13.1 Bacterial Skin & Soft Tissue Infections

13.1 Bacterial Skin & Soft Tissue Infections

Overview of Bacterial Skin & Soft Tissue Infections

Bacterial skin and soft tissue infections (SSTIs) are among the most frequent clinical presentations in both ambulatory and inpatient dermatology across Europe. Pathophysiologically, SSTIs depend on the delicate equilibrium between the cutaneous physical and immunological barrier (acid mantle, stratum corneum integrity, antimicrobial peptides such as cathelicidin LL-37 and human beta-defensins) and bacterial virulence factors (exotoxins, proteases, superantigens, adhesins).

Clinically, SSTIs are classified according to their anatomical depth of involvement:

1. Epidermal (Superficial pyodermas): Impetigo (non-bullous and bullous), ecthyma, Staphylococcal Scalded Skin Syndrome (SSSS).
2. Follicular & Appendageal: Superficial folliculitis, furuncles, carbuncles, abscesses.
3. Dermal & Lymphatic: Erysipelas.
4. Subcutaneous & Deep Dermal: Cellulitis.
5. Fascial & Muscular (Necrotising Soft Tissue Infections): Necrotising fasciitis, Fournier gangrene, myonecrosis.
6. Superficial Cutaneous Corynebacterioses: Erythrasma, pitted keratolysis, trichobacteriosis.

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Superficial Pyodermas

1. Impetigo

Impetigo is the most common superficial bacterial skin infection in children aged 2 to 5 years, though it can occur at any age, particularly in settings of poor hygiene, tropical climates, or underlying pre-existing dermatoses (secondary impetiginisation / eczema impetiginatum).

Non-Bullous Impetigo (Impetigo Contagiosa)

• Etiology: Staphylococcus aureus is the predominant pathogen in Europe (accounting for ~70–80% of cases), either alone or in co-infection with Group A beta-hemolytic Streptococcus (Streptococcus pyogenes / GAS). Primary S. pyogenes impetigo accounts for the remaining cases.
• Pathogenesis: Inoculation occurs into microtrauma, abrasions, or eczematous lesions. Streptococcal strains involved are primarily nephritogenic skin strains (M types 49, 55, 57, 60), which carry a risk of triggering post-streptococcal glomerulonephritis (PSGN), but notably not acute rheumatic fever (which follows pharyngeal, not cutaneous, streptococcal infections).
• Clinical Presentation: Commences as transient, thin-walled vesicles or pustules on an erythematous base that rapidly rupture, releasing purulent exudate that dries into classic meliceric (honey-coloured) crusts. Predilection sites are exposed facial areas, especially the perioral, perinasal, and chin regions, as well as the extremities. Lesions are pruritic, and auto-inoculation via scratching produces satellite clusters. Regional lymphadenopathy is frequent.
• Management:
  • Localized disease (limited number of lesions, no systemic signs): Gentle soaking and removal of crusts with saline compresses, followed by topical mupirocin 2% ointment or fusidic acid 2% cream/ointment applied 2 to 3 times daily for 5 to 7 days. Topical retapamulin 1% ointment is an approved pleuromutilin alternative.
  • Widespread or bullous disease, daycare/school outbreaks, or systemic symptoms: Oral beta-lactamase-resistant penicillins (flucloxacillin 250–500 mg q6h in adults; 25–50 mg/kg/day in children divided q6h) or first-generation cephalosporins (cefalexin 500 mg q6h in adults). In penicillin-allergic patients or documented MRSA, oral clindamycin, trimethoprim-sulfamethoxazole (TMP-SMX), or macrolides (clarithromycin) are indicated.

Bullous Impetigo

• Etiology: Exclusively caused by Staphylococcus aureus strains belonging to phage group II (predominantly types 71 and 55).
• Pathogenesis: These strains produce exfoliative toxins A and B (ETA and ETB). ETA (chromosomally encoded, heat-stable) and ETB (plasmid-encoded, heat-labile) are serine proteases that specifically cleave the extracellular domain of Desmoglein 1 (Dsg1)—a desmosomal cadherin mediating cell-cell adhesion exclusively in the superficial granular layer (stratum granulosum) of the epidermis. Dsg1 cleavage causes intraepidermal acantholysis, creating subcorneal cleavage without dermal-epidermal separation.
• Clinical Presentation: Presents as flaccid, clear to turbid bullae (1–3 cm) on previously intact skin, most frequently in the trunk, intertriginous folds (axillae, groin), and buttocks. Because the roof of the blister is thin stratum corneum, blisters rupture readily, leaving a moist, glistening red erosion surrounded by a characteristic narrow peripheral collarette of scale. Honey-coloured crusts are absent; crusts are thin, varnish-like, and moist. Blister fluid contains abundant viable S. aureus (in contrast to SSSS).
• Management: Systemic oral antimicrobial therapy is preferred because multiple cutaneous sites are typically involved. Oral flucloxacillin or cefalexin for 7 days is first-line.

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2. Staphylococcal Scalded Skin Syndrome (SSSS / Ritter von Rittershain Disease)

SSSS represents the severe, generalized systemic counterpart to bullous impetigo, occurring primarily in neonates and young children under 5 years of age, or in adults with severe renal insufficiency, end-stage kidney disease, or cellular immunodeficiency.

Pathogenesis

Unlike bullous impetigo (where exfoliative toxins act locally at the infection site), in SSSS, Staphylococcus aureus phage group II colonizes a distant focal infection—typically the nasopharynx, conjunctiva, umbilicus (in neonates), otitis media, or an occult cutaneous abrasion.

• The bacteria proliferate locally and secrete exfoliative toxins ETA and ETB into the bloodstream.
• The toxins disseminate hematogenously throughout the entire body to reach the cutaneous microvasculature of the upper dermis and epidermis.
• Circulating ETA/ETB binds and specifically cleaves Desmoglein 1 in the granular layer of the entire integument.
• Why neonates and renal patients? Neonates lack mature neutralizing maternal anti-ETA/ETB antibodies and possess immature renal glomerular clearance mechanisms, allowing circulating toxin concentrations to rise dramatically. Adults with renal failure cannot clear the low-molecular-weight protein toxins (27–30 kDa), predisposing them to SSSS despite prior antibody exposure.

Clinical Manifestations

1. Prodrome: Irritability, malaise, restlessness, high fever, and profound, exquisite cutaneous tenderness (the child cries violently when touched).
2. Erythroderma Stage: Diffuse, tender, macular faint erythema begins periorificially on the face (perioral, perinasal, periocular) and in flexural folds (neck, axillae, groin) before generalizing within 24 to 48 hours to the entire cutaneous surface.
3. Bullous & Desquamative Stage: Large, very flaccid, clear fluid-filled bullae form rapidly and rupture with minimal friction, leading to extensive epidermal sloughing that resembles a severe thermal burn (scalded appearance). Moist, denuded, red glistening skin is exposed.
4. Facial Characteristics: Prominent perioral crusting and radial fissuring (rhagades) giving an appearance resembling a "sunburst" or "sad mouth".
5. Pathognomonic Physical Signs:
   • Nikolsky Sign Positive: Gentle lateral tangential shear pressure on perilesional or normal-appearing skin causes the epidermis to slide and shear off.
   • Mucous Membrane Sparing: The buccal mucosa, tongue, pharynx, and genital mucosal surfaces are strictly spared (may show mild conjunctival hyperaemia without erosion). Key Reason: Desmoglein 3 (Dsg3) is co-expressed with Dsg1 throughout the mucosal epithelium, providing mechanical adhesive compensation when Dsg1 is cleaved; in the superficial epidermis, Dsg1 is the sole expressed isoform, making it selectively vulnerable to exfoliative cleavage.
   • Sterile Blister Fluid: Because the blistering is a toxin-mediated phenomenon from a distant site, cultures of blister fluid or intact bullae are consistently sterile. Cultures must be obtained from the primary colonized site (nasopharynx, conjunctiva, umbilicus, ears, blood).

Diagnostic Confirmation & Histopathology

• Frozen Section / Tzanck Smear: Rapid differentiation from Toxic Epidermal Necrolysis (TEN) is life-saving. Frozen section of a blister roof shows intraepidermal cleavage at the subcorneal / granular layer with intact basal and spinous layers. In TEN, the entire full-thickness epidermis is necrotic (subepidermal split with necrotic keratinocytes).

Treatment Protocol

• Hospital Admission: Usually pediatric intensive care or a burn unit for fluid resuscitation, temperature control, and barrier protection.
• Antimicrobial Therapy: Immediate intravenous antistaphylococcal beta-lactams: Flucloxacillin (100–200 mg/kg/day IV divided q6h) or Cefazolin (50–100 mg/kg/day IV divided q8h). Addition of intravenous Clindamycin (30–40 mg/kg/day IV divided q8h) is strongly recommended for its potent ribosomal protein-synthesis-inhibiting effect, rapidly halting bacterial production of exfoliative toxins.
• In communities with elevated MRSA prevalence or culture-confirmed MRSA: IV Vancomycin (40–60 mg/kg/day) or Linezolid.
• Supportive Care: Gentle handling, non-adherent silicone/petrolatum dressings, analgesia (avoid NSAIDs due to renal impact), fluid and electrolyte management.
• Systemic Corticosteroids are Contraindicated: Corticosteroids impair host clearance of S. aureus and worsen mortality.

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Comparison: SSSS vs Toxic Epidermal Necrolysis (TEN)

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Ecthyma, Folliculitis, Furuncles & Carbuncles

1. Ecthyma

• Definition: A deep, ulcerative form of impetigo extending entirely through the epidermis into the dermis.
• Etiology: Streptococcus pyogenes (GAS) alone or combined with Staphylococcus aureus.
• Pathogenesis: Arises from pre-existing minor trauma, excoriations, insect bites, or neglected non-bullous impetigo, frequently exacerbated by poor hygiene, malnutrition, diabetes, or peripheral vascular insufficiency.
• Clinical Presentation: Commences as a vesicle or pustule that erodes deeply into the dermis, forming a characteristic punched-out circular ulcer (0.5–3 cm) covered by an extremely thick, hard, adherent, greenish-black or dirty-grey crust. The ulcer margins are raised, indurated, and violaceous with surrounding erythema and edema. Most commonly affects the lower extremities (shins, dorsal feet).
• Distinction from Impetigo: Because it penetrates the basement membrane into the vascularized dermis, ecthyma always heals with permanent scarring and post-inflammatory pigmentary alterations.
• Management: Requires systemic oral antistaphylococcal/streptococcal antibiotics (oral flucloxacillin, cefalexin) for 10 to 14 days, combined with gentle soaking to debride the adherent crusts and topical antiseptics.

2. Folliculitis, Furuncles & Carbuncles

• Superficial Folliculitis (Bockhart Impetigo): Tiny, dome-shaped yellow pustules centered exactly on hair follicles, surrounded by a narrow erythematous rim. Predominantly S. aureus. Non-infectious or fungal mimics include Malassezia folliculitis, eosinophilic folliculitis, and pseudofolliculitis barbae.
• Furuncle (Boil): A deep, necrotizing perifollicular and follicular infection extending into the deep dermis and subcutaneous adipose tissue, forming an exquisitely painful, fluctuant inflammatory nodule with a central necrotic core or "plug". Most common on the neck, face, axillae, perineum, and buttocks.
• Carbuncle: An extensive, highly confluent, interconnected conglomeration of several adjacent furuncles that drain through multiple follicular openings onto the skin surface. Characterized by severe localized throbbing pain, dense induration, high fever, chills, and leukocytosis. Predilection for the thick, fibrous skin of the posterior neck, upper back, and lateral thighs, particularly in patients with poorly controlled diabetes mellitus.

3. Panton-Valentine Leukocidin (PVL) Cytotoxin

• Microbiology: Panton-Valentine leukocidin (PVL) is a pore-forming, two-component cytotoxin (composed of proteins LukS-PV and LukF-PV) encoded by the pvl genes carried on a lysogenic bacteriophage integrated into the S. aureus genome.
• Pathogenicity: PVL specifically binds to complement receptors on polymorphonuclear neutrophils, monocytes, and macrophages, assembling into octameric pores that induce rapid leukocyte lysis and profound tissue necrosis.
• Clinical Phenotype: PVL-producing S. aureus (which may be either MSSA or community-associated MRSA [CA-MRSA], notably clone USA300 in the Americas or ST80 in Europe) is strongly associated with:
  • Recurrent, severe, highly necrotic furunculosis and cutaneous abscesses in young, otherwise healthy individuals.
  • Severe local tissue destruction, extensive central necrosis, and violaceous border hemorrhage.
  • Lethal necrotising hemorrhagic pneumonia (often preceded by an influenza-like viral illness with hemoptysis, leukopenia, and high mortality).
• Decolonization Protocol: For patients with recurrent PVL-positive furunculosis and their household contacts:
  • Intranasal mupirocin 2% nasal ointment applied twice daily to both anterior nares for 5 days.
  • Daily whole-body washes with chlorhexidine 4% or octenidine wash lotion for 5 to 7 days.
  • Decontamination of bed linens, towels, and clothing by washing at ≥ 60°C.
  • Systemic antibiotics when indicated: Clindamycin, trimethoprim-sulfamethoxazole, or linezolid (which suppress PVL toxin synthesis via ribosomal inhibition).

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Dermal & Soft-Tissue Infections: Erysipelas vs Cellulitis

+--------------------------------------------------------------------------+
|                     ANATOMICAL LEVEL OF INFECTION                        |
+--------------------------------------------------------------------------+
| [Epidermis]      Impetigo / SSSS (Subcorneal layer)                      |
| [Basement Memb]  Ecthyma (Ulcerates through BM into dermis)              |
| [Upper Dermis]   ERYSIPELAS (Superficial dermis + superficial lymphatics)|
|                  -> Sharply demarcated, raised flame-like margins        |
| [Deep Dermis]    CELLULITIS (Deep dermis + subcutaneous fat)             |
| [Subcutis]       -> Ill-defined, indistinct, flat spreading margins      |
| [Deep Fascia]    NECROTISING FASCIITIS (Fascial necrosis + thrombosis)   |
|                  -> Wooden hardness, skin anesthesia, purple bullae      |
+--------------------------------------------------------------------------+

1. Erysipelas

• Etiology: Predominantly Streptococcus pyogenes (Group A beta-hemolytic Streptococcus, >80–85%), followed by Group C and Group G streptococci, and rarely S. aureus.
• Anatomical Level: Infection is localized to the superficial papillary and reticular dermis with prominent, intense involvement of the cutaneous lymphatic vessels.
• Clinical Presentation:
  • Onset: Extremely abrupt onset over hours, heralded by systemic symptoms: high fever (39–40°C), rigors, shaking chills, nausea, and headache—often preceding cutaneous signs by several hours.
  • Cutaneous Morphology: A bright red, intensely erythematous, warm, tensely indurated, and painful plaque with sharply demarcated, elevated, step-like advancing borders ("flame-like" borders). Dermal lymphatic obstruction produces cutaneous edema with surface pitting around follicular openings, creating a classic peau d'orange (orange-peel) texture.
  • Distribution: Lower extremities (approx. 75–80% of cases) and the face (approx. 10–15%).
  • Milian's Ear Sign: Involvement of the external ear pinna. Because the pinna consists of skin closely adherent to cartilage with virtually no subcutaneous fat, any cutaneous infection of the ear pinna must be an infection of the dermis—confirming erysipelas and ruling out cellulitis (which requires subcutaneous tissue).
  • Complications: Bullae or petechiae (bullous/hemorrhagic erysipelas), chronic recurrent erysipelas leading to irreversible obstructive lymphatic destruction and secondary elephantiasis nostras verrucosa.
• Treatment:
  • Uncomplicated oral therapy: Phenoxymethylpenicillin (Penicillin V) 1.0–1.5 million IU (600–1000 mg) orally q6h for 7–10 days, or Amoxicillin 1 g q8h.
  • Severe disease / inpatient: Intravenous Benzylpenicillin (Penicillin G) 2–4 million IU IV q4–6h. Once clinical improvement and fever resolution occur, step down to oral penicillin.
  • Penicillin allergy: Macrolides (clarithromycin 500 mg q12h), oral/IV clindamycin (300–600 mg q8h), or cefazolin/ceftriaxone (if non-anaphylactic).

2. Cellulitis

• Etiology: Most commonly Streptococcus pyogenes and Staphylococcus aureus (MSSA and MRSA). Gram-negative bacilli (Pseudomonas aeruginosa, Escherichia coli, Klebsiella) occur in neutropenic, cirrhotic, or diabetic patients; Aeromonas hydrophila following freshwater exposure; Vibrio vulnificus following warm saltwater or raw seafood exposure.
• Anatomical Level: Infection involves the deep reticular dermis and the subcutaneous adipose tissue.
• Clinical Presentation:
  • Onset: More indolent and progressive onset over days compared to erysipelas.
  • Cutaneous Morphology: Spreading area of erythema, local warmth, swelling, and tenderness with ill-defined, indistinct, non-elevated margins that blend imperceptibly into surrounding normal skin. The skin is flat or indurated, but lacks the sharp, step-like ridge seen in erysipelas.
  • Predisposing Factors: Disruption of cutaneous integrity (tinea pedis in toe webs—the single most common portal of entry in lower-limb cellulitis), chronic venous insufficiency, lymphedema, obesity, and prior saphenous vein harvesting.
• Treatment:
  • Mild to moderate: Oral Flucloxacillin (500–1000 mg q6h) or Cefalexin (500 mg q6h) to cover both S. aureus and streptococci.
  • Severe / hospitalized: IV Flucloxacillin (1–2 g IV q6h), Cefazolin (1–2 g IV q8h), or Ampicillin-sulbactam (1.5–3 g IV q6h).
  • Essential adjunctive measures: Strict limb elevation, treatment of interdigital tinea pedis (maceration) to eliminate the portal of entry, and long-term compression therapy once acute inflammation resolves.

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Life-Threatening Soft Tissue Infections: Necrotising Fasciitis

Necrotising Soft Tissue Infections (NSTIs) encompass necrotising fasciitis, necrotising cellulitis, and myonecrosis. They are rapidly progressive, destructive bacterial infections characterized by widespread necrosis of the subcutaneous tissues and fascia, with secondary thrombotic infarction of the overlying skin.

Classification

1. Type I (Polymicrobial, 70–80%):
   • Mixed synergistic infection involving aerobes (Enterobacteriaceae such as E. coli, Klebsiella, Proteus; Streptococcus species; Enterococcus) and obligate anaerobes (Bacteroides fragilis, Peptostreptococcus, Clostridium species).
   • Typically occurs in patients with predisposing comorbidities: diabetes mellitus, peripheral arterial disease, end-stage renal disease, immunosuppression, postoperative abdominal/perineal surgical wounds.
   • Fournier Gangrene: Specific Type I necrotising fasciitis localized to the perineum, scrotum, and perianal region, originating from colorectal, urogenital, or perianal foci.
2. Type II (Monomicrobial, 20–30%):
   • Caused by Group A beta-hemolytic Streptococcus (Streptococcus pyogenes), either alone or in combination with Staphylococcus aureus (MSSA or MRSA).
   • Known colloquially as "flesh-eating bacteria".
   • Frequently affects young, previously healthy individuals following minor trauma, lacerations, burns, childbirth, or blunt muscle injury without skin breach.
   • Produces Streptococcal Pyrogenic Exotoxins (SpeA, SpeB, SpeC), functioning as superantigens that induce massive non-specific T-cell activation, profound capillary leak, and Streptococcal Toxic Shock Syndrome (STSS) in over 50% of cases.
3. Type III (Vibrio & Marine): Caused by Vibrio vulnificus or Aeromonas, associated with marine trauma, saltwater exposure, or ingestion of raw oysters in patients with chronic liver disease/cirrhosis.
4. Type IV (Fungal): Rare, aggressive fungal forms (Mucorales, Aspergillus) occurring in severely immunocompromised or polytrauma burn patients.

Clinical Presentation: Early Warning Signs vs Late Manifestations

• The Hallmark Early Sign: Severe, excruciating pain that is completely out of proportion to the subtle cutaneous physical findings. A patient may present with mild, ill-defined erythema resembling early cellulitis, but writhing in agony.
• Early Features: Rapid spread along fascial planes (often extending tens of centimeters within hours); shiny, tense, pale or erythematous edema with a characteristic "wooden-hard" (woody) subcutaneous induration beyond the visible border of erythema; unresponsiveness to standard antibiotic therapy.
• Late / Definite Features:
  • Cutaneous Anesthesia: Disappearance of local pain and development of circumscribed skin numbness due to ischemic necrosis and infarction of cutaneous nerves crossing the superficial fascia.
  • Dusky, Violaceous Ecchymotic Discoloration: Skin turns from dusky grey to violaceous and purple.
  • Bullae: Development of large, flaccid bullae containing brown, foul-smelling, "dishwater"-like serosanguinous fluid.
  • Crepitus: Palpable gas in soft tissues (present in ~30% of Type I polymicrobial infections due to anaerobic fermentation; rare in Type II streptococcal necrotising fasciitis).
  • Systemic Collapse: High fever, tachycardia, profound hypotension, lactic acidosis, multiorgan failure, and septic shock.

The LRINEC Score (Laboratory Risk Indicator for Necrotizing Fasciitis)

Developed to assist in distinguishing severe necrotising soft tissue infections from non-necrotising cellulitis or abscess at initial presentation:

• Interpretation:
  • LRINEC Score < 6: Low risk (probability < 50%), but clinical suspicion always overrides the score.
  • LRINEC Score 6–7: Intermediate risk; suspicious for necrotising infection.
  • LRINEC Score ≥ 8: High risk (> 75% probability of necrotising fasciitis).
• Critical Clinical Caveat: While a high LRINEC score strongly supports necrotising fasciitis, a low score does not rule it out, especially in early Type II streptococcal infections. Never delay surgical exploration to await blood results or imaging.

Diagnostic "Finger Test"

Under local anaesthesia at the bedside or in the operating suite, a 2-cm incision is made down to the deep fascia. If necrotising fasciitis is present:

• There is an absence of normal bleeding and lack of muscular/fascial resistance.
• The examining gloved index finger slides effortlessly along the fascial plane without resistance ("positive finger test").
• Foul-smelling, dishwater-like, turbid exudate discharges freely.

Emergency Management Protocol

1. Immediate Radical Surgical Debridement: The absolute cornerstone of therapy. Complete surgical excision of all non-viable, necrotic skin, subcutaneous tissue, and fascia back to healthy, bleeding tissue. Re-exploration and "second-look" debridement in the operating room every 24 to 48 hours is mandatory until all tissue necrosis ceases.
2. Empiric Broad-Spectrum Intravenous Antibiotics:
   • Broad-spectrum cover for Gram-negatives and anaerobes: Meropenem (1 g IV q8h) OR Piperacillin-tazobactam (4.5 g IV q6h).
   • PLUS cover for MRSA: Vancomycin (15–20 mg/kg IV q8–12h) OR Daptomycin (6–8 mg/kg IV q24h).
   • PLUS Clindamycin (600–900 mg IV q8h): Non-negotiable component. Clindamycin acts at the bacterial 50S ribosomal subunit to inhibit bacterial protein synthesis (translation), shutting down production of streptococcal pyrogenic exotoxins (SpeA, SpeB) and staphylococcal toxins, overcoming the "Eagle effect" (where high bacterial inocula render cell-wall active beta-lactams ineffective due to stationary bacterial growth phase).
3. Intravenous Immunoglobulin (IVIG): High-dose IVIG (commonly a total of about 2 g/kg over 2–3 days) may be considered in Group A streptococcal necrotising fasciitis with streptococcal toxic shock syndrome; evidence is limited, so it is an adjunct to surgery and antibiotics, neutralizing circulating superantigens and down-regulating inflammatory cytokines.
4. ICU Resuscitation: Aggressive crystalloid fluid therapy, vasopressors for septic shock, correction of coagulopathy, and metabolic monitoring.

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Superficial Corynebacterioses & Plantar Bacterial Dermatoses

1. Erythrasma

• Etiology: Corynebacterium minutissimum, an aerobic, Gram-positive, non-spore-forming bacillus that constitutes normal human cutaneous microbiota.
• Pathogenesis: In humid, warm microenvironments with skin occlusion and friction, C. minutissimum proliferates within the stratum corneum, synthesizing water-soluble porphyrins—predominantly coproporphyrin III.
• Clinical Presentation: Sharply circumscribed, thin, reddish-brown, pink, or brownish macules and patches with a finely wrinkled surface, mild cigarette-paper scaling, and minimal to mild pruritus. Located in intertriginous flexural folds: genitocrural/inguinal folds, axillae, submammary spaces, umbilicus, and toe web spaces (interdigital erythrasma, often presenting as asymptomatic maceration and scale between the 4th and 5th toes).
• Wood's Lamp Examination (Diagnostic Gold Standard): Illuminating lesions under Wood's lamp (long-wave UVA light, peak 365 nm) produces a pathognomonic brilliant coral-red fluorescence due to coproporphyrin III. Distinguishes erythrasma instantly from tinea cruris (no red fluorescence) and intertrigo.
• Management:
  • Localized: Topical fusidic acid 2% cream, topical clindamycin 1% lotion/gel, or topical erythromycin 2% applied twice daily for 2 to 3 weeks.
  • Extensive or refractory: Single-dose oral clarithromycin (1 g stat) or erythromycin 500 mg q6h for 10–14 days.

2. Pitted Keratolysis (Keratolysis Plantare Sulcatum)

• Etiology: Kytococcus sedentarius (formerly Micrococcus sedentarius), Corynebacterium species, Dermatophilus congolensis, and Actinomyces species.
• Pathogenesis: Prolonged occlusion, hyperhidrosis, and elevated stratum corneum pH allow these bacteria to proliferate on the plantar skin. K. sedentarius secretes keratin-degrading serine proteases (protease P1 and P2) that selectively digest the keratin of the stratum corneum, eroding pits. Simultaneous production of volatile sulfur compounds (methanethiol, thiols, thioesters) produces a characteristic pungent, foul foot odor.
• Clinical Presentation: Multiple discrete, crateriform, punched-out superficial pits (1–7 mm wide, 1–2 mm deep) that coalesce into irregular, sieve-like erosions and sulci on weight-bearing plantar surfaces (heels, metatarsal heads, plantar surface of toes). Accompanied by intense plantar malodour (bromhidrosis), white waterlogged maceration, and burning or discomfort during prolonged standing. Highly prevalent in athletes, military personnel, and industrial workers wearing occlusive waterproof boots.
• Management:
  • Topical antibiotics: Topical clindamycin 1% solution/gel, fusidic acid 2% cream, or erythromycin twice daily for 2 to 4 weeks.
  • Control hyperhidrosis: Plantar aluminium chloride hexahydrate 20% solution applied at bedtime to clean, dry feet.
  • Hygiene measures: Moisture-wicking socks (wool or synthetic, avoiding cotton), rotating leather/breathable shoes, avoiding continuous rubber boot wear.

3. Trichobacteriosis (Trichomycosis Axillaris)

• Etiology: Corynebacterium flavescens (formerly Corynebacterium tenuis).
• Presentation: Asymptomatic yellow (flava, 98%), red (rubra), or black (nigra) granular concretions, nodules, and sheaths firmly adhering along the shafts of axillary and pubic hair, sparing the hair root. Accompanied by axillary hyperhidrosis and malodorous perspiration.
• Management: Shaving the involved axillary/pubic hair is curative. Adjunctive washing with chlorhexidine or benzoyl peroxide wash, followed by topical clindamycin or fusidic acid.