Antimicrobials in dermatology

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Meet the patient

A 54-year-old with type 2 diabetes arrives with a hot, red, spreading left leg over 36 hours — well-demarcated edge, tender, no pus, systemically well. The first question is not "which antibiotic" but "is this even infected?" because the mimic — bilateral red legs from stasis dermatitis — is not, and flucloxacillin will not fix compression stockings.^[1]

A second patient, 19, asks for "the antibiotic that worked last year" for her acne. The teaching moment is that her doxycycline worked as an anti-inflammatory, not a bactericide, and that every oral acne antibiotic must travel with benzoyl peroxide or it breeds resistant Cutibacterium acnes. Hold both patients and the whole topic turns on three sentences.^[6][18]

Three principles that run the whole topic

Topical for localised disease, oral for extensive or deep. A few impetigo lesions get mupirocin; a leg of cellulitis gets flucloxacillin. Crossing that line unnecessarily is how resistance and C. difficile are made.^[1]

Narrowest effective spectrum for the shortest effective time. Five to seven days of flucloxacillin for uncomplicated cellulitis; three to six months capped for an acne antibiotic; reassess at 48 hours if nothing has changed.^[1]

No acne antibiotic is ever prescribed alone. Every topical or oral antibiotic for acne travels with benzoyl peroxide, which kills C. acnes by free-radical chemistry that resistance mechanisms cannot touch. This single rule is the difference between stewardship and its opposite.^[6][18]

Classification — two axes, three organism families

Every antimicrobial on the skin falls into one of three organism families, and within each a topical and a systemic branch. Hold the taxonomy and the drug list becomes a prescribing map.^[1]

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How common, who, and why resistance is now your problem

Skin infections are among the commonest reasons antibiotics are prescribed worldwide, and dermatologists write a disproportionate share — acne alone sustains years of tetracycline exposure in young adults. Staphylococcus aureus colonises the anterior nares of about a third of healthy people and drives most purulent SSTI; Streptococcus pyogenes drives most non-purulent cellulitis and erysipelas. Diabetes, chronic oedema, tinea pedis, and immunosuppression are the host factors that turn a portal of entry into a spreading infection.^[2][3]

The counterpoint is resistance. C. acnes resistance to topical erythromycin and clindamycin has climbed wherever those agents are used without benzoyl peroxide, and prolonged tetracycline courses select resistant staphylococci and streptococci in skin and oropharyngeal flora. Community-acquired MRSA, once confined to defined risk groups, is now endemic in many regions and must be on the list whenever a purulent infection fails first-line therapy.^[17][18]

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Mechanisms — four bacterial targets, and why resistance follows

Antibiotics kill or disable bacteria through four classical targets, and the target predicts both spectrum and toxicity. Beta-lactams (flucloxacillin, cefalexin, cefaclor) bind penicillin-binding proteins and wreck the cell wall — bactericidal and inherently non-toxic to human cells, which is why they head anti-staphylococcal therapy and lead the pregnancy list. Protein-synthesis inhibitors crowd the ribosome: tetracyclines and macrolides hit the 30S and 50S subunits, clindamycin and fusidic acid block translation, and mupirocin is distinctive in disabling isoleucyl-tRNA synthetase.^[1]

Resistance comes in four flavours. Enzymatic inactivation — beta-lactamase, the reason plain penicillin fails against S. aureus and the reason flucloxacillin is beta-lactamase-stable. Target modification — the mecA gene encoding PBP2a is the molecular basis of MRSA. Efflux pumps drive tetracycline resistance. Reduced permeability closes the door. The dermatology-specific trap is inducible clindamycin resistance in staphylococci, detected by the D-test — an apparently sensitive isolate can still fail clindamycin therapy, so check the D-test before you rely on it.^[3]

Antifungals attack the wall and membrane. The allylamine terbinafine inhibits squalene epoxidase, depleting ergosterol and stacking toxic squalene — a fungicidal mechanism against dermatophytes. The azoles (clotrimazole through itraconazole) inhibit lanosterol 14-alpha-demethylase, a cytochrome P450 enzyme, and are fungistatic — and that same P450 inhibition is the engine of their drug-interaction load. Griseofulvin disrupts microtubule-mediated mitosis. Antivirals against HSV and VZV are nucleoside analogues — aciclovir and penciclovir are preferentially phosphorylated by viral thymidine kinase and then terminate viral DNA polymerase.^[10]

The clinical scenarios — match the picture to the first-line drug

Impetigo is honey-coloured crusts (non-bullous, S. aureus and S. pyogenes) or flaccid bullae (bullous, S. aureus exfoliative toxin); localised disease is topical, extensive disease oral. Cellulitis is a warm, spreading, poorly demarcated erythema of dermis and subcutis, usually unilateral on a leg, from S. pyogenes and MSSA — flucloxacillin first-line. Acne vulgaris is the papulopustular and nodulocystic disease of pilosebaceous units driven by C. acnes, treated with a tetracycline plus BPO for moderate-to-severe inflammatory disease. Rosacea is centrofacial erythema with papules and pustules and no comedones — topical metronidazole or low-dose doxycycline.^{[13][14][6][8]}

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Differential reasoning — three traps that waste antibiotics

The recurring trainee error is to reach for flucloxacillin before asking whether the leg is infected at all. Three traps deserve a named warning.^[1]

Pseudocellulitis — bilateral red legs from stasis dermatitis or contact dermatitis — is not infected and improves with compression and emollient. The discriminator: true cellulitis is unilateral, warm, spreading, and tender with systemic upset; pseudocellulitis is bilateral, cool, and symmetrical.^[1][4]

Infected versus colonised eczema — atopic eczema is nearly always colonised by S. aureus, so swabs grow staphylococci by default. Weeping, crusting, and sudden deterioration signal true infection and earn flucloxacillin; after which eczema therapy — emollient, topical steroid — must resume or the patient returns.^[4]

Acne versus folliculitis versus rosacea — acne shows comedones, folliculitis shows pustules centred on hairs often after hot tubs or shaving, and rosacea shows centrofacial erythema with telangiectasia and no comedones. Treating rosacea with an acne regimen misses the diagnosis.^[8]

At the bedside — four questions before the prescription

Run four questions before you write anything: the infection itself (extent, depth, purulence, systemic signs), the portal of entry (tinea pedis fissure, ulcer, cannula, eczema — treat the portal or the infection recurs), the host (pregnancy, age, renal function, immunocompromise, drug list), and whether to sample. Mark the leading edge of cellulitis with a datable pen line to track response; measure limb circumference to catch deterioration; check for fluctuance to find the abscess that needs surgery more than antibiotics.^[1]

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Investigations — usually none, sometimes decisive

Most uncomplicated skin infections are diagnosed clinically and need no test. Investigations earn their place when the organism is in doubt, the infection is severe or recurrent, or resistance is suspected. A bacterial swab of pus or exudate — not dry intact skin — guides therapy in abscess, purulent cellulitis, infected ulcer, and recurrent SSTI; blood cultures are reserved for severe sepsis, immunocompromise, and atypical infection.^[1][11]

Potassium hydroxide microscopy of skin scrapings confirms a dermatophyte within minutes and spares an unnecessary oral antifungal; fungal culture and PCR speciate the organism and belong before any long terbinafine course. Wood's lamp shows Microsporum fluorescing green in tinea capitis (rare now) and coral-red in erythrasma. For a chronic non-healing ulcer or nodular lesion unresponsive to standard antibiotics, extend the workup to atypical mycobacteria and deep fungi — tissue biopsy for AFB and culture at the right temperature is the only reliable answer.^[11][5]

Time-critical situations — when narrow therapy is the wrong answer

A few presentations override the routine logic and demand immediate broad action. Severe SSTI with sepsis or suspected necrotising fasciitis needs IV antibiotics and urgent surgical exploration — never delay surgery for imaging. Empiric cover combines a beta-lactam or beta-lactamase inhibitor or carbapenem with clindamycin for toxin suppression and MRSA cover with vancomycin, linezolid, or daptomycin.^[1]

Sepsis itself triggers the hour-1 bundle — cultures, lactate, broad antibiotics, fluids. A severe drug reaction — DRESS or Stevens-Johnson syndrome or toxic epidermal necrolysis, most often from co-trimoxazole, sulfonamides, or nevirapine — demands immediate withdrawal of the culprit and every unnecessary drug, supportive care, and burn-unit referral for TEN.^[1]

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Topical antibacterials — high local concentration, low systemic exposure

Topical therapy delivers a high local concentration with low systemic exposure, which is why it leads localised superficial infection and the chronic anti-inflammatory use in acne and rosacea. The cardinal acne rule returns: no topical antibiotic travels alone — always pair it with benzoyl peroxide.^[6][18]

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Topical antifungals — allylamine or azole, by site

Topical antifungals lead localised superficial fungal infection — tinea corporis, cruris, and pedis, cutaneous candidiasis, and pityriasis versicolor — leaving oral therapy for nail disease, tinea capitis, extensive or refractory infection, and the immunocompromised host. The allylamine terbinafine is fungicidal and may cure tinea pedis in one to two weeks; the azoles are fungistatic and need two to four weeks.^[11]

Topical antivirals — a small role for early labial HSV

Topical antivirals have a modest place in early, limited herpes labialis; systemic therapy wins for genital HSV, extensive disease, and the immunocompromised. Aciclovir 5% cream at the prodrome trims healing by about half a day; penciclovir 1% is similar; docosanol 10% is a barrier cream available without prescription. None helps once vesicles have crusted, because recurrent labial HSV is self-limiting and oral valaciclovir outperforms them for anything beyond the mildest episode.^[16]

Systemic antibacterials — flucloxacillin and the anti-staphylococcal backbone

When infection is extensive, deep, or systemic, oral replaces topical and IV replaces oral. The first-line oral agent for MSSA and streptococcal SSTI across most of the world is flucloxacillin, a beta-lactamase-stable penicillin.^[1][3]

For cellulitis and erysipelas, a 2024 network meta-analysis of randomised trials found no significant differences in cure rates among the evaluated oral antibiotics — flucloxacillin, cloxacillin, cefalexin, cefaclor, erythromycin, roxithromycin, clindamycin, and pristinamycin among them — so choice follows severity, allergy, and tolerability rather than ranked efficacy.^[26] For staphylococcal SSTI, response is expected within the first days and 5 to 7 days of therapy is typically adequate to achieve cure.^[3] The class-defining toxicity of the isoxazolyl penicillins is cholestatic hepatitis: roughly 1 in 15,000 flucloxacillin users, with age over 55 years and intake beyond 14 days as particular risk factors, and jaundice and pruritus that may first appear several weeks after the drug has been stopped, with liver tests abnormal for months.^[19]

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Tetracyclines — the acne and rosacea workhorses (used as anti-inflammatories)

Tetracyclines are the workhorses of inflammatory acne and papulopustular rosacea. The 2024 American Academy of Dermatology guideline makes oral doxycycline the only strongly recommended oral antibiotic for acne, while minocycline and sarecycline receive conditional recommendations — and its good practice statements require that systemic antibiotics are always combined with topical therapy and that systemic antibiotic use is limited.^[6] In rosacea, oral tetracyclines are a mainstay of treatment and low-dose modified-release tetracycline is among the established options.^[8]

The safety list every candidate must own. Tetracyclines are contraindicated in pregnancy (Category D) for fetal bone and tooth deposition, and in children under 8 years for the same reason. They cause photosensitivity (sunscreen mandatory), benign intracranial hypertension (stop for headache and blurred vision), oesophageal irritation (take with water, upright, not at bedtime), and they are chelated by calcium, iron, and antacids (separate by 2 hours). Vaginal candidiasis is common. Doxycycline is the preferred agent for its favourable profile.^[6]

Macrolides — the penicillin-allergy and pregnancy-acne option

Macrolides remain useful oral options for impetigo and for cellulitis in the penicillin-allergic, with erythromycin among the antibiotics showing no significant difference in cellulitis cure rates.^[13][26] Their class hazard is QT prolongation with a risk of torsade de pointes — rare, but concentrated in patients with existing QT prolongation, hypokalaemia, hypomagnesaemia, bradycardia, cardiovascular disease, and concomitant QT-prolonging drugs.^[25]

Resistant Gram-positive cover — linezolid and the rifampicin rule

Linezolid is an alternative to vancomycin for skin and soft tissue infections, including those caused by MRSA: a Cochrane review of nine randomised trials found linezolid achieved better clinical and microbiological cure rates than vancomycin, with a shorter hospital stay and cheaper outpatient oral therapy — at the cost of more thrombocytopenia and nausea than vancomycin.^[20]

Clindamycin plus rifampicin is an effective combination for hidradenitis suppurativa — a 2017 JAMA review of treatment studies identified clindamycin-rifampicin among the antibiotic combinations with evidence of effectiveness — alongside ertapenem followed by rifampicin, moxifloxacin, and metronidazole, adalimumab, and tissue-sparing surgery.^[21]

Systemic antifungals — terbinafine first for the nail

Oral antifungals are reserved for onychomycosis, tinea capitis, extensive or refractory dermatophytosis, deep or cutaneous candidiasis, and Malassezia folliculitis. Terbinafine leads dermatophyte onychomycosis; the azoles are alternatives and preferred for candidiasis and certain non-dermatophyte moulds.^[10][11]

Terbinafine 250 mg continuously leads toenail onychomycosis: in the 2020 network meta-analysis, the odds of mycological cure with continuous terbinafine 250 mg were significantly greater than with topical treatments, and oral terbinafine is first-line therapy for onychomycosis on tolerability, cure rate, and cost.^[10][11] Its principal toxicity is hepatotoxicity: severe cholestatic hepatitis has been reported, and the published analysis supports confirming normal liver function at the onset of therapy and measuring liver biochemistry with periodic blood tests during treatment.^[24]

Itraconazole 200 mg continuously matched continuous terbinafine in the network meta-analysis — both had significantly greater odds of mycological cure than topical treatments for toenail onychomycosis — whereas fluconazole and the pulse regimens of terbinafine and itraconazole did not differ significantly from topical treatment.^[10] For tinea capitis with a kerion, griseofulvin is preferred unless Trichophyton has been documented as the pathogen.^[11]

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Systemic antivirals — the 72-hour window for zoster

Systemic antivirals treat HSV and VZV. The nucleoside analogues aciclovir, valaciclovir (a prodrug with better bioavailability), and famciclovir (a prodrug of penciclovir) are all virostatic, working only in infected cells after phosphorylation by viral thymidine kinase.^[15][16]

For herpes zoster, antiviral treatment with aciclovir, valaciclovir, or famciclovir should be started ideally within 72 hours of the development of the rash.^[15] In zoster ophthalmicus, oral acyclovir 800 mg five times daily was superior to placebo for preventing ocular manifestations, with oral famciclovir 500 mg three times daily for 7 days and valaciclovir 1000 mg three times daily for 7 days giving comparable results to acyclovir 800 mg five times daily.^[22] For frequently recurrent genital herpes, long-term suppressive therapy with aciclovir 400 mg twice daily cut the mean number of recurrences from 12.9 to 1.7 per year in the first year, with no emerging aciclovir resistance over five years.^[23] In neonatal HSV, intravenous acyclovir is mandatory, and suppressive oral acyclovir after completion of parenteral therapy further improves the long-term prognosis.^[16]

Stewardship — the competency that is no longer optional

The mantra: topical for local, oral for deep, BPO with every acne antibiotic, short courses, culture-guided. Five principles, tested repeatedly.^[17]

1. Topical for localised disease — impetigo, folliculitis, localised tinea, infected wounds.^[13][18]
2. Oral for extensive or deep disease — cellulitis, extensive impetigo, abscess with surrounding cellulitis, onychomycosis.^[1]
3. Always combine a topical antibiotic with benzoyl peroxide for acne — BPO generates free radicals that kill C. acnes independent of resistance, suppressing the emergence of resistant strains.^[6][18]
4. Limit duration — acne antibiotics to 3 to 6 months then review; cellulitis 5 to 7 days; reassess at 48 hours if there is no response (resistant organism, abscess, wrong diagnosis).^[1]
5. Culture-guided therapy — swab pus from abscesses, cellulitis, and infected wounds; MRSA nasal screen for decolonisation; KOH or culture before any long antifungal course; tailor to sensitivities.^[3]

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Adverse effects — the signature toxicity of each class

Adverse effects fall into three groups: direct drug toxicity, ecological effects (resistance and C. difficile), and idiosyncratic reactions (SJS or TEN, DRESS, drug-induced lupus). Every prescriber must own the signature toxicity of each class — this is core exam and viva material.^[17]

Prognosis, duration, and the 48-hour checkpoint

Response to appropriate therapy is usually evident within 48 to 72 hours for bacterial SSTI. Failure to improve by then demands reassessment for a resistant organism, an undrained abscess, a deep infection (osteomyelitis, necrotising fasciitis), or a non-infectious diagnosis. Uncomplicated cellulitis resolves on 5 to 7 days of flucloxacillin; severe disease may need 10 to 14 days.^[1]

Acne antibiotics show benefit over 6 to 8 weeks and are capped at 3 to 6 months, with a maintenance plan of topical retinoid plus BPO and a switch to hormonal or isotretinoin therapy if response is inadequate. Onychomycosis cure with terbinafine is confirmed at 12 weeks (toenail) by clinical improvement and repeat KOH or culture, recognising that the nail grows out slowly.^[6]

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Special populations — pregnancy, children, the old, the failing organ, the immunocompromised

Pregnancy reshapes the choice sharply. Penicillins (flucloxacillin) and cephalosporins (cefalexin) are safe and remain first-line for SSTI. Tetracyclines are Category D and absolutely contraindicated — for acne in pregnancy use erythromycin (topical or oral), topical azelaic acid, or topical BPO. Co-trimoxazole is avoided (folate antagonism in the first trimester; kernicterus risk in the third). Aciclovir and valaciclovir are Category B and used for HSV and VZV in pregnancy, including suppression near term to prevent neonatal HSV.^[6][16]

Children need weight-based dosing and never receive tetracyclines under 8 years (permanent tooth discolouration). Paediatric impetigo gets topical mupirocin or oral weight-based flucloxacillin; tinea capitis gets oral griseofulvin or terbinafine for 6 to 12 weeks.^[12][13]

The elderly may blunt fever and present with confusion, and they are at higher risk of C. difficile (clindamycin, co-trimoxazole) and hyperkalaemia (co-trimoxazole with ACE inhibitors). Renal impairment forces dose adjustment of aciclovir, valaciclovir, fluconazole, co-trimoxazole, and cefalexin; terbinafine needs reduction in moderate-to-severe CKD. The immunocompromised — neutropenic, transplant, HIV, and the diabetic foot — need broader empiric cover, culture-guided de-escalation, and a low threshold for IV therapy and surgical review.^[2]

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Evidence, guidelines, and the settled controversies

The American Academy of Dermatology 2024 acne guideline makes strong recommendations for benzoyl peroxide, topical retinoids, topical antibiotics, and oral doxycycline, with oral isotretinoin strongly recommended for acne that is severe, causing psychosocial burden or scarring, or failing standard therapy; minocycline and sarecycline are conditional. Its good practice statements call for combining topical therapies with multiple mechanisms of action, limiting systemic antibiotic use, and combining systemic antibiotics with topical therapies.^[6] The network meta-analysis by Mavranezouli and colleagues found that for moderate-to-severe acne the combination of BPO with a topical retinoid and an oral tetracycline was among the most effective treatments (mean lesion-count reduction 43.5 percent), and that oral antibiotics combined with topical treatment outperformed oral antibiotics alone; oral isotretinoin at a cumulative dose of 120 mg per kg or more was the most effective oral agent.^[7] For rosacea, treatment is guided by phenotype: topical metronidazole, azelaic acid, and ivermectin, brimonidine for erythema, and oral tetracyclines including low-dose modified-release formulations.^[8][9] For onychomycosis, the network meta-analysis found that continuous terbinafine 250 mg and continuous itraconazole 200 mg both achieved significantly greater odds of mycological cure than topical treatments, with no significant difference in adverse-event odds between oral and topical agents.^[10] The withdrawal of oral ketoconazole for dermatophytosis, on hepatotoxicity grounds, is a settled controversy — topical ketoconazole remains safe. Open questions include the optimal duration of cellulitis therapy (short courses increasingly supported), the role of empiric anti-MRSA cover in low-prevalence settings, and the place of topical antiseptics (chlorhexidine, hypochlorous acid) as antibiotic-sparing alternatives for decolonisation and infected eczema.^[17][18]

Exam pearls

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Ward-round test

A 54-year-old diabetic has a unilateral hot red leg, well-demarcated edge, no pus, systemically well. First-line drug and duration?ShowHide

This is non-purulent cellulitis — unilateral, warm, spreading erythema is the classic picture, and antibiotic selection is determined by history, risk factors, severity, and the most likely organism. An oral agent active against streptococci and staphylococci is standard, with 5 to 7 days typically adequate and response expected within the first days; failure to respond demands reassessment for a resistant organism, an undrained abscess, or a mimic. Empiric MRSA cover belongs to purulent infection, where S. aureus dominates. Bilateral red legs point away from cellulitis toward a mimic such as stasis dermatitis — that leg needs compression and emollient, not antibiotics.

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A 19-year-old wants doxycycline for acne. What must travel with it, and for how long?ShowHide

Benzoyl peroxide, always. Every oral or topical acne antibiotic must be paired with BPO to suppress resistant C. acnes, and the tetracycline course is capped at 3 to 6 months before review and a switch to maintenance topical therapy or hormonal or isotretinoin. Tetracyclines are also contraindicated in pregnancy (Category D) and under age 8.

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A patient on clindamycin for an abscess develops profuse diarrhoea. What do you do?ShowHide

Stop the clindamycin immediately and send a C. difficile toxin assay. Clindamycin's signature harm is C. difficile-associated diarrhoea, which can progress to pseudomembranous colitis. Switch to a non-clindamycin agent guided by culture, and treat confirmed C. diff per local protocol (oral vancomycin or fidaxomicin).

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A returned traveller from an endemic region has a large painless ulcer with undermined edges. Which organism, and what is the trap?ShowHide

This is Buruli ulcer from Mycobacterium ulcerans — its mycolactone toxin causes painless tissue necrosis with undermined edges. The trap is treating with standard anti-TB RHZE: NTM are largely resistant. Diagnosis is tissue biopsy with AFB stain and culture at the right temperature; treatment is WHO rifampicin plus clarithromycin for 8 weeks with surgical debridement for advanced disease.

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References27ShowHide

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