Bacterial Skin Infections

Pyodermas are among the commonest dermatology vignettes in NEET PG, and they reward a student who can map a clinical picture to the right organism, the right anatomical depth, and the right first-line antibiotic. This note builds the whole spectrum — impetigo, folliculitis, furuncle, carbuncle, ecthyma, erysipelas and cellulitis — around two organisms: Staphylococcus aureus and Streptococcus pyogenes (Group A beta-haemolytic streptococcus, GABHS).

Definition & classification

Bacterial skin infections (pyodermas) are infections of the skin and soft tissue caused chiefly by Gram-positive cocci. The single most useful organising principle is anatomical depth — it predicts the morphology, the likely organism, and the complications.

Depth involved	Condition	Hallmark
Epidermis (superficial)	Impetigo, ecthyma	Honey-coloured crust / punched-out ulcer
Hair follicle (ostium)	Folliculitis	Follicular pustule
Hair follicle + perifollicular dermis	Furuncle (boil)	Tender nodule, single follicle
Several adjacent follicles + deep subcutis	Carbuncle	Multi-loculated mass, multiple pus points
Upper dermis + superficial lymphatics	Erysipelas	Sharply demarcated, raised, fiery red
Deep dermis + subcutaneous fat	Cellulitis	Ill-defined, flat, warm erythema
Fascia / muscle	Necrotising fasciitis	Pain out of proportion, crepitus (separate emergency)

High-yield: The clean mental rule — superficial spreading lateral = impetigo; follicle-centred = folliculitis → furuncle → carbuncle; dermal/lymphatic = erysipelas; deep dermis/fat = cellulitis.

Etiology & pathophysiology

The two protagonists:

• Staphylococcus aureus — coagulase-positive, catalase-positive Gram-positive cocci in clusters. Causes bullous impetigo, folliculitis, furuncle, carbuncle, and most non-bullous impetigo today. Virulence via coagulase, Panton-Valentine leucocidin (PVL — associated with recurrent furunculosis and abscesses, classically community-acquired MRSA), and exfoliative/epidermolytic toxins A and B.
• Streptococcus pyogenes (GABHS) — catalase-negative, beta-haemolytic, bacitracin-sensitive cocci in chains. Causes erysipelas, ecthyma, and a share of non-bullous impetigo. Virulence via M protein, streptolysin O/S, streptokinase, hyaluronidase, and pyrogenic exotoxins.

Bullous impetigo and Staphylococcal Scalded Skin Syndrome (SSSS) share a mechanism worth memorising: exfoliative toxins A/B are serine proteases that cleave desmoglein-1, the desmosomal adhesion protein of the superficial granular layer. This produces a subcorneal split and flaccid bullae. In bullous impetigo the toxin acts locally (skin culture positive); in SSSS the toxin is haematogenously disseminated from a distant focus (skin culture negative, blood/focus culture positive). The same target (desmoglein-1) is destroyed immunologically in pemphigus foliaceus — a favourite linkage.

Predisposing factors: minor trauma/insect bites, poor hygiene, warm humid climate, atopic dermatitis (breached barrier + staph colonisation), diabetes mellitus, obesity, lymphoedema/venous stasis (recurrent cellulitis), and nasal carriage of S. aureus (recurrent furunculosis).

Clinical features — entity by entity

Impetigo

The commonest paediatric bacterial skin infection; highly contagious; favours face (peri-oral, peri-nasal) and limbs.

• Non-bullous (impetigo contagiosa) — ~70% of cases. Starts as a vesicle/pustule that ruptures to leave the classic honey-coloured (golden) crust on an erythematous base. Now predominantly S. aureus; GABHS or mixed in a minority. Minimal systemic upset.
• Bullous impetigo — S. aureus exfoliative toxin. Flaccid, fragile bullae with clear→turbid fluid that rupture leaving a collarette of scale and a shiny erythematous base. Trunk and intertriginous sites; common in neonates/infants.

High-yield: Honey-coloured crusts = non-bullous impetigo. The most feared sequela of streptococcal impetigo is post-streptococcal glomerulonephritis (PSGN) — and crucially, treating impetigo does NOT prevent PSGN (unlike rheumatic fever after strep pharyngitis, which antibiotics do prevent). Acute rheumatic fever does NOT follow streptococcal skin infection.

Ecthyma

A deeper form of impetigo extending into the dermis. Begins like impetigo but evolves into a punched-out ulcer with a thick adherent crust and heals with scarring (impetigo does not scar). Usually GABHS, often on the legs, in poor hygiene/malnutrition. Distinguish from ecthyma gangrenosum (a separate entity — Pseudomonas aeruginosa septicaemia in neutropenic patients; necrotic ulcer with surrounding erythema).

Folliculitis

Inflammation of the hair follicle ostium → pustule pierced by a hair. Usually superficial (Bockhart impetigo) and staphylococcal.

• "Hot tub" folliculitis — Pseudomonas aeruginosa, follows whirlpool/swimming-pool exposure; pruritic follicular papulopustules in swimwear distribution.
• Sycosis barbae — deep staphylococcal folliculitis of the beard.
• Gram-negative folliculitis — complicates prolonged antibiotic therapy for acne.

Furuncle (boil) and Carbuncle

• Furuncle — deep infection of a single follicle forming a tender, fluctuant perifollicular nodule with central necrosis; almost always S. aureus. Furunculosis = recurrent crops (think nasal carriage, diabetes, PVL-positive CA-MRSA).
• Carbuncle — coalescence of several adjacent furuncles into a deep, multi-loculated mass with multiple draining pus points (sieve-like); favours thick skin of the nape of neck, back, thighs; often with fever and malaise; frequent in diabetics.

High-yield: A furuncle/carbuncle of the central face (danger triangle — nose to lip) can spread via the facial→angular→ophthalmic veins to the cavernous sinus → cavernous sinus thrombosis. Never squeeze; treat with antibiotics ± drainage.

Erysipelas vs Cellulitis

Both present as spreading red, warm, tender skin, but depth differs and so do the cardinal signs. This comparison is the single most tested item in this topic.

Feature	Erysipelas	Cellulitis
Depth	Upper dermis + superficial lymphatics	Deep dermis + subcutaneous fat
Border	Sharply demarcated, raised, palpable edge	Ill-defined, flat, indistinct
Colour/surface	Fiery red, "peau d'orange", may blister	Pinkish-red, less brilliant
Usual organism	Strep. pyogenes (GABHS)	S. aureus and/or streptococci
Onset/systemic	Abrupt, high fever, chills, toxic	More gradual, fever variable
Classic sites	Face (butterfly) and legs	Lower limbs
Lymphatic streaking	Common (lymphangitis)	Variable

High-yield: Erysipelas = sharply raised demarcated border + Streptococcus; cellulitis = ill-defined flat margin + Staphylococcus. If the question stem stresses a clear-cut raised edge and a brilliant red plaque on the face/shin with sudden high fever, answer erysipelas.

Erysipeloid is a different beast: Erysipelothrix rhusiopathiae, a violaceous plaque on the hand/finger in fish/meat handlers — drug of choice penicillin.

Nikolsky sign and friends

A recurring MCQ favourite is the link between toxin-mediated staph disease and blistering signs.

• Nikolsky sign positive — lateral pressure/shear on normal-looking perilesional skin causes the epidermis to slough → indicates intra-epidermal loss of cohesion. Seen in SSSS, pemphigus vulgaris/foliaceus, and toxic epidermal necrolysis (TEN).
• Asboe-Hansen (bulla-spread) sign — pressing a bulla makes it extend laterally; same mechanistic family.
• Bullous impetigo blisters are flaccid and rupture easily but Nikolsky is localised to lesional skin; SSSS gives generalised Nikolsky positivity.

High-yield: SSSS spares mucous membranes (toxin targets desmoglein-1, which is not the dominant desmoglein in mucosa) — this clinically separates SSSS from TEN, which has prominent mucosal involvement and a deeper, full-thickness (subepidermal/DEJ) split with a poorer prognosis. SSSS occurs in neonates/young children (immature renal toxin clearance, lack of antibody) and heals without scarring.

Diagnosis & investigation of choice

Most pyodermas are clinical diagnoses. Investigations are reserved for severe, atypical, recurrent, or treatment-failing cases.

1. Gram stain + culture/sensitivity of pus or exudate → the investigation of choice when an organism/sensitivity is needed (abscess, carbuncle, MRSA suspicion, treatment failure). Aspirate or swab the leading edge/pus.
2. Blood cultures — only in toxic/septic patients, immunocompromised, or extensive cellulitis with systemic signs (low yield otherwise).
3. SSSS — diagnosis confirmed by skin biopsy/frozen section showing a high subcorneal (granular layer) split; culture the focus (nasopharynx, conjunctiva, umbilicus), not the bullae.
4. ASO / anti-DNase B titres — evidence of recent streptococcal infection; anti-DNase B is the better marker after skin (pyoderma) infection (ASO often does not rise well after skin strep). Useful in suspected PSGN.
5. Nasal swab for S. aureus carriage in recurrent furunculosis; screen blood sugar for diabetes.

Differentiating SSSS from TEN — the bedside flow: Mucosa involved? → yes ⇒ favours TEN · no ⇒ favours SSSS → Level of split on biopsy? → subcorneal/granular ⇒ SSSS · subepidermal/full-thickness with necrotic keratinocytes ⇒ TEN → Drug history & age? → drug + adult ⇒ TEN · staph focus + neonate/child ⇒ SSSS.

Management & drug of choice

General measures: soak and gently remove crusts, hygiene, keep area clean and dry, treat predisposing dermatoses (e.g., eczema), control diabetes, and decolonise carriers when recurrent.

Condition	First-line / drug of choice
Limited impetigo	Topical mupirocin (or fusidic acid / retapamulin)
Extensive/bullous impetigo	Oral antibiotic — cloxacillin/dicloxacillin or cephalexin (amoxicillin–clavulanate alternative)
Folliculitis (simple)	Topical antiseptics/mupirocin; oral antistaph if extensive
Hot-tub (Pseudomonas) folliculitis	Usually self-limiting; ciprofloxacin if needed
Furuncle	Warm compresses; incision & drainage is primary for fluctuant lesions; antibiotic if cellulitis/systemic
Carbuncle	Incision & drainage + systemic antistaph antibiotic
Erysipelas	Penicillin (penicillin V/amoxicillin oral; penicillin G IV if severe) — Streptococcus
Cellulitis (non-purulent)	Cover strep + MSSA: cephalexin / cloxacillin / amoxicillin–clavulanate
Cellulitis (purulent) / suspected MRSA	Doxycycline, clindamycin, or co-trimoxazole (oral); vancomycin/linezolid (IV)
Ecthyma	Oral antistaph/antistrep antibiotic (cloxacillin/cephalexin) + crust care
SSSS	IV antistaphylococcal penicillin (cloxacillin/nafcillin) + fluids/skin care; add vancomycin if MRSA

High-yield: The cornerstone of a fluctuant abscess/furuncle is incision and drainage — antibiotics are adjunctive, not a substitute. "Pus somewhere, pus nowhere, pus under a diaphragm — let it out."

High-yield: Erysipelas → penicillin; staphylococcal pyoderma → penicillinase-resistant penicillin (cloxacillin) or a first-generation cephalosporin (cephalexin). Choose I&D first for boils and carbuncles.

MRSA pointers: community-acquired MRSA (often PVL+) causes recurrent abscesses/furuncles. Oral options — clindamycin, co-trimoxazole, doxycycline; severe/inpatient — vancomycin (or linezolid/daptomycin). Decolonisation for recurrence: intranasal mupirocin + chlorhexidine body wash ± oral regimen.

Penicillin allergy: use clindamycin or a macrolide (with rising macrolide resistance noted).

Complications

• Post-streptococcal glomerulonephritis (PSGN) — after streptococcal impetigo/pyoderma (nephritogenic M-types); antibiotics do not prevent it.
• Acute rheumatic fever — follows strep pharyngitis, NOT skin infection (high-yield negative).
• Cellulitis → abscess, lymphangitis, lymphoedema, recurrent cellulitis, bacteraemia/sepsis.
• Necrotising fasciitis — rapidly spreading deep infection; pain out of proportion, dusky skin, bullae, crepitus, systemic toxicity → surgical emergency (urgent debridement + broad-spectrum antibiotics).
• Cavernous sinus thrombosis — from danger-triangle furuncles.
• Scarlet fever / streptococcal toxic shock / staphylococcal toxic shock — toxin-mediated.
• SSSS — dehydration, secondary infection, temperature instability (neonates).
• Scarring — ecthyma and carbuncle scar; impetigo and erysipelas usually do not.

Key differentials

• Cellulitis vs Deep vein thrombosis — both give a red, swollen, warm calf; cellulitis is usually unilateral with a portal of entry and more sharply tender erythema; image if DVT suspected.
• Cellulitis vs Stasis dermatitis / contact dermatitis — bilateral lower-leg erythema is rarely bilateral cellulitis; itch favours dermatitis, pain/fever favours infection ("pseudocellulitis" is a common over-diagnosis).
• Bullous impetigo vs SSSS vs Bullous pemphigoid vs TEN — see split level, mucosa, Nikolsky, age, drug history.
• Erysipelas vs Contact dermatitis vs Angioedema (face) — erysipelas is hot, tender, febrile with a raised border; angioedema is non-tender and non-erythematous.
• Ecthyma vs Ecthyma gangrenosum — the latter is Pseudomonas sepsis in neutropenics.
• Furuncle vs Hidradenitis suppurativa vs Epidermoid cyst (infected) — recurrent painful nodules/sinuses in axillae/groin favour hidradenitis.
• Erythrasma (intertriginous, Corynebacterium minutissimum, coral-red on Wood's lamp) and pitted keratolysis (also corynebacterial) — Gram-positive but distinct.

Mnemonics & named points

• Depth ladder: "Folliculitis is the seed, Furuncle the plant, Carbuncle the bush" — single ostium → single follicle nodule → cluster of follicles.
• Erysipelas = "Edges Raised" (sharp), strEptococcus, Eruptive high fever.
• Nikolsky-positive trio: "SPT" — SSSS, Pemphigus, TEN.
• Desmoglein-1 is the shared villain of bullous impetigo, SSSS, and pemphigus foliaceus.
• "Pus = drain it" for furuncle/carbuncle/abscess; antibiotic alone is not enough.

Recently asked / exam angle

• Photograph/description of a sharply marginated, raised, fiery-red plaque on the cheek or shin with sudden fever → identify erysipelas, organism Strep. pyogenes, DOC penicillin.
• Honey-coloured crust on a child's face → non-bullous impetigo; topical mupirocin; the complication that antibiotics will not prevent → PSGN.
• A neonate with diffuse erythema, flaccid blisters, positive Nikolsky, sparing mucosa, culture-negative skin → SSSS; toxin cleaves desmoglein-1 at the granular layer; treat with IV cloxacillin.
• "Pain out of proportion to skin findings + crepitus + rapidly dusky skin" → necrotising fasciitis, not simple cellulitis → emergency surgical debridement.
• Recurrent boils with PVL-positive culture → CA-MRSA; manage with I&D + clindamycin/co-trimoxazole and decolonisation (nasal mupirocin + chlorhexidine).
• Differentiate SSSS from TEN on split level (subcorneal vs subepidermal), mucosa, age, and drug history.
• Distinguish the investigation of choice (pus Gram stain & culture) versus when blood cultures are warranted.

Rapid revision

1. Erysipelas = upper dermis/lymphatics, sharply raised border, GABHS, DOC penicillin.
2. Cellulitis = deep dermis/fat, ill-defined flat margin, S. aureus/strep; cover MRSA if purulent (doxycycline/clindamycin/co-trimoxazole).
3. Honey-coloured crust = non-bullous impetigo; topical mupirocin for limited disease.
4. Bullous impetigo & SSSS = S. aureus exfoliative toxin cleaving desmoglein-1 (subcorneal split).
5. SSSS spares mucosa, occurs in neonates, Nikolsky positive, skin culture negative (culture the focus).
6. Nikolsky positive in SSSS, Pemphigus, TEN.
7. Furuncle = single follicle; carbuncle = multiple follicles (nape of neck, diabetics); I&D is primary.
8. Danger-triangle facial furuncle → cavernous sinus thrombosis — never squeeze.
9. Ecthyma = ulcerative, scarring impetigo (dermal); ecthyma gangrenosum = Pseudomonas sepsis.
10. Streptococcal impetigo → PSGN (antibiotics don't prevent it); never rheumatic fever from skin.
11. Anti-DNase B beats ASO as marker after streptococcal skin infection.
12. Hot-tub folliculitis = Pseudomonas; erysipeloid (fish handlers) = Erysipelothrix, DOC penicillin.