What it is:A grab-bag of infections that all involve skin or the tissue beneath it, from a superficial crusty rash in a toddler up to a surgical emergency that kills tissue by the hour. The chapter is really seven different diseases (impetigo, erysipelas, folliculitis/furuncles/carbuncles, cellulitis, necrotizing fasciitis, diabetic foot infections, pressure injuries, bite wounds) that share one organizing question.
The core problem:Gram-positive skin flora, mostly Staphylococcus aureus and Streptococcus pyogenes, breaches a barrier.Everything else, depth of spread, whether it's purulent, whether anaerobes and gram-negatives join in, is a variation on that theme.
What you do about it:Answer two questions before picking a drug: (1) is there pus to drain, and (2) does this patient need MRSA coverage?Then match severity to route (oral vs IV) and match the wound type to the extra bugs (anaerobes for bites and diabetic feet, Pseudomonas only with specific risk factors).
Worth knowing
Every SSTI question on this chapter reduces to a 2x2 grid: purulent or not, MRSA risk or not.Nonpurulent, no MRSA risk → cover strep with a beta-lactam. Purulent or MRSA risk present → you need an anti-MRSA agent, and a beta-lactam alone will fail you. Hold that grid in your head through the whole chapter.
Primary vs Secondary, and Who Causes What
The chapter splits SSTIs into primaryinfections (a single organism attacking previously healthy skin) and secondaryinfections (polymicrobial, developing in skin that's already damaged by an ulcer, wound, or bite). Five conditions predispose skin to infection in the first place: a high bacterial load, excess moisture, poor blood supply, available nutrients for bacteria, and any break in the stratum corneum that lets organisms in.
Type
Condition
Usual organism(s)
Primary infections
Erysipelas
Superficial dermis + lymphatics
Group A strep (S. pyogenes), almost exclusively
Impetigo
Superficial epidermis
S. aureus (incl. MRSA) ± group A strep
Lymphangitis
Lymphatic channels
Group A strep, occasionally S. aureus
Cellulitis
Dermis + subcutaneous fat
Group A strep, S. aureus (incl. MRSA); occasionally other gram-positive cocci, gram-negative rods, anaerobes
S. aureus, strep, Enterobacteriaceae, Bacteroides, Peptostreptococcus, P. aeruginosa
Pressure injury
Ulcer-based, polymicrobial
Same list plus MRSA
Animal bite
Puncture/laceration
Pasteurellaspp., S. aureus, strep, Bacteroides
Human bite
Puncture/laceration
Eikenella corrodens, S. aureus, strep, Corynebacterium, Bacteroides, Peptostreptococcus
Burn wound
Thermal injury
P. aeruginosa, Enterobacteriaceae, S. aureus, strep
The gram-positive baseline
Regardless of type, S. aureus and S. pyogenes cause the majority of SSTIs. Community-associated MRSA has changed empiric therapy for nearly every category on this list, which is why "does this need MRSA coverage" is the single most tested decision point in the chapter.
Pathophysiology - Why the Drug Choices Split the Way They Do
Almost all the mechanistic reasoning in this chapter boils down to matching the antibiotic's spectrum to which organisms are actually present, since SSTIs aren't really one pathophysiologic process, they're one anatomic location with several different bugs finding several different ways in.
Why nonpurulent and purulent infections get different regimens
Nonpurulent cellulitis(no abscess, no drainable pus) is overwhelmingly a streptococcaldisease, because strep spreads diffusely through tissue via secreted enzymes (hyaluronidase, streptokinase) rather than walling itself off. That's why a plain beta-lactam active against streptococci, without added MRSA coverage, is usually enough. Purulent infections(abscesses, furuncles, carbuncles, purulent cellulitis) form because S. aureustriggers a localized, walled-off suppurative response, pus is a staph signature. Since community-MRSA is now a leading cause of purulent SSTI, purulent disease automatically earns anti-MRSA coverage regardless of culture status.
Why beta-lactams alone fail against MRSA
Penicillinase-resistant penicillins (dicloxacillin, nafcillin) and first-generation cephalosporins (cephalexin, cefazolin) work by binding penicillin-binding proteins to block cell wall synthesis. MRSA expresses an altered PBP (PBP2a, via the mecAgene) that these drugs can't bind, so no beta-lactam in that list touches it no matter how purulent the infection looks. You need drugs that hit MRSA through a different route entirely: folate synthesis (TMP-SMX), protein synthesis (doxycycline, clindamycin, linezolid), or the cell membrane/wall by other mechanisms (vancomycin, daptomycin, ceftaroline, the only beta-lactam that does cover MRSA).
Why anaerobes show up in bites and diabetic feet but not simple cellulitis
Anaerobes need an oxygen-poor niche to thrive, deep puncture wounds (bites), macerated tissue under an ulcer (diabetic feet, pressure injuries), and necrotic tissue (necrotizing fasciitis) all provide that. Simple cellulitis on intact-ish skin doesn't create that environment, which is why routine cellulitis regimens skip anaerobic coverage but bite and DFI regimens build it in (metronidazole, clindamycin, or a beta-lactam/beta-lactamase inhibitor that already covers anaerobes).
The unlock
Stop memorizing regimens as arbitrary lists. Ask three questions for any SSTI: (1) purulent → think staph/MRSA. (2) diffusely spreading, no pus → think strep. (3) deep wound, ulcer, or bite → add anaerobic coverage.Almost every regimen in this chapter falls out of those three answers.
These are a spectrum of the same process, infection of a hair follicle, at increasing depth and severity. Folliculitis is superficial and usually needs nothing but warm compresses. A furuncle is a deeper, more painful nodule; a carbuncle is multiple furuncles coalescing into one inflamed mass with multiple drainage points, usually on the neck, back, or thighs.
Incision and drainage is the treatment
Carbuncles, abscesses, and large furuncles are treated primarily with incision and drainage, not antibiotics. Antibiotics are an adjunct, added only when there are systemic signs of infection, the lesion is severe, the patient is immunocompromised, or I&D alone already failed. This is a common exam trap: don't reach for an antibiotic first.
When antibiotics are warranted, TMP-SMX, doxycycline, or minocycline cover community MRSA empirically in adults; clindamycin or TMP-SMX in children.
Impetigo
A superficial epidermal infection, mostly in kids, spread by close contact in households, daycares, and schools. Nonbullous impetigostarts as small vesicles that rupture into pus-filled lesions drying into the classic golden-yellow crust. Bullous impetigois caused by exfoliative-toxin-producing S. aureus strains, forms larger fluid-filled bullae that rupture into thin light-brown crusts, and can come with fever, weakness, and diarrhea from the systemic toxin effect.
Extent
Preferred treatment
Duration
Limited lesions, not on the face
Topical mupirocinor retapamulin ointment
5 days
Multiple lesions, facial involvement, or systemic therapy needed
Dicloxacillin or cephalexin (S. pyogenes alone → penicillin); penicillin-allergic: doxycycline, clindamycin, or TMP-SMX
7 days
Penicillinase-resistant penicillins and first-generation cephalosporins are preferred over plain penicillin because S. aureus, not just strep, is now a major cause of impetigo.
Erysipelas
A distinct, superficial variant of cellulitis confined to the upper dermis and cutaneous lymphatics, almost always caused by group A strep. Classically hits the lower extremities, preceded by flu-like symptoms (fever, chills, malaise), then a painful, intensely erythematous, edematous lesion with a sharply demarcated, raised border, sometimes with visible lymphatic streaking. Leukocytosis and elevated CRP are common.
Erysipelas vs cellulitis: the border is the tell
Erysipelas has a raised, sharply demarcated borderbecause it's confined to the superficial dermis and lymphatics. Cellulitis has a flat lesion with poorly defined, blending marginsbecause it involves the deeper dermis and subcutaneous fat, which doesn't hold a crisp edge. This distinction is a classic distractor pair.
Mild-to-moderate erysipelas in adults: IM procaine penicillin G or oral penicillin VK for 7-10 days. Severe disease: hospitalize, IV aqueous penicillin G. Penicillin-allergic patients get clindamycin.
Cellulitis
An acute, spreading infection of the epidermis and dermis that can extend into the superficial fascia, considered serious because it spreads through lymphatics and into the bloodstream. Mostly caused by group A strep or S. aureus. Mixed aerobic/anaerobic cellulitis shows up in diabetics, after trauma, and at abdominal or perineal surgical sites.
Clinical presentation
Erythema and edema with nonelevated, poorly defined margins(the key contrast with erysipelas above). Tender lymphadenopathy, malaise, fever, and chills are common. There's usually an antecedent minor trauma, ulcer, or surgical wound. A Gram stain of fluid aspirated from the advancing edge can help identify the organism but is frequently negative, and routine cultures of blood, aspirates, or swabs are not routinely recommendedfor typical cases.
When cultures ARE worth it
Blood cultures (and consideration of cutaneous cultures) are recommended for patients with malignancy on chemo, neutropenia, severe cell-mediated immunodeficiency, immersion injuries, or animal bites, situations where an unusual or resistant organism is more likely.
Treatment logic: purulent vs nonpurulent, mild vs severe
Local care (elevation, immobilization) reduces swelling in every case. Incision and drainage plus antibiotics is reserved for complicated abscesses: extensive or multi-site disease, rapidly progressive infection, systemic illness, difficult-to-drain locations (hands, face, genitalia), immunosuppression, extremes of age, or failure of drainage alone.
Mild
Moderate
Severe
Nonpurulent(cover strep only, no systemic signs)
PO penicillin VK, cephalexin, dicloxacillin, or clindamycin
Same PO options; add MRSA coverage if risk factors present
Hospitalize. IV penicillin, cefazolin, ceftriaxone, or clindamycin; add vancomycin if MRSA risk (penetrating trauma, MRSA elsewhere/nasal colonization, IV drug use, SIRS criteria)
Purulent(assume MRSA)
I&D only, no antibiotics needed
PO TMP-SMX or doxycycline; linezolid/tedizolid work but cost more with no efficacy edge
Hospitalize. IV vancomycin, daptomycin, linezolid, or tedizolid; children: vancomycin, linezolid, or clindamycin
Duration is shorter than most people guess
5 daysis the recommended treatment duration for cellulitis, extended only if there's no clinical response by then. Diabetic foot infections and necrotizing fasciitis run much longer (see below), don't apply the 5-day rule across the whole chapter.
For severely immunocompromised patients with severe nonpurulent cellulitis, broad empiric coverage (vancomycin plus piperacillin-tazobactam, imipenem, or meropenem) may be used, and a short course of systemic corticosteroids (7 days) can be considered as an adjunct in nondiabetic patients.
Necrotizing Fasciitis - Don't Miss This
An aggressive, rapidly progressive infection along the fascial planes with systemic toxicity, tissue necrosis, and sometimes gas formation. It can look like severe cellulitis early on, which is exactly why any severe nonpurulent cellulitis with signs of systemic toxicity needs to trigger suspicion.
Prompt surgical consult is not optional
Early and aggressive surgical debridementof all necrotic tissue is the single most essential intervention. Antibiotics alone will not save these patients; delay in surgical source control is the deadliest mistake.
Empiric and directed therapy
Empiric (unknown organism):vancomycin or linezolid pluspiperacillin-tazobactam or a carbapenem, or vancomycin/linezolid plus ceftriaxone and metronidazole.
Confirmed group A strep:clindamycin plus penicillin. Clindamycin is added on top of a penicillin that strep is already exquisitely susceptible to, because clindamycin works by inhibiting bacterial protein synthesis, which suppresses toxin and exotoxin production, something a cell-wall active drug like penicillin can't do on its own, and matters enormously in a toxin-driven, tissue-destroying infection like this.
Clostridial gas gangrene (myonecrosis):also clindamycin plus penicillin.
Vancomycin trough target changes here
Routine MRSA SSTI wants a vancomycin trough >10 mg/Lto avoid resistance. For MRSA necrotizing fasciitis specifically, the target rises to 15-20 mg/L. Same drug, different disease severity, different number, a favorite way to test whether you're reading the question carefully.
Diabetic Foot Infections
Three converging problems set these up: neuropathy(patients don't feel the injury), angiopathy/ischemia(poor perfusion impairs healing and antibiotic delivery), and immunologic defects. They usually present as one of three patterns: deep abscess, dorsal cellulitis, or a mal perforans ulcer on the sole. Osteomyelitis complicates 30-40%of infections, always think about bone involvement in a chronic, non-healing wound.
Mild infections tend to be monomicrobial (staph or strep); severe infections are usually polymicrobial, up to 60% of hospitalized patients, with gram-negative rods and anaerobes present in about half. Because of neuropathy, patients often present with swelling or drainage rather than pain; a foul odor suggests anaerobes.
Uninfected wounds don't get antibiotics
Clinically uninfected diabetic wounds should notbe treated with antibiotics regardless of how they look otherwise. Antibiotic therapy is for infection, not for the ulcer itself, and empiric regimen selection should always be based on infection severity and likely pathogens, not applied blanket-style.
Ampicillin-sulbactam, cefoxitin, ceftriaxone, imipenem-cilastatin, ertapenem, or a fluoroquinolone + clindamycin
Moderate: 1-3 wk; severe: 2-4 wk
+ MRSA risk
Add if: prior MRSA history/colonization in the last year, local prevalence ≥30-50%, or recent hospitalization
Add vancomycin, linezolid, or daptomycin to the base regimen
Per base regimen
+ Pseudomonas risk
Add only if: feet soaked in water, failed a nonpseudomonal regimen already, or severe infection
Piperacillin-tazobactam, or cefepime/ceftazidime/aztreonam + metronidazole or clindamycin
Per base regimen
Don't reflexively cover Pseudomonas
Empiric antipseudomonal coverage is usually unnecessaryin DFI, it's reserved for specific risk factors (feet soaked in water, prior nonpseudomonal treatment failure, or clinically severe disease). Same logic applies to MRSA coverage, it's risk-factor driven, not automatic just because the patient is diabetic.
Goals of therapy:clear the infection, prevent complications, preserve as much limb function as possible, avoid unnecessary antibiotic exposure that drives resistance, and minimize toxicity/cost. Up to 90%of DFIs resolve with a comprehensive approach combining wound care (debridement, drainage, sometimes amputation) with antimicrobials. Glycemic control should be maximized, and the limb should be rested and elevated. Therapy continues until signs and symptoms resolve, not necessarily until the wound is fully healed.
Infected Pressure Injuries
Pressure injuries ("pressure sores," "decubitus ulcers," "bed sores") form over bony prominences (sacrum, coccyx, ischial tuberosities, greater trochanter) from a mix of pressure, shearing, friction, and moisture, in patients predisposed by paralysis, immobility, malnutrition, anemia, or advanced age. Most are heavily colonized with a broad mix of aerobes, gram-negatives, and anaerobes, so colonization alone doesn't mean active infection; look for surrounding erythema, warmth, purulence, foul odor, or systemic signs.
Stage
Findings
1
Intact skin, localized nonblanchable erythema. No open wound.
2
Partial-thickness loss with exposed dermis; pink/red, moist wound bed, may be an intact or ruptured blister. No fat or deeper tissue visible.
Full-thickness loss with exposed fascia, muscle, tendon, ligament, cartilage, or bone.
Unstageable
Full-thickness loss obscured by slough or eschar; would reveal a stage 3 or 4 wound once debrided.
Deep-tissue injury
Intact or nonintact skin with a persistent, nonblanchable deep red/maroon/purple area or blood-filled blister, from intense/prolonged pressure and shear at the bone-muscle interface.
Prevention is the actual goal
Reposition to relieve pressure for just 5 minutes every 2 hoursto meaningfully protect against formation. Once a sore exists, therapy goals shift to preventing infection, preventing growth, and preventing new lesions elsewhere.
Management by stage:stage 1-2 lesions, not over a bony prominence, are usually managed medically (cleaning, debridement, dressing selection). Stage 3, stage 4, and unstageable lesions almost always need surgical intervention. Debridement can be surgical, mechanical (wet-to-dry dressings), or chemical; wounds should be cleaned with normal saline. A short 2-week trial of topical antibiotic (silver sulfadiazine or triple antibiotic) is reasonable for a clean, non-healing, or moderately exudative ulcer. Once there's clinical evidence of systemic infection (positive blood cultures, cellulitis, fasciitis, osteomyelitis, SIRS, sepsis), systemic antibiotics covering MRSA, anaerobes, enterococci, and Pseudomonasare warranted, using the same regimen logic as severe DFI.
Bite Wounds
Bite infections come from the biter's mouth flora plus the victim's own skin flora, and are usually polymicrobial. Risk factors for infection: puncture wound, more than 8 hours since injury without care, or age over 50.
Animal bites
Dog and cat bites are mostly polymicrobial; Pasteurella multocidais the most frequently isolated organism, especially from cats. Wounds need thorough irrigation with sterile water or saline plus washing with soap or povidone-iodine; surgical debridement and immobilization for more extensive dog/human bite injuries.
Pasteurella breaks the "usual" empiric choices
Penicillinase-resistant penicillins, first-generation cephalosporins, macrolides, and clindamycin all have poor activity against Pasteurellaand should not be used for infected animal bite wounds, even though they're your go-to agents everywhere else in this chapter. Amoxicillin-clavulanateis the outpatient drug of choice specifically because it covers Pasteurella along with strep, staph, and anaerobes.
IV options for serious infections: a beta-lactam/beta-lactamase inhibitor (ampicillin-sulbactam, piperacillin-tazobactam) or a second-generation cephalosporin with anaerobic activity (cefoxitin).
Prophylaxis(3-5 days) is recommended for high-risk patients: immunocompromised, asplenic, advanced liver disease, existing edema at the site, moderate-severe injury (especially hands/face), or a bite that penetrated periosteum or a joint capsule. Update tetanus/diphtheria toxoid if immunization status is unknown, incomplete, or more than 10 years old; rabies postexposure management should follow current guidelines if exposure risk exists.
Human bites
Eikenella corrodensis the signature organism, found in roughly 30% of infections, alongside S. aureus and beta-lactamase-producing anaerobes. Primary wound closure is generally notrecommended. Every human bite injury gets prophylactic antibiotics for 3-5 days ("early preemptive therapy") given the high infection risk, typically amoxicillin-clavulanate 500 mg every 8 hours. Clenched-fist injuries or serious wounds need IV therapy: ampicillin-sulbactam, piperacillin-tazobactam, cefoxitin, or ertapenem. Because bloodborne virus transmission (HIV, hepatitis B/C, herpes) is possible, assess exposure risk and consider antiretroviral post-exposure prophylaxis case by case.
Bite wound duration
Established infections are typically treated for 7-14 days, longer than the 5-day cellulitis rule, because these are polymicrobial, deep, and harder to sterilize.
Dosing Table
Doses below assume normal renal function; adjust for renal impairment per institutional protocol.
Drug
Adult dose
Notes
Topical
Mupirocin ointment
Apply every 8 h
Impetigo, 5 days
Retapamulin ointment
Apply every 12 h
Impetigo, 5 days
Oral - streptococcal / MSSA coverage
Penicillin VK
250-500 mg every 6 h
Erysipelas, nonpurulent cellulitis
Dicloxacillin
250-500 mg every 6 h
Not MRSA active
Cephalexin
250-500 mg every 6 h
Not MRSA active
Cefadroxil
250-500 mg every 12 h
Cefuroxime axetil
250-500 mg every 12 h
Cefaclor
500 mg every 8 h
Erythromycin
250-500 mg every 6 h
Penicillin-allergic option
Oral - MRSA coverage
Trimethoprim-sulfamethoxazole
160/800 mg every 12 h
Up to double dose for MRSA; no reliable strep coverage alone
Doxycycline
100-200 mg every 12 h
Clindamycin
300-600 mg every 6-8 h
Covers both MRSA and strep
Linezolid
600 mg every 12 h
Expensive, no efficacy edge over cheaper options
Tedizolid
200 mg once daily
Delafloxacin
450 mg every 12 h
Covers MRSA, unlike most fluoroquinolones
Oral - bite wounds / anaerobic coverage
Amoxicillin-clavulanate
875/125 mg every 12 h
Drug of choice for animal and human bites
Metronidazole
250-500 mg every 8 h
Combine with a fluoroquinolone or TMP-SMX for anaerobic coverage
Parenteral - streptococcal / MSSA coverage
Penicillin G
1-2 million units every 4-6 h
Nafcillin
1-2 g every 4-6 h
Cefazolin
1 g every 6-8 h
Ceftriaxone
1 g once daily
Parenteral - MRSA coverage
Vancomycin
30-40 mg/kg/day in 2 divided doses; trough-guided
Trough >10 mg/L standard; 15-20 mg/L for necrotizing fasciitis
Daptomycin
4 mg/kg once daily
Linezolid
600 mg every 12 h
Ceftaroline
600 mg every 12 h
Only beta-lactam with MRSA activity
Telavancin
10 mg/kg once daily
Dalbavancin
1000 mg day 1, then 500 mg day 8; or 1500 mg once
Long half-life, good for outpatient/one-time dosing
Pseudomonas coverage, pair with clindamycin/metronidazole for anaerobes
Ceftazidime
1-2 g every 8 h
Pseudomonas coverage, weak gram-positive
Metronidazole
500 mg every 8 h
Clindamycin
300-600 mg every 6-8 h (600-900 mg for necrotizing fasciitis)
Tigecycline
100 mg once, then 50 mg every 12 h
Broad gram-positive/negative/anaerobic, no Pseudomonas
Class-by-Class Notes
Beta-lactams: who they cover, who they miss
Penicillin VK and penicillin G remain first-line for pure streptococcal disease (erysipelas, strep-confirmed impetigo) because strep has never developed meaningful penicillin resistance. Penicillinase-resistant penicillins (dicloxacillin, nafcillin) and first-generation cephalosporins (cephalexin, cefazolin) extend coverage to methicillin-susceptibleS. aureus by resisting staphylococcal penicillinase, but none of them touch MRSA, PBP2a simply doesn't bind them. Ceftarolineis the outlier: a 5th-generation cephalosporin engineered with high affinity for PBP2a, making it the only beta-lactam with real anti-MRSA activity.
Amoxicillin-clavulanate and ampicillin-sulbactam add a beta-lactamase inhibitor, which is what gives them anaerobic and Pasteurella/Eikenella coverage that plain aminopenicillins lack, this is exactly why they're the bite-wound drugs of choice.
Anti-MRSA agents compared
TMP-SMX and doxycyclineare the standard oral outpatient choices for purulent/MRSA-risk SSTI, cheap and effective, but neither reliably covers streptococci, so if strep coverage is also wanted, combine with amoxicillin or a beta-lactam. Clindamycinis unique among the oral options in covering both MRSA and strep in one drug, useful when you don't want to add a second agent, though inducible clindamycin resistance in some staph strains is a real limitation.
Vancomycinis the IV workhorse for hospitalized MRSA SSTI, trough-monitored to balance efficacy against nephrotoxicity. Daptomycin, linezolid, and tedizolidare comparable-efficacy alternatives; daptomycin is inactivated by pulmonary surfactant so it's never used for pneumonia, but that's not a limitation for skin infections. Linezolid/tedizolidinhibit protein synthesis at the 50S ribosome and work well orally or IV, but cost more without outperforming cheaper options, so they're reserved rather than first-line.
The long-acting lipoglycopeptides dalbavancin, oritavancin, and telavancinexist mainly to enable single-dose or once-weekly outpatient therapy, avoiding a PICC line and home infusion nursing for patients who'd otherwise need days of IV vancomycin.
Fluoroquinolones in SSTI: not interchangeable
Levofloxacin, ciprofloxacin, and moxifloxacin show up mainly in diabetic foot and bite-wound regimens for their gram-negative and (for moxifloxacin) some anaerobic coverage. Ciprofloxacin has the weakest gram-positive activity of the group and is usually paired with clindamycin or metronidazole when anaerobes need covering. Delafloxacinis the exception in this class: unlike its relatives, it has real anti-MRSA activity, making it usable as monotherapy in situations where older fluoroquinolones would need an add-on agent.
Monitoring - What, When, Why
Parameter
When
Watching for
Clinical response(erythema, edema, pain, fever)
Daily to every few days depending on setting
Improvement expected within the treatment window; lack of response by day 3-5 in cellulitis should prompt reassessment, not just a duration extension
Vancomycin trough
Before 4th-5th dose at steady state
>10 mg/L for standard MRSA SSTI; 15-20 mg/L for MRSA necrotizing fasciitis
SCr/renal function
Baseline and periodically on vancomycin, aminoglycosides, or high-dose beta-lactams
Nephrotoxicity, need for dose adjustment
WBC, CRP, systemic signs (SIRS criteria)
Baseline and with clinical change
Progression to systemic infection, sepsis, or (in nonpurulent cellulitis) an evolving picture that suggests necrotizing fasciitis
Wound/ulcer exam(DFI, pressure injury)
Every visit or dressing change
Depth progression, new necrotic tissue, signs bone may be involved (probes-to-bone, chronic non-healing wound)
Culture/susceptibility data
As soon as available
De-escalate empiric broad-spectrum therapy once organism and sensitivities are known
Glycemic control(DFI)
Ongoing
Hyperglycemia impairs healing and immune function
Patient Counseling - What You'll Actually Say
"Finish the whole course, even once it looks better."Especially important for the shorter regimens (5-day cellulitis, 5-day impetigo) where it's tempting to stop early once the redness fades.
Impetigo:"This spreads easily to other people, especially kids in the same house. Wash your hands after touching the lesions, don't share towels, and try not to scratch, scratching is how it spreads to new areas of your own skin."
Mupirocin/retapamulin:"Apply a thin layer directly on the crusted areas, not a big glob, and keep going for the full 5 days even if it looks clear by day 3."
Cellulitis:"Keep the leg (or arm) elevated above your heart when you can, it helps the swelling go down faster than the antibiotic alone."
Cellulitis red flags to call about:"If the redness is spreading fast, you develop a fever, the pain feels way worse than the redness looks, or you see blistering or dark/purple skin, go to the ER, don't wait for your next dose."
MRSA-active oral drugs (TMP-SMX, doxycycline):"These make you sunburn more easily, use sunscreen and cover up outdoors while you're on it."
Diabetic foot infections:"Check your feet every single day, even the bottoms and between the toes, because you may not feel a new sore forming if you have nerve damage."
Diabetic foot infections:"Keep your blood sugar as controlled as you can right now, it directly affects how fast this heals and whether the infection responds to the antibiotic."
Animal or human bite:"Even if this looks minor, infection risk is real, especially on the hand. Finish the prescribed course and come back if swelling or pain increases instead of decreasing."
Pressure injury prevention (for caregivers):"Reposition every 2 hours if the person can't do it themselves, that alone prevents a lot of these from ever forming."
High-Yield Recall Sheet
The master question for every SSTI:purulent (think staph/MRSA) or nonpurulent (think strep)? Then layer on anaerobic coverage for bites/ulcers/necrotic tissue.
Erysipelas:raised, sharp border, group A strep almost exclusively, penicillin is first-line.
Cellulitis:flat, poorly demarcated margins; treat 5 days(extend only if not improving).
Carbuncles/large furuncles/abscesses:incision and drainage is the primary treatment, antibiotics are an adjunct.
Impetigo:topical mupirocin/retapamulin x 5 days for limited disease; oral dicloxacillin/cephalexin x 7 days for extensive or facial disease.
Beta-lactams that do NOT cover MRSA:dicloxacillin, cephalexin, nafcillin, cefazolin. Ceftaroline is the exceptionthat does.
Necrotizing fasciitis from group A strep:clindamycin + penicillin, clindamycin suppresses toxin production, penicillin doesn't.
Necrotizing fasciitis:surgical debridement is essential, not optional, antibiotics alone will not cure it.
Animal bites:Pasteurella is resistant to penicillinase-resistant penicillins, 1st-gen cephalosporins, macrolides, and clindamycin. Amoxicillin-clavulanateis the answer.
Human bites:Eikenella corrodens in ~30%; amoxicillin-clavulanate again; primary closure generally avoided; all human bites get 3-5 days of prophylaxis.