Skin, Bone & Soft Tissue Infections
From cellulitis to the surgical emergencies you cannot miss
Cellulitis, erysipelas and abscess
Cellulitis. Warm, tender, poorly demarcated erythema involving the deep dermis and subcutaneous fat, often with fever. Nonpurulent cellulitis is usually caused by β-hemolytic streptococci, chiefly Streptococcus pyogenes, entering through tinea pedis, venous stasis skin, lymphedema or minor trauma. The diagnosis is clinical; blood cultures are reserved for systemic toxicity or immunocompromise. For recurrent cellulitis, treat predisposing tinea pedis, edema and lymphedema first; with 3 to 4 episodes a year despite this, consider prophylactic oral penicillin or erythromycin.
Erysipelas. A superficial streptococcal infection of the upper dermis and its lymphatics, typically on the face or shins, forming a raised, sharply demarcated "orange-peel" plaque. Cellulitis borders, by contrast, are indistinct.
| Feature | Nonpurulent cellulitis, erysipelas | Purulent cellulitis, abscess |
|---|---|---|
| Usual organism | β-hemolytic streptococci | S. aureus, including MRSA |
| Key step | Antibiotics; elevate the limb, treat tinea pedis | Incision and drainage |
| Oral therapy | Cephalexin or dicloxacillin | TMP-SMX, doxycycline or clindamycin |
| Severe or inpatient | IV cefazolin | IV vancomycin, linezolid or daptomycin |
Abscess. A fluctuant, walled-off collection of pus is cured by incision and drainage (I&D); antibiotics without drainage will not resolve it. Add antibiotics only for systemic signs (SIRS), surrounding cellulitis, large or multiple abscesses, immunocompromise, or failure of I&D alone. Bedside ultrasound helps confirm a drainable collection.
MRSA agents. Community MRSA (SCCmec type IV, Panton-Valentine leukocidin toxin) causes recurrent boils and abscesses in healthy people; for recurrent MRSA abscesses, consider decolonization (intranasal mupirocin plus chlorhexidine washes) and hygiene measures. Oral options are TMP-SMX, doxycycline or clindamycin; for clindamycin, check a D-test, because erythromycin-resistant strains can harbor inducible clindamycin resistance. Hospital-acquired or severe MRSA is treated with IV vancomycin (dosed by trough or AUC), linezolid or daptomycin.
Daptomycin is inactivated by pulmonary surfactant, so it is never used for MRSA pneumonia.
Necrotizing soft-tissue infections
Recognition. Necrotizing fasciitis spreads along fascial planes faster than the skin reveals. Red flags are pain out of proportion to the exam, rapid spread, systemic toxicity, tense edema beyond the erythema, bullae, skin anesthesia and crepitus. Imaging may show gas, but it must never delay surgery; the diagnosis is confirmed in the operating room.
| Feature | Type I fasciitis | Type II fasciitis | Gas gangrene |
|---|---|---|---|
| Organisms | Polymicrobial aerobes and anaerobes | Group A Strep (± S. aureus) | Clostridium perfringens |
| Setting | Diabetics, postoperative wounds, perineum (Fournier gangrene) | Healthy hosts after minor trauma, varicella or injection drug use | Traumatic or contaminated deep wounds |
| Hallmarks | Pain out of proportion, crepitus, toxicity | Rapid spread, streptococcal toxic shock | Soft-tissue gas, brown "dishwater" discharge, rapid myonecrosis |
| Antibiotics | Vancomycin + piperacillin-tazobactam | Same, with clindamycin | Penicillin + clindamycin |
- Recognizepain out of proportion, crepitus, toxicity
- Emergent surgeryimmediate wide debridement, repeated as needed
- Broad antibioticsvancomycin plus piperacillin-tazobactam
- Add clindamycinsuppresses streptococcal and clostridial toxin production
Gas gangrene. Clostridial myonecrosis follows trauma or contamination; C. perfringens alpha toxin (a lecithinase) destroys muscle, and x-ray or CT shows gas in tissue. Treatment is surgical debridement plus penicillin and clindamycin. Spontaneous gas gangrene from C. septicum should prompt a search for colon cancer.
Fournier gangrene is necrotizing fasciitis of the perineum and scrotum, often in diabetics; it needs the operating room, not a trial of antibiotics.
Osteomyelitis and the diabetic foot
Routes and organisms. Hematogenous spread seeds the long-bone metaphysis in children and the vertebrae in adults; contiguous spread comes from ulcers, open fractures and surgery. S. aureus is the most common cause overall.
| Host or exposure | Classic organism | Note |
|---|---|---|
| Sickle cell disease | Salmonella | S. aureus remains common |
| Injection drug use | Pseudomonas, S. aureus | Vertebral, sternoclavicular sites |
| Nail through a shoe | Pseudomonas | Foot puncture osteomyelitis |
| Prosthetic joint, hardware | S. epidermidis | Biofilm; hardware usually removed |
| Cat or dog bite | Pasteurella multocida | Amoxicillin-clavulanate |
| Diabetic foot | Polymicrobial | Gram-positive cocci, gram-negative rods, anaerobes |
| Young, sexually active | Neisseria gonorrhoeae | Septic arthritis, tenosynovitis |
Diagnosis. Plain films lag 1–2 weeks because lucency needs roughly 50% bone loss. MRI (marrow edema) is the most sensitive and specific imaging and is the next step when films are normal but suspicion persists. Bone biopsy with culture is the gold standard for the organism and ideally precedes antibiotics in a stable patient. ESR and CRP are elevated and useful for tracking response.
Treatment. Prolonged antibiotics, typically about 6 weeks, are tailored to the biopsy culture. Chronic osteomyelitis forms a sequestrum (necrotic bone nidus) encased by an involucrum (reactive new periosteal bone); cure usually requires debridement of dead bone and removal of infected hardware. A long-standing draining sinus can transform into squamous cell carcinoma (Marjolin ulcer).
Diabetic foot. Infections are often polymicrobial on a background of neuropathy and vascular disease. A positive probe-to-bone test, an ulcer over bone, an ulcer larger than 2 cm², or an ESR above 70 mm/h raises concern for underlying osteomyelitis. Assess perfusion, image if bone involvement is suspected, and combine antibiotics with debridement, offloading and glycemic control.
Septic and gonococcal arthritis
Septic arthritis. Any acute monoarthritis mandates arthrocentesis (cell count, Gram stain, culture, crystals), ideally before antibiotics. S. aureus is the most common cause. Treat with joint drainage (serial aspiration, arthroscopic or open washout) plus IV antibiotics chosen by the Gram stain; delay causes rapid cartilage destruction.
Disseminated gonococcal infection. In young, sexually active patients, Neisseria gonorrhoeae presents either as a triad of migratory polyarthralgia, tenosynovitis (often of the wrist) and pustular dermatitis, or as a purulent monoarthritis, often of the knee. Synovial cultures are often negative, so send urethral, cervical and pharyngeal NAATs. Treat with ceftriaxone 1 g IV or IM every 24 hours for at least 7 days in total, adding doxycycline only if chlamydia has not been excluded. Recurrent neisserial infection suggests a terminal complement deficiency.