12.2 Acne, Rosacea & Cutaneous Infections
Key Takeaways
- Acne vulgaris and rosacea are the two topics enumerated under acne and rosacea.
- Dermatophytes, herpes zoster and varicella, viral exanthems, cellulitis, necrotizing infection, lymphadenitis and ectoparasites are enumerated under skin and soft tissue infections.
- Isotretinoin requires pregnancy prevention with monitoring because of severe teratogenicity.
- Eczema herpeticum is a dermatologic emergency in which herpes simplex disseminates across eczematous skin and requires prompt systemic acyclovir.
- Topical corticosteroids applied to undiagnosed dermatophyte infection produce tinea incognito with an altered, less recognizable appearance.
Last updated: August 2026
Rosacea
- Pathophysiology: A chronic centrofacial inflammatory disorder characterized by abnormal neurovascular reactivity, innate immune hyperreactivity (upregulation of toll-like receptor 2 [TLR2] and cathelicidin antimicrobial peptides [LL-37]), and proliferation of Demodex folliculorum mites within sebaceous follicles.
- Clinical Subtypes & Differentiation:
| Rosacea Subtype | Primary Clinical Features | Common Triggers | First-Line Management |
|---|---|---|---|
| 1. Erythematotelangiectatic (ETR) | Persistent central facial erythema, flushing episodes, and fine branching telangiectasias across cheeks, nose, and chin | Hot beverages, spicy foods, alcohol, temperature changes, emotional stress, UV light | Avoid known triggers; broad-spectrum SPF >=30 sunscreen; topical alpha-adrenergic vasoconstrictors (Brimonidine 0.33% gel or Oxymetazoline 1% cream); Pulsed-dye laser (PDL) for fixed telangiectasias |
| 2. Papulopustular | Central facial erythema with dome-shaped inflammatory papules and pustules; NO comedones (distinguishes from acne vulgaris) | Same dietary, thermal, and UV triggers | Mild/Moderate: Topical Metronidazole 0.75-1% gel/cream, Topical Ivermectin 1% cream (anti-parasitic against Demodex + anti-inflammatory), or Topical Azelaic acid 15% gel.<br/>Moderate/Severe: Add Oral Doxycycline (sub-antimicrobial dose 40 mg daily [30 mg IR / 10 mg DR] or 50-100 mg daily) |
| 3. Phymatous | Marked sebaceous gland hyperplasia and fibrous connective tissue hypertrophy leading to irregular, thickened, lobulated skin; most commonly affects nose (rhinophyma), predominantly in men | Chronic progressive inflammation | Early: Oral Isotretinoin; Advanced: Surgical debulking, electrosurgery, or ablative CO2 laser resurfacing |
| 4. Ocular Rosacea | Blepharitis, conjunctival hyperemia, chalazia/styes, gritty foreign-body sensation, dry eyes, photophobia; can lead to corneal vascularization/ulceration | Meibomian gland dysfunction | Eyelid hygiene, warm compresses, artificial tears, oral Doxycycline, topical ophthalmic Cyclosporine |
Acne Vulgaris
- Pathophysiology: A multifactorial disorder of the pilosebaceous unit involving 4 primary pathogenic events: (1) Follicular hyperkeratinization obstructing the pilosebaceous follicle (forming microcomedones); (2) Androgen-stimulated excess sebum production; (3) Proliferation of Cutibacterium acnes (formerly Propionibacterium acnes) within sebum-rich microenvironments; (4) Follicular rupture and innate immune inflammation mediated by neutrophils and lymphocytes.
- Morphology: Non-inflammatory comedones (open [blackheads] vs closed [whiteheads]) and inflammatory lesions (erythematous papules, pustules, deep tender nodules, and pseudocysts). May heal with post-inflammatory hyperpigmentation or atrophic/hypertrophic scarring.
- Stepwise Treatment Algorithm:
- Mild Comedonal Acne: Topical Retinoid monotherapy (Adapalene 0.1-0.3%, Tretinoin 0.025-0.1%, or Tazarotene 0.05-0.1%) applied once nightly. Normalizes follicular desquamation, prevents new microcomedones, and promotes lesion clearance.
- Mild-to-Moderate Inflammatory Acne: Combination of Topical Retinoid + Benzoyl Peroxide (BPO 2.5-5%) +/- Topical Antibiotic (Clindamycin 1%).
- Crucial Rule: Never prescribe topical antibiotic monotherapy (e.g., clindamycin alone) due to rapid development of bacterial resistance; always combine with Benzoyl Peroxide, which generates bactericidal reactive oxygen species with zero bacterial resistance.
- Moderate-to-Severe Inflammatory Acne: Topical Retinoid + BPO + Oral Antibiotic (Doxycycline 50-100 mg PO BID or Minocycline 50-100 mg PO BID). Limit oral antibiotic duration to <=3 to 4 months to prevent systemic resistance. In post-pubertal females, consider antiandrogenic hormonal therapies: Combined Oral Contraceptives (COCs) containing drospirenone or norgestimate, or Spironolactone (50-100 mg daily).
- Severe Nodulocystic, Scarring, or Treatment-Refractory Acne: Oral Isotretinoin (13-cis-retinoic acid) (cumulative target dose 120-150 mg/kg over 4-6 months). Isotretinoin is the only curative monotherapy that addresses all 4 pathogenic mechanisms.
- Safety, Monitoring & Regulations: Extreme teratogenicity (hydrocephalus, microtia, conotruncal cardiac defects); mandates enrollment in the iPLEDGE Risk Evaluation and Mitigation Strategy (REMS) program requiring two negative pregnancy tests prior to initiation, two forms of contraception, and monthly negative pregnancy tests before each 30-day prescription. Baseline and periodic monitoring: Liver Function Tests (LFTs), fasting lipid panel (triglycerides/cholesterol), and screening for depressive symptoms/mood changes. Common side effects: severe cheilitis, xerosis, epistaxis, myalgias, and elevated liver enzymes/triglycerides.
1. Infectious Dermatoses & Mimickers
Cellulitis vs. Erysipelas vs. Stasis Dermatitis
Differentiating acute bacterial dermohypodermal infections from chronic vascular pseudocellulitis is among the most heavily tested dermatology topics in hospital and outpatient internal medicine.
| Clinical Parameter | Cellulitis | Erysipelas | Stasis Dermatitis (Pseudocellulitis) |
|---|---|---|---|
| Anatomical Depth | Deep dermis and subcutaneous fat | Superficial dermis and upper dermal lymphatics | Epidermis and superficial dermis secondary to chronic venous hypertension |
| Typical Etiology | Beta-hemolytic Streptococci (S. pyogenes, Group G/C/B) > Staphylococcus aureus | Group A Beta-hemolytic Streptococcus (Streptococcus pyogenes) | Chronic venous insufficiency, valvular incompetence, capillary leakage, hemosiderin deposition |
| Laterality | Unilateral (>98% of cases) | Unilateral | Bilateral (symmetric lower extremities) |
| Margin & Appearance | Poorly demarcated, spreading flat erythematous border; warm, tender, edematous | Sharply demarcated, raised, indurated border; fiery red, orange-peel (peau d'orange) texture; prominent facial (malar) or lower leg involvement | Poorly demarcated, brown-red hemosiderin hyperpigmentation, eczematous scaling, xerosis, varicose veins, pitting edema, lipodermatosclerosis ("inverted champagne bottle" leg) |
| Onset & Systemic Signs | Subacute (days), moderate fever/leukocytosis | Acute, explosive onset (hours) with high fever, chills, rigors, systemic toxicity | Chronic, indolent (months to years), afebrile, normal WBC count |
| First-Line Treatment | Oral Cephalexin 500 mg QID or IV Cefazolin 1-2 g q8h (non-purulent).<br/>Add MRSA coverage (TMP-SMX, Doxycycline, or IV Vancomycin) if purulent drainage, abscess, injection drug use, or severe toxicity | Oral Penicillin VK 500 mg QID, Amoxicillin 500 mg TID, or IV Cefazolin / Penicillin G | Leg elevation, graduated compression stockings (20-30 mmHg), thick emollients, mid-potency topical steroids (Triamcinolone 0.1%) for acute eczematous flare. NO SYSTEMIC ANTIBIOTICS |
Test Your Knowledge
A 26-year-old woman with a longstanding history of atopic dermatitis and allergic rhinitis presents with a 2-day history of acute painful facial skin eruptions, malaise, and a fever of 38.9°C (102.0°F). Physical examination reveals widespread, monomorphic, punched-out, umbilicated vesicles and shallow crusted erosions superimposed over excoriated eczematous plaques on her cheeks, perioral area, and forehead. Cervical lymph nodes are enlarged and tender. What is the most appropriate next step in management?
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