996426.
  13. Kostman JR, DiNubile MJ (1993). "Nodular lymphangitis: a distinctive but often unrecognized syndrome". Ann. Intern. Med. 118 (11): 883–8. PMID 8480962.
  14. Arosemena R, Booth SA, Su WP (1993). "Cutaneous myiasis". J. Am. Acad. Dermatol. 28 (2 Pt 1): 254–6. PMID 8432924.
  15. Holsenback H, Smith L, Stevenson MD (2012). "Cutaneous abscesses in children: epidemiology in the era of methicillin-resistant Staphylococcus aureus in a pediatric emergency department". Pediatr Emerg Care. 28 (7): 684–6. doi:10.1097/PEC.0b013e31825d20e1. PMID 22743746.
  16. McNamara DR, Tleyjeh IM, Berbari EF, Lahr BD, Martinez J, Mirzoyev SA, Baddour LM (2007). "A predictive model of recurrent lower extremity cellulitis in a population-based cohort". Arch. Intern. Med. 167 (7): 709–15. doi:10.1001/archinte.167.7.709. PMID 17420430.
  17. Gordon RJ, Lowy FD (2005). "Bacterial infections in drug users". N. Engl. J. Med. 353 (18): 1945–54. doi:10.1056/NEJMra042823. PMID 16267325.
  18. Llera JL, Levy RC, Staneck JL (1984). "Cutaneous abscesses: natural history and management in an outpatient facility". J Emerg Med. 1 (6): 489–93. PMID 6444142.
  19. Raff AB, Kroshinsky D (2016). "Cellulitis: A Review". JAMA. 316 (3): 325–37. doi:10.1001/jama.2016.8825. PMID 27434444.
  20. Rajendran PM, Young D, Maurer T, Chambers H, Perdreau-Remington F, Ro P, Harris H (2007). "Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection". Antimicrob. Agents Chemother. 51 (11): 4044–8. doi:10.1128/AAC.00377-07. PMC 2151464. PMID 17846141.
  21. 21.0 21.1 Schmitz GR, Bruner D, Pitotti R, Olderog C, Livengood T, Williams J, Huebner K, Lightfoot J, Ritz B, Bates C, Schmitz M, Mete M, Deye G (2010). "Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection". Ann Emerg Med. 56 (3): 283–7. doi:10.1016/j.annemergmed.2010.03.002. PMID 20346539.
  22. Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, J Rybak M, Talan DA, Chambers HF (2011). "Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children". Clin. Infect. Dis. 52 (3): e18–55. doi:10.1093/cid/ciq146. PMID 21208910.
  23. Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC (2014). "Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America". Clin. Infect. Dis. 59 (2): e10–52. doi:10.1093/cid/ciu444. PMID 24973422.
  24. Talan DA, Mower WR, Krishnadasan A, Abrahamian FM, Lovecchio F, Karras DJ, Steele MT, Rothman RE, Hoagland R, Moran GJ (2016). "Trimethoprim-Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess". N. Engl. J. Med. 374 (9): 823–32. doi:10.1056/NEJMoa1507476. PMC 4851110. PMID 26962903.
  25. Talan DA, Krishnadasan A, Gorwitz RJ, Fosheim GE, Limbago B, Albrecht V, Moran GJ (2011). "Comparison of Staphylococcus aureus from skin and soft-tissue infections in US emergency department patients, 2004 and 2008". Clin. Infect. Dis. 53 (2): 144–9. doi:10.1093/cid/cir308. PMID 21690621.
  26. Singer AJ, Talan DA (2014). "Management of skin abscesses in the era of methicillin-resistant Staphylococcus aureus". N. Engl. J. Med. 370 (11): 1039–47. doi:10.1056/NEJMra1212788. PMID 24620867.