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Skin And Soft Tissue InfectionEdit

Skin and soft tissue infections (SSTIs) comprise a wide spectrum of bacterial infections affecting the skin and underlying soft tissues. They range from non-purulent cellulitis and erysipelas, in which inflammation is driven mainly by streptococcal species and skin barrier disruption, to purulent infections such as abscesses caused by Staphylococcus aureus, including methicillin-resistant strains, and even to rapidly progressive necrotizing infections that require emergent surgical intervention. Most episodes are managed in the outpatient setting, but certain presentations necessitate hospital admission for intravenous antibiotics, imaging-guided drainage, or urgent surgery. The two most common pathogens in community-acquired SSTIs are Staphylococcus aureus and Streptococcus pyogenes, with MRSA becoming a significant consideration in many regions. The clinical approach hinges on the pattern of infection (purulent vs non-purulent), depth of involvement, patient comorbidities (e.g., diabetes mellitus or other states of immunocompromised), and risk factors for antibiotic resistance. For a broad view of the organisms and clinical spectrum, see the discussions in Staphylococcus aureus and Streptococcus pyogenes.

SSTIs are not purely a medical curiosity; they carry substantial consequences for patient outcomes and health care costs. Chronic conditions such as diabetes and peripheral vascular disease increase risk and complicate healing, while wounds, ulcers, and skin barrier disruptions create portals for infection. In the modern era, attention to antibiotic stewardship—balancing prompt, effective treatment with restraint to limit resistance—has become a central part of management, alongside emphasis on adequate drainage of purulent collections and appropriate wound care. See antibiotic stewardship for a broader discussion of balancing effectiveness with longer-term public health concerns.

The following article outlines the clinical features, microbiology, diagnosis, and management of SSTIs, with attention to how a clinician evaluates risk, selects therapy, and uses non-drug interventions to improve outcomes. It also addresses some contemporary debates about treatment approaches and the rationale behind evidence-based guidelines.

Clinical presentation

SSTIs present with a variety of patterns, and distinguishing among them guides initial management decisions.

Non-purulent SSTIs

Non-purulent cellulitis and erysipelas typically present with diffuse or poorly demarcated redness, warmth, swelling, and tenderness of the affected area. Fever and systemic symptoms may occur but are not universal. The infection is usually caused by streptococci and sometimes by MSSA, and it commonly arises after skin barrier breakdown, tinea pedis, or minor trauma. Management focuses on anti-streptococcal or anti-staphylococcal therapy when indicated, along with wound care and monitoring for progression. See cellulitis.

Purulent SSTIs

Purulent SSTIs are characterized by abscess formation or purulent drainage, often with localized signs of infection such as fluctuance, pain, and erythema. Staphylococcus aureus is the leading culprit, including MRSA in many communities. Management prioritizes drainage of abscesses when feasible and, if antibiotics are indicated, selection depends on local resistance patterns and patient risk factors. See abscess and Staphylococcus aureus.

Necrotizing SSTIs and severe soft tissue infections

Necrotizing infections, including necrotizing fasciitis, are medical emergencies. They present with severe pain disproportionate to exam findings, rapid progression, systemic toxicity, crepitus or anesthesia in affected tissues, and sometimes bullae or anesthesia. Immediate surgical exploration and broad surgical debridement, combined with broad-spectrum antibiotics, are required. See necrotizing fasciitis.

Microbiology

Common pathogens

Antibiotic resistance and stewardship

Rising rates of resistance, including MRSA, have influenced empirical therapy in many regions. Stewardship aims to use the narrowest effective antibiotic spectrum for the shortest effective duration, guided by clinical response and culture data when available. See antibiotic stewardship and antibiotics.

Diagnosis

Diagnosis is primarily clinical, supported by imaging and laboratory data when deeper tissue involvement or atypical features are suspected.

  • Cultures from drained purulent material or wound swabs can identify causative organisms and guide de-escalation.
  • Imaging (ultrasound, CT, or MRI) is helpful when abscesses are not readily accessible for drainage, or when deeper infection such as necrotizing fasciitis is suspected.
  • Laboratory tests (e.g., complete blood count, C-reactive protein) may assist in assessing inflammatory burden or systemic involvement, though they are not diagnostic on their own. See immunocompromised states and diabetes mellitus as risk factors that influence diagnostic interpretation.

Management

General approach

  • Determine the pattern (non-purulent vs purulent), depth, and systemic illness to decide on outpatient vs inpatient management.
  • Drainage is essential for abscesses; antibiotic therapy complements source control.
  • Wound care and proper cleansing, dressing, and attention to diabetes control and vascular health support healing. See wound.

Antimicrobial therapy

  • Non-purulent cellulitis (low risk of MRSA): first-line selective therapy often targets streptococci and MSSA, such as cephalexin or amoxicillin-clavulanate where appropriate. See cephalexin.
  • Non-purulent cellulitis with higher risk of MRSA or in areas with elevated MRSA prevalence: consider agents with MRSA activity or local guidelines, such as doxycycline, TMP-SMX, or clindamycin, with transition to narrower-spectrum therapy as indicated. See doxycycline and trimethoprim-sulfamethoxazole and clindamycin.
  • Purulent SSTIs: management typically includes antibiotics with MRSA coverage when drainage alone is unlikely to suffice (e.g., larger abscesses or systemic symptoms). Options include TMP-SMX, doxycycline, or linezolid; severe cases may require IV therapy with vancomycin or linezolid, often followed by step-down to oral therapy. See vancomycin and linezolid.
  • Severe, life-threatening infections or necrotizing fasciitis: broad-spectrum IV antibiotics (e.g., a beta-lactam with activity against Gram-positives and anaerobes) plus MRSA coverage, with urgent surgical consultation for debridement. See piperacillin-tazobactam and MRSA.

Drainage and wound management

  • Drainage of abscesses is a mainstay of therapy and may obviate the need for antibiotics in small, well-formed abscesses after adequate drainage. See surgical debridement and abscess.
  • Wound care, dressing changes, and management of chronic conditions (like diabetes) support healing and reduce recurrence risk. See wound and diabetes mellitus.

Duration and follow-up

  • Duration depends on clinical response, infection severity, and microbial findings but often ranges from 5 to 10 days for uncomplicated cases and longer for complicated infections. De-escalation to narrow-spectrum antibiotics should occur when culture data permit and the patient improves. See antibiotics.

Complications and prognosis

Untreated or inadequately treated SSTIs can lead to local tissue damage, septicemia, or the spread of infection to deeper structures such as muscle or bone. Necrotizing infections carry particularly high mortality risk without prompt surgical intervention. Early recognition, appropriate drainage, and timely antibiotic therapy improve outcomes. Chronic comorbidities like diabetes or vascular disease can complicate healing and increase recurrence risk, underscoring the importance of comprehensive management that includes control of underlying conditions. See diabetes mellitus and peripheral vascular disease.

Controversies and debates

  • Antibiotic stewardship versus rapid empirical therapy: Clinicians continuously balance the risks of under-treating a bacterial infection against overusing broad-spectrum antibiotics that promote resistance. Proponents of stewardship emphasize de-escalation and culture-guided therapy, while others argue for broader empiric coverage in high-risk patients or regions with high resistance. See antibiotic stewardship.
  • Outpatient management versus hospitalization: For many uncomplicated SSTIs, outpatient therapy is safe and cost-effective. Critics contend that a subset of patients might benefit from earlier inpatient observation in order to ensure complete source control and adherence, particularly in high-risk groups such as those with diabetes or immunosuppression. See outpatient care and hospitalization.
  • The role of social determinants in care: Some commentators urge guidelines to address access, affordability, and social factors that influence outcomes. Proponents argue these considerations improve equity, while detractors contend that core principles should remain rooted in pathogen-directed therapy and measurable clinical endpoints. From a conservative, clinically driven perspective, the priority remains timely, evidence-based treatment that yields the best patient outcomes, with contingency plans to meet patients where they are. See antibiotic stewardship and diabetes mellitus.
  • Woke criticisms of medical guidelines: Critics sometimes claim that emphasis on equity or political correctness diverts attention from scientific rigor. The counterpoint is that guidelines should remain anchored in robust evidence while acknowledging real-world barriers to care; neglecting either aspect risks worse outcomes. In practice, SSTI management targets proven microbiology and patient-specific risks while allowing flexibility to address access and comorbidity considerations. See Staphylococcus aureus and Streptococcus pyogenes.

See also