Skin and soft tissue infections

My patient complains of severe facial scarring from childhood acne that is not improving. How should I advise her?

FA Manian MD, MPH, , , , Leave a comment

Severe facial scarring after childhood acne is not uncommon, having been shown to affect 43% of acne patients.1 Fortunately, there are several evidence-based treatments available to improve their appearance.

One procedure that you could recommend to your patient is microneedling, also known as percutaneous collagen induction or collagen induction therapy.2 This therapy works by using extremely fine needles to create small puncture wounds in the epidermis and superficial dermis, leading to tissue proliferation and collagen remodeling with subsequent enhancement in scar appearance.3 In fact, one randomized clinical trial showed a statistically significant 41% mean improvement following the procedure4. Adverse effects are limited with this treatment, with participants experiencing no issues other than mild erythema and edema.4

Another highly effective solution is laser therapy, which includes resurfacing (carbon dioxide, CO2; erbium-doped yttrium aluminum garnet, Er:YAG) and fractional (nonablative, NAFL; and ablative, AFL) lasers. One study compared the efficacy of these different lasers. Improvement in scar appearance was measured with a scale graded from 0 to 10. The mean improvement scores of the CO2, Er:YAG, NAFL, and AFL groups were 6.0, 5.8, 2.2, and 5.2, respectively.5 The Er:YAG laser has even been shown to have significantly better results than microneedling (70% improvement vs 30% improvement).6 The biggest downside to laser therapy is that patients reported more erythema, swelling, and crusting when compared to microneedling; however, they experienced significantly less pain.6

Other potentially effective treatments for acne scars include dermal fillers and chemical peels, neither of which have been shown to be superior to microneedling or laser therapy individually. However, certain peels do seem to significantly improve the effects of microneedling when used together.7 The good news is that all four can be performed easily in the office setting, so a referral to a board-certified dermatologist or plastic surgeon would be a good first step to addressing your patient’s problem.

Request for treatment of scars years after onset of acne should not be surprising in a general medicine practice. Acne is the most common skin condition in the United States, affecting over 50 million people.8 Unfortunately, in severe cases, inflammation can lead to scarring in cosmetically sensitive areas, leading to a lower quality of life and higher rates of anxiety and depression.9

Bonus Pearl: Did you know that platelet-rich plasma (PRP), a concentrate of platelets and growth factors obtained from venipuncture, has been shown to enhance the effects of microneedling and laser therapy through increased protein synthesis, collagen remodeling, and accelerated wound healing? 10

Contributed by Aditya Nellore, MD,  St. Louis, Missouri

 

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References:

  1. Tan J, Kang S, Leyden J. Prevalence and Risk Factors of Acne Scarring Among Patients Consulting Dermatologists in the USA. J Drugs Dermatol. 2017 Feb 1;16(2):97-102. PMID: 28300850. https://pubmed.ncbi.nlm.nih.gov/28300850/
  2. Orentreich DS, Orentreich N. Subcutaneous incisionless (subcision) surgery for the correction of depressed scars and wrinkles. Dermatol Surg. 1995 Jun;21(6):543-9. doi: 10.1111/j.1524-4725.1995.tb00259.x. PMID: 7773602. https://pubmed.ncbi.nlm.nih.gov/7773602/
  3. Fabbrocini G, Fardella N, Monfrecola A, Proietti I, Innocenzi D. Acne scarring treatment using skin needling. Clin Exp Dermatol. 2009 Dec;34(8):874-9. doi: 10.1111/j.1365-2230.2009.03291.x. Epub 2009 May 22. PMID: 19486041. https://pubmed.ncbi.nlm.nih.gov/19486041/
  4. Alam M, Han S, Pongprutthipan M, Disphanurat W, Kakar R, Nodzenski M, Pace N, Kim N, Yoo S, Veledar E, Poon E, West DP. Efficacy of a needling device for the treatment of acne scars: a randomized clinical trial. JAMA Dermatol. 2014 Aug;150(8):844-9. doi: 10.1001/jamadermatol.2013.8687. PMID: 24919799. https://pubmed.ncbi.nlm.nih.gov/24919799/
  5. You HJ, Kim DW, Yoon ES, Park SH. Comparison of four different lasers for acne scars: Resurfacing and fractional lasers. J Plast Reconstr Aesthet Surg. 2016 Apr;69(4):e87-95. doi: 10.1016/j.bjps.2015.12.012. Epub 2016 Jan 7. PMID: 26880620. https://pubmed.ncbi.nlm.nih.gov/26880620/
  6. Osman MA, Shokeir HA, Fawzy MM. Fractional Erbium-Doped Yttrium Aluminum Garnet Laser Versus Microneedling in Treatment of Atrophic Acne Scars: A Randomized Split-Face Clinical Study. Dermatol Surg. 2017 Jan;43 Suppl 1:S47-S56. doi: 10.1097/DSS.0000000000000951. PMID: 28009690. https://pubmed.ncbi.nlm.nih.gov/28009690/
  7. El-Domyati M, Abdel-Wahab H, Hossam A. Microneedling combined with platelet-rich plasma or trichloroacetic acid peeling for management of acne scarring: A split-face clinical and histologic comparison. J Cosmet Dermatol. 2018 Feb;17(1):73-83. doi: 10.1111/jocd.12459. Epub 2017 Dec 10. PMID: 29226630. https://pubmed.ncbi.nlm.nih.gov/29226630/
  8. Bickers DR, Lim HW, Margolis D, Weinstock MA, Goodman C, Faulkner E et al. The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology Association and the Society for Investigative Dermatology. Journal of the American Academy of Dermatology 2006;55:490-500. https://pubmed.ncbi.nlm.nih.gov/16908356/
  9. Yazici K, Baz K, Yazici AE, Köktürk A, Tot S, Demirseren D, Buturak V. Disease-specific quality of life is associated with anxiety and depression in patients with acne. J Eur Acad Dermatol Venereol. 2004 Jul;18(4):435-9. doi: 10.1111/j.1468-3083.2004.00946.x. PMID: 15196157. https://pubmed.ncbi.nlm.nih.gov/15196157/
  10. Hashim PW, Levy Z, Cohen JL, Goldenberg G. Microneedling therapy with and without platelet-rich plasma. Cutis. 2017 Apr;99(4):239-242. PMID: 28492598. https://pubmed.ncbi.nlm.nih.gov/28492598/

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

 

My patient complains of severe facial scarring from childhood acne that is not improving. How should I advise her?

My 19-year-old patient wishes treatment for his chronic acne while waiting for his dermatology appointment. What treatment should I recommend?

FA Manian MD, MPH, , , , , , , , , , , , , Leave a comment

Irrespective of your patient’s acne severity, a good starting point is over-the-counter topical benzoyl peroxide.1 Benzoyl peroxide not only kills the bacteria that causes acne (Cutibacterium acnes) through the release of free oxygen radicals, but also functions as a comedolytic.2

If your patient’s acne is mild to moderate (defined as non-inflammatory lesions [comedones] or less than 5 inflammatory lesions [papulopustules]), you may consider prescribing a topical retinoid such as tretinoin 0.025%, adapalene 0.1%, or tazarotene 0.05% in combination with the benzoyl peroxide.1,3 These agents have been shown to have both comedolytic and anti-inflammatory effects, and are the cornerstone of topical therapy for all acne cases, save for the most mild.1,4

In moderate to severe acne (defined as multiple inflammatory lesions), you can consider prescribing an oral antibiotic in combination with the retinoid and benzoyl peroxide.1,3 The first-line therapy in this situation is often a tetracycline, such as daily doxycycline in the 1.7 to 2.4 mg/kg dose range.5,6 

As with all medications, please familiarize yourself with contraindications and adverse side effects of these drugs before prescribing (eg, doxycycline-related photosensitivity or adverse impact on GI flora, or avoiding tretinoin in pregnancy).

For extremely severe acne (defined as widespread inflammatory lesions, nodules, and/or scarring), you should consider referral to a dermatologist for Accutane (isotretinoin) treatment.3 However, the aforementioned treatment options should be sufficient to control your patient’s symptoms until seen by a dermatologist!           

Bonus Pearl: Did you know that besides anabolic-androgenic steroids, dietary supplements containing vitamins B6/B12, iodine and whey have also been linked to acne?7

Contributed by Aditya Nellore, Fourth-Year Medical Student, St. Louis University Medical School, St. Louis, Missouri   

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References:

  1. Zaenglein AL, Pathy AL, Schlosser BJ, Alikhan A, Baldwin HE, Berson DS, Bowe WP, Graber EM, Harper JC, Kang S, Keri JE, Leyden JJ, Reynolds RV, Silverberg NB, Stein Gold LF, Tollefson MM, Weiss JS, Dolan NC, Sagan AA, Stern M, Boyer KM, Bhushan R. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol. 2016 May;74(5):945-73.e33. doi: 10.1016/j.jaad.2015.12.037. Epub 2016 Feb 17. Erratum in: J Am Acad Dermatol. 2020 Jun;82(6):1576. PMID: 26897386. https://www.jaad.org/article/S0190-9622(15)02614-6/fulltext#tbl6
  2. Cunliffe WJ, Holland KT. The effect of benzoyl peroxide on acne. Acta Derm Venereol. 1981;61(3):267-9. PMID: 6167116. https://pubmed.ncbi.nlm.nih.gov/6167116/
  3. Purdy S, Deberker D. Acne vulgaris. BMJ Clin Evid. 2008 May 15;2008:1714. PMID: 19450306; PMCID: PMC2907987. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907987/
  4. Cunliffe WJ, Caputo R, Dreno B, Förström L, Heenen M, Orfanos CE, Privat Y, Robledo Aguilar A, Meynadier J, Alirezai M, Jablonska S, Shalita A, Weiss JS, Chalker DK, Ellis CN, Greenspan A, Katz HI, Kantor I, Millikan LE, Swinehart JM, Swinyer L, Whitmore C, Czernielewski J, Verschoore M. Clinical efficacy and safety comparison of adapalene gel and tretinoin gel in the treatment of acne vulgaris: Europe and U.S. multicenter trials. J Am Acad Dermatol. 1997 Jun;36(6 Pt 2):S126-34. doi: 10.1016/s0190-9622(97)70056-2. PMID: 9204091. https://pubmed.ncbi.nlm.nih.gov/9204091/
  5. Tan J, Humphrey S, Vender R, Barankin B, Gooderham M, Kerrouche N, Audibert F, Lynde C; POWER study group. A treatment for severe nodular acne: a randomized investigator-blinded, controlled, noninferiority trial comparing fixed-dose adapalene/benzoyl peroxide plus doxycycline vs. oral isotretinoin. Br J Dermatol. 2014 Dec;171(6):1508-16. doi: 10.1111/bjd.13191. Epub 2014 Oct 28. PMID: 24934963. https://pubmed.ncbi.nlm.nih.gov/24934963/
  6. Leyden, James J., et al. “A randomized, phase 2, dose-ranging study in the treatment of moderate to severe inflammatory facial acne vulgaris with doxycycline calcium.” Journal of Drugs in Dermatology: JDD6 (2013): 658-663. https://pubmed.ncbi.nlm.nih.gov/23839182/
  7. Zamil DH, Perez-Sanchez A, Katta R. Acne related to dietary supplements. Dermatol Online J. 2020 Aug 15;26(8):13030/qt9rp7t2p2. PMID: 32941710. https://pubmed.ncbi.nlm.nih.gov/32941710/

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My 19-year-old patient wishes treatment for his chronic acne while waiting for his dermatology appointment. What treatment should I recommend?

My patient with history of intravenous drug use has noticed excessive growth of thick hair at the site of a previous abscess on her arm. Is there a connection between skin and soft tissue infections and localized hypertrichosis?

FA Manian MD, MPH, , , , , , , , , , Leave a comment

Localized hypertrichosis after infectious rash or “HAIR”, has been reported following a variety of skin and soft tissue infections (SSTIs), including sites of previous septic thrombophlebitis, cellulitis and olecranon bursitis. 1,2  A similar phenomenon has also been described in infants with recent chicken pox, as well non-infectious skin conditions arising from repeated irritation, friction, burns, excoriated insect bites, and fractures with cast application.1,2

Although heat and hyperemia have been implicated as growth stimulants for the hair follicle, 3 the exact mechanism of this intriguing phenomenon is unclear. It is possible that the sustained inflammatory process associated with chronic or more severe SSTIs leads to protracted stimulation of certain growth receptors in the human hair follicles (eg, transient vanilloid receptor-1) through heat and inflammation, as observed in mice in vivo.4

Aside from its possibly undesirable esthetic effects, localized HAIR appears to have no adverse health consequences, is reversible, and should require no further evaluation.

Note: 2 of the publications cited were written by the author of this post.

References

  1. Manian, FA. Localized hypertrichosis after infectious rash in adults. JAAD Case Reports 2015; 1:106-7. https://www.jaadcasereports.org/article/S2352-5126(15)00051-X/pdf
  2. Manian, FA. Localized hypertrichosis after infectious rash (“HAIR”) in adults: a report of 5 cases. Open Forum Infect Dis 2014;1 (Suppl 1):S195-S195. http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC5782143&blobtype=pdf
  3. Leung AK, Kiefer GN. Localized acquired hypertrichosis associated with fracture and cast application. J Natl Med Assoc 1989;81:65-7. https://www.ncbi.nlm.nih.gov/pubmed/2724357
  4. Bodo E, Biro T, Telek A, et al. A hot new twist to hair biology; involvement of vanilloid receptor-1 (VR1/TRPV1) signaling in human hair growth control. Am J Pathol 1005;166:985-8. https://www.sciencedirect.com/science/article/pii/S0002944010623206

 

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My patient with history of intravenous drug use has noticed excessive growth of thick hair at the site of a previous abscess on her arm. Is there a connection between skin and soft tissue infections and localized hypertrichosis?

My elderly patient on chronic warfarin with recent hospitalization for soft tissue infection is now readmitted with gastrointestinal bleed and a newly-discovered supra-therapeutic INR? Why did her INR jump?

FA Manian MD, MPH, , , , , , , , , , , , , , , , , , , , Leave a comment

Assuming no recent changes in the dose of warfarin, one potential culprit may be her recent antibiotic exposure. Of the long list of antibiotics associated with elevated INR, quinolones (e.g. ciprofloxacin, levofloxacin), trimethoprim-sulfamethoxazole, macrolides (e.g. azithromycin), and azole antifungals (e.g. fluconazole) are generally thought to carry the highest risk of warfarin toxicity, while amoxacillin and cephalexin may be associated with a more modest risk. 1-3

Other drugs such as amiodarone (Did she have atrial fibrillation during her recent hospitalization?), acetaminophen (Has she been receiving at least 2 g/day for several consecutive days?), and increasing dose of levothyroxine (Was she thought to be hypothyroid recently?) should also be considered.3,4

Also remember to ask about herbal supplements (eg, boldo-fenugreek, dong quai, danshen) that may potentiate the effect of warfarin. 3 Of course, poor nutrition in the setting of recent illness might have also played a role.5

As far as the mechanisms for drug interaction with warfarin, some drugs act as cytochrome p450 inhibitors (thus reducing the metabolism of warfarin), while others influence the pharmacodynamics of warfarin by inhibiting the synthesis or increasing the clearance of vitamin K-2 dependent coagulation factors.3

Antibiotics may increase the risk of major bleeding through disruption of intestinal flora that synthesize vitamin K-2 with or without interference with the metabolism of warfarin through cytochrome p450 isozymes inhibition.

Check out a related pearl on P4P: https://pearls4peers.com/2015/06/25/is-there-anyway-to-predict-a-significant-rise-in-inr-from-antibiotic-use-in-patients-who-are-also-on-warfarin  

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References

  1. Baillargeon J, Holmes HM, Lin Y, et al. Concurrent use of warfarin and antibiotics and the risk of bleeding in older adults. Am J Med. 2012 February ; 125(2): 183–189. https://www.ncbi.nlm.nih.gov/pubmed/22269622
  2. Juurlink DN. Drug interactions with warfarin: what every physician should know. CMAJ, 2007;177: 369-371. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1942100/pdf/20070814s00018p369.pdf
  3. Ageno W, Gallus AS, Wittkowsky A, et al. Oral anticoagulant therapy: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e44S-e88S. doi:10.1378/chest.11-2292.  https://www.ncbi.nlm.nih.gov/pubmed/22315269
  4. Hughes GJ, Patel PN, Saxena N. Effect of acetaminophen on international normalized ratio in patients receiving warfarin therapy. Pharmacotherapy 2011;31:591-7. https://www.ncbi.nlm.nih.gov/pubmed/21923443
  5. Kumar S, Gupta D, Rau SS. Supratherapeutic international normalized ratio: an indicator of chronic malnutrition due to severely debilitating gastrointestinal disease. Clin Pract. 2011;1:e21. doi:10.4081/cp.2011.e21. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3981245

 

Contributed by Rachel Weitzman, Medical Student, Harvard Medical School, Boston, MA.

My elderly patient on chronic warfarin with recent hospitalization for soft tissue infection is now readmitted with gastrointestinal bleed and a newly-discovered supra-therapeutic INR? Why did her INR jump?

My patient has a sacral decubitus ulcer that can be probed to the bone. Should I assume she has osteomyelitis?

FA Manian MD, MPH, , Leave a comment

When dealing with pressure sores, there is no definitive way of making a diagnosis of osteomyelitis short of a biopsy of the involved bone1. 

In fact, only about a third of stage IV pressure ulcers (those extending to the bone) may be associated with osteomyelitis2. In a study of pressure sores related to spinal cord injury or cerebrovascular accident, the clinical judgement of physicians with respect to the presence of osteomyelitis was accurate in only 56% of patients.  Only 3 of 21 patients with exposed bone had a diagnosis of osteomyelitis confirmed on biopsy3.

The “Probe to the Bone” bedside procedure has been studied primarily in diabetic foot infections with a recent systematic review reporting pooled sensitivity and specificity of 0.87 (95% confidence interval [CI], .75-.93) and 0.83 (95% CI, .65-.93), respectively4. Its performance in non-diabetic patients or those without a foot infection needs further study.

So in our patient, we should not assume a diagnosis of osteomyelitis; a bone biopsy is necessary for a definitive diagnosis.

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References

  1. Larson DL, Gilstrap J, Simonelic K, et al. Is there a simple, definitive, and cost-effective way to diagnose osteomyelitis in the pressure ulcer patient? Plast Reconstr Surg 2011; 127:67.  https://www.ncbi.nlm.nih.gov/pubmed/21285771
  2. Bodavula P, Liang SY, Wu J et al. Pressure ulcer-related pelvic osteomyelitis: a neglected disease? Open Forum Infect Dis 2015. DOI:10.1093/ofid/ofv112. https://www.ncbi.nlm.nih.gov/pubmed/26322317
  3. Darouiche RO, Landon GC, Klima M et al. Osteomyelitis associated with pressure sores. Arch Intern Med 1994;154:753-58. https://www.ncbi.nlm.nih.gov/pubmed/8147679
  4. Lam K, van Asten SA, Nguyen T, et al. Diagnostic accuracy of probe to bone to detect osteomyelitis in the diabetic foot: a systematic review. Clin Infect Dis 2016;63:944-8. https://www.ncbi.nlm.nih.gov/pubmed/27369321
My patient has a sacral decubitus ulcer that can be probed to the bone. Should I assume she has osteomyelitis?

Is clindamycin an acceptable empiric monotherapy for Staphylococcus aureus (SA) infections in adults?

FA Manian MD, MPH, , Leave a comment

Clindamycin is active in-vitro against many strains of SA and is indicated in the treatment of SA mild-to-moderate skin and soft tissue infections (SSTIs), including some methicillin-resistant strains 1,2.  However, evidence for its use as monotherapy against SA infections in other body sites is limited or lacking.   For example, in adults with pneumonia, efficacy of clindamycin is based solely on case series that excluded monotherapy3.  For bone and joint infections, clindamycin has limited evidence of efficacy in adults, and is not recommended in the treatment of endovascular or central nervous system infections2.

 Emergence of resistance to clindamycin in previously susceptible SA isolates may also occur during therapy conferred by erythromycin resistance methylase (erm) gene which is typically screened for by the “D-zone” test2 (Figure).  Increasing resistance of SA to clindamycin has led to recommendation against its empiric use for severe or complicated SSTIs (e.g. large abscess or deep infections)4.  

dzoneclindapcrop

Fig. The “E” disk (on left) contains erythromycin; “CC” disk (on right) contains clindamycin. The test detects inducible clindamycin resistance in erythromycin-resistant , clindamycin- susceptible isolates (http://www.cdc.gov/groupbstrep/images/lab-positivegbs-lg.jpg).

References:

  1. Miller LG, Daum RS, Creech CB, Young D, Downing MD, Eells SJ, Pettibone S, Hoagland RJ, Chambers HF. Clindamycin versus trimethoprim–sulfamethoxazole for uncomplicated skin infections. N Engl J Med 2015;372:1093-103. 
  2. Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, Rybak MJ. 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 2011;52:e18-55. 
  3. Lobo LJ, Reed KD, Wunderink RG. Expanded clinical presentation of community-acquired methicillin-resistant Staphylococcus aureus pneumonia. Chest 2010; 138:130-6. 
  4. VanEperen AS, Segreti J. Empirical therapy in Methicillin-resistant Staphylococcus Aureus infections: An Up-To-Date approach. J Infect Chemother 2016;22:351-9.

Contributed by Nathan T. Georgette, 4th year, Harvard Medical School student

 

Is clindamycin an acceptable empiric monotherapy for Staphylococcus aureus (SA) infections in adults?

Should we routinely use broad spectrum empiric antibiotic therapy in our diabetic patients with cellulitis of the lower extremities?

FA Manian MD, MPH, , Leave a comment

The short answer is “No”!

The myth that diabetics with acute bacterial skin and skin structure infections should be routinely placed on antibiotics against gram-positives as well as gram-negatives and/or anaerobes probably originates from the extrapolation of data revolving around the frequent polymicrobial nature of diabetic foot infections.  These infections often originate from chronic ulcers and are complicated by deep tissue infection or gangrene (1), which is often not the case in our diabetic patients with cellulitis alone.  

In a recent study of the microbiology of cellulitis or cutaneous abscess in hospitalized patients, Staphylococcus and Streptococcus sp. accounted for 90% of cultured organisms in  diabetic patients, not significantly different than that of non-diabetics (1).

These finding support national guidelines which do not recommend routine use of broader spectrum antibiotics in diabetics with cellulitis or cutaneous abscess (2).  

References

1. Jenkins TC, Knepper BC, Moore SJ, et al. Comparison of the microbiology and antibiotic treatment among diabetic and nondiabetic patients hospitalized for cellulitis or cutaneous abscess. J Hosp Med 2014;9:788-794. https://www.ncbi.nlm.nih.gov/pubmed/25266293

2. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections. Clin Infect Dis 2014;59:e10-e52. https://www.ncbi.nlm.nih.gov/pubmed/24973422

Should we routinely use broad spectrum empiric antibiotic therapy in our diabetic patients with cellulitis of the lower extremities?

Is there any utility in screening for methicillin-resistant Staphylococcus aureus (MRSA) colonization when selecting empiric antibiotic therapy for skin and soft tissue infections (SSTIs)?

FA Manian MD, MPH, , Leave a comment

The reported rates of MRSA colonization in patients with community-associated MRSA SSTI have been surprisingly low, ranging from 7% to 41% (55% among hospitalized patients) (1), making it difficult to exclude MRSA as a causative pathogen based on a negative screening test alone.

The concordance between what grows from the nares and what is isolated from the SSTI site is also far from ideal.  Among patients with methicillin-sensitive S. aureus (MSSA) SSTI , 12% may be colonized with MRSA and of those with MRSA SSTI, 32% may be colonized with MSSA (1). 

In the absence of a reliable screening test to help us select an empiric antibiotic regimen in patients with SSTI, we should pay special attention to the clinical features of the SSTI.  Empiric MRSA antibiotic coverage should be considered for patients with purulent SSTIs, deep tissue infections, or those with systemic toxicity( 2), irrespective of colonization status.  

References

1. Ellis MW, Schlett CD, Millar EV, et al. Prevalence of nasal colonization and strain concordance in patients with community-associated Staphylococcus aureus skin and soft tissue infections. Infect Control Hosp Epidemiol 2014;35:1251-6. https://www.ncbi.nlm.nih.gov/pubmed/25203178  

2. Liu C, Bayer A, Cosgrove SE, et al. 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 2011;52:e18-55.2. https://www.ncbi.nlm.nih.gov/pubmed/21208910 

 

Is there any utility in screening for methicillin-resistant Staphylococcus aureus (MRSA) colonization when selecting empiric antibiotic therapy for skin and soft tissue infections (SSTIs)?

Should we routinely cover for methicillin-resistant Staphylococcus aureus (MRSA) when treating patients for cellulitis?

FA Manian MD, MPH, , , Leave a comment

No! Despite the MRSA epidemic, β-hemolytic streptococci (BHS) are still considered the primary cause of non-purulent cellulitis (e.g. without abscesses, or infections involving deep soft tissues, wounds, or ulcer).

In a prospective study of patients admitted to the hospital for “diffuse,  non-culturable “(i.e. many of our patients), most had serological evidence of acute  BHS, and >95% responded to a β-lactam antibiotic treatment (1) . 

The current Infectious Diseases Society of America guidelines do not endorse empiric coverage of  MRSA for non-purulent cellulitis,  unless there is systemic toxicity or poor response to  β-lactam  monotherapy (2). More specifically, the guidelines recommend a  β-lactam antibiotic for treatment of non-purulent cellulitis in hospitalized patients with modification to MRSA coverage if no clinical response.

One advantage to β-lactam monotherapy is the ease of switch to an equivalent oral antibiotic (e.g. cephalexin) when transitioning from parenteral antibiotic therapy.  

References

1. Jeng A, Beheshti M, Li J, et al. The role of beta-hemolytic streptococci in causing diffuse nonculturable cellulitis: a prospective investigation. Medicine (Baltimore) 2010;89:217-26. https://www.ncbi.nlm.nih.gov/pubmed/20616661

2. Liu C, Bayer A, Cosgrove SE, et al. 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 2011;52:e18-55. https://www.ncbi.nlm.nih.gov/pubmed/21208910

 

Should we routinely cover for methicillin-resistant Staphylococcus aureus (MRSA) when treating patients for cellulitis?