BEST PRACTICES FOR THE MANAGEMENT OF SKIN AND SOFT TISSUE INFECTIONS
Faculty:
L. Austin Fredrickson, MD, FACP
L. Austin Fredrickson is an Associate Professor of Internal Medicine at Northeast Ohio Medical University, where he serves as core faculty and teaches diagnostics, therapeutics, clinical skills, and health humanities. He is board-certified in general internal medicine and practices rural primary care.
Liz Fredrickson, PharmD, BCPS
Liz Fredrickson, PharmD, BCPS, is an Associate Professor of Pharmacy Practice and Pharmaceutical Sciences at the Northeast Ohio Medical University (NEOMED) College of Pharmacy, where she is course director of the Parenteral Products and Basic Pharmaceutics Lab courses.
Pamela Sardo, PharmD, BS
Pamela Sardo, PharmD, BS, is a freelance medical writer and licensed pharmacist. She is the founder and principal at Sardo Solutions in Texas. Pam received her BS from the University of Connecticut and her PharmD from the University of Rhode Island. Pam’s career spans many years in retail, clinics, hospitals, long-term care, Veterans Affairs, and managed health care responsibilities across a broad range of therapeutic classes and disease states.
Abstract
Skin and soft tissue infections (SSTIs) pose significant challenges for patients in community and hospital settings. The effective management of SSTIs requires a strong understanding of their associated risk factors and pathophysiology, as well as knowledge of diagnosis and management strategies. Pharmacy team members play crucial roles in preventing and managing SSTIs via interprofessional collaboration with healthcare teams and providing patient and caregiver education. This continuing education presentation will discuss common risk factors for SSTIs, as well as the related pathophysiology, etiology, and epidemiology. Additionally, this program will review SSTI classification and management strategies.
Accreditation Statements
In support of improving patient care, RxCe.com LLC is jointly accredited by the Accreditation CouncilTM for Continuing Medical Education (ACCME®), the Accreditation Council for Pharmacy Education (ACPE®), and the American Nurses Credentialing Center (ANCC®), to provide continuing education for the healthcare team.
Joint Universal Activity Number: The Joint Accreditation Universal Activity Numbers assigned to this activity are as follows:
Pharmacists: JA4008424-0000-26-091-H01-P
Pharmacy Technicians: JA4008424-0000-26-091-H01-T
Credits: 2 contact hour(s) (0.2 CEU(s)) of continuing education credit.
Credit Types:
Pharmacy - 2 Credits
Type of Activity: Knowledge
Media: Computer-Based Training (i.e., online courses)
Estimated time to complete activity: 2 contact hour(s) (0.2 CEU(s)), including Course Test and course evaluation
Release Date: June 16, 2026 Expiration Date: June 27, 2027
Target Audience: This educational activity is for Pharmacists and Pharmacy Technicians
How to Earn Credit: From June 16, 2026, through June 27, 2027, participants must:
Read the “learning objectives” and “author and planning team disclosures;”
Take the “Educational Activity Pre-Test;”
Study the section entitled “Educational Activity;” and
Complete the Educational Activity Post-Test and Activity Evaluation. The Educational Activity Post-Test will be graded automatically. Following successful completion of the Educational Activity Post-Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)
CE Credits: Credits for this course will be uploaded to CPE Monitor® for pharmacists and pharmacy technicians.
Statement of Need
The management of skin and soft tissue infections requires a strong understanding of their associated risk factors and pathophysiology, as well as knowledge pertaining to diagnosis and effective management strategies. An understanding of common risk factors for SSTIs, as well as the related pathophysiology, etiology, and epidemiology, is necessary for effective management strategies.
Learning Objectives: Upon completion of this educational activity, participants should be able to:
Describe risk factors for the development of skin and soft tissue infections (SSTIs)
Classify SSTIs based on their severity, need for therapeutic intervention, and the presence of comorbidities
Describe treatment strategies for SSTIs
Compare and Contrast antibiotics utilized in the management of SSTIs in terms of mechanism of action, dosing, and side effects
Disclosures
The following individuals were involved in planning, developing, and/or authoring this activity: L. Austin Fredrickson, MD, FACP; and Pamela Sardo, PharmD, BS. None of the individuals involved in developing this activity has any conflicts of interest or financial relationships related to the subject matter. There are no financial relationships or commercial or financial support relevant to this activity to report or disclose by RxCe.com or any of the individuals involved in the development of this activity.
© RxCe.com LLC 2026: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.
Educational Activity Pre-Test
Of the following, which is the most significant risk factor for developing community-acquired methicillin-resistant S. aureus (MRSA) infections?
Being age 65 years or older
Having lymphedema
A recent exposure to the beach
Being a healthcare professional
Which of the following is a potential treatment option for a patient with folliculitis?
Clindamycin, applied topically twice daily
Cephalexin 500 mg given every 6-12 hours
Vancomycin 15 mg/kg IV Q8H
Amoxicillin 875 mg PO Q12H
Which of the following antibiotic combinations is recommended for confirmed type 3 (clostridial) necrotizing fasciitis?
Piperacillin/tazobactam + vancomycin
Penicillin + clindamycin
Linezolid + amoxicillin
Meropenem + ertapenem
Educational Activity
Best Practices for the Management of Skin and Soft Tissue Infections
Introduction
The management of skin and soft tissue infections requires a strong understanding of their associated risk factors and pathophysiology, as well as knowledge pertaining to diagnosis and effective management strategies. Pharmacy team members play crucial roles in preventing and managing SSTIs via interprofessional collaboration with healthcare teams and providing patient and caregiver education. This continuing education presentation will discuss common risk factors for SSTIs, as well as the related pathophysiology, etiology, and epidemiology. Additionally, this program will review the classification of SSTIs and management strategies in detail, focusing on folliculitis, furuncles and carbuncles, cellulitis, and necrotizing soft-tissue infections.
Classification of SSTIs
Skin and soft tissue infections (SSTIs) are a heterogeneous group of diseases that can pose significant challenges for patients in community and hospital settings.1 Although the incidence rate of SSTIs has remained stable, effective treatment of SSTIs can significantly reduce disease morbidity and the utilization of healthcare services.2
Skin and soft tissue infections are associated with important terminology (and abbreviations) with which pharmacy personnel should be familiar. These are defined in Table 1.2
Table 1
SSTI Terminology2-5
| Term | Abbreviation | Definition | Examples |
| Skin and soft tissue infections | SSTI | Infections of various etiology and severity that involve the skin, subcutaneous tissue, fascia, and muscle. | Cellulitis, impetigo, abscesses |
| complicated SSTIs | cSSTIs | Severe infections that involve deeper soft tissues and rapid progression | Complicated cellulitis, complex abscesses |
| Necrotizing soft tissue infections | NSTI | A severe form of SSTI characterized by rapidly progressing infection leading to necrosis. | Necrotizing cellulitis, Fourier’s gangrene |
| Acute bacterial skin and skin structure infections | ABSSI | A subset of SSTIs that encompasses more severe bacterial infection with a lesion size area of ≥75 cm2 | Cellulitis, erysipelas, major cutaneous abscess, wound infections |
Skin and soft tissue infections can be categorized as primary or secondary (Table 2).3 In the case of primary bacterial skin infections, areas of skin that were once healthy are infected by a single pathogen.3 Conversely, secondary skin infections involve infection of previously damaged skin and are typically caused by multiple bacteria (polymicrobial).3 SSTIs can also be classified as uncomplicated (simple) or complicated (necrotizing or non-necrotizing).3,6 Examples of simple infections include cellulitis, erysipelas, folliculitis, furuncles, and carbuncles.6 With complicated infections, deeper skin structures, such as fascia, are infected, and patients often require surgery.2 Examples include deep abscesses, decubitus ulcers, and necrotizing fasciitis.6 Patients with complicated infections are also commonly immunocompromised in some manner and may have conditions such as diabetes or human immunodeficiency virus (HIV).3
Table 2
Bacterial Classification of Skin and Soft-Tissue Infections3
| Primary Infections | |
| Erysipelas | Group A streptococci (Streptococcus pyogenes) |
| Impetigo | Staphylococcus aureus (including methicillin-resistant strains), group A streptococci |
| Lymphangitis | Group A streptococci; occasionally S. aureus |
| Cellulitis | Group A streptococci, S. aureus (potentially including methicillin-resistant strains); occasionally other gram-positive cocci, gram-negative bacilli, and/or anaerobes |
| Necrotizing fasciitis | |
| Type I | Anaerobes (Bacteroides spp., Peptostreptococcus spp.) and facultative bacteria (streptococci, Enterobacterales) |
| Type II | Group A streptococci |
| Type III | Clostridioides perfringens |
| Secondary Infections | |
| Diabetic foot infections | S. aureus, streptococci, Enterobacteriaceae, Bacteroides spp., Peptostreptococcus spp., Pseudomonas aeruginosa |
| Pressure sores | S. aureus, including methicillin-resistant strains, streptococci, Enterobacterales, Bacteroides spp., Peptostreptococcus spp., P. aeruginosa |
| Bite wounds | |
| Animal | Pasteurella spp., S. aureus, streptococci, Bacteroides spp. |
| Human | Eikenella corrodens, S. aureus, streptococci, Corynebacterium spp., Bacteroides spp., Peptostreptococcus spp. |
| Burn wounds | P. aeruginosa, Enterobacterales, S. aureus, streptococci |
Finally, these infections can be classified according to their severity, need for therapeutic intervention, and the presence of comorbidities. Table 3 details this classification system.
Table 3
Classification of SSTIs6
| Class | Description |
| 1 | Simple infection with no systemic signs or symptoms indicating spread and no uncontrolled comorbidities that could complicate treatment. Infection is amenable to outpatient management with either topical or oral antimicrobials |
| 2 | Infection with systemic signs or symptoms indicating spread or with stable comorbidities or infection without systemic spread but with uncontrolled comorbidities. May require either inpatient treatment with parenteral antibiotics |
| 3 | Infection with signs and symptoms of systemic spread or uncontrolled comorbidities. Inpatient treatment with parenteral antibiotics is required. |
| 4 | Infection with signs of potentially fatal sepsis that requires parenteral antibiotics. Inpatient management is required, and surgery may be indicated. |
Etiology and Epidemiology
Within the United States (US), SSTIs result in over 14 million outpatient visits and nearly 900,000 inpatient admissions annually.2,3 Over the last few decades, there has been a rise in the incidence and associated costs of cellulitis, which has an incidence of approximately 200 cases per 100,000-person years.2,7 Cellulitis tends to occur more frequently during warmer months in nontropical regions.7
Skin and soft tissue infections account for 3% to 30% of all emergency department (ED) visits.2 Approximately 12-40% of SSTI cases in the ED are admitted to the hospital, and 0.7% to the intensive care unit (ICU).2 Severe SSTIs with sepsis happen somewhat frequently and are estimated to be the cause of approximately 10% of all septic shock cases.2 Complicated SSTIs are the third most frequent cause of severe sepsis or septic shock, following pneumonia and abdominal infections.2
Current evidence indicates that the primary pathogens of SSTIs are Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA]) and Streptococcus pyogenes, along with other β-hemolytic streptococci.2,3 Cellulitis is most commonly caused by beta-hemolytic streptococci, including groups A, B, C, G, and F.7 S. aureus and S. pyogenes are the most common causes of simple, community-acquired SSTIs.6 Up to 30% of individuals may be colonized with S. aureus.3 Gram-negative bacteria are far less common; however, in some regions, they are increasingly reported as the cause of these infections, accounting for up to 30% of cases in certain studies.3 P. aeruginosa, enterococcus, and E. coli are common causes among hospitalized patients.6 Common microorganisms of normal skin are summarized in Table 4.3
Table 4
Common Microorganisms of Normal Skin3
Bacteria Gram-positive Coagulase-negative staphylococci Micrococci (Micrococcus luteus) Corynebacterium species (diphtheroids) Propionibacterium species Gram-negative Acinetobacter species Fungi Malassezia species Candida species |
Risk Factors of SSTIs
Numerous factors may increase patients' risk of developing an SSTI. Examples of predisposing factors include reduced tissue vascularity, increased peripheral fluid stasis, and a decreased ability to fight off infections. Often, a patient’s comorbidities help determine the bacterial cause of SSTIs.6 As an example, Pseudomonas aeruginosa is linked to intravenous drug use.6 Risk factor examples are presented in Table 5.
Table 5
Risk Factors for SSTIs
| Age (children,* older adults) | Human or animal bites | Peripheral arteriovenous insufficiency |
| Alcohol misuse+ | Immunocompromised | Peripheral neuropathy |
| Asplenia | Immunosenescence | Poor nutrition+ |
| Cardiopulmonary disease | Long-term care~ | Prolonged hospital stays~ |
| Debility | Long-term intravascular access~ | Sports participation+ |
| Diabetes mellitus~ | Lymphedema | Intravenous drug use |
| Health care professional* | Military personnel | Trauma (including surgery)+ |
| Hepatorenal disease | Obesity | Water exposure (hot tub) |
*Risk factor for community-acquired MRSA infection
+Predisposes patient to necrotizing fasciitis
~Risk factor for hospital-acquired methicillin-resistant S. aureus infection
Pathophysiology of SSTIs
Healthy skin is a primary defense mechanism against infections, serving as a barrier between humans and their environment.3 It supports a diverse microbiome of bacteria and fungi and several host factors that protect against infections.3 The continuous renewal of the epidermal layer leads to the shedding of skin bacteria, and sebaceous secretions are hydrolyzed to form free fatty acids, inhibiting bacterial growth.3 Additionally, the commensal skin microbiome prevents colonization by more pathogenic bacteria.3
Factors that can predispose a person to skin infections include the following:3
High concentrations of bacteria (more than 105 microorganisms)
Excessive moisture of the skin
Inadequate blood supply
Availability of bacterial nutrients
Damage to the corneal layer, allowing bacterial penetration
Although the skin and subcutaneous tissues are typically highly resistant to infections, under certain conditions, they can become vulnerable.3 Intact skin is the best defense against SSTIs, as most occur due to the disruption of normal host defenses through skin puncture, surgery, increased tissue tension secondary to fluid stasis, or underlying diseases such as diabetes.3,6 Skin and soft tissue infections can either initiate from a neighboring site or be due to embolic spread from a site further away.6
Clinical Presentation and Diagnosis
Patients with an SSTI may have either cellulitis or an abscess.7 Common signs and symptoms of SSTIs include erythema (redness), warmth, edema, and pain at the affected site.6 Patients may have systemic signs of infection as well, which is indicative of the severity and magnitude of the infection.6 Such signs include fever and other systemic manifestations.7
The diagnosis of SSTIs should begin with a thorough patient history to identify potential risk factors.6 The physical examination involves inspecting the affected area for signs of infection, including erythema, edema, tenderness, and the presence of any lesions or abscesses.6 Laboratory testing is not indicated for uncomplicated infections or for patients without complications or comorbidities.7 However, for patients with suspected severe infections, such as complete blood count (CBC) with differential, C-reactive protein (CRP), and kidney and liver function tests.6 Clinicians can use the Laboratory Risk Factor Indicator for Necrotizing Fasciitis to stratify patients into either low or high risk categories for necrotizing fasciitis.6 This scoring system utilizes the following lab values: C-reactive protein, creatinine, glucose, hemoglobin, sodium, and total white blood cells.6 A score of at least six is indicative of necrotizing fasciitis, while a score of eight or more is highly suggestive, with a positive predictive value of 93.4%.6
In healthy individuals (non-immunocompromised), blood cultures are generally not necessary, but they may be needed in patients presenting with severe infections or signs suggestive of systemic involvement.6 Older patients and those who are immunocompromised may also require blood cultures, in addition to those with animal bites, or failure of antibiotic therapy.6,7 Wound cultures are useful for immunocompromised patients, patients with significant cellulitis, lymphangitis, sepsis, infection from a human or animal bite, and those with recurrent, large abscesses.6
Imaging is typically not required for simple SSTIs. Magnetic resonance imaging (MRI) has 100% sensitivity for necrotizing fasciitis and 86% specificity.6 The use of ultrasound can assist with determining the extent and depth of an infection, with a sensitivity of 77.6% and specificity of 43.7% for the extent of infection.6
General Management of SSTIs
The general management of SSTIs involves determining the severity and location of the infection.6 A patient’s comorbidities also need to be taken into consideration.6 The initial strategy depends on whether there is purulence, the acuity of the infection, and the type of infection.6 Mild-to-moderate infections can be treated with topical antibiotics, such as mupirocin.6 Adults with mild-moderate infections and no suppuration can utilize beta-lactam antibiotics.6 If the SSTI is mildly purulent and there is no significant cellulitis, incision and drainage may be all that is required.6
Abscesses with extensive cellulitis or that are rapidly progressing or do not respond to drainage will require the use of antibiotics.6 If cellulitis is uncomplicated, the duration is five days.6 Treatment of severe infections requires inpatient management with initial use of broad-spectrum, intravenous antibiotics until pathogen-specific sensitivities have been obtained.6 Antibiotics should be continued for 7-14 days until the patient clinically improves and can tolerate oral intake.6
Folliculitis, Furuncles, and Carbuncles
Overview
Folliculitis is defined as inflammation of hair follicles that may be caused by infection, physical injury, or chemical irritation.3 This type of superficial infection involving pus occurs only in the epidermis.3
In contrast, furuncles and carbuncles occur when follicular infections extend to the subcutaneous area of the skin.3 Furuncles, in particular, are walled-off masses of purulent material arising from hair follicles, while carbuncles occur when furuncles merge to form a single inflamed area.3 The most common cause of these infections is S. aureus.3 The clinical presentation of these infections is presented in Table 6.
Table 6
Clinical Presentation of Folliculitis, Furuncles, and Carbuncles
| Condition | Clinical Presentation |
| Folliculitis | Clustering, pruritic papules localized to hair follicles. Generally, develop in areas subject to friction and perspiration. Papules are generally 5 mm or less in diameter and erythematous. Papules evolve into pustules, which generally rupture spontaneously within several days. Systemic signs (fever, malaise) are uncommon. |
| Furuncles | Inflammatory, draining nodule involving a hair follicle. Develop in areas subject to friction and perspiration. Lesions are discrete, whether occurring as singular or multiple nodules. Lesion starts as a firm, tender, red nodule that becomes painful and fluctuant. Lesions often drain spontaneously. Lesions caused by CA-MRSA often have necrotic centers Systemic signs are uncommon |
| Carbuncles | Formed when adjacent furuncles coalesce to form a single inflamed area Form broad, swollen, erythematous, deep, and painful follicular masses Commonly develops on the back of the neck Commonly associated with systemic signs (fever, chills, malaise) Bacteremia with secondary spread to other tissues is common |
Treatment
The main goals of treating skin infections are to relieve discomfort, stop the infection from spreading, and prevent it from coming back.3 Managing recurrent furunculosis is crucial because chronic cases are challenging to treat.3 Additionally, pharmacists can work with the care team to ensure treatments are effective, affordable, and have minimal side effects.3
Management recommendations include the following:3
Gram stain and culture of pus from carbuncles and abscesses are recommended, but treatment without cultures is reasonable in most patients
Carbuncles, abscesses, and large furuncles of mild severity should be treated with incision and drainage
Administration of antibiotics with activity against S. aureus as an adjunct to incision and drainage should be based on the presence or absence of systemic signs of infection
Antibiotics with activity against MRSA are recommended for patients with carbuncles or abscesses of higher severity who have failed initial antibiotic therapy, have severe systemic signs of infection, or are immunocompromised
Treating these infections involves using local care measures, such as warm, moist compresses.3 Topical therapies can be tried, including clindamycin, erythromycin, mupirocin, or benzoyl peroxide.3 These should be applied 2-4 times a day for one week.3 If furuncles are small, they can be treated with moist heat to encourage pus drainage, while larger furuncles and carbuncles may need to be incised and drained.3 More severe infections require antibiotic therapies. Options include trimethoprim-sulfamethoxazole, doxycycline, or minocycline for 5-10 days.3 These antibiotics will cover any potential MRSA.3 Oftentimes, these infections will resolve without the use of medical or surgical involvement.3 Patients who require but do not respond to systemic antibiotic therapies or have recurrent infections will need culture and sensitivity testing to guide further antibiotic therapies.3
Table 7
Treatment of Folliculitis
| Generic Name | Brand Name | Mechanism of Action | Dose | Adverse Effects |
| Mupirocin | Bactroban | Inhibits bacterial protein synthesis | Apply topically 2-3 times daily | Local irritation, rash |
| Clindamycin | Cleocin | Inhibits bacterial protein synthesis | Apply topically twice daily | Dryness, redness, burning |
Table 8
Treatment of Furuncles and Carbuncles
| Generic Name | Brand Name | Mechanism of Action | Dose | Adverse Effects |
| Dicloxacillin | Dynapen | Inhibits bacterial cell wall synthesis | 250-500 mg orally every 6 hours | Nausea, vomiting, diarrhea |
| Cephalexin | Keflex | Inhibits bacterial cell wall synthesis | 500 mg orally every 6-12 hours | Diarrhea, nausea, allergic reactions |
| Trimethoprim-sulfamethoxazole | Bactrim, Septra | Inhibits folic acid synthesis (two mechanisms) | 1-2 tablets (800 mg/160 mg) orally twice daily | Rash, nausea, hyperkalemia |
Cellulitis
Overview
Cellulitis is a serious SSTI that begins in the epidermis and dermis and may spread to the superficial fascia, potentially spreading to the bloodstream.3 The most common bacterial causes include S. aureus and S. pyogenes; however, many different bacteria can be potential culprits.3 There has been a specific increase in the number of MRSA infections in both community and hospital settings.3 Depending on the patient’s comorbidities and risk factors, several other types of bacteria may be causal. Injection drug users may have cellulitis that is polymicrobial and caused by S. aureus, including MRSA, and/or anaerobic bacteria.3 Individuals with diabetes mellitus are also prone to polymicrobial infections.3 These can occur post-surgery or in areas with vascular insufficiency.3 Cellulitis tends to develop over the course of a few days.7 The clinical presentation of cellulitis is detailed in Table 9.
Table 9
Clinical Presentation of Cellulitis3
| General | Symptoms | Signs |
| A history of an antecedent wound from minor trauma, abrasion, ulcer, or surgery is often present | -Patients often experience fever, chills, or malaise and complain that the affected area feels hot and painful. -Systemic findings such as hypotension, dehydration, and altered mental status are common. | -Characterized by erythema and edema of the skin. -Lesions are non-elevated and have poorly defined margins. -Affected areas are warm to the touch. -Inflammation is present with little or no necrosis or suppuration of soft tissue. -Lesions may be associated with purulent drainage, exudates, and/or abscesses. -Tender lymphadenopathy associated with lymphatic involvement is common. |
Treatment
Treatment goals for patients with acute bacterial cellulitis include quickly eradicating the infection and preventing further complications.3 The management of cellulitis involves decreasing swelling by elevating and immobilizing the affected area.3 Cool, sterile saline dressings can help decrease pain and swelling initially, and this can be followed by moist heat after one to three days.3 Uncomplicated cellulitis rarely requires surgical intervention, which may be essential for more severe cases.3 Antimicrobial therapy is guided by the type of bacteria identified or suspected, with particular attention to resistant pathogens like MRSA, Gram-negative bacteria, and anaerobes.3 In particular, clinicians should consider whether coverage is needed for MRSA or atypical bacteria.7 Empiric antibiotics should always cover MSSA and beta-hemolytic streptococci.7 Conditions that warrant MRSA coverage include systemic signs of toxicity (e.g., fever >100.5°F/38°C, hypotension, sustained tachycardia), cellulitis with purulent wound drainage, known MRSA colonization or infection, injection drug use, and high-risk neutropenia.7
Cellulitis can be categorized as purulent or non-purulent to determine treatment strategies.3 Purulent infections are associated with purulent drainage without a simple, drainable abscess.3 Per the IDSA, purulent cellulitis often requires incision and drainage, and systemic antibiotics may be unnecessary for mild cases.3 Oral antibiotics such as trimethoprim-sulfamethoxazole and doxycycline are recommended for moderate to severe purulent cellulitis, with linezolid or tedizolid as alternatives, though linezolid is more expensive.3 Severe purulent cellulitis, characterized by systemic infection signs or immunocompromised status, requires hospitalization and parenteral antibiotics such as vancomycin, daptomycin, linezolid or tedizolid, telavancin or ceftaroline.3 Antibiotics like dalbavancin and oritavancin—both glycopeptide drugs— have indications for treating complicated SSTI, but are costly and best used for specific cases.3 Delafloxacin, a fluoroquinolone, and certain carbapenems may be options for severe polymicrobial infections, though their roles are not well-defined.3 Treatment duration typically ranges from 5 to 14 days, which depends on the infection's severity and patient response.3
Non-purulent cellulitis, which lacks drainage or an abscess, is typically treated with oral β-lactams, such as penicillin VK or cephalexin, for mild cases.3 Severe non-purulent cellulitis may require hospitalization and a combination of antibiotics effective against MRSA and streptococci.3 Treatment of cellulitis is summarized in Table 10, and doses are provided in Table 11.
Table 10
Treatment Strategies for Cellulitis
| Category | Recommended Antibiotics | Alternative Antibiotic Therapies |
| Cellulitis with no abscess present in an immunocompetent patient | Dicloxacillin, cephalexin, cefadroxil | If severe beta-lactam allergy: trimethoprim-sulfamethoxazole, linezolid, clindamycin |
| Indication for MRSA coverage | Trimethoprim-sulfamethoxazole, amoxicillin + doxycycline, linezolid, clindamycin | |
| Concerning conditions (i.e., toxic shock syndrome, necrotizing infection, wound or injury) without severe sepsis but indication for parenteral antibiotics (systemic toxicity, rapid erythema progression, inability to tolerate oral therapy) + no MRSA coverage needed | Cefazolin, nafcillin, oxacillin, flucloxacillin | Severe beta-lactam allergy: vancomycin |
| Concerning conditions (i.e., toxic shock syndrome, necrotizing infection, wound or injury) without severe sepsis but indication for parenteral antibiotics (systemic toxicity, rapid erythema progression, inability to tolerate oral therapy) + MRSA coverage needed | Vancomycin, daptomycin | |
| Concerning conditions (i.e., toxic shock syndrome, necrotizing infection, wound or injury) with severe sepsis | Vancomycin or daptomycin + one of the following: cefepime or meropenem |
Table 11
Antibiotic Dosing for Cellulitis
| Oral Antibiotics | Parenteral Antibiotics |
| Amoxicillin 875 mg Q12H | Cefazolin 1-2 g Q8H |
| Cefadroxil 500 mg Q12H or 1 g daily | Cefepime 2 g Q8H |
| Cephalexin 500 mg Q6H | Daptomycin 4-6 mg/kg Q24H |
| Clindamycin 450 mg Q8H | Flucloxacillin 2 g Q6H |
| Dicloxacillin 500 mg Q6H | Meropenem 1 g Q8H |
| Flucloxacillin 500-1000 mg Q6H | Nafcillin 1-2 g Q4H |
| Linezolid 600 mg Q12H | Oxacillin 1-2 g Q4H |
| Trimethoprim-sulfamethoxazole 1-2 double-strength tablets BID | Vancomycin 20-35 mg/kg one-time loading dose, then 15-20 mg/kg IV Q8H (adjust via blood levels) |
In terms of follow-up, clinicians should thoroughly evaluate culture and sensitivity results to identify resistant organisms.3 High-quality additional samples may be needed for thorough microbiologic analysis. If there is no response to therapy, it might indicate an underlying local or systemic issue or a possible misdiagnosis.3
Pharmacists can assist with tailoring the appropriate selection and duration of antibiotics to individual patient needs with the goal of effectively treating the infection while minimizing resistance and adverse effects.3 Pharmacists can also assist the care team with avoiding the use of unnecessary antibiotics, thereby reducing antibiotic resistance and side effects, and keeping the cost of therapy low for the patient.3
Necrotizing Soft Tissue Infections
Overview
Necrotizing soft-tissue infections are extremely severe and are characterized by high morbidity and mortality.3 They require early surgical debridement along with appropriate antibiotics and supportive care.3 The epidermis, dermis, subcutaneous tissue, fascia, and muscle all may be involved.8,9 These infections include necrotizing forms of fasciitis, cellulitis, and myositis.10 They are classified based on predisposing conditions, symptom onset, pain, skin appearance, etiologic agents, gas production, muscle involvement, and systemic toxicity.3,8,9 The major clinical NSTIs include necrotizing fasciitis and clostridial myonecrosis, or gas gangrene.3
Necrotizing fasciitis is a rare and severe infection of the subcutaneous tissue.3 It is caused by aerobic and/or anaerobic bacteria, which progressively destroy superficial fascia and subcutaneous fat.3 Because muscle tissue has a sufficient blood supply, it is typically not infected.9 Type I necrotizing fasciitis typically follows trauma or surgery and is polymicrobial in nature, involving a mixture of anaerobes (i.e., Bacteroides, Clostridium, Peptostreptococcus) and facultative bacteria (i.e., E. Coli, enterococci).3 This type is more common among injection drug users.3 It tends to spread slower than Type II, which is caused by virulent strains of S. pyogenes and is often referred to as streptococcal gangrene or “flesh-eating bacteria.”3 Type II infections are monomicrobial and progress rapidly, with extensive tissue necrosis, severe pain, systemic toxicity, and a high risk of shock and organ failure.3,8,9 They are typically caused by group A streptococci or another beta-hemolytic streptococcus, but may be caused by S. aureus.11 Critical risk factors for Type 1 infections include diabetes, particularly those with peripheral vascular disease.8,10 Type 2 necrotizing fasciitis may occur in individuals of any age, even those without comorbidities.12 Clostridial myonecrosis, or type III necrotizing fasciitis, involves skeletal muscle.3 Known as gas gangrene, it is characterized by gas production and muscle necrosis, advancing rapidly within hours.3 Most cases occur post-surgery or trauma, with Clostridium perfringens being the most common causative agent.3
Table 12
Clinical Presentation of Necrotizing Fasciitis
| General | Symptoms | Signs |
|
|
|
|
|
|
|
|
|
|
Table 13
Features Associated with Necrotizing Skin Infections
| Clinical characteristics | Laboratory parameters |
| Rapid progression of cellulitis or fasciitis | Progressive hyperlactatemia |
| Cellulitis refractory to antimicrobial treatment | Renal failure (decreased creatinine clearance or glomerular filtrate abnormalities) |
| Pain out of proportion to examination | Hyponatremia (serum sodium < 135 mmol/l) |
| Tenderness beyond the area of erythema | Leukocytosis (white blood cell count > 15,000 cells/µl) or leukopenia (< 3.000 cell/µl) |
| Cutaneous anesthesia | Hemostasis disorders, prolonged clotting times |
| Bullae, hemorrhagic blisters | Elevated C-reactive protein, together with probably very high procalcitonin values |
| Dusky appearance of skin | Rhabdomyolysis (creatine phosphokinase elevations and/or lactodehydrogenase) |
| Crepitus | Hyperglycemia or hypoglycemia (underlying diabetes mellitus decompensation) |
| Systemic toxicity | |
| Fever that does not respond to treatment or unexplained hypothermia | |
Treatment
Therapy goals for necrotizing soft tissue infections include rapid eradication of the infection, prevention of complications, reduction of mortality, avoidance of unnecessary antibiotic use, and minimization of side effects of antibiotic therapy.3
Patients should be quickly evaluated for surgery.2,3 Delays in initial surgical intervention, particularly beyond 14 hours after diagnosis, are associated with significantly increased mortality.3 Type I necrotizing fasciitis requires empiric broad-spectrum antibiotics covering gram-positive, gram-negative, and anaerobic bacteria.8 Options include a carbapenem, such as meropenem or piperacillin-tazobactam, plus an antibiotic with MRSA coverage, such as vancomycin or daptomycin plus clindamycin, which has antitoxin properties.8 The antibiotic regimen should be adjusted following Gram stain, culture, and sensitivity results.8
If a GAS or beta-hemolytic infection is present, penicillin and clindamycin can be given. Vancomycin with a beta-lactam/beta-lactamase inhibitor or a carbapenem can be given for polymicrobial infections.8
If type II (streptococcal) or type III (clostridial) necrotizing fasciitis is diagnosed, therapy should switch to penicillin plus clindamycin.3 Clindamycin is more effective due to its inhibition of protein synthesis, reduced bacterial exotoxin production, and immunomodulatory properties.3 It is also effective against some MRSA strains.3 This combination can be continued for 48-72 hours, after which penicillin can be given alone.8 Linezolid may be considered, but it lacks extensive clinical data.3 While hyperbaric oxygen may benefit clostridial myonecrosis, and intravenous immunoglobulin (IVIG) may help necrotizing streptococcal infections, neither is recommended due to insufficient evidence of improved outcomes.3
Table 14
Treatment of Necrotizing Fasciitis
| Generic Name | MOA | Dose | Adverse Effects |
| Piperacillin- tazobactam | Inhibits bacterial cell wall synthesis (piperacillin); beta-lactamase inhibitor (tazobactam) | 3.375-4.5 g IV every 6-8 hours | Diarrhea, allergic reactions |
| Vancomycin | Inhibits bacterial cell wall synthesis | 15-20 mg/kg IV every 8-12 hours | Nephrotoxicity, ototoxicity, "red man" syndrome |
| Clindamycin | Inhibits bacterial protein synthesis | 600-900 mg IV every 8 hours | Diarrhea, colitis, rash |
| Penicillin G | Inhibits bacterial cell wall synthesis | 4 million units IV every 4 hours | Allergic reactions, nausea |
| Imipenem | Inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins, preventing the final step of peptidoglycan synthesis and inhibiting cell wall biosynthesis. | 1 gram IV every 6-8 hours | Diarrhea, nausea, headache, hypersensitivity reactions |
| Meropenem | Inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins, preventing the final step of peptidoglycan synthesis and inhibiting cell wall biosynthesis. | I g IV every 8 hours | Diarrhea, nausea, headache, hypersensitivity reactions |
| Ertapenem | Inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins, preventing the final step of peptidoglycan synthesis and inhibiting cell wall biosynthesis. | 1 g IV every 24 hours | Diarrhea, nausea, headache, hypersensitivity reactions |
| Daptomycin | Binds to components of the cell membrane of susceptible organisms and causes rapid depolarization | 4-6 mg/kg IV once daily | Vomiting, hypersensitivity reactions, eosinophilia, myopathy |
The Roles of Pharmacy Teams
Pharmacists
Pharmacists play a crucial role in the treatment and prevention of SSTIs, working with other healthcare providers to ensure optimal patient outcomes and minimize therapy-related complications. A vital role in medication management involves selecting appropriate empiric antibiotic therapy based on likely pathogens, local resistance patterns, and patient-specific factors such as allergies and comorbidities. Pharmacists can also work with physicians to assist in monitoring antibiotic levels, such as vancomycin, and in switching from IV to PO therapies when appropriate. Additionally, they can educate patients and/or caregivers on proper medication use, the importance of completing antibiotic courses, and recognizing side effects.
Pharmacy Technicians
Pharmacy technicians play a vital role in supporting patients with SSTIs by performing tasks that ensure the smooth functioning of pharmacy operations and enhance patient care. They assist pharmacists by accurately filling prescriptions and ensuring that patients receive the correct medications in the appropriate doses. In addition to filling prescriptions, pharmacy technicians help manage inventory, ensuring that essential antibiotics and other related supplies are readily available. This involves monitoring stock levels, placing orders, and checking for expired medications, thereby maintaining a reliable supply of necessary treatments for SSTIs. By keeping the pharmacy well-stocked and organized, they help prevent treatment delays and contribute to the overall efficiency of pharmacy services.
In their administrative capacity, pharmacy technicians manage patient records, ensuring that all documentation is accurate and up to date. This meticulous record-keeping supports continuity of care, as accurate records are essential for monitoring treatment progress and making informed decisions about ongoing care. They also assist with billing and insurance processing, helping patients navigate the complexities of medication coverage and reducing financial barriers to accessing necessary treatments.
Summary
Skin and soft tissue infections pose significant challenges for patients in community and hospital settings. The effective management of SSTIs requires a strong understanding of their associated risk factors and pathophysiology, as well as knowledge of diagnosis and management strategies. Pharmacy team members play crucial roles in preventing and managing SSTIs via interprofessional collaboration with healthcare teams and providing patient and caregiver education.
References
Bouza E, Burillo A. Current international and national guidelines for managing skin and soft tissue infections. Curr Opin Infect Dis. 2022;35(2):61-71. doi:10.1097/QCO.0000000000000814
Blanes Hernández R, Rodríguez Pérez M, Fernández Navarro J, Salavert Lletí M. Current approach to skin and soft tissue infections. Thinking about continuity of care. Rev Esp Quimioter. 2023;36 Suppl 1(Suppl 1):37-45. doi:10.37201/req/s01.10.2023
Fish DN. Skin and Soft Tissue Infections. In: DiPiro JT, Yee GC, Haines ST, Nolin TD, Ellingrod VL, Posey L. eds. DiPiro’s Pharmacotherapy: A Pathophysiologic Approach, 12th Edition. McGraw Hill; 2023.
Ki V, Rotstein C. Bacterial skin and soft tissue infections in adults: A review of their epidemiology, pathogenesis, diagnosis, treatment and site of care. Can J Infect Dis Med Microbiol. 2008;19(2):173-184. doi:10.1155/2008/846453
Wingate B, Kehr H. Management of Complicated Skin and Soft Tissue Infections in Hospitalized Patients. US Pharm. 2007;32(4):HS5-HS12
Ramakrishnan K et al. Skin and Soft Tissue Infections. Am Fam Physician. 2015;92(6):474-483.
Spelman D, et al. Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis. Uptodate. 2024.
Hua C, Urbina T, Bosc R, et al. Necrotising soft-tissue infections. Lancet Infect Dis. 2023;23(3):e81-e94. doi:10.1016/S1473-3099(22)00583-7
Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America [published correction appears in Clin Infect Dis. 2015 May 1;60(9):1448. doi: 10.1093/cid/civ114. Dosage error in article text]. Clin Infect Dis. 2014;59(2):e10-e52. doi:10.1093/cid/ciu444
Gozal D, Ziser A, Shupak A, Ariel A, Melamed Y. Necrotizing fasciitis. Arch Surg. 1986;121(2):233-235. doi:10.1001/archsurg.1986.01400020119015
Miller LG, Perdreau-Remington F, Rieg G, et al. Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles. N Engl J Med. 2005;352(14):1445-1453. doi:10.1056/NEJMoa042683
Wong CH, Chang HC, Pasupathy S, Khin LW, Tan JL, Low CO. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;85(8):1454-1460.
DISCLAIMER
The information provided in this course is general in nature, and it is designed solely to provide participants with continuing education credit(s). This course and materials are not meant to substitute for the independent, professional judgment of any participant regarding that participant’s professional practice, including but not limited to patient assessment, diagnosis, treatment, and/or health management. Medical and pharmacy practices, rules, and laws vary from state to state, and this course does not cover the laws of each state; therefore, participants must consult the laws of their state as they relate to their professional practice.
Healthcare professionals must consult their employer, healthcare facility, hospital, or other organization for guidelines, protocols, and procedures to follow. The information provided in this course does not replace those guidelines, protocols, and procedures, but is for academic purposes only, and this course’s limited purpose is for the completion of continuing education credits.
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