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Home , Abscess, Boil, Carbuncle, Cellulitis, Clostridium, Erysipelas

Karl T. Clebak, MD, MHA, FAAFP; Alexis Reedy-Cooper, MD, MPH; A guide to the Tx of Michael T. Partin, MD; Christopher R. Davis, MD Penn State Health Milton and other soft-tissue S. Hershey Medical Center, Hershey (Drs. Clebak, Partin, and Davis); Penn State Diagnostic and therapeutic priorities vary for the 8 types Health St. Joseph Medical Center, Reading (Dr. Reedy- of reviewed. Cooper).

kclebak@ pennstatehealth.psu.edu kin and soft-tissue infections, frequently encountered in PRACTICE The authors reported no primary care, range from the uncomplicated potential conflict of interest RECOMMENDATIONS relevant to this article. to the life-threatening necrotizing . This review ❯ Start - S draws from the latest evidence and guidelines to help guide doi: 10.12788/jfp.0198 , , , the care you provide to patients with cellulitis, , , or a third- erysipelas, , furuncles, , , and or fourth-generation . fluoroquinolone for patients with cellulitis likely caused by community Cellulitis acquired - Cellulitis, an infection of the deep dermal and subcutaneous resistant layers of the , has become increasingly common in recent aureus (MRSA). A years, with both incidence and hospitalization rates rising.1 ❯ Consider culturing for Cellulitis occurs when enter the through MRSA and treating with oral breaks in the skin barrier due to cutaneous fungal infections, doxycycline or trimethoprim- trauma, pressure sores, venous stasis, or . The sulfamethoxazole for resistant diagnosis is often made clinically based on characteristic cases of folliculitis. C skin findings—classically an acute, poorly demarcated area ❯ Perform complete of , warmth, swelling, and tenderness. Lymphangitic surgical streaking and local may also be present. In- promptly if necrotizing fection often occurs on an extremity (although it can be found fasciitis is suspected. C on other areas of the body) and is usually unilateral. may ❯ Prescribe broad- or may not be present.2 for necrotizing ❚ Likely responsible . Staphylococcus au- fasciitis, covering both reus and Group A streptococci (often pyogenes) anaerobes and aerobes are common culprits. One systematic review that examined including MRSA. C cultures taken of intact skin in cellulitis patients found S aureus Strength of recommendation (SOR) to be about twice as common as S pyogenes, with both bacte- A Good-quality patient-oriented ria accounting for a little more than 70% of cases. Of the re- evidence maining positive cultures, the most common were B Inconsistent or limited-quality patient-oriented evidence alpha-­hemolytic streptococcus, group B streptococcus, Pseu-  C Consensus, usual practice, domonas aeruginosa, perfringens, Escherichia opinion, -oriented 3 evidence, case series coli, multocida, and Proteus mirabilis. Similarly, a systematic review of bacteremia in patients with cellulitis and erysipelas found that S pyogenes, other beta-hemolytic strep, and S aureus account for about 70% of cases (although S au- reus was responsible for just 14%), with the remainder of cases

214 THE JOURNAL OF FAMILY PRACTICE | JUNE 2021 | VOL 70, NO 5 caused by gram-negative organisms such as posterior to the orbital septum.6,7 Periorbital, E coli and P aeruginosa.4 or preseptal, cellulitis occurs anterior to the ❚ Treatment considerations. Strict orbital septum and is the more common of treatment guidelines for cellulitis are lack- the 2 infections—84% compared with 16% for ing, but general consensus encourages the orbital cellulitis.6 However, orbital cellulitis, use of antibiotics and occasionally . which affects mainly children at a median age For mild and moderate cases of cellulitis, of 7 years,6 must be detected and treated early prescribe oral and parenteral antibiotics due to the potential for serious complications to cover for streptococci and methicillin- such as cavernous sinus , men- susceptible S aureus, respectively. Expand ingitis, intracranial , and vision loss.7 coverage to include if nasal Chemosis (conjunctival ) and diplopia colonization shows methicillin-resistant are more commonly associated with orbital S aureus (MRSA) or if you otherwise sus- cellulitis and are seldom seen with preseptal pect prior MRSA exposure. Expanded cov- cellulitis. erage will also be needed if there is severe ❚ Predominant causative organisms are nonpurulent infection associated with S pneumoniae, Moraxella catarrhalis, non- penetrating trauma or a history of intrave- typeable , and group nous drug use, or the patient meets criteria A streptococcus. The most common mecha- for systemic inflammatory response syn- nism of infection is tracking from periorbital drome. If patients are severely compromised structures (eg, paranasal and ethmoid sinus- For orbital (eg, neutropenic), it is reasonable to further itis). Other causes include orbital trauma/ cellulitis, choose add broad-spectrum coverage (eg, intrave- fracture, periorbital surgery, and bacterial antibiotics nous -tazobactam­ or carbape- . Clinically, patients present with effective against nem). Typical duration of treatment is 5 to limited ocular motility and proptosis associ- -related 7 days, although this should be extended if ated with inflamed conjunctiva, orbital , pathogens (eg, there is no clinical improvement. , , fever, edema, and S pneumoniae, Generally, cellulitis can be managed in possible decrease in visual acuity. The diag- H influenzae, the outpatient setting, although hospitaliza- nosis is often made clinically and confirmed M catarrhalis), tion is recommended if there are concerns for with orbital computed tomography (CT) with S aureus, and deep or necrotizing infection, if patients are contrast, which can assist in ruling out intra- anaerobes. nonadherent to therapy or are immunocom- cranial involvement such as abscess. promised, or if outpatient therapy has failed.5 ❚ therapy, generally admin- Furthermore, in an observational study of istered intravenously, is recommended for 606 adult patients, prior episodes of cellulitis, at least 3 days or until orbital symptoms venous insufficiency, and immunosuppres- begin to resolve. Choose antibiotics effec- sion were all independently associated with tive against sinusitis-related pathogens poorer clinical outcomes.2 Also treat underly- (eg, S pneumoniae, H influenzae, M catarrha- ing predisposing factors such as edema, obe- lis), S aureus, and anaerobes.8 For instance, a sity, eczema, venous insufficiency, and toe regimen may include vancomycin for MRSA web abnormalities such as fissures, scaling, coverage, a third-generation , or maceration.5 Consider the use of prophy- or for anaerobic coverage if lactic antibiotics for patients who have had there is concern about intracranial involve- 3 to 4 episodes of cellulitis despite attempts ment. Surgical intervention is often reserved to treat predisposing conditions. Prophylac- for patients with inadequate response to tic antibiotic regimens include or antibiotic therapy, necessitating biopsy for orally and penicillin G benza- identification, as well as drainage thine intramuscularly.5 Antibiotic regimens of large abscesses refractory to antibiotics. are summarized in the TABLE.5

Erysipelas Orbital cellulitis Erysipelas, a related yet distinct form of cellu- Orbital cellulitis is an infection of the tissues litis, is a bacterial infection of the superficial

MDEDGE.COM/FAMILYMEDICINE VOL 70, NO 5 | JUNE 2021 | THE JOURNAL OF FAMILY PRACTICE 215 TABLE Antibiotic regimens for skin and soft-tissue infections5 ANTIBIOTIC ADULT DOSAGE Mild infection: Treat 5-7 days; extend if clinical improvement is insufficient Penicillin V 250-500 mg po q6h 500 mg po tid, or 875 mg po bid Cephalexin 500 mg po q6h 500 mg po q6h 500 mg po bid Clindamycin* 300 po qid, or 450 mg po tid Doxycycline* 100 mg po bid Trimethoprim-sulfamethoxazole* 1-2 DS tablets po bid Minocycline* 100 mg po daily Moderate systemic infection: Treat until there is clinical improvement and the patient is able to take oral antibiotics Penicillin G 2-4 million units IV q4-6h Ceftriaxone 1-2 g IV daily When clinical Vancomycin* 15 mg/kg IV bid exam alone is inconclusive * 600 mg po bid when evaluating Daptomycin* 4 mg/kg IV q24h skin and soft- Ceftaroline* 600 mg IV bid tissue infections Severe systemic infection: Treat until there is clinical improvement in children and Vancomycin + piperacillin-tazobactam 15 mg/kg IV bid + 4.5 g IV q8h adolescents, Vancomycin + -cilastatin 15 mg/kg IV bid + 500 mg IV q6h or 1 g q8h IV for consider using fully susceptible organisms ultrasound Recurrent infections: Treat 4-52 weeks or as long as predisposing risk factors are present to improve Penicillin V 250-500 mg po q6h diagnostic accuracy. Benzathine penicillin 1.2 million units IM q2-4 weeks Erythromycin 250 mg po bid * Coverage for suspected MRSA. bid, twice a day; DS, double strength; IM, intramuscularly; IV, intravenously; MRSA, methicillin-resistant ; po, by mouth; qid, 4 times a day; q6h, every 6 hours; tid, 3 times a day.

dermis and hypodermis and is commonly and, rarely, bacteremia. caused by group A streptococcus.5,9 Other ❚ Antibiotic treatment regimens include less common organisms include S aureus, penicillin G, macrolides (reserved for those P aeruginosa, and enterobacteria. Erysipelas with penicillin ), fluoroquinolones, predominantly affects the lower extremities and , with duration of treat- unilaterally (~90%); the arms and the face ment ranging from 10 to 14 days depending on are the next most common locations. In ad- infection severity. Fever, pain, and erythema dition to the rapid onset of well-demarcated generally improve within 48 to 72 hours of an- erythema, pain, and swelling, patients tibiotic therapy. If there is no improvement, may have fever and regional lymphade- consider alternative diagnoses, such as nec- nopathy. Risk factors include portal of entry rotizing fasciitis. Recurrence rates following (eg, tinea pedis, ulceration), , the initial episode of erysipelas are estimated and . Complications of erysipelas in- at 10% of patients at 6 months and 30% at clude bullae from edema, abscess formation, 3 years.10

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Folliculitis If you suspect pseudomonas, consider Inflammation of follicles is characterized giving ciprofloxacin for 10 to 14 days for by superficial inflammation with the devel- persistent lesions or if the patient is immuno- opment of perifollicular or pustules compromised.13,15 Consider obtaining bacte- on an erythematous base.11,12 Folliculitis most rial, fungal, or viral cultures for lesions that fail commonly affects the face, scalp, thighs, but- to respond to initial treatment. tocks, axillae, and inguinal areas.13 It may be caused by infection, an inflammatory reac- tion, or physical injury. Diagnosis is typically Furuncles/carbuncles/abscesses based on the patient’s history and physical A furuncle, commonly referred to as a , examination. is an infected that becomes en- ❚ are the most common cause closed, creating a collection of . A carbun- of infection, although fungi, viruses, and cle is a collection of furuncles that converge other entities can cause folliculitis. S aureus and drain through a single opening. An ab- (methicillin sensitive or methicillin resistant) scess is a localized collection of pus arising is the most common pathogen; in the past, from within the dermis that can extend within superficial pustular folliculitis attributed to deeper tissues.5 Furuncles, carbuncles, and S aureus was referred to as Bockhart impe- abscesses are managed similarly with drain- tigo. Folliculitis secondary to P aeruginosa, age and consideration for MRSA risk factors. often seen after exposure to contaminated ❚ S aureus is the most common cause Do not routinely water or hot tubs, is frequently referred to as of these infections; 59% of skin abscesses are order cultures “.” , a reported due to community-acquired MRSA.16 Anaer- or prescribe cause of , tends to occur in obes may contribute to the polymicrobial flo- antibiotics for adolescents of either sex and men with high ra of skin abscesses.17 Risk factors for MRSA uncomplicated sebum production, is common in tropical infection include a history of previous MRSA abscesses. climates, and can be associated with HIV or infection, diabetes, dialysis or renal failure, .11,12,14 placement of an indwelling or medi- of folliculitis in- cal device, drug use, incarcera- cludes pseudofolliculitis barbae, eosino- tion, close contact with a person with known philic folliculitis, , MRSA infection or colonization, long-term vulgaris, , contact , im- care residence, hospitalization or surgery petigo, and .13 Pseudofolliculitis bar- within the past 12 months, and high preva- bae is an inflammatory reaction to shaving, lence of MRSA in the community.5 more commonly seen in darkly pigmented ❚ Ultrasound improves diagnostic accu- skin. Pseudofolliculitis develops when the racy. One study showed that when a clinical hair shaft penetrates the wall of the follicle or exam alone was inconclusive in evaluating directly enters the . skin and soft-tissue infections in children ❚ Initial treatment for mild disease and adolescents, an ultrasound-assisted ex- includes the elimination of predisposing amination improved diagnostic accuracy.18 factors such as occlusion, moisture, and Sensitivity of the clinical examination was abrasion. The area should be kept clean and 43.7%, compared with 77.6% for the clinical dry, avoiding friction. For localized disease, examination plus ultrasound.18 prescribe topical clindamycin, ❚ first. Ultra- ointment, or benzoyl peroxide. If symptoms sound-guided needle aspiration, however, has fail to respond, prescribe a 7-day course of not improved treatment efficacy compared antibiotic that targets methicillin-sensitive with incision and drainage,19 the mainstay ap- S aureus—eg, cephalexin or dicloxacil- proach for abscesses.17 The procedure to drain lin. Also consider doxycycline, which a furuncle, , or abscess should in- has anti-inflammatory effects and is clude the expression of all purulent material effective against MRSA. For refractory and the removal of all loculations if possible. lesions, trimethoprim-sulfamethoxazole,­ Wound culture is recommended during in- clindamycin, or minocycline may be useful. cision and drainage per current guidelines.5 CONTINUED

MDEDGE.COM/FAMILYMEDICINE VOL 70, NO 5 | JUNE 2021 | THE JOURNAL OF FAMILY PRACTICE 217 Simple dry dressings are convenient and ef- per wound, although in some cases up to fective, although some wounds may require 15 organisms have been identified in a single packing. Tap water (that is potable) is suit- wound.5 Type I infection is often associated able for wound cleansing. However, there is with tissue injury, abscess, or abdominal sur- no strong evidence that irrigating wounds in- gery. The majority of cases of necrotizing fas- creases healing or reduces infection.20 ciitis are polymicrobial.27,28 ❚ Routine use of antibiotics is not recom- Monomicrobial infection, also referred mended for simple cutaneous abscesses.5,17,21 to as type II, is often due to group A strep- Evidence has been conflicting regarding em- tococcus, S aureus, vibrio spp, piric antibiotic coverage of MRSA following hyrophilio, or an anaerobic streptococci like incision and drainage.22-25 Guidelines recom- spp. Typically monomi- mend considering the initiation of antibiotics crobial infections, which account for 20% to if there are multiple abscesses, , sur- 30% of cases of necrotizing fasciitis, are com- rounding cellulitis, or systemic signs of infec- munity acquired.5,26,29,30 tion, or if the host is immunocompromised.5 ❚ Clinical presentation. In the early stag- If MRSA is suspected, recommended es of disease, patients commonly complain antibiotic coverage includes trimethoprim-­ of flu-like symptoms and extreme pain that sulfamethoxazole, clindamycin, doxycy- is out of proportion to findings on the exam. cline, or minocycline.5 If MRSA is identified, Additional warning signs include and Monomicrobial treatment options include dicloxacillin or other symptoms of toxicity such as tachy- infections, which cephalexin. For severe infections persist- cardia, , , , and account for 20% ing after incision and drainage, in addition diarrhea. Later in the course, symptoms may to 30% of cases to oral antibiotic therapy, consider intrave- localize to the affected area and include ery- of necrotizing nous antibiotic options for MRSA: , thema, tense swelling, development of blis- fasciitis, are clindamycin, linezolid, , , ters or bullae, blackish blue discoloration of community or vancomycin.5 the skin, severe pain, and loss of sensation. In acquired. some cases involving gas-forming bacteria, tissue crepitus may be noted on exam.5,27-31 Necrotizing fasciitis ❚ Rely on clinical judgment to hasten Necrotizing fasciitis is a rare but potentially surgical intervention. Laboratory or imaging deadly infection of the skin and . It findings may augment clinical judgment. But progresses rapidly and spreads along fascial if you suspect necrotizing fasciitis, obtaining planes, leading to the of the super- blood tests and imaging should not delay sur- ficial . The infection often is more -ex gery. Blood tests that may aid in the diagno- tensive than is indicated by superficial signs. sis of necrotizing fasciitis include a complete Prompt diagnosis is imperative as necrotiz- blood count with differential; coagulation ing fasciitis is a surgical emergency.5,26 In the studies; a comprehensive metabolic panel; as- United States, 500 to 1500 cases of necrotiz- says of lactate, C-reactive (CRP), and ing fasciitis occur each year.27 Risk factors creatinine kinase; and blood cultures. Most of- for necrotizing fasciitis include diabetes, pe- ten, patients with necrotizing fasciitis will have ripheral vascular disease, malignancy, obe- leukocytosis or leukopenia, evidence of hemo- sity, cirrhosis, renal failure, injection drug lysis, thrombocytopenia, acute renal failure, use, chronic therapy, alcohol and significantly elevated CRP. abuse, , and iatrogenic immu- On any imaging modality, indications of nosuppression.26,28 necrotizing fasciitis are inflammatory infil- Necrotizing fasciitis may be polymicro- tration of the deep fascia on the affected side bial or monomicrobial. Polymicrobial infec- that is absent on the contralateral side, and tion, also referred to as type I, is often due the presence of subcutaneous air (which is a to multiple bacteria that originate from the specific but rare finding). Imaging modalities bowel flora, typically including a mix of an- may include CT or magnetic resonance imag- aerobic and aerobic organisms. On average, ing. A definitive diagnosis can only be made there can be 5 infecting organisms identified with surgical exploration of the involved area.

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Definitive microbiologic diagnosis will require A reasonable initial empiric regimen in culture of organisms from affected tissue or adults would include an agent that is effective blood.5,26,30,31 against group A streptococcus, gram-nega- ❚ First address any hemodynamic in- tive pathogens, and anaerobes, such as a car- stability (hypotension is frequently en- bapenem or a beta-lactam-beta-lactamase­ countered), followed by urgent surgical inhibitor such as piperacillin-­tazobactam. exploration, debridement of the wound, and Additionally, include an agent that targets antimicrobial therapy. Antibiotic treatment MRSA, such as vancomycin, linezolid, or should align with probable pathogens and clindamycin.5 JFP treatment should be continued until repeat- CORRESPONDENCE ed surgical debridement is no longer neces- Karl T. Clebak, MD, Department of Family and Community sary, clinical improvement is evident, and 48 Residency Program, Penn State Health M.S. Hershey Medical Center, 500 University Drive, H154/C1613, Hershey, to 72 hours have passed since defervescence. PA 17033; [email protected]

References 1. Raff AB, Kroshinsky D. Cellulitis: a review. JAMA. 2016;316: Ann Intern Med. 1977;87:145-149. 325-337. 18. Marin JR, Dean AJ, Bilker WB, et al. Emergency ultrasound- 2. Collazos J, de la Fuente B, García A, et al. Cellulitis in adult pa- assisted examination of skin and soft tissue infections in the tients: a large, multicenter, observational, prospective study of pediatric emergency department. Acad Emerg Med. 2013;20: 606 episodes and analysis of the factors related to the response to 545-553. treatment. PLoS One. 2018;13:e0204036. 19. Gaspari RJ, Resop D, Mendoza M, et al. A randomized controlled If you suspect 3. Chira S, Miller LG. Staphylococcus aureus is the most common trial of incision and drainage versus ultrasonographically guided identified cause of cellulitis: a systematic review. Epidemiol Infect. needle aspiration for skin abscesses and the effect of methicil- necrotizing 2010;138:313-317. lin-resistant Staphylococcus aureus. Ann Emerg Med. 2011;57: fasciitis, 4. Gunderson CG, Martinello RA. A systematic review of bactere- 483-491. obtaining mias in cellulitis and erysipelas. J Infect. 2012;64:148-155. 20. Fernandez R, Griffiths R, Ussia C. Water for wound cleansing. Co- 5. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for chrane Database Syst Rev. 2002: CD003861. blood tests the diagnosis and management of skin and soft tissue infections: 21. Llera JL, Levy RC. Treatment of cutaneous abscess: a double- and imaging 2014 update by the Infectious Society of America. Clin blind clinical study. Ann Emerg Med. 1985;14:15-19. Infect Dis. 2014;59:147-159. 22. Talan DA, Mower WR, Krishnadasan A, et al. Trimethoprim-­ should not delay 6. Jain A, Rubin PA. Orbital cellulitis in children. Int Ophthalmol sulfamethoxazole versus placebo for uncomplicated skin abscess. surgery. Clin. 2001;41:71-86. N Engl J Med. 2016;374:823-832. 7. Seltz LB, Smith J, Durairaj VD, et al. and antibiotic 23. Korownyk C, Allan GM. Evidence-based approach to abscess management of orbital cellulitis. Pediatrics. 2011;127:e566-e572. management. Can Fam Physician. 2007;53:1680-1684. 8. Nageswaran S, Woods CR, Benjamin DK, et al. Orbital cellulitis in 24. Schmitz GR, Bruner D, Pitotti R, et al. Randomized controlled children. Pediatr Infect Dis J. 2006;25:695-699. trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicil- 9. Bonnetblanc J-M, Bédane C. Erysipelas. Am J Clin Dermatol. lin-resistant Staphylococcus aureus infection. Ann Emerg Med. 2003;4:157-163. 2010;56:283-287. 10. Jorup-Rönström C, Britton S. Recurrent erysipelas: predisposing 25. Rajendran PM, Young D, Maurer T, et al. Randomized, double- factors and costs of prophylaxis. Infection. 1987;15:105-106. blind, placebo-controlled trial of cephalexin for treatment of 11. Clebak KT, Malone MA. Skin Infections. Prim Care. 2018;45: uncomplicated skin abscesses in a population at risk for commu- 433-454. nity-acquired methicillin-resistant Staphylococcus aureus infec- 12. Luelmo-Aguilar J, Santandreu MS. Folliculitis: recognition and tion. Antimicrob Agents Chemother. 2007;51:4044-4048. management. Am J Clin Dermatol. 2004;5:301-310. 26. Hunter J, Quarterman C, Waseem M, et al. Diagnosis and man- 13. Mengesha YM, Bennett ML. Pustular skin disorders: diagnosis agement of necrotizing fasciitis. Br J Hosp Med. 2011;72:391-395. and treatment. Am J Clin Dermatol. 2002;3:389-400. 27. Hussein QA, Anaya DA. Necrotizing soft tissue infections. Crit 14. Akaza N, Akamatsu H, Sasaki Y, et al. is Care Clin. 2013;29:795-806. caused by cutaneous resident Malassezia species. Med Mycol. 28. Puvanendran R, Huey JCM, Pasupathy S. Necrotizing fasciitis. 2009;47:618-624. Can Fam Physician. 2009;55:981-987. 15. Berger RS, Seifert MR. Whirlpool folliculitis: a review of its cause, 29. Raven MC, Billings JC, Goldfrank LR, et al. Medicaid patients at treatment, and prevention. Cutis. 1990;45:97-98. high risk for frequent hospital admission: real-time identification 16. Fridkin SK, Hageman JC, Morrison M, et al. Methicillin-resistant and remediable risks. J Urban Health. 2009;86:230-241. Staphylococcus aureus disease in three communities. N Engl 30. Ustin JS, Malangoni MA. Necrotizing soft-tissue infections: Crit J Med. 2005;352:1436-1444. Care Med. 2011;39:2156-2162. 17. Meislin HW, Lerner SA, Graves MH, et al. Cutaneous abscesses: 31. Bystritsky R, Chambers H. Cellulitis and soft tissue infections. anaerobic and aerobic bacteriology and outpatient management. Ann Intern Med. 2018;168:ITC17- ITC32.

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