MedMentor EDU

Medicine / Infectious Diseases  —  Study Notes Series

BACTERIAL INFECTIONS OF THE SKIN, SOFT TISSUES AND BONES

Part 2  —  Complete Exam-Oriented Notes

Classification  •  Impetigo  •  Cellulitis  •  Necrotising Infections  •  Diabetic Foot  •  Osteomyelitis  •  Septic Arthritis  •  Prosthetic-Joint Infection

MBBS  |  NEET-PG  |  INI-CET  |  DNB  |  FMGE

Based on Harrison’s, Davidson’s, Kumar & Clark and the API Textbook of Medicine

CONTENTS AT A GLANCE

1.   Classification of Skin and Soft-Tissue Infections 2.   Impetigo 3.   Ecthyma 4.   Follicular Infections 5.   Cutaneous Abscess 6.   Cellulitis 7.   Erysipelas 8.   Staphylococcal Scalded Skin Syndrome 9.   Localised Bacterial Skin Disorders 10.  Necrotising Soft-Tissue Infections 11.  Clostridial Myonecrosis (Gas Gangrene) 12.  Pyomyositis and Infectious Myositis 13.  Bite-Wound and Inoculation Infections 14.  Diabetic Foot Infection 15.  Osteomyelitis 16.  Septic Arthritis 17.  Prosthetic-Joint and Orthopaedic-Device Infection 18.  Master Comparison Tables 19.  Important Diagrams, Figures and Algorithms 20.  Important Clinical Photographs 21.  Important Radiology Images 22.  Important Microbiology and Histopathology Slides 23.  Rapid Revision — High-Yield One-Liners

 

SECTION 1  |  Classification of Skin and Soft-Tissue Infections

Skin and soft-tissue infections (SSTIs) are infections involving the epidermis, dermis, subcutaneous fat, superficial and deep fascia, or skeletal muscle. They form one of the commonest reasons for outpatient antibiotic prescription and hospital admission in India, and range from trivial impetigo to fulminant necrotising fasciitis with mortality exceeding 25%. [VERY HIGH-YIELD]

WHY CLASSIFICATION MATTERS ▪  Determines empirical antibiotic choice (Gram-positive vs polymicrobial cover). ▪  Determines need for surgery — purulent and necrotising infections need drainage/debridement, not antibiotics alone. ▪  Determines site of care — outpatient oral therapy vs inpatient IV therapy vs ICU. ▪  Provides the framework used by IDSA 2014 and IWGDF guidelines for all treatment algorithms.

1.1  By Anatomical Depth

The single most useful classification for the exam — depth predicts both the organism and the need for surgery. [COMMON MCQ]

Anatomical depth-based classification of SSTIs
Depth / Layer	Representative Infections
Epidermal	Impetigo (non-bullous, bullous), erythrasma, pitted keratolysis
Dermal	Ecthyma, erysipelas, cellulitis (upper dermis + superficial lymphatics for erysipelas)
Follicular	Folliculitis (superficial/deep), furuncle, carbuncle, sycosis barbae
Subcutaneous	Cellulitis, cutaneous abscess, subcutaneous abscess, panniculitis-like infection
Fascial	Necrotising fasciitis (Type I, II, III), Fournier gangrene, synergistic necrotising cellulitis
Muscular	Pyomyositis, streptococcal myositis, clostridial myonecrosis (gas gangrene)
Anatomical Depth — Infection Ladder (memorise top-to-bottom)
EPIDERMIS  →  Impetigo ↓ DERMIS  →  Ecthyma  |  Erysipelas ↓ HAIR FOLLICLE  →  Folliculitis → Furuncle → Carbuncle ↓ SUBCUTANEOUS FAT  →  Cellulitis  |  Abscess ↓ SUPERFICIAL & DEEP FASCIA  →  Necrotising fasciitis ↓ MUSCLE  →  Pyomyositis  |  Clostridial myonecrosis

1.2  By Clinical Morphology

• Purulent — furuncle, carbuncle, cutaneous abscess. Pus is present; Staphylococcus aureus (including CA-MRSA) predominates. Incision and drainage is the primary therapy. [VERY HIGH-YIELD]
• Non-purulent — cellulitis, erysipelas, necrotising infections without collection. β-haemolytic streptococci (mainly Streptococcus pyogenes) predominate; antibiotics are primary therapy.
• Necrotising — necrotising fasciitis, myonecrosis, Fournier gangrene. Tissue death with systemic toxicity; surgery is life-saving.
• Toxin-mediated — staphylococcal scalded skin syndrome (SSSS), staphylococcal and streptococcal toxic shock syndrome, scarlet fever. Skin damage is caused by circulating toxin rather than local invasion.

IDSA PURULENT VS NON-PURULENT RULE ▪  The purulent/non-purulent divide is the backbone of the IDSA 2014 algorithm and the single most examined classification in SSTI. ▪  Purulent → think Staphylococcus aureus / MRSA → drain first. ▪  Non-purulent → think Streptococcus pyogenes → penicillin-class antibiotic.

1.3  By Severity

Severity classification (IDSA)
Severity	Defining Features
Mild	Local signs only; no systemic features of infection
Moderate	Systemic signs present — temperature >38°C, pulse >90/min, respiratory rate >24/min, WBC >12,000 or <4,000/mm³
Severe	Failed incision and drainage plus oral antibiotics, OR systemic inflammatory response with hypotension, OR immunocompromise, OR clinical signs of deeper infection (bullae, skin sloughing, organ dysfunction)

• Complicated SSTI (cSSTI) — deep soft-tissue involvement, requires significant surgical intervention, or occurs in a host with significant comorbidity (diabetes mellitus, peripheral arterial disease, immunosuppression). Includes infected ulcers, burns and major abscesses.
• Uncomplicated SSTI — simple abscess, impetigo, furuncle, superficial cellulitis.
• ABSSSI (Acute Bacterial Skin and Skin-Structure Infection) — regulatory (US FDA) term requiring a lesion area ≥75 cm²; comprises cellulitis/erysipelas, wound infection and major cutaneous abscess. Used in modern drug trials (dalbavancin, oritavancin, tedizolid). [IMPORTANT]

1.4  By Mode of Acquisition

Acquisition-based classification and predicted organisms
Acquisition	Typical Organisms
Community-acquired	S. pyogenes, MSSA, community-associated MRSA (CA-MRSA)
Healthcare-associated	HA-MRSA, Pseudomonas aeruginosa, Enterobacterales, Enterococcus
Postoperative	MSSA/MRSA, coagulase-negative staphylococci; bowel/genital surgery → polymicrobial with anaerobes
Post-traumatic	S. aureus, streptococci, Clostridium spp., environmental Gram-negatives
Bite-related	Pasteurella multocida (cat/dog), Eikenella corrodens (human), Capnocytophaga canimorsus, anaerobes
Water-related	Aeromonas hydrophila (fresh water), Vibrio vulnificus (salt/brackish water), Mycobacterium marinum
Immunocompromised host	Above plus Pseudomonas, fungi (Mucor, Aspergillus, Fusarium), Cryptococcus, atypical mycobacteria
INDIAN CONTEXT — THE EPIDEMIOLOGY YOU MUST QUOTE ▪  S. aureus remains the commonest SSTI isolate in India; ICMR AMR Surveillance Network data show MRSA in roughly 35–45% of clinical S. aureus isolates, with wide inter-hospital variation. ▪  India has the world’s largest diabetic population — diabetic foot infection is the leading cause of non-traumatic lower-limb amputation and of SSTI-related admissions. ▪  Tropical (temperate-uncommon) entities are common here: tropical pyomyositis, Fournier gangrene, and post-traumatic tetanus following soil-contaminated wounds. ▪  Coastal states (Kerala, Tamil Nadu, Andhra, West Bengal, Odisha, Gujarat) see Vibrio vulnificus wound infection after sea-water exposure or fish-handling injury. ▪  Rabies risk assessment is mandatory in all mammalian bites under the National Rabies Control Programme (NRCP); India accounts for a substantial share of global rabies deaths.

 

SECTION 2  |  Impetigo

2.1  Definition

Impetigo is a contagious superficial bacterial infection confined to the epidermis, characterised by vesicles/pustules that rupture to leave the classical golden-yellow (honey-coloured) crust. It is the commonest bacterial skin infection of children worldwide. [VERY HIGH-YIELD]

Simple explanation: the infection stays above the basement membrane — that is why impetigo heals without scarring, unlike ecthyma which extends into the dermis and scars.

2.2  Types

Non-bullous versus bullous impetigo
Feature	Non-bullous (Impetigo contagiosa)	Bullous impetigo
Frequency	~70% — commonest form	~30%
Organism	S. aureus (commonest), S. pyogenes, or mixed	S. aureus only (phage group II, types 71/55)
Mechanism	Direct epidermal invasion through a breach	Local exfoliative toxin A/B cleaving desmoglein-1
Lesion	Thin-walled vesicle/pustule → honey-coloured crust	Flaccid bulla with clear→turbid fluid → collarette of scale
Site	Face — perioral, perinasal; limbs	Trunk, axillae, groin, neck folds; neonatal periumbilical
Age	Children 2–5 years	Neonates and infants <2 years
Mucosa	Spared	Spared
Nikolsky sign	Negative	Negative (positive only in SSSS)

2.3  Causative Organisms

• Staphylococcus aureus — now the predominant organism in both forms worldwide, including India.
• Streptococcus pyogenes (Group A Streptococcus, GAS) — historically dominant; still important in hot, humid, crowded settings and in tropical India.
• Mixed staphylococcal–streptococcal infection is frequent in non-bullous disease.
• Bullous impetigo is exclusively staphylococcal — a favourite one-liner. [FAVORITE EXAM QUESTION]

2.4  Predisposing Factors

• Breach of skin barrier: insect bite, scabies, pediculosis, eczema (impetiginised atopic dermatitis), minor trauma, burns.
• Hot humid climate, poor hygiene, overcrowding, low socio-economic status — highly relevant in Indian slum and school populations.
• Nasal carriage of S. aureus (anterior nares are the principal reservoir).
• Malnutrition, immunosuppression, diabetes mellitus.
• Close contact settings: schools, hostels, day-care, contact sports (wrestling — impetigo contagiosa outbreaks).

2.5  Pathogenesis

Pathogenesis of Impetigo

Nasal / skin colonisation by S. aureus or S. pyogenes ↓ Breach in epidermal barrier (bite, scratch, eczema, trauma) ↓ Bacterial adherence and superficial epidermal invasion ↓ NON-BULLOUS: neutrophilic subcorneal pustule → rupture → serum + neutrophils dry → HONEY-COLOURED CRUST ↓ BULLOUS: exfoliative toxin A/B (serine protease) cleaves DESMOGLEIN-1 ↓ Loss of keratinocyte adhesion in the granular layer → subcorneal split → FLACCID BULLA

DESMOGLEIN-1 — THE UNIFYING CONCEPT ▪  Desmoglein-1 is the desmosomal adhesion protein of the superficial epidermis. ▪  Cleaved by staphylococcal exfoliative toxin → bullous impetigo (localised) and SSSS (generalised, toxin is haematogenous). ▪  Attacked by autoantibodies → pemphigus foliaceus. ▪  All three diseases therefore produce a subcorneal/granular-layer split with no mucosal involvement. [VERY HIGH-YIELD]

2.6  Clinical Features

Non-bullous impetigo

• Begins as a small erythematous macule → thin-walled vesicle/pustule → ruptures within hours.
• Honey-coloured (golden-yellow) adherent crust on an erythematous base — the diagnostic hallmark.
• Lesions enlarge by peripheral extension and satellite lesions appear by autoinoculation.
• Mild itching; pain is unusual. Regional lymphadenopathy in up to 90%.
• Systemic symptoms are absent or minimal. Heals in 2–3 weeks even untreated, without scarring (may leave post-inflammatory hypo/hyperpigmentation).

Bullous impetigo

• Flaccid, superficial bullae 1–2 cm, initially clear then turbid/purulent fluid.
• Bullae rupture easily leaving a shallow moist erosion with a rim (collarette) of scale and a thin varnish-like crust.
• Little surrounding erythema — a useful discriminator from SSSS.
• Lymphadenopathy uncommon. Neonatal form (impetigo neonatorum) may present periumbilically and can disseminate.

2.6.1  Distribution

• Non-bullous: exposed areas — face (around nose and mouth), extremities; peri-orificial predilection.
• Bullous: intertriginous/moist areas — axillae, groin, neck folds, trunk, buttocks, perineum, diaper area.
• Any site of prior trauma or dermatosis (impetiginisation) — scabies burrows, eczema, herpes labialis, pediculosis capitis.

2.7  Diagnosis

• Essentially clinical — appearance and distribution are characteristic.
• Gram stain of exudate: Gram-positive cocci in clusters (staphylococci) or chains (streptococci) with neutrophils.
• Culture and sensitivity of vesicle fluid/crust base — indicated when lesions are extensive, recurrent, treatment-fails, or MRSA is suspected (recommended in Indian practice given high MRSA rates).
• Anti-DNase B and anti-hyaluronidase titres are better than ASO for skin streptococcal infection; ASO response is poor in impetigo because skin lipids inhibit streptolysin O. [COMMON MCQ]
• Skin biopsy is rarely needed — shows subcorneal pustule/bulla with neutrophils and Gram-positive cocci.

2.8  Differential Diagnosis

Differential diagnosis of impetigo
Condition	Distinguishing Feature
Herpes simplex	Grouped vesicles on erythematous base, scalloped border, Tzanck smear shows multinucleate giant cells
Varicella / herpes zoster	Dermatomal (zoster) or centripetal crops in different stages (varicella)
Tinea corporis / faciei	Annular lesion with active scaly raised edge; KOH mount positive
Contact / atopic dermatitis	Itching dominant, ill-defined erythema; may be secondarily impetiginised
Scabies	Burrows, night-time itch, family history; frequently impetiginised in India
Pemphigus foliaceus	Chronic, adult, widespread superficial erosions; direct immunofluorescence positive
Bullous pemphigoid	Tense bullae, elderly, subepidermal split, DIF linear IgG/C3 at basement membrane
SSSS	Diffuse tender erythema, Nikolsky positive, systemic upset, cultures from skin sterile
Cutaneous leishmaniasis / ecthyma	Deeper, ulcerated, punched-out, heals with scar

2.9  Complications

• Local: cellulitis, lymphangitis, ecthyma (deeper extension), scarlet fever, secondary eczematisation, bacteraemia (rare).
• Post-streptococcal glomerulonephritis (PSGN) — see below.
• Staphylococcal scalded skin syndrome — from bullous impetigo in neonates/infants.
• Toxic shock syndrome — rare, toxin-mediated.
• Guttate psoriasis may be triggered by streptococcal infection.
• Acute rheumatic fever does NOT follow skin infection — only pharyngeal GAS infection causes ARF. [FAVORITE EXAM QUESTION]

2.9.1  Post-streptococcal Glomerulonephritis

• Follows infection with nephritogenic GAS strains — skin (impetigo) strains classically M types 49, 55, 57, 60; pharyngeal strains M types 1, 4, 12.
• Latent period: 3–6 weeks after impetigo (vs 1–3 weeks after pharyngitis). [VERY HIGH-YIELD]
• Presents with acute nephritic syndrome — haematuria (smoky/cola urine), oliguria, oedema (periorbital, early morning), hypertension.
• Investigations: low C3 (normalises by 6–8 weeks), raised anti-DNase B, red-cell casts and dysmorphic RBCs on urine microscopy, raised urea/creatinine.
• Histology: diffuse endocapillary proliferative GN; electron microscopy shows subepithelial "humps"; immunofluorescence shows granular C3 ± IgG ("starry sky").
• Management is supportive — salt and fluid restriction, diuretics, antihypertensives. Antibiotic treatment of impetigo does NOT reliably prevent PSGN (unlike ARF prevention after pharyngitis). [IMPORTANT]
• Prognosis excellent in children (>95% complete recovery); worse in adults.

2.10  Treatment

2.10.1  Topical Treatment

• Indicated for limited disease — few lesions, no systemic features, no outbreak.
• Gently remove crusts with saline soaks/soap and water before applying medication (crust harbours bacteria and blocks drug penetration).
• Mupirocin 2% ointment — three times daily for 5 days. First-line; active against MSSA, MRSA and streptococci.
• Fusidic acid 2% cream — three times daily for 5–7 days. Widely used in India; resistance is rising with over-the-counter misuse.
• Retapamulin 1% ointment — twice daily for 5 days; active against mupirocin-resistant strains.
• Ozenoxacin 1% cream — twice daily 5 days; newer non-fluorinated quinolone.
• Avoid neomycin (contact sensitisation) and topical gentamicin (drives resistance).

2.10.2  Systemic Treatment

• Indications: numerous/widespread lesions, bullous impetigo, deep lesions, systemic symptoms, lymphadenopathy, immunosuppression, failure of topical therapy, outbreaks (schools, households), or suspected PSGN cluster.
• Duration: 7 days (typical).
• MSSA / streptococcal cover: Cloxacillin/dicloxacillin 250–500 mg QID, Cephalexin 250–500 mg QID (children 25–50 mg/kg/day), or Amoxicillin–clavulanate.
• Streptococcal only: Penicillin V or amoxicillin.
• Penicillin allergy: Clindamycin, or a macrolide (azithromycin/clarithromycin) — but macrolide resistance in Indian GAS and S. aureus is high; use only guided by sensitivity.
• Suspected/proven MRSA: Clindamycin, cotrimoxazole, doxycycline (avoid <8 years), or linezolid. Note cotrimoxazole and doxycycline have poor GAS activity — add a β-lactam if streptococcal disease is also possible. [IMPORTANT]

ANTIBIOTIC PITFALLS IN IMPETIGO ▪  Do not use topical mupirocin/fusidic acid indiscriminately — mupirocin resistance (mupA) and fusidic-acid resistance are climbing sharply in India. ▪  Doxycycline is contraindicated under 8 years of age. ▪  Cotrimoxazole and doxycycline do not reliably cover Streptococcus pyogenes. ▪  Treating impetigo does not prevent post-streptococcal glomerulonephritis — do not reassure the family otherwise.

2.10.3  Infection-Control Measures

• Exclude child from school/day-care until 24–48 hours of effective therapy or until lesions have crusted and dried.
• Keep lesions covered; separate towels, linen and clothing; hot-wash and sun-dry.
• Frequent hand washing; short, clean fingernails to limit autoinoculation and scratching.
• Screen and treat household contacts with lesions; treat concurrent scabies/pediculosis — a major driver of recurrence in Indian households.
• For recurrent staphylococcal impetigo, consider nasal decolonisation: mupirocin 2% nasal ointment BD × 5 days + chlorhexidine 4% body wash × 5–14 days ± dilute-bleach baths.

2.11  Prognosis

• Excellent — most cases resolve in 7–10 days with therapy; spontaneous resolution in 2–3 weeks.
• Heals without scarring; transient post-inflammatory pigment change is common in Indian skin.
• Recurrence is common with persistent nasal carriage, untreated scabies or ongoing overcrowding.
• PSGN is the main determinant of long-term outcome; overall renal prognosis in children is excellent.

 

SECTION 3  |  Ecthyma

3.1  Definition

Ecthyma is a deep, ulcerative pyoderma in which infection penetrates through the epidermis into the dermis, producing a punched-out ulcer covered by a thick adherent crust and healing with scarring. It is best regarded as "impetigo that has gone deep". [IMPORTANT]

ECTHYMA VS ECTHYMA GANGRENOSUM — DO NOT CONFUSE ▪  Ecthyma — streptococcal/staphylococcal, dermal pyoderma, on legs of malnourished children, non-fulminant. ▪  Ecthyma gangrenosum — haemorrhagic bulla → necrotic ulcer with black eschar and erythematous halo, caused by Pseudomonas aeruginosa bacteraemia in neutropenic/immunocompromised patients; anogenital and axillary predilection; a marker of septicaemia with high mortality. [FAVORITE EXAM QUESTION]

3.2  Organisms

• Streptococcus pyogenes — classical and commonest primary pathogen.
• Staphylococcus aureus — frequent co-pathogen or sole pathogen.
• Mixed streptococcal–staphylococcal infection is usual in practice.
• (Pseudomonas aeruginosa causes the distinct entity ecthyma gangrenosum — see box above.)

3.3  Clinical Appearance

• Begins as a vesicle or vesicopustule on an erythematous base, often at a site of trauma or an insect bite.
• Enlarges and extends deeply → thick, hard, adherent greyish-yellow crust.
• Removal of the crust reveals a "punched-out" ulcer with raised, indurated, violaceous margins and a purulent, granulating base. [VERY HIGH-YIELD]
• Usually few lesions (fewer than in impetigo), 0.5–3 cm, on the lower legs, dorsa of feet, thighs and buttocks.
• Painful and slow to heal (weeks); regional lymphadenopathy common.
• Always heals with a scar — the key clinical discriminator from impetigo.

3.4  Risk Factors

• Malnutrition, poor hygiene, overcrowding, hot humid tropical climate.
• Pre-existing pruritic dermatoses and excoriation — scabies, pediculosis, insect bites, eczema (very common precursors in India).
• Minor trauma and neglected wounds; barefoot walking.
• Immunosuppression: HIV, diabetes mellitus, chronic renal failure, neutropenia, corticosteroids.
• Injection drug use ("skin popping").
• Venous insufficiency and lymphoedema of the legs; advanced age.

3.5  Differential Diagnosis

Differential diagnosis of a crusted punched-out leg ulcer
Condition	Distinguishing Feature
Impetigo	Superficial, honey crust, no ulcer, heals without scar
Ecthyma gangrenosum	Black necrotic eschar with erythematous halo, neutropenic host, Pseudomonas bacteraemia
Cutaneous leishmaniasis	Endemic area (Bihar, Rajasthan, Gujarat), chronic painless ulcer with raised edge, LD bodies on slit-skin smear
Cutaneous tuberculosis / TB verrucosa cutis	Chronic, verrucous or undermined edge, granuloma with AFB, Mantoux positive
Cutaneous diphtheria	Punched-out ulcer with grey membrane; travel/endemic exposure
Pyoderma gangrenosum	Rapidly enlarging ulcer, undermined violaceous border, pathergy, associated IBD/RA; culture-negative
Venous / arterial ulcer	Medial malleolus + stasis changes (venous); punched-out, painful, absent pulses (arterial)
Tropical / phagedenic ulcer	Fusobacterium + spirochaete, foul-smelling, rapidly enlarging, malnourished tropical patient
Anthrax (cutaneous)	Painless black eschar with marked non-pitting oedema, animal-handling history

3.6  Complications

• Scarring and post-inflammatory pigmentary change (cosmetically significant in Indian skin).
• Extension to cellulitis, lymphangitis, deep soft-tissue infection or osteomyelitis.
• Bacteraemia and sepsis.
• Post-streptococcal glomerulonephritis — recognised sequela.
• Chronic non-healing ulceration; rarely Marjolin ulcer (squamous cell carcinoma) in long-standing ulcers.

3.7  Treatment

• Systemic antibiotics are mandatory — topical therapy alone is inadequate because infection is dermal. [IMPORTANT]
• First line: Cloxacillin/dicloxacillin or cephalexin 500 mg QID for 7–10 days, or amoxicillin–clavulanate.
• If streptococcal only: penicillin V or benzathine penicillin.
• Penicillin allergy: clindamycin (also covers many CA-MRSA strains).
• Suspected MRSA: clindamycin, cotrimoxazole, doxycycline or linezolid, guided by culture.
• Local care: saline/antiseptic soaks or compresses to debride crust, gentle mechanical debridement, non-adherent dressing.
• Treat the underlying cause — scabies (permethrin 5% / ivermectin), pediculosis, eczema, nutritional deficiency, anaemia, glycaemic control.
• Address hygiene, footwear and household contacts to prevent recurrence.

 

SECTION 4  |  Follicular Infections

Follicular infections form a continuum of increasing depth: folliculitis (ostium) → deep folliculitis → furuncle (whole follicle + perifollicular tissue) → carbuncle (several adjacent follicles coalescing into a deep multiloculated abscess). S. aureus is the dominant organism throughout. [VERY HIGH-YIELD]

Spectrum of Follicular Infection
SUPERFICIAL FOLLICULITIS  —  pustule at follicular ostium, no induration ↓ DEEP FOLLICULITIS (sycosis)  —  whole follicle inflamed, tender papulopustule ↓ FURUNCLE (boil)  —  perifollicular abscess with central necrotic core ↓ CARBUNCLE  —  coalescence of multiple furuncles, multiple draining sinuses, systemic upset
Folliculitis, furuncle and carbuncle — the core comparison
Feature	Folliculitis	Furuncle	Carbuncle
Depth	Follicular ostium ± upper follicle	Entire follicle + perifollicular dermis	Multiple follicles + subcutaneous tissue
Follicles	Single/multiple, superficial	Single follicle	Multiple contiguous follicles
Lesion	Small pustule with central hair	Tender erythematous nodule with pustular apex	Large indurated plaque, multiple pustular points
Necrotic core	Absent	Present (single)	Present (multiple)
Discharge	Minimal	Single pus point	Cribriform / sieve-like multiple sinuses
Systemic upset	Absent	Usually absent	Fever, malaise, toxaemia common
Common site	Any hair-bearing area	Face, neck, axilla, buttock, thigh	Nape of neck, back, thighs
Scarring	None	Small scar	Significant scar
Treatment	Topical antiseptic/antibiotic	Warm compress ± I&D ± antibiotic	I&D/excision + systemic antibiotics

4.1  Superficial Folliculitis

• Etiology: S. aureus commonest; also Pseudomonas aeruginosa, Gram-negatives (in acne patients on long-term antibiotics), Malassezia (fungal), Demodex, and viral (herpes) mimics.
• Risk factors: occlusion, humidity and sweating (major in Indian climate), shaving/waxing/hair removal, topical corticosteroids and oils, obesity, diabetes, hyperhidrosis, tight clothing.
• Clinical features: crops of small dome-shaped pustules pierced by a hair, on an erythematous base; mildly itchy or tender; scalp, beard, axillae, buttocks, thighs.
• Diagnosis: clinical; Gram stain/culture of pustule contents if recurrent or resistant; KOH mount and fungal culture if Malassezia suspected.
• Differential diagnosis: acne vulgaris (comedones present), pseudofolliculitis barbae (ingrown hairs, no infection), keratosis pilaris, Malassezia folliculitis (monomorphic itchy papulopustules on trunk in young adults), miliaria pustulosa, drug-induced acneiform eruption, eosinophilic folliculitis (HIV).
• Complications: progression to furuncle/abscess, recurrence, post-inflammatory pigmentation, scarring alopecia if deep.
• Treatment: antiseptic wash (chlorhexidine 4%, povidone-iodine), topical mupirocin/fusidic acid/clindamycin; avoid shaving affected areas; loose cotton clothing; treat hyperhidrosis. Systemic antibiotic only if extensive or recurrent.

4.2  Deep Folliculitis

• Involves the entire follicle and adjacent dermis.
• Presents as a tender, deep, erythematous papule or nodule with a pustular apex; heals with scarring.
• Includes sycosis barbae, folliculitis decalvans (scarring alopecia of scalp) and folliculitis of the nape (acne keloidalis nuchae in predisposed individuals).
• Requires systemic anti-staphylococcal therapy (cloxacillin/cephalexin ± clindamycin) with prolonged courses in chronic forms.

4.3  Furuncle (Boil)

• Etiology: S. aureus — increasingly CA-MRSA, characteristically carrying Panton–Valentine leukocidin (PVL) genes. [VERY HIGH-YIELD]
• Risk factors: nasal/perineal S. aureus carriage, diabetes mellitus, obesity, poor hygiene, friction and occlusion, atopic dermatitis, iron deficiency, immunosuppression (HIV), chronic kidney disease, hyper-IgE (Job) syndrome and chronic granulomatous disease in recurrent childhood cases.
• Clinical features: firm, tender, red perifollicular nodule → enlarges, becomes fluctuant → yellow pustular apex → discharges pus and a central necrotic core (slough) → heals with a small scar.
• Sites: face, neck, axillae, buttocks, thighs, perineum — friction and sweat-prone regions.
• Diagnosis: clinical; pus for Gram stain, culture and sensitivity (essential given Indian MRSA rates); blood glucose/HbA1c in recurrent disease; ultrasound if fluctuance is uncertain.
• Differential diagnosis: epidermoid cyst (inflamed), hidradenitis suppurativa (axilla/groin, sinus tracts, chronic recurrent), cystic acne, myiasis/furuncular myiasis, kerion, insect-bite reaction, bacterial abscess.
• Complications: cellulitis, abscess, bacteraemia, metastatic seeding (osteomyelitis, endocarditis, septic arthritis), scarring, and — for the "danger area of the face" (upper lip, nose, medial canthus) — cavernous sinus thrombosis via the angular and ophthalmic veins. Never squeeze a boil in this zone. [FAVORITE EXAM QUESTION]

DANGER AREA OF THE FACE ▪  Furuncles of the nose, upper lip and medial canthal region drain via the angular vein → superior/inferior ophthalmic veins → cavernous sinus (valveless). ▪  Manipulation may cause cavernous sinus thrombosis: fever, proptosis, chemosis, ophthalmoplegia (III, IV, VI), V1/V2 sensory loss, headache. ▪  Management: no squeezing, high-dose parenteral anti-staphylococcal antibiotics, MR venography, and anticoagulation in consultation with neurology.

4.4  Carbuncle

• Etiology: S. aureus — a deep interconnecting abscess of several adjacent hair follicles in thick inelastic skin.
• Risk factors: diabetes mellitus (classic association), elderly males, malnutrition, obesity, chronic kidney disease, immunosuppression, corticosteroid therapy.
• Clinical features: large, hard, exquisitely tender, dusky-red indurated plaque, most often on the nape of the neck, upper back or thigh; suppurates through multiple pustular openings — the "cribriform" or sieve-like appearance; fever, chills and prostration are common; sloughing leaves a deep crateriform ulcer that heals with a significant scar. [VERY HIGH-YIELD]
• Diagnosis: clinical; pus culture and blood culture; blood glucose and HbA1c in every patient — a carbuncle is a classic presenting feature of undiagnosed type 2 diabetes in India; ultrasound/CT if deep extension suspected.
• Differential diagnosis: cutaneous anthrax (painless black eschar with oedema), hidradenitis suppurativa, ruptured epidermoid cyst, kerion, deep fungal infection, necrotising fasciitis (early).
• Complications: sepsis and bacteraemia, endocarditis, osteomyelitis, extension to necrotising infection, extensive scarring and contracture.
• Treatment: incision and drainage / saucerisation with deloculation and debridement of necrotic tissue plus systemic antibiotics (IV cloxacillin/cefazolin; vancomycin, teicoplanin or linezolid if MRSA), analgesia, glycaemic control, dressings, and nutritional support.

4.5  Sycosis Barbae

• Chronic deep folliculitis of the beard area in adult males caused by S. aureus.
• Risk factors: shaving (autoinoculation by razor), nasal carriage, seborrhoea, hot humid climate.
• Clinical: perifollicular papules and pustules studded with hairs over the upper lip, chin and jaw; hairs are not easily epilated (unlike tinea barbae); may scar.
• Differential: tinea barbae (kerion-like, boggy, hair epilates easily, KOH positive), pseudofolliculitis barbae (ingrown hair, no pus), acne vulgaris, herpetic sycosis.
• Treatment: stop shaving temporarily or use a clean electric razor; antiseptic wash; topical mupirocin/fusidic acid; systemic cloxacillin or cephalexin for 2–3 weeks in extensive disease; nasal mupirocin decolonisation to prevent recurrence.

4.6  Hot-Tub Folliculitis

• Etiology: Pseudomonas aeruginosa, characteristically serotype O:11. [COMMON MCQ]
• Risk factors: inadequately chlorinated hot tubs, whirlpools, swimming pools, water slides, loofah sponges; prolonged immersion; occlusive swimwear.
• Clinical: pruritic follicular erythematous papules and pustules appearing 8–48 hours after exposure, maximal in areas covered by swimwear (trunk, buttocks, axillae) with sparing of head and neck; may be accompanied by mild fever, malaise and "Pseudomonas hot-foot syndrome".
• Diagnosis: exposure history is diagnostic; culture of pustules and of the water source.
• Treatment: usually self-limiting in 7–14 days without antibiotics; symptomatic treatment with antipruritics and dilute acetic acid compresses; ciprofloxacin for severe, extensive or immunocompromised cases; disinfect/re-chlorinate the water source.

4.7  Periporitis

• Also called periporitis staphylogenes / multiple sweat gland abscesses of infancy (pseudofurunculosis).
• Staphylococcal infection of eccrine sweat glands and ducts, typically complicating miliaria (prickly heat) — highly relevant to Indian summers.
• Occurs in malnourished infants, especially on the scalp, forehead, neck, back and buttocks.
• Clinical: multiple firm, non-follicular, dusky-red nodules that become fluctuant and discharge pus; no central necrotic core (differentiating from furuncle); little pain; may be accompanied by fever.
• Treatment: systemic anti-staphylococcal antibiotics, aspiration/drainage of larger lesions, cooling and avoidance of over-clothing, treatment of miliaria, and correction of malnutrition.

4.8  Recurrent Furunculosis

Defined as three or more episodes in 12 months. Driven overwhelmingly by persistent S. aureus carriage plus a host or environmental factor.

Evaluation

• Culture pus and screen for carriage — anterior nares, axillae, groin, perineum, throat.
• Blood glucose / HbA1c — exclude diabetes mellitus.
• Full blood count, ferritin/iron studies (iron deficiency), HIV serology, immunoglobulins (hyper-IgE syndrome in children with eczema, recurrent cold abscesses and pneumonia), nitroblue tetrazolium / dihydrorhodamine test for chronic granulomatous disease if childhood onset.
• Screen household contacts; look for PVL-positive CA-MRSA, which characteristically causes recurrent boils in families and closed communities.

Decolonisation regimen [VERY HIGH-YIELD]

• Mupirocin 2% nasal ointment to both anterior nares twice daily for 5 days (may be repeated monthly).
• Chlorhexidine gluconate 4% body wash daily for 5–14 days, or dilute sodium hypochlorite (bleach) baths — ½ cup of 6% bleach in a full bathtub, twice weekly.
• Rifampicin 600 mg daily for 7–10 days combined with a second agent (cloxacillin, doxycycline, cotrimoxazole or clindamycin) for refractory carriage — never rifampicin monotherapy (rapid resistance). [IMPORTANT]
• Environmental measures: hot-wash linen and towels, separate personal items, treat all colonised household members simultaneously, clip nails, avoid sharing razors.
• Correct predisposing factors: glycaemic control, iron repletion, treat eczema and hyperhidrosis, weight reduction.

FOLLICULAR INFECTIONS — RAPID VIVA ▪  Commonest organism in furuncle and carbuncle? — Staphylococcus aureus. ▪  Which toxin marks CA-MRSA causing recurrent boils? — Panton–Valentine leukocidin (PVL). ▪  Commonest site of carbuncle? — Nape of the neck. ▪  Which systemic disease must be excluded in every carbuncle? — Diabetes mellitus. ▪  Organism and serotype of hot-tub folliculitis? — Pseudomonas aeruginosa serotype O:11. ▪  Why must a furuncle on the upper lip never be squeezed? — Risk of cavernous sinus thrombosis. ▪  Definition of recurrent furunculosis? — ≥3 episodes in 12 months.

 

SECTION 5  |  Cutaneous Abscess

5.1  Definition

A cutaneous abscess is a localised collection of pus within the dermis and subcutaneous tissue, walled off by a pyogenic membrane of inflammatory granulation tissue. It presents as a painful, fluctuant, erythematous nodule, often with a surrounding rim of cellulitis. [IMPORTANT]

5.2  Common Organisms

• Staphylococcus aureus — isolated in ~75% of cutaneous abscesses; CA-MRSA is the single commonest identified organism in many series.
• Streptococci (Groups A, B, C, G).
• Polymicrobial with anaerobes at specific sites: perianal, perirectal, vulvovaginal, buttock and axillary abscesses — Bacteroides, Peptostreptococcus, Prevotella, Enterobacterales.
• Injection drug users: S. aureus, oral streptococci (needle-licking), anaerobes, Clostridium spp., Eikenella.
• Sterile ("culture-negative") abscess should prompt consideration of tuberculosis (cold abscess), atypical mycobacteria, fungal infection or a foreign body, and of hidradenitis suppurativa.

5.3  Clinical Features

• Painful, tender, warm, erythematous, fluctuant swelling; may point and discharge spontaneously.
• Surrounding cellulitic rim; regional lymphadenopathy.
• Fluctuation is the classical sign but is unreliable in deep or early abscesses — hence the role of ultrasound.
• Fever and systemic signs are usually absent in simple abscess; their presence signals moderate/severe disease or bacteraemia.
• Cardinal features of inflammation: rubor, calor, dolor, tumor, functio laesa.

5.4  Ultrasound Findings

• Point-of-care ultrasound (POCUS) is the investigation of choice to distinguish abscess from cellulitis and changes management in ~15–25% of cases. [VERY HIGH-YIELD]
• Abscess: anechoic or hypoechoic collection with irregular walls, posterior acoustic enhancement, internal debris/septations, and "squish sign" (swirling of contents on probe compression).
• Cellulitis: diffuse subcutaneous thickening with hyperechoic fat and hypoechoic septal fluid → "cobblestone" appearance, without a drainable collection.
• Doppler shows peripheral hyperaemia with an avascular centre in abscess (helps exclude pseudoaneurysm — important before incising a groin swelling in an injection drug user). [IMPORTANT]
• Ultrasound also identifies foreign bodies and guides the optimal incision site.

5.5  Management

5.5.1  Indications for Incision and Drainage

Incision and drainage (I&D) is the definitive and primary treatment of every cutaneous abscess — "ubi pus, ibi evacua". Antibiotics alone will not cure a walled-off collection. [FAVORITE EXAM QUESTION]

• Any fluctuant or ultrasound-proven collection.
• Non-resolving induration after 48–72 hours of antibiotics.
• Technique: adequate analgesia/anaesthesia (field block; abscess pH limits local anaesthetic efficacy), generous incision along skin tension lines over the point of maximal fluctuance, complete evacuation of pus, breakdown of loculi with a finger or blunt forceps, irrigation, and packing or a loop drain in large cavities.
• Loop drainage and simple I&D have comparable outcomes; routine packing of small abscesses is not required and increases pain.
• Special sites need specialist care: perianal, breast, hand (felon, tenosynovitis), face/danger area, neck, and abscesses adjacent to major vessels.

5.5.2  Indications for Culture

• Severe or extensive local disease; systemic inflammatory response.
• Failure of initial antibiotic therapy; recurrent abscess.
• Immunocompromised host; suspected unusual organism (water, bite, injection exposure).
• Local MRSA prevalence high or unknown — essentially all Indian hospital practice.
• Abscess in a patient with an implanted prosthesis or on chemotherapy.

5.5.3  Indications for Adjunctive Antibiotics

After adequate drainage, antibiotics add benefit in defined situations (IDSA 2014; supported by two large randomised trials showing higher cure with cotrimoxazole or clindamycin after I&D).

• Abscess >2 cm, or multiple abscesses.
• Surrounding cellulitis or extensive induration.
• Systemic features of infection (fever, tachycardia, leukocytosis) — i.e. moderate/severe SSTI.
• Immunocompromised host, diabetes mellitus, extremes of age.
• Abscess in a difficult-to-drain site — face, hand, genitalia, perianal region.
• Associated septic phlebitis, indwelling device, or failure to respond to drainage alone.
• Typical choice: cotrimoxazole, doxycycline or clindamycin (MRSA-active) for 5–7 days; add a β-lactam if streptococcal cellulitis coexists; IV vancomycin/teicoplanin/linezolid/daptomycin in severe disease.

Purulent SSTI / Abscess Management Algorithm (IDSA-based)

Purulent lesion — suspected abscess ↓ Clinical assessment ± Point-of-care ULTRASOUND ↓ No collection → treat as cellulitis          Collection present → INCISION AND DRAINAGE + culture ↓ Assess severity after drainage ↓ MILD (no systemic signs, small, no cellulitis) → I&D alone, review in 48 h ↓ MODERATE (systemic signs / >2 cm / cellulitis) → I&D + ORAL MRSA-active antibiotic (cotrimoxazole or doxycycline) ↓ SEVERE (failed I&D + orals, SIRS, immunocompromised) → Admit, culture, IV VANCOMYCIN / TEICOPLANIN / LINEZOLID / DAPTOMYCIN ↓ Consider imaging & surgical review if no improvement in 48–72 h — exclude deep or necrotising infection

5.6  Recurrent Abscess

• Search for a local cause: pilonidal sinus, hidradenitis suppurativa, epidermoid cyst, retained foreign body, fistula-in-ano (perianal), inflammatory bowel disease, sinus tract, or an underlying osteomyelitis.
• Search for a host cause: diabetes mellitus, HIV, neutrophil disorders (chronic granulomatous disease, hyper-IgE syndrome, Chédiak–Higashi), injection drug use, obesity.
• Search for a microbial cause: persistent S. aureus carriage, PVL-positive CA-MRSA.
• Obtain culture at every recurrence; consider excision of the abscess cavity/sinus once quiescent.
• Institute decolonisation (Section 4.8) for the patient and household.

5.7  Community-Associated MRSA

• CA-MRSA arises in people without healthcare exposure; typically carries SCCmec type IV or V (small, mobile cassette) and PVL genes.
• Clinically: recurrent purulent skin abscesses often mistaken for "spider bites", necrotising pneumonia after influenza, and severe necrotising SSTI.
• PVL is a pore-forming leukocidin causing neutrophil lysis and tissue necrosis — the basis of the abscess-forming and necrotising phenotype. [VERY HIGH-YIELD]
• CA-MRSA usually remains susceptible to clindamycin, cotrimoxazole, doxycycline and rifampicin, unlike multiresistant HA-MRSA (SCCmec I–III).
• Test for inducible clindamycin resistance with the D-test before using clindamycin for an erythromycin-resistant, clindamycin-susceptible isolate. [COMMON MCQ]
• Indian relevance: rising CA-MRSA in community pyoderma; ICMR surveillance guides local empirical policy.

5.8  Household Transmission

• Spread occurs by direct skin contact and contaminated fomites — towels, razors, bed linen, sports equipment, wrestling mats, gym benches.
• Recognised "5 Cs" of transmission: Crowding, frequent skin Contact, Compromised skin integrity, Contaminated items, lack of Cleanliness. [COMMON MCQ]
• Asymptomatic colonised household members act as a reservoir and cause "ping-pong" reinfection.
• Household-wide (rather than index-patient-only) decolonisation gives the best recurrence-free outcome.

5.9  Decolonisation Measures

• Nasal mupirocin 2% BD × 5 days to all colonised household members simultaneously.
• Chlorhexidine 4% body wash daily × 5–14 days, or dilute bleach baths twice weekly for 3 months.
• Cover draining lesions; hand hygiene with soap or alcohol rub after dressing changes.
• Hot-wash (≥60°C) and sun-dry clothing, towels and linen; do not share personal items.
• Clean high-touch surfaces with a detergent–disinfectant.
• Re-screen and consider systemic rifampicin-based combination therapy for persistent carriage.

SECTION 2–5 RAPID RECALL ▪  Honey-coloured crust = impetigo; punched-out ulcer with scar = ecthyma; black eschar + halo in neutropenia = ecthyma gangrenosum. ▪  Bullous impetigo & SSSS = exfoliative toxin vs desmoglein-1; Nikolsky positive only in SSSS. ▪  PSGN after skin infection = 3–6 weeks, M types 49, 55, 57, 60; no ARF after skin infection. ▪  Carbuncle = nape of neck + diabetes + cribriform pus discharge. ▪  Ubi pus, ibi evacua — I&D is the treatment of abscess; antibiotics are adjunctive. ▪  CA-MRSA = SCCmec IV/V + PVL; check D-test before using clindamycin.

 

SECTION 6  |  Cellulitis

6.1  Definition

Cellulitis is an acute, spreading, non-purulent pyogenic infection of the deep dermis and subcutaneous tissue, characterised by erythema, warmth, swelling and tenderness with poorly demarcated, non-elevated borders. [VERY HIGH-YIELD]

Key contrast: erysipelas involves the upper dermis and superficial lymphatics and therefore has a raised, sharply demarcated border; cellulitis is deeper and its edge fades into normal skin.

6.2  Etiology

• β-haemolytic streptococci — Group A (S. pyogenes) commonest; also Groups B, C, G. Predominant cause of non-purulent cellulitis. [VERY HIGH-YIELD]
• Staphylococcus aureus (MSSA and MRSA) — especially with a penetrating injury, abscess, ulcer or indwelling device (purulent cellulitis).
• Group B Streptococcus (S. agalactiae) — neonates, elderly, diabetics.
• Haemophilus influenzae type b — facial/periorbital cellulitis in unimmunised children (now rare after Hib introduction in the Universal Immunisation Programme).
• Gram-negative bacilli (E. coli, Klebsiella, Pseudomonas) — immunocompromised, neutropenic, cirrhotic and diabetic patients.
• Pasteurella multocida (animal bite), Vibrio vulnificus (salt water, cirrhosis), Aeromonas hydrophila (fresh water), Erysipelothrix rhusiopathiae (fish/meat handlers — erysipeloid), Mycobacterium marinum (fish-tank granuloma).
• Cryptococcus neoformans — cellulitis in transplant recipients and other profoundly immunosuppressed patients.

6.3  Portal of Entry

• Interdigital toe-web intertrigo / tinea pedis — the commonest identifiable portal in lower-limb cellulitis and a modifiable risk factor that must be actively sought and treated. [FAVORITE EXAM QUESTION]
• Traumatic wounds, abrasions, insect bites, burns, surgical incisions.
• Chronic leg ulcers (venous, arterial, diabetic), pressure sores.
• Eczema, psoriasis, scabies, impetigo and other breached dermatoses.
• Injection sites in people who inject drugs; intravenous cannulae and catheters.
• Onychomycosis and paronychia; barefoot walking (highly relevant in rural India).
• No portal is identified in up to one-third of cases.

6.4  Risk Factors

• Lymphoedema — the single strongest risk factor for recurrence (filarial lymphoedema is a major Indian cause). [VERY HIGH-YIELD]
• Chronic venous insufficiency, oedema of any cause, previous saphenous vein harvesting, prior groin/axillary lymph-node dissection or radiotherapy.
• Obesity, diabetes mellitus, peripheral arterial disease.
• Previous episode of cellulitis at the same site (strongest predictor of another episode).
• Immunosuppression: HIV, chemotherapy, corticosteroids, transplantation, cirrhosis, chronic kidney disease.
• Injection drug use, alcohol misuse, malnutrition.

6.5  Pathogenesis

Pathogenesis of Cellulitis

Breach in skin barrier (toe-web intertrigo, ulcer, trauma, bite) ↓ Bacterial entry into dermis and subcutaneous tissue ↓ Streptococcal virulence factors — M protein, hyaluronidase, streptokinase, streptolysin, DNase, exotoxins ↓ Rapid horizontal spread through tissue planes and lymphatics (no abscess wall formed) ↓ Neutrophil influx, cytokine release (TNF-α, IL-1, IL-6) → erythema, warmth, oedema, pain ↓ Lymphatic obstruction and damage → persistent lymphoedema ↓ Impaired lymphatic clearance → PREDISPOSITION TO RECURRENT CELLULITIS (vicious cycle)

THE LYMPHOEDEMA–CELLULITIS VICIOUS CYCLE ▪  Cellulitis damages dermal lymphatics → lymphoedema. ▪  Lymphoedema impairs local immune surveillance and bacterial clearance → further episodes. ▪  Each episode causes more lymphatic damage → progressive elephantiasis nostras verrucosa. ▪  This is why antibiotic prophylaxis plus lifelong compression is central to recurrent cellulitis management.

6.6  Clinical Features

• Acute onset of erythema, warmth, swelling and tenderness with an ill-defined, non-elevated advancing margin.
• Commonest site: lower limb (unilateral); bilateral simultaneous lower-limb cellulitis is very rare and should prompt reconsideration of the diagnosis. [IMPORTANT]
• Peau d’orange dimpling from dermal oedema; vesicles, bullae, petechiae or superficial haemorrhage may develop.
• Lymphangitis (tender red streaks) and tender regional lymphadenopathy.
• Fever, chills and malaise may precede skin findings; systemic upset is variable.
• Skin desquamation during recovery is common.

6.6.1  Facial Cellulitis

• Organisms: S. pyogenes, S. aureus; H. influenzae type b in unimmunised children.
• Sources: dental infection, sinusitis, facial trauma, furuncle, skin lesions.
• Requires exclusion of odontogenic deep-space infection (Ludwig angina) and orbital involvement.
• Risk of cavernous sinus thrombosis with midface involvement.

6.6.2  Periorbital (Preseptal) versus Orbital (Postseptal) Cellulitis

This distinction is an examination favourite and a genuine ophthalmic emergency. The orbital septum — a fibrous sheet from the orbital rim periosteum to the tarsal plates — is the anatomical divider. [FAVORITE EXAM QUESTION]

Preseptal versus orbital cellulitis
Feature	Preseptal (Periorbital)	Orbital (Postseptal)
Site	Anterior to orbital septum	Posterior to orbital septum
Source	Skin trauma, insect bite, hordeolum, dacryocystitis, impetigo	Ethmoid sinusitis (commonest), dental infection, trauma
Organisms	S. aureus, S. pyogenes	S. aureus, streptococci, H. influenzae, anaerobes (polymicrobial)
Lid swelling / erythema	Present	Present
Proptosis	Absent	Present
Ophthalmoplegia / painful eye movement	Absent	Present
Chemosis	Absent/minimal	Present
Visual acuity	Normal	Reduced; RAPD may be present
Fever / toxicity	Mild	Marked
Imaging	Usually not required	Contrast CT orbit + sinuses is mandatory
Treatment	Oral antibiotics, outpatient (children may need admission)	Admit, IV antibiotics, ENT/ophthalmology review, drain abscess
Complications	Progression to orbital cellulitis	Subperiosteal/orbital abscess, cavernous sinus thrombosis, meningitis, brain abscess, blindness
CHANDLER CLASSIFICATION OF ORBITAL COMPLICATIONS OF SINUSITIS ▪  Group I — Preseptal (periorbital) cellulitis. ▪  Group II — Orbital cellulitis. ▪  Group III — Subperiosteal abscess. ▪  Group IV — Orbital abscess. ▪  Group V — Cavernous sinus thrombosis. ▪  Any proptosis, ophthalmoplegia, chemosis or reduced acuity = urgent contrast CT and admission. [VERY HIGH-YIELD]

6.6.3  Breast Cellulitis

• Occurs in lactational mastitis, after breast surgery, and notably after breast-conserving surgery with axillary dissection and radiotherapy (lymphatic disruption).
• Organisms: S. aureus, streptococci.
• Always exclude inflammatory breast carcinoma in a non-lactating woman with a red, oedematous, peau d’orange breast that fails to respond to antibiotics — mammography, ultrasound and skin punch biopsy. [IMPORTANT]
• Exclude an underlying breast abscess by ultrasound.

6.6.4  Recurrent Cellulitis

• Defined as ≥2 episodes at the same site; occurs in ~20–30% within 3 years.
• Predictors: lymphoedema, venous insufficiency, obesity, tinea pedis, prior cellulitis, chronic ulcer.
• Managed with treatment of the portal of entry, compression therapy, weight reduction and long-term antibiotic prophylaxis.

6.6.5  Lymphoedema-Associated Cellulitis

• Common in post-filarial lymphoedema (Wuchereria bancrofti) — a major cause in endemic Indian states, in post-mastectomy arms, and after pelvic surgery/radiotherapy.
• Acute dermatolymphangioadenitis (ADLA) — recurrent febrile attacks of cellulitis that drive progression of filarial lymphoedema to elephantiasis.
• Management combines antibiotics, limb hygiene and skin care (the cornerstone of the WHO/National Filaria morbidity-management package), exercise, elevation and compression.

6.6.6  Water-Exposure Cellulitis

Water-exposure and animal-associated cellulitis
Exposure	Organism / Clinical Clue
Sea water, brackish water, raw seafood	Vibrio vulnificus — haemorrhagic bullae, rapid necrosis, sepsis; high mortality in cirrhosis and haemochromatosis (iron-loving). Treat with doxycycline + ceftriaxone/ceftazidime. [VERY HIGH-YIELD]
Fresh water, leeches, mud	Aeromonas hydrophila — rapidly progressive cellulitis/myonecrosis; treat with ciprofloxacin or third-generation cephalosporin ± aminoglycoside
Fish tank, swimming pool	Mycobacterium marinum — chronic nodular sporotrichoid lesions; treat with clarithromycin ± ethambutol/rifampicin
Fish, shellfish, meat, poultry handling	Erysipelothrix rhusiopathiae (erysipeloid) — violaceous non-suppurative plaque of the hand; penicillin (intrinsically resistant to vancomycin)
Hot tub / pool	Pseudomonas aeruginosa — folliculitis, hot-foot syndrome

6.6.7  Animal-Associated Cellulitis

• Cat bite/scratch → Pasteurella multocida — rapid-onset cellulitis within 12–24 hours; amoxicillin–clavulanate is drug of choice.
• Dog bite → Pasteurella canis, Capnocytophaga canimorsus — fulminant sepsis with purpura fulminans in asplenic, cirrhotic and alcoholic patients.
• Cat scratch disease → Bartonella henselae — regional lymphadenopathy with a papule at the scratch site.
• Rabbits/tick exposure → Francisella tularensis (ulceroglandular tularaemia).
• Sheep/goat/cattle contact → cutaneous anthrax (Bacillus anthracis) — painless black eschar with extensive non-pitting oedema; important in Indian anthrax-endemic districts of Odisha, Andhra Pradesh, Karnataka, Tamil Nadu.

6.7  Investigations

• Cellulitis is a clinical diagnosis; investigations are for severity, complications and atypical cases.
• Full blood count, CRP/ESR, renal function, blood glucose and HbA1c.
• Creatine kinase and lactate if a necrotising infection is suspected.
• Swab/aspirate: needle aspiration of the advancing edge and punch biopsy have low yield (<20%) and are not routine; culture any pus, ulcer base or bulla fluid.
• Ultrasound to exclude an abscess or deep collection; Doppler ultrasound to exclude DVT where the clinical picture is ambiguous.
• Plain radiograph if osteomyelitis, gas or foreign body is suspected; MRI is the imaging of choice for deep or necrotising infection.

6.7.1  Indications for Blood Culture

• Blood cultures are positive in <5% of uncomplicated cellulitis — do not take them routinely. [COMMON MCQ]
• Take when: systemic toxicity/sepsis or SIRS, immunocompromise or neutropenia, extensive/rapidly spreading disease, suspected necrotising infection, malignancy on chemotherapy, animal bite or water immersion injury, lymphoedema-associated cellulitis, chills and high fever, or failure of first-line therapy.

6.7.2  Indications for Imaging

• Suspected abscess or undrained collection (ultrasound first).
• Suspected necrotising soft-tissue infection — CT/MRI, but do not delay surgery for imaging. [VERY HIGH-YIELD]
• Suspected osteomyelitis or septic arthritis (X-ray then MRI).
• Suspected DVT (Doppler ultrasound).
• Diabetic foot infection with deep ulcer or probe-to-bone positive.
• Retained foreign body; periorbital swelling with any red-flag eye sign (contrast CT orbit).

6.8  Differential Diagnosis — "Pseudocellulitis"

Approximately 30% of patients admitted with "cellulitis" have a mimic. Bilateral involvement, absence of fever, itching rather than pain, and failure to respond to antibiotics should trigger reconsideration. [VERY HIGH-YIELD]

Cellulitis mimics
Mimic	Discriminating Features
Deep-vein thrombosis	Calf swelling and tenderness without sharp erythema or warmth gradient; risk factors present; Doppler ultrasound diagnostic — always exclude before compression therapy
Stasis dermatitis	Bilateral, chronic, itchy, hyperpigmented, scaly medial lower legs; afebrile; normal inflammatory markers — the commonest single mimic
Lipodermatosclerosis	Chronic venous disease; woody induration; "inverted champagne bottle" leg; painful in acute phase
Contact dermatitis	Itching predominates, sharply demarcated to contact area, vesicles, afebrile
Gout	Acute severe pain of first MTP/ankle with overlying erythema; hyperuricaemia; negatively birefringent needle-shaped crystals
Erythema nodosum	Tender bilateral subcutaneous nodules over shins; associated with TB, sarcoidosis, streptococcal infection, drugs, IBD; septal panniculitis on biopsy
Necrotising infection	Pain out of proportion, systemic toxicity, bullae, crepitus, skin anaesthesia, rapid progression — a surgical emergency
Others	Superficial thrombophlebitis, insect-bite hypersensitivity, drug reaction, cutaneous lymphoma, calciphylaxis, Sweet syndrome, carcinoma erysipeloides

6.9  Severity Assessment and Site of Care

The Eron classification (CREST) is the standard tool for deciding site of care.

Eron classification of cellulitis severity
Class	Description and Site of Care
Class I	No systemic toxicity, no comorbidity — oral antibiotics as outpatient
Class II	Systemically unwell or systemically well with comorbidity (diabetes, PVD, obesity, venous insufficiency) that may delay resolution — short admission or outpatient parenteral antibiotic therapy (OPAT)
Class III	Significant systemic upset (confusion, tachycardia, tachypnoea, hypotension) or unstable comorbidity — admit for IV antibiotics
Class IV	Sepsis or life-threatening/necrotising infection — admit, IV antibiotics, urgent surgical opinion, consider ICU

6.9.1  Outpatient versus Inpatient Treatment

• Outpatient oral therapy: Eron class I; reliable patient, able to take orals, no vomiting, no rapidly advancing margin, no immunosuppression.
• Inpatient/IV therapy: Eron class III–IV; failure of ≥48 h oral therapy; extensive or rapidly spreading disease; facial/periorbital/hand/perineal involvement; immunocompromise, neutropenia, poorly controlled diabetes; suspected necrotising infection; inability to tolerate orals; social factors preventing follow-up.
• Mark the erythema margin with an indelible pen and date it — the simplest and most useful bedside monitoring tool. [IMPORTANT]
• Elevate the limb, rest, analgesia, treat oedema, and treat the portal of entry (antifungal for tinea pedis).
• Expect erythema may transiently worsen in the first 24–48 h due to bacterial lysis — this is not treatment failure.

6.10  Empirical Antibiotics

Empirical antibiotic therapy for cellulitis
Setting	Regimen
Non-purulent, mild (oral)	Penicillin V, amoxicillin, cephalexin 500 mg QID, cloxacillin/dicloxacillin, or amoxicillin–clavulanate — 5–7 days
Non-purulent, moderate (IV)	IV penicillin G, ceftriaxone, cefazolin, or ampicillin–sulbactam
Non-purulent, severe	Broad-spectrum: piperacillin–tazobactam or meropenem + vancomycin/teicoplanin, plus urgent surgical assessment
Purulent (abscess-associated)	Drainage + MRSA-active agent: cotrimoxazole, doxycycline, clindamycin (oral); vancomycin, teicoplanin, linezolid, daptomycin (IV)
Penicillin allergy	Clindamycin, macrolide (resistance-dependent), linezolid, vancomycin
Diabetic / immunocompromised	Broad Gram-positive + Gram-negative + anaerobic cover (piperacillin–tazobactam, or a carbapenem in severe disease)
Water exposure	Add doxycycline + ceftazidime/ceftriaxone (Vibrio) or ciprofloxacin (Aeromonas)
Animal/human bite	Amoxicillin–clavulanate (drug of choice)

• Standard duration: 5–7 days; extend to 10–14 days for slow response, severe disease or immunocompromise. Trials show 5 days is non-inferior to 10 days in uncomplicated cellulitis. [COMMON MCQ]

6.10.1  MRSA Coverage — when to add it

• Purulent cellulitis or associated abscess.
• Penetrating trauma, injection drug use.
• Known MRSA colonisation or previous MRSA infection.
• Failure of β-lactam therapy.
• SIRS/sepsis, or systemic toxicity.
• Nasal MRSA carriage; recent hospitalisation, surgery, dialysis or residence in a care facility.
• High local MRSA prevalence — relevant across most Indian tertiary centres.

6.11  Complications

• Local: abscess, bullae, skin necrosis, ulceration, lymphangitis, progression to necrotising fasciitis.
• Systemic: bacteraemia and sepsis, infective endocarditis, metastatic infection (osteomyelitis, septic arthritis).
• Toxin-mediated: streptococcal toxic shock syndrome.
• Post-streptococcal: glomerulonephritis.
• Chronic: persistent lymphoedema and recurrent cellulitis; elephantiasis nostras verrucosa.
• Thrombophlebitis and DVT.

6.12  Recurrent Cellulitis Prophylaxis

• Indication: ≥2 episodes per year despite control of predisposing factors.
• Benzathine penicillin G 1.2 million units IM every 2–4 weeks, or Penicillin V 250–500 mg orally twice daily, or Erythromycin 250 mg twice daily in penicillin allergy. Continue for at least 12 months (PATCH trial evidence: prophylaxis roughly halves recurrence, but benefit wanes after stopping). [VERY HIGH-YIELD]
• Non-antibiotic measures are equally essential: treat tinea pedis and onychomycosis; daily emollients and meticulous skin hygiene; graduated compression stockings/bandaging (after excluding arterial disease and DVT); leg elevation; weight reduction; glycaemic control; management of venous insufficiency and lymphoedema (manual lymphatic drainage).

6.13  Prognosis

• Most uncomplicated cellulitis resolves within 7–10 days of appropriate therapy.
• Erythema regresses more slowly than systemic features; residual pigmentation and desquamation are expected.
• Recurrence in 20–30% within 3 years; each episode increases lymphatic damage.
• Mortality is low in simple cellulitis but rises sharply with bacteraemia, necrotising progression, diabetes, cirrhosis or immunosuppression.

 

SECTION 7  |  Erysipelas

7.1  Definition

Erysipelas ("St Anthony's fire") is an acute superficial bacterial infection of the upper dermis and superficial lymphatics producing a fiery-red, raised, sharply demarcated, indurated plaque with an abrupt palpable step-off from normal skin. [VERY HIGH-YIELD]

7.2  Etiology

• Streptococcus pyogenes (Group A Streptococcus) — the cause in the great majority of cases. [FAVORITE EXAM QUESTION]
• Groups B, C and G streptococci — particularly in neonates (GBS), diabetics and the elderly.
• Staphylococcus aureus — occasional, especially when a wound or abscess is present.

7.3  Pathogenesis

Pathogenesis of Erysipelas

Streptococcal entry through a skin breach (toe-web fissure, ulcer, nasal vestibulitis, surgical scar) ↓ Invasion of the UPPER DERMIS and SUPERFICIAL LYMPHATIC VESSELS ↓ Streptococcal M protein, hyaluronidase, streptokinase, exotoxins → intense inflammation ↓ Dense dermal oedema with marked lymphatic dilatation and neutrophil infiltrate ↓ RAISED, SHARPLY DEMARCATED, INDURATED PLAQUE with abrupt edge (superficial plane = sharp border) ↓ Lymphatic obstruction → lymphoedema → predisposition to recurrence

7.4  Clinical Features

• Abrupt onset with high fever, rigors, headache and vomiting preceding the rash by 4–48 hours — systemic upset is more prominent and earlier than in cellulitis.
• Typical raised, sharply demarcated border — the lesion is elevated above normal skin with a palpable "step" at the margin; brilliant erythema, warmth, tenderness and peau d’orange texture. [VERY HIGH-YIELD]
• Bullae, vesicles and superficial petechiae/ecchymoses may develop.
• Sites: lower limb is now commonest (~80%); face is the classic site.
• Facial erysipelas — characteristic "butterfly" distribution across the cheeks and bridge of the nose, often following streptococcal pharyngitis or nasal vestibulitis; must be distinguished from SLE (non-tender, no fever spike, nasolabial sparing) and from herpes zoster.
• Ear (pinna) involvement — "Milian ear sign" — favours erysipelas over cellulitis, because the pinna has almost no subcutaneous tissue for cellulitis to occupy. [COMMON MCQ]
• Lymphangitic streaking and tender regional lymphadenopathy are common.
• Desquamation occurs during recovery.

Cellulitis versus erysipelas
Feature	Cellulitis	Erysipelas
Depth	Deep dermis + subcutaneous fat	Upper dermis + superficial lymphatics
Border	Ill-defined, flat, blends into normal skin	Sharply demarcated, raised, palpable step
Colour	Dull pink-red	Fiery/salmon red
Onset	Gradual (days)	Abrupt (hours), fever precedes rash
Usual organism	Streptococci; S. aureus if purulent	Streptococcus pyogenes
Peau d’orange	Sometimes	Characteristic
Ear involvement (Milian sign)	No	Yes
Systemic toxicity	Variable, later	Early and marked
Abscess formation	More common	Uncommon
First-line therapy	Anti-staphylococcal ± anti-streptococcal	Penicillin

7.5  Differential Diagnosis

• Cellulitis — deeper, indistinct margin (see table above).
• Necrotising fasciitis — pain out of proportion, systemic toxicity, crepitus, skin anaesthesia, rapid progression.
• Contact dermatitis / angio-oedema — itching rather than pain, afebrile.
• Herpes zoster (early) — dermatomal, prodromal neuralgia, vesicles appear later.
• SLE malar rash — non-tender, photosensitive, spares the nasolabial folds, no fever spike.
• Erysipeloid (Erysipelothrix rhusiopathiae) — violaceous, non-suppurative, on the hand of a fish/meat handler, no fever.
• Carcinoma erysipeloides — cutaneous lymphatic infiltration by breast carcinoma; painless, non-resolving.
• Acute lipodermatosclerosis and stasis dermatitis — chronic, bilateral, afebrile.

7.6  Complications

• Local: abscess, bullae, superficial necrosis, gangrene, progression to necrotising fasciitis.
• Systemic: bacteraemia, sepsis, streptococcal toxic shock syndrome, endocarditis, septic arthritis.
• Facial disease: cavernous sinus thrombosis, orbital involvement.
• Post-streptococcal glomerulonephritis (acute rheumatic fever does not follow skin infection).
• Chronic: persistent lymphoedema, recurrence (up to 30%), elephantiasis nostras verrucosa.

7.7  Treatment

• Penicillin is the drug of choice — erysipelas is essentially a streptococcal disease. [VERY HIGH-YIELD]
• Mild disease: Penicillin V 500 mg QID or amoxicillin 500 mg TDS orally for 7–10 days.
• Moderate–severe/facial disease: IV benzylpenicillin (penicillin G) 1.2–2.4 g 6-hourly or ceftriaxone 1–2 g daily, switching to orals on clinical response.
• Penicillin allergy: clindamycin, or a macrolide guided by sensitivity.
• If S. aureus is suspected (bullae, pus, wound): cloxacillin/cefazolin; add MRSA cover if risk factors present.
• Adjuncts: rest and limb elevation, analgesia (paracetamol/NSAIDs), cool compresses, treatment of the portal of entry (tinea pedis, fissures, nasal vestibulitis), and management of oedema.
• Mark the margin and review at 48 hours; failure to improve should prompt reassessment for abscess, resistant organism, mimic, or necrotising infection.

7.8  Recurrence Prevention

• Recurrence rate up to 30% within 3 years; each episode worsens lymphoedema.
• Benzathine penicillin G 1.2 MU IM every 3–4 weeks, or penicillin V 250–500 mg BD, for ≥12 months in patients with ≥2 episodes per year.
• Aggressive treatment of tinea pedis, onychomycosis and interdigital maceration.
• Compression therapy, skin emollients, weight reduction, glycaemic control and lymphoedema care.

7.9  Prognosis

• Excellent with prompt penicillin — fever settles in 24–48 hours; erythema regresses over 5–10 days with desquamation.
• Mortality low in healthy adults; higher in the elderly, diabetics, immunosuppressed and those with bacteraemia.
• Long-term morbidity is dominated by recurrence and chronic lymphoedema.

 

SECTION 8  |  Staphylococcal Scalded Skin Syndrome

8.1  Definition and Concept

Staphylococcal scalded skin syndrome (SSSS, Ritter disease in neonates) is a toxin-mediated blistering disease in which haematogenously disseminated staphylococcal exfoliative toxins cleave desmoglein-1 in the superficial epidermis, producing widespread superficial denudation resembling a scald. The skin lesions themselves are sterile — the infection focus is elsewhere. [VERY HIGH-YIELD]

8.2  Exfoliative Toxins

• Produced by phage group II Staphylococcus aureus (types 71, 55, 3A, 3B).
• Exfoliative toxin A (ETA) — chromosomally/phage encoded, heat-stable; Exfoliative toxin B (ETB) — plasmid encoded, heat-labile; ETD also described.
• They are glutamate-specific serine proteases that cleave desmoglein-1, the desmosomal cadherin of the superficial epidermis. [COMMON MCQ]
• Result: split at the granular layer (stratum granulosum) — an intraepidermal, subcorneal cleavage plane.
• Desmoglein-3 (deeper epidermis and mucosa) is not affected → mucous membranes are spared, and the deeper epidermis remains intact so healing occurs without scarring.
• Toxin is cleared renally — hence the predilection for neonates and children with immature renal clearance and for adults with renal failure.

8.3  Neonatal and Childhood Disease

• >95% of cases occur in children under 5 years, with peak incidence in neonates and infants.
• Reasons: immature renal toxin clearance, absent protective anti-exfoliative-toxin antibodies.
• Primary focus: umbilical stump (omphalitis), conjunctivitis, nasopharynx, ear, circumcision site, or bullous impetigo.
• Ritter disease — the severe generalised neonatal form; nursery outbreaks occur from a colonised healthcare worker or mother.
• Mortality in children with modern care is low (<5%).

8.4  Adult Disease

• Rare; occurs almost exclusively with renal impairment (impaired toxin clearance) and/or immunosuppression — HIV, malignancy, chemotherapy, transplantation, alcoholic liver disease.
• Bacteraemia is frequent in adults (unlike children) and blood cultures are often positive.
• Mortality in adults is high — 40–60% — because of underlying disease and sepsis. [VERY HIGH-YIELD]

8.5  Clinical Features

• Prodrome: fever, irritability, malaise, poor feeding; a preceding purulent focus (conjunctivitis, omphalitis, ear discharge).
• Stage 1 (erythematous): diffuse, tender, macular scarlatiniform erythema starting on the face (perioral), neck, axillae and groin — exquisite skin tenderness is a hallmark.
• Stage 2 (exfoliative/blistering): within 24–48 h, flaccid, thin-walled, sterile bullae; large sheets of superficial epidermis peel away leaving moist, red, "scalded" skin.
• Perioral radial crusting and fissuring ("radial furrows") with a characteristic sad-looking facies — a classic sign. [FAVORITE EXAM QUESTION]
• Mucous membranes are SPARED — the key differentiator from toxic epidermal necrolysis. [VERY HIGH-YIELD]
• Stage 3 (desquamative/recovery): drying and generalised branny desquamation over 5–7 days; heals without scarring.

8.5.1  Nikolsky Sign

• Definition: gentle lateral shearing pressure on apparently normal-looking perilesional skin causes the epidermis to slide off — i.e. an extension of the blister.
• Positive in SSSS, pemphigus vulgaris, pemphigus foliaceus, TEN/Stevens–Johnson syndrome.
• Negative in bullous impetigo and in bullous pemphigoid (subepidermal, tense blisters).
• Asboe-Hansen (bulla spread) sign — pressure on an intact bulla extends it laterally; same disease group.

8.6  Differential Diagnosis from Toxic Epidermal Necrolysis

SSSS versus toxic epidermal necrolysis — the classic comparison
Feature	SSSS	TEN
Cause	Staphylococcal exfoliative toxin	Drug reaction (sulphonamides, anticonvulsants, allopurinol, NSAIDs, nevirapine)
Age	Neonates, children <5 y; adults with renal failure	Any age, mostly adults
Level of split	Intraepidermal — granular layer (subcorneal)	Subepidermal — dermo-epidermal junction (full-thickness epidermal necrosis)
Mucosal involvement	Absent (spared)	Present in >90% — oral, ocular, genital
Nikolsky sign	Positive	Positive
Skin tenderness	Marked	Marked, with painful erosions
Skin biopsy / frozen section	Split at granular layer, few inflammatory cells	Full-thickness epidermal necrosis, subepidermal split
Bacterial culture of skin	Sterile (organism at distant focus)	Sterile unless superinfected
Healing	Without scarring, 5–7 days	Slow; scarring, ocular sequelae
Treatment	Anti-staphylococcal antibiotics + supportive care	Stop the culprit drug; burns-unit care, supportive; ciclosporin/IVIG debated
Mortality	Children <5%; adults 40–60%	25–35% (SCORTEN-dependent)
FROZEN-SECTION BIOPSY — THE FASTEST DISCRIMINATOR ▪  When SSSS and TEN cannot be separated clinically, a frozen section of the sloughed skin (blister roof) gives an answer within an hour. ▪  SSSS — the roof is only stratum corneum ± granular layer (thin, no nucleated cells at the base). ▪  TEN — the roof is the full-thickness epidermis with necrotic keratinocytes. ▪  This distinction changes management completely: antibiotics vs drug withdrawal and burns-unit care. [VERY HIGH-YIELD]

8.7  Investigations

• Cultures from the primary focus — nasopharynx, conjunctiva, umbilicus, throat, ear, any wound. Blister fluid and denuded skin are sterile. [COMMON MCQ]
• Blood culture — usually negative in children, frequently positive in adults.
• Skin biopsy / frozen section (see box).
• Full blood count, CRP, electrolytes, renal function (toxin clearance and fluid loss), blood glucose.
• Toxin detection by PCR (eta, etb genes) or ELISA where available.

8.8  Management

• Admit; manage as a partial-thickness burn — a paediatric burns/high-dependency setting is ideal for extensive disease.
• Anti-staphylococcal antibiotics: IV cloxacillin/flucloxacillin or cefazolin; vancomycin, teicoplanin, linezolid or clindamycin if MRSA is suspected or prevalent (relevant in Indian units). Adding clindamycin is advocated for toxin suppression via inhibition of bacterial protein synthesis. [IMPORTANT]
• Fluid and electrolyte replacement — transepidermal loss can be substantial; monitor input/output and temperature (thermoregulation is impaired).
• Analgesia — the skin is exquisitely tender; handle minimally.
• Non-adherent, soft paraffin-based emollient dressings; avoid adhesive tapes; nurse on a non-adherent surface.
• Nutritional support; ophthalmology review if the eyelids are involved.
• Avoid corticosteroids — they worsen staphylococcal infection.
• Infection control: isolate the patient; search for and treat the colonised source in nursery outbreaks (staff and mothers); hand hygiene; cohort nursing.

8.9  Prognosis

• Children: excellent — mortality <5%, complete healing without scarring in 1–2 weeks.
• Adults: mortality 40–60%, largely determined by comorbidity, sepsis and renal failure.
• Complications: dehydration, electrolyte imbalance, hypothermia, secondary infection, sepsis, pneumonia, cellulitis.
• Recurrence is rare once protective antitoxin antibodies develop.

 

SECTION 9  |  Localised Bacterial Skin Disorders

This group comprises anatomically-defined pyogenic infections, several of which are surgical rather than medical problems. For each, note the organism, the predisposing factor and — critically — whether drainage is required.

9.1  Erythrasma

• Etiology: Corynebacterium minutissimum — a Gram-positive, non-spore-forming diphtheroid.
• Predisposing factors: hot humid climate (very common in India), obesity, diabetes mellitus, hyperhidrosis, poor hygiene, immunosuppression, occlusive clothing.
• Clinical features: well-demarcated, red-brown, finely scaly or wrinkled patches in intertriginous sites — toe webs (commonest, especially 4th web space), groin, axilla, inframammary and intergluteal folds; usually asymptomatic or mildly itchy.
• Diagnostic findings: Wood's lamp shows CORAL-RED fluorescence due to coproporphyrin III produced by the organism. [FAVORITE EXAM QUESTION] Gram stain of scales shows Gram-positive filamentous rods and coccobacilli; KOH mount is negative (excludes fungus).
• Differential diagnosis: tinea cruris/pedis (active scaly edge, KOH positive, green fluorescence with Microsporum only), candidal intertrigo (satellite pustules), inverse psoriasis, seborrhoeic dermatitis, pitted keratolysis.
• Treatment: topical fusidic acid, clindamycin, erythromycin or 2% miconazole cream for 2 weeks; oral erythromycin 250 mg QID for 5–14 days or single-dose clarithromycin 1 g for extensive disease; benzoyl peroxide wash; keep areas dry, weight reduction, glycaemic control, absorbent powders.
• Surgical indications: none.

9.2  Pitted Keratolysis

• Etiology: Kytococcus sedentarius (formerly Micrococcus), Dermatophilus congolensis, Corynebacterium spp. — organisms producing keratin-degrading proteases.
• Predisposing factors: hyperhidrosis and prolonged occlusive footwear — classic in soldiers, farmers, athletes, and in monsoon conditions; barefoot walking in wet fields.
• Clinical features: multiple discrete crater-like pits (1–7 mm) coalescing into erosions on the pressure-bearing plantar surfaces (heel, forefoot); malodour (bromhidrosis) and sliminess are the usual complaints; may be asymptomatic.
• Diagnostic findings: clinical; KOH mount negative; Wood’s lamp may show faint coral-red fluorescence if erythrasma coexists; Gram stain shows Gram-positive cocci/filaments in the pits.
• Differential diagnosis: plantar warts, tinea pedis, punctate palmoplantar keratoderma, basal cell naevus syndrome pits, arsenical keratoses.
• Treatment: control hyperhidrosis — 20% aluminium chloride hexahydrate, absorbent socks, alternate footwear, sun-dry shoes; topical clindamycin, erythromycin, mupirocin, fusidic acid or benzoyl peroxide for 2–4 weeks; treat coexisting erythrasma/tinea; botulinum toxin for refractory hyperhidrosis.
• Surgical indications: none.

9.3  Trichomycosis Axillaris

• Etiology: Corynebacterium tenuis and related corynebacteria colonising the hair shaft (a misnomer — it is bacterial, not fungal).
• Predisposing factors: hyperhidrosis, poor hygiene, obesity, humid climate, lack of shaving.
• Clinical features: adherent yellow (commonest), red or black concretions/nodules along axillary or pubic hair shafts; sweat may be stained; malodour; skin is normal.
• Diagnostic findings: clinical; Wood's lamp — pale yellow fluorescence; microscopy of hair shows bacterial concretions cementing the cuticle; KOH negative.
• Differential diagnosis: pediculosis pubis (nits are ovoid and attached to one side of the shaft), white/black piedra (fungal — Trichosporon, Piedraia), hair casts, monilethrix.
• Treatment: shave the affected hair (most effective single measure); topical erythromycin/clindamycin, benzoyl peroxide, or 2% fusidic acid for 2 weeks; antiperspirants; antiseptic soap.
• Surgical indications: none.

9.4  Perianal Streptococcal Dermatitis

• Etiology: Streptococcus pyogenes (Group A) — occasionally S. aureus.
• Predisposing factors: children 6 months–10 years; autoinoculation from the pharynx (concurrent or recent streptococcal pharyngitis); household spread.
• Clinical features: sharply demarcated, bright/beefy-red, tender perianal erythema extending 2–3 cm from the anal verge; painful defaecation with stool withholding and constipation; blood-streaked stools; anal fissures; pruritus ani; may be accompanied by guttate psoriasis flare or balanitis/vulvovaginitis.
• Diagnostic findings: perianal swab culture or rapid streptococcal antigen test is diagnostic — the crucial step, because the condition is routinely misdiagnosed as candidiasis, threadworm or sexual abuse. [IMPORTANT]
• Differential diagnosis: candidal dermatitis (satellite lesions, KOH positive), threadworm (nocturnal pruritus, tape test), irritant/seborrhoeic dermatitis, inverse psoriasis, inflammatory bowel disease, child sexual abuse, lichen sclerosus.
• Treatment: oral penicillin V or amoxicillin for 10 days (some advocate 14–21 days for cure), or cephalexin/clindamycin in allergy; topical mupirocin as adjunct; treat pharyngeal carriage and household contacts; relapse is common — re-culture after treatment.
• Surgical indications: none.

9.5  Bacterial Intertrigo

• Etiology: Streptococcus pyogenes, S. aureus, Corynebacterium, Gram-negatives (Pseudomonas, Proteus); frequently mixed with Candida albicans and dermatophytes.
• Predisposing factors: obesity, diabetes mellitus, heat and humidity, occlusive clothing, incontinence, immobility, poor hygiene, hyperhidrosis.
• Clinical features: erythematous, macerated, moist, malodorous, sometimes eroded or fissured plaques in skin folds — inframammary, axillary, inguinal, abdominal panniculus, interdigital; burning and itching; satellite pustules suggest candidal involvement.
• Diagnostic findings: Gram stain, bacterial culture; KOH mount for Candida/dermatophyte; Wood's lamp (coral-red = erythrasma; green fluorescence = Pseudomonas pyoverdin).
• Differential diagnosis: erythrasma, candidal intertrigo, tinea cruris, inverse psoriasis, seborrhoeic dermatitis, Hailey–Hailey disease, extramammary Paget disease (unilateral, non-resolving — biopsy).
• Treatment: drying measures are the mainstay — barrier creams (zinc oxide), absorbent powders, cotton clothing, weight reduction, glycaemic control; topical antibacterial (mupirocin, fusidic acid, clindamycin) ± topical azole; short course of low-potency topical steroid for inflammation; systemic antibiotics if cellulitic.
• Surgical indications: panniculectomy/reduction surgery occasionally for intractable disease in morbid obesity.

9.6  Acute Paronychia

• Etiology: Staphylococcus aureus (commonest); streptococci; anaerobes and mixed flora in nail-biters and finger-suckers; Pseudomonas (greenish discolouration) in chronic water exposure.
• Predisposing factors: nail biting, thumb sucking, manicure and cuticle trimming, hangnails, ingrown nail, finger trauma, occupational wet work (housemaids, cooks, dishwashers), diabetes mellitus.
• Clinical features: acute painful, throbbing, red, swollen nail fold; pus may track around the nail ("run-around" or horseshoe abscess) or beneath the nail plate (subungual abscess); fluctuance; nail-plate elevation.
• Diagnostic findings: clinical; digital pressure test (light pressure on the volar pulp blanches and outlines the collection); pus for Gram stain and culture; ultrasound in doubtful cases; X-ray if bone involvement or foreign body suspected.
• Differential diagnosis: herpetic whitlow — vesicles, no pus, DO NOT INCISE [VERY HIGH-YIELD]; felon (pulp space, not nail fold); chronic paronychia (candidal, occupational); squamous cell carcinoma of the nail unit; psoriatic nail disease; acute gout.
• Treatment: early/cellulitic stage — warm soaks 3–4 times daily, elevation, oral anti-staphylococcal antibiotic (cloxacillin/cephalexin; add anaerobic cover with amoxicillin–clavulanate or clindamycin in nail-biters).
• Surgical indications: any fluctuant collection requires incision and drainage — elevation of the eponychial fold with a blunt instrument (no anaesthesia may be needed for simple decompression), or a longitudinal incision; partial/complete nail-plate removal for subungual pus; drain and irrigate; do not close.

9.7  Felon

• Etiology: Staphylococcus aureus (including MRSA); streptococci; mixed flora after penetrating injury.
• Predisposing factors: penetrating pulp injury — finger-prick blood glucose testing in diabetics (a very common Indian cause), splinters, thorns, minor trauma.
• Anatomy — the crux of the disease: the distal pulp space is divided into 15–20 closed compartments by fibrous septa running from periosteum to skin; pus therefore cannot decompress and produces a closed-space abscess with rapidly rising pressure. [VERY HIGH-YIELD]
• Clinical features: intense, throbbing, unremitting pain, marked tense swelling of the distal pulp (proximal to the distal interphalangeal flexion crease it is spared), erythema, exquisite tenderness; pointing may occur; fever.
• Diagnostic findings: clinical; pus culture; radiograph to exclude foreign body and osteomyelitis of the distal phalanx (a common complication because septa attach to periosteum); ultrasound to localise pus.
• Differential diagnosis: herpetic whitlow (clear vesicles, less tense, DO NOT incise), acute paronychia (nail fold), cellulitis, gout, foreign-body granuloma.
• Complications: osteomyelitis of the distal phalanx, septic arthritis of the DIP joint, flexor tenosynovitis, pulp necrosis and skin sloughing, "fish-mouth" deformity from bad incisions.
• Treatment: IV/oral anti-staphylococcal antibiotics with MRSA cover as indicated; elevation and splinting; analgesia.
• Surgical indications: a felon is a surgical emergency — decompress early. Preferred approaches: unilateral longitudinal (high lateral) incision on the ulnar side of the index/middle/ring fingers and radial side of the thumb/little finger, kept dorsal to the neurovascular bundle and not crossing the DIP crease; or a volar longitudinal incision. Avoid "fish-mouth" and transverse incisions (unstable pulp, neuroma, anaesthetic fingertip). Break down all septa, irrigate, pack loosely, and leave open.

9.8  Infectious Flexor Tenosynovitis

• Etiology: S. aureus (including MRSA), streptococci; penetrating trauma is the usual mechanism; disseminated Neisseria gonorrhoeae causes a non-penetrating haematogenous form; Pasteurella after cat bite; Mycobacterium marinum and atypical mycobacteria in chronic cases.
• Predisposing factors: penetrating injury of the volar finger, animal/human bite, diabetes mellitus, immunosuppression, injection drug use.
• Kanavel's four cardinal signs — must be memorised: [FAVORITE EXAM QUESTION]
  • 1. Fusiform ("sausage") swelling of the whole digit
  • 2. Finger held in slight flexion (position of comfort)
  • 3. Tenderness along the entire course of the flexor tendon sheath
  • 4. Severe pain on PASSIVE EXTENSION of the digit — the earliest and most reliable sign
• Diagnostic findings: clinical (Kanavel signs); raised WBC/CRP; ultrasound or MRI shows fluid within the sheath; radiograph for foreign body/osteomyelitis; operative sheath fluid for Gram stain and culture; add gonococcal NAAT if disseminated gonococcal infection is possible.
• Anatomical danger — spread patterns: the little-finger sheath communicates with the ulnar bursa and the thumb sheath with the radial bursa; these connect through Parona's space in the distal forearm, producing a "horseshoe abscess". [IMPORTANT]
• Differential diagnosis: cellulitis, felon, septic arthritis of a finger joint, acute gout/pseudogout, inflammatory (rheumatoid) tenosynovitis, herpetic whitlow.
• Treatment: hand-surgical emergency — admit, IV broad-spectrum antibiotics (anti-staphylococcal + MRSA cover; add amoxicillin–clavulanate/anaerobic cover for bites), splint in the position of function, elevate.
• Surgical indications: presentation within 24 h with mild signs may be tried on IV antibiotics with strict 12–24-hour review; all others require urgent sheath drainage — proximal (A1 pulley) and distal (distal sheath) incisions with closed catheter irrigation, or open mid-lateral drainage; delay leads to tendon necrosis, adhesions and permanent stiffness.

9.9  Omphalitis

• Etiology: S. aureus, Group A and B streptococci, E. coli, Klebsiella, Proteus; anaerobes (Bacteroides fragilis, Clostridium tetani) — often polymicrobial.
• Predisposing factors: unhygienic cord care — application of cow dung, ash, oil or turmeric to the stump (a persisting rural Indian practice), home delivery by untrained attendants, prolonged rupture of membranes, low birth weight, prematurity, umbilical catheterisation. [IMPORTANT]
• Clinical features: periumbilical erythema, induration and tenderness with purulent or foul-smelling discharge from the stump; systemic features — fever or hypothermia, poor feeding, lethargy, abdominal distension; may progress with alarming speed to necrotising fasciitis of the abdominal wall, peritonitis, portal vein thrombophlebitis and neonatal sepsis.
• Diagnostic findings: discharge for Gram stain and culture; blood culture; full blood count, CRP; abdominal ultrasound for abscess, umbilical vein thrombosis or urachal/vitelline duct remnant; lumbar puncture if sepsis suspected.
• Differential diagnosis: normal cord separation (some serous discharge is physiological), umbilical granuloma (pink friable tissue, no cellulitis — treat with silver nitrate), patent urachus (urine leak), patent vitellointestinal duct (faeculent discharge), umbilical polyp, umbilical hernia.
• Treatment: admit — omphalitis in a neonate is treated as sepsis; IV cloxacillin + gentamicin (add metronidazole/clindamycin if foul-smelling or necrotising), 10–14 days; supportive neonatal care; tetanus prophylaxis considerations and maternal Td/TT immunisation status (neonatal tetanus prevention under India’s Universal Immunisation Programme; India was validated as having eliminated maternal and neonatal tetanus in 2015).
• Prevention: clean cord care; WHO/Government of India recommend 7.1% chlorhexidine digluconate application to the cord in home-birth/high-mortality settings.
• Surgical indications: abscess drainage; urgent debridement if necrotising fasciitis develops (mortality up to 60–80%).

9.10  Mastitis

• Etiology: Staphylococcus aureus (commonest), including MRSA; streptococci; E. coli, Bacteroides in non-lactational and periductal disease; anaerobes in smokers.
• Predisposing factors — lactational: milk stasis (the fundamental cause), cracked/fissured nipple, poor latch, missed feeds, abrupt weaning, primiparity, maternal fatigue and anaemia; commonest in the first 6 weeks of lactation.
• Predisposing factors — non-lactational: smoking (periductal mastitis), nipple piercing, diabetes mellitus, duct ectasia, prior radiotherapy; granulomatous mastitis and tuberculous mastitis are important Indian differentials.
• Clinical features: unilateral, wedge-shaped, tender, red, hot, swollen segment of the breast with fever, rigors and flu-like malaise; the breast is engorged and feeding is painful.
• Diagnostic findings: clinical; breast-milk culture and sensitivity in severe, recurrent, hospital-acquired or non-responding cases; ultrasound to exclude abscess in any case not improving within 48–72 hours; mammography ± core biopsy in non-lactational and non-resolving disease.
• Differential diagnosis: breast abscess, engorgement, blocked duct, galactocele, inflammatory breast carcinoma (must be excluded in non-lactational disease), tuberculous mastitis (India-specific: chronic, sinus formation, AFB/GeneXpert on aspirate), idiopathic granulomatous mastitis.
• Treatment: CONTINUE BREASTFEEDING or express milk — effective milk drainage is the single most important therapy and is safe for the baby. [VERY HIGH-YIELD] Warm compresses before and cold compresses after feeds, analgesia (paracetamol/ibuprofen — both safe in lactation), fluids, rest, correct latch with lactation-consultant support.
• Antibiotics (10–14 days): cloxacillin/dicloxacillin 500 mg QID or cephalexin 500 mg QID; clindamycin in penicillin allergy; MRSA-suspected: cotrimoxazole (avoid <1 month old or in G6PD deficiency/jaundiced infants), clindamycin, or vancomycin.
• Surgical indications: none for uncomplicated mastitis; drainage if abscess develops.

9.11  Breast Abscess

• Etiology: S. aureus (including MRSA) predominates; anaerobes and mixed flora in non-lactational/periductal abscess.
• Types: lactational (puerperal) — usually peripheral; non-lactational (periductal/subareolar) — associated with smoking and duct ectasia, prone to recurrence and mammary duct fistula; retromammary; neonatal (mastitis neonatorum); tuberculous cold abscess (India-relevant).
• Predisposing factors: untreated or inadequately treated mastitis, delayed presentation, diabetes, smoking, immunosuppression, MRSA.
• Clinical features: persistent fever and a tender fluctuant breast lump with overlying erythema; fluctuance may be absent in deep/retromammary abscess; failure of mastitis to improve after 48–72 h of antibiotics is the classic history.
• Diagnostic findings: ultrasound is the investigation of choice — anechoic/hypoechoic collection with debris and posterior enhancement; guides aspiration; pus for Gram stain, culture and AFB/GeneXpert and cytology where tuberculosis or malignancy is possible.
• Treatment / Surgical indications: ultrasound-guided needle aspiration (with an 18–19 G needle) plus antibiotics is the first-line treatment for most abscesses — repeat aspirations every 2–3 days as required; percutaneous catheter drainage for collections >3–5 cm; formal incision and drainage reserved for very large, multiloculated, skin-necrotic or failed-aspiration cases (use a circumareolar or cosmetically placed incision, break loculi, avoid injuring lactiferous ducts). [VERY HIGH-YIELD]
• Continue breastfeeding/expression from the affected breast unless the incision makes it impossible.
• For recurrent subareolar abscess with fistula: total duct excision (Hadfield procedure) once quiescent plus smoking cessation.

9.12  Pilonidal Abscess

• Etiology: infected pilonidal sinus — a foreign-body granulomatous reaction to hair penetrating the natal-cleft skin; polymicrobial — anaerobes (Bacteroides), S. aureus, streptococci, coliforms.
• Predisposing factors: young hirsute males (peak 15–30 y), deep natal cleft, prolonged sitting (drivers — "jeep bottom" — IT and desk workers), obesity, poor local hygiene, sweating, family history. Also occurs interdigitally in barbers (hair-cutters' sinus).
• Clinical features: painful, tender, fluctuant swelling in the natal cleft, typically 4–5 cm above the anus and often off the midline, with midline pits containing hair; purulent/serosanguinous discharge; fever.
• Diagnostic findings: clinical — identify midline pits; MRI or fistulography only if a complex or recurrent sinus, or if a fistula-in-ano is suspected.
• Differential diagnosis: perianal/ischiorectal abscess, fistula-in-ano, hidradenitis suppurativa, furuncle, sacrococcygeal teratoma or dermoid, tuberculous sinus, osteomyelitis of the sacrum.
• Treatment / Surgical indications: incision and drainage under anaesthesia is the treatment of an acute pilonidal abscess — an off-midline incision heals better than a midline one; curette the cavity, remove all hair and debris, leave open to granulate; antibiotics only as an adjunct (systemic upset, cellulitis, immunocompromise, diabetes).
• Definitive treatment of the underlying sinus is performed after the acute episode settles — options include pit-picking (Bascom), laying open with secondary healing, excision with primary midline closure (highest recurrence), or flap procedures (Karydakis, Limberg/rhomboid, Bascom cleft-lift) which off-midline the wound and lower recurrence. Adjuncts: hair removal (laser is superior to shaving), hygiene, weight loss.

9.13  Bartholin Abscess

• Etiology: polymicrobial — anaerobes (Bacteroides, Peptostreptococcus), E. coli, S. aureus; screen for Neisseria gonorrhoeae and Chlamydia trachomatis, though these are less often isolated than previously taught.
• Anatomy: Bartholin (greater vestibular) glands lie at the 4 and 8 o'clock positions of the vestibule; duct obstruction → cyst → secondary infection → abscess.
• Predisposing factors: reproductive age (20–30 y), sexually transmitted infection, prior Bartholin cyst, trauma, episiotomy, poor hygiene.
• Clinical features: rapidly enlarging, exquisitely painful unilateral labial swelling in the posterior third of the labium majus, with erythema, fluctuance, dyspareunia and difficulty sitting or walking; fever if extensive.
• Diagnostic findings: clinical; pus for culture and NAAT for gonorrhoea/chlamydia; biopsy or excision is mandatory in women over 40 years with a Bartholin mass to exclude adenocarcinoma of the gland. [IMPORTANT]
• Differential diagnosis: Bartholin cyst (non-tender), Skene duct cyst, epidermal inclusion cyst, vulval haematoma, hidradenitis suppurativa, Gartner duct cyst, vulval carcinoma, folliculitis/furuncle.
• Treatment / Surgical indications: drainage is the definitive treatment; simple incision alone has a high recurrence rate. Preferred: incision + insertion of a Word catheter left in situ for 4–6 weeks to epithelialise a new tract, or marsupialisation (suturing the cyst wall to vestibular skin). Gland excision is reserved for recurrent disease or suspected malignancy (risk of haemorrhage and dyspareunia). Antibiotics (amoxicillin–clavulanate or ceftriaxone + azithromycin/doxycycline for STI cover) when cellulitis, systemic signs, pregnancy, recurrence, immunosuppression or proven STI. Sitz baths and analgesia as adjuncts.

9.14  Perianal Abscess

• Etiology: originates from infection of the anal crypt glands (cryptoglandular theory) at the dentate line — polymicrobial: E. coli, Bacteroides fragilis, Enterococcus, Klebsiella, streptococci, S. aureus.
• Classification by space: perianal (~60%, commonest and most superficial), ischiorectal (~20%), intersphincteric (~5%), supralevator (~4%), and horseshoe abscess encircling the anus through the deep postanal space.
• Predisposing factors: Crohn disease, diabetes mellitus, immunosuppression/HIV, malignancy, trauma, anal fissure, haemorrhoid surgery, tuberculosis (India-relevant), obesity, smoking.
• Clinical features: severe constant throbbing perianal pain, worse on sitting and defaecation, with a tender, indurated, fluctuant perianal swelling; fever and malaise; deep (intersphincteric/supralevator) abscesses may show little external swelling but severe pain, urinary retention and rectal fullness — digital rectal examination is essential. [IMPORTANT]
• Diagnostic findings: clinical + digital rectal examination ± examination under anaesthesia; MRI pelvis is the gold standard for deep, recurrent, horseshoe and Crohn-related abscess and for delineating a fistula; endoanal ultrasound as an alternative; pus culture (growth of gut organisms predicts an underlying fistula-in-ano; skin organisms suggest a simple cutaneous abscess).
• Differential diagnosis: pilonidal abscess, hidradenitis suppurativa, Bartholin abscess, Crohn perianal disease, thrombosed external haemorrhoid, anal fissure with sentinel pile, Fournier gangrene (a surgical emergency — look for crepitus, necrosis, systemic toxicity), anal carcinoma, tuberculous perianal sinus.
• Treatment / Surgical indications: prompt incision and drainage is the treatment — antibiotics alone are inadequate and delay is dangerous. Drain under anaesthesia with a cruciate or elliptical incision as close to the anal verge as possible; deloculate; consider a drainage (mushroom) catheter for deep cavities; do not perform primary fistulotomy routinely (sphincter injury risk) — a loose seton may be placed if a fistula is obvious. Antibiotics as an adjunct in cellulitis, systemic sepsis, diabetes, immunosuppression, prosthetic valves or Crohn disease.
• Follow-up: 30–50% develop a fistula-in-ano; review at 6 weeks and manage per Parks classification. Investigate for Crohn disease and tuberculosis in recurrent or complex disease.

LOCALISED BACTERIAL DISORDERS — ONE-LINERS ▪  Coral-red Wood’s lamp fluorescence — erythrasma (C. minutissimum). ▪  Pale-yellow fluorescing axillary hair concretions — trichomycosis axillaris. ▪  Crater-like plantar pits with malodour — pitted keratolysis. ▪  Beefy-red perianal erythema with painful defaecation in a child — perianal streptococcal dermatitis. ▪  Four Kanavel signs — fusiform swelling, flexed posture, tenderness along sheath, pain on passive extension. ▪  Fifteen to twenty septa create a closed space in the fingertip — felon. ▪  Word catheter or marsupialisation — Bartholin abscess. ▪  Off-midline incision preferred — pilonidal abscess. ▪  Continue breastfeeding — lactational mastitis. ▪  30–50% of perianal abscesses are followed by — fistula-in-ano.

 

SECTION 10  |  Necrotising Soft-Tissue Infections

Necrotising soft-tissue infections (NSTIs) are rapidly progressive infections causing necrosis of fascia, subcutaneous tissue and/or muscle with severe systemic toxicity. They are surgical emergencies: mortality is 20–40% overall and approaches 100% without operation. Every hour of delay to debridement increases mortality. [VERY HIGH-YIELD]

THE SINGLE MOST IMPORTANT STATEMENT IN THIS CHAPTER ▪  Necrotising fasciitis is a CLINICAL diagnosis and a SURGICAL disease. ▪  Do NOT delay surgical exploration for imaging, scores or antibiotics. ▪  The LRINEC score and CT/MRI support but never exclude the diagnosis. ▪  If you are considering the diagnosis seriously, call the surgeon now.

10.1  Types of Necrotising Soft-Tissue Infection

Types of necrotising soft-tissue infection
Type / Entity	Microbiology and Characteristic Setting
Type I — Polymicrobial	Commonest (~70–80%). Mixed aerobes + anaerobes (Enterobacterales, Bacteroides, Peptostreptococcus, enterococci). Elderly, diabetes mellitus, postoperative abdominal/perineal, immunocompromised. Trunk, abdomen, perineum
Type II — Monomicrobial	Streptococcus pyogenes ± S. aureus (including CA-MRSA). Young, previously healthy patients; limbs; may follow minor trauma, varicella, NSAID use, IV drug use. Associated with streptococcal toxic shock syndrome
Type III — Marine / Gram-negative	Vibrio vulnificus (sea water, raw shellfish, cirrhosis, haemochromatosis), Aeromonas hydrophila (fresh water). Haemorrhagic bullae, fulminant course, very high mortality
Type IV — Fungal	Candida, Mucorales (mucormycosis), Aspergillus — immunocompromised, burns, penetrating trauma. Highly relevant in India post-COVID and in uncontrolled diabetes
Clostridial myonecrosis (gas gangrene)	Clostridium perfringens, C. septicum — muscle necrosis with gas (see Section 11)
Non-clostridial anaerobic myonecrosis	Anaerobic streptococci + Gram-negatives; "synergistic" necrotising myositis in diabetics
Streptococcal myositis	S. pyogenes invading muscle directly; rare, fulminant, mortality up to 80–100%
Synergistic necrotising cellulitis	Anaerobes + facultative Gram-negatives; perineum/lower limb in diabetics; foul "dishwater" pus, skin and muscle both involved
Fournier gangrene	Necrotising fasciitis of the perineum, genitalia and perianal region; polymicrobial; diabetes is the leading risk factor; male predominance ~10:1; sources — anorectal, urogenital, cutaneous
Cervicofacial necrotising fasciitis	Odontogenic (lower molars) or peritonsillar origin; spreads along deep cervical fascial planes; risk of descending mediastinitis, airway loss and jugular vein thrombosis (Lemierre)

10.2  Etiology — Key Organisms

• Streptococcus pyogenes (Group A Streptococcus) — the classic monomicrobial cause; virulence from M protein (M1, M3), streptococcal pyrogenic exotoxins (SpeA, SpeB, SpeC) acting as superantigens, streptolysin O/S, hyaluronidase and streptokinase. Causes streptococcal toxic shock syndrome. [VERY HIGH-YIELD]
• Staphylococcus aureus — increasingly CA-MRSA with PVL, causing monomicrobial necrotising infection.
• Anaerobes — Bacteroides fragilis, Peptostreptococcus, Prevotella, Fusobacterium; produce foul odour and gas; thrive in the hypoxic necrotic environment.
• Enterobacterales — E. coli, Klebsiella pneumoniae (an important cause of Type I NSTI and liver-abscess-associated invasive syndrome in Asia), Proteus, Enterobacter.
• Clostridium species — C. perfringens (traumatic gas gangrene), C. septicum (spontaneous gas gangrene; strong association with colonic malignancy and neutropenia).
• Vibrio vulnificus — halophilic Gram-negative rod; sea water/raw oyster exposure; haemorrhagic bullae and fulminant sepsis in cirrhotics (iron overload enhances virulence); mortality >50%.
• Aeromonas hydrophila — fresh water, mud, leech therapy, penetrating injury in paddy fields; rapidly progressive myonecrosis.

10.3  Risk Factors

• Diabetes mellitus — the commonest predisposing factor overall. [VERY HIGH-YIELD]
• Trauma (even trivial), surgery, burns, injection drug use, insect bites, childbirth.
• Varicella (chickenpox) in children — a classic antecedent of GAS necrotising fasciitis.
• NSAID use — implicated in masking early signs and possibly promoting GAS invasion (association debated but examinable).
• Chronic liver disease/cirrhosis (especially Vibrio), chronic kidney disease, malignancy, neutropenia, chemotherapy, corticosteroids, HIV.
• Peripheral vascular disease, obesity, malnutrition, alcohol misuse, advanced age.
• Perineal/anorectal disease, urethral stricture, perianal abscess (Fournier); poor dental hygiene (cervicofacial).

10.4  Pathogenesis

Pathogenesis of Necrotising Fasciitis

Inoculation of organisms into subcutaneous tissue (trauma, surgery, haematogenous, or cryptogenic) ↓ Bacterial proliferation along the AVASCULAR, LOW-RESISTANCE FASCIAL PLANE ↓ Release of exotoxins, superantigens (SpeA/SpeB), hyaluronidase, lipases, collagenase ↓ FASCIAL THROMBOSIS — thrombosis of nutrient perforating vessels crossing the fascia ↓ Ischaemic necrosis of fascia, subcutaneous fat, nerves and overlying skin ↓ Destruction of cutaneous nerves → SKIN ANAESTHESIA;  Tissue hypoxia → anaerobic growth → GAS ↓ Antibiotics cannot penetrate thrombosed, avascular tissue → ANTIBIOTICS ALONE FAIL ↓ Superantigen-driven massive cytokine release (TNF-α, IL-1, IL-6) → capillary leak, shock, multi-organ failure ↓ STREPTOCOCCAL TOXIC SHOCK SYNDROME  →  DEATH unless urgent DEBRIDEMENT

10.4.1  Fascial Thrombosis

• Bacteria spread horizontally along the superficial fascia, releasing enzymes that cause thrombosis of the perforating vessels supplying the overlying skin.
• Consequence 1: skin appears deceptively normal early, because it is supplied separately — the fascia is already destroyed beneath ("the disease is worse than it looks").
• Consequence 2: as thrombosis progresses, the skin becomes dusky, bullous, ecchymotic and finally gangrenous.
• Consequence 3: avascularity prevents antibiotic delivery — the pharmacological basis for mandatory surgical debridement. [IMPORTANT]

10.4.2  Toxin-Mediated Injury

• Streptococcal pyrogenic exotoxins (SpeA, SpeB, SpeC) and staphylococcal TSST-1 act as SUPERANTIGENS — they bridge MHC class II to the T-cell receptor Vβ region outside the antigen-binding groove, activating up to 20–30% of the T-cell repertoire (vs ~0.01% for a conventional antigen). [VERY HIGH-YIELD]
• Result: a cytokine storm (TNF-α, IL-1, IL-2, IL-6, IFN-γ) → capillary leak, vasodilatation, shock and multi-organ failure.
• SpeB is a cysteine protease that degrades tissue and activates inflammatory mediators; streptolysin O is cytolytic; M protein–fibrinogen complexes activate neutrophils and damage endothelium.
• C. perfringens alpha toxin (phospholipase C/lecithinase) and theta toxin (perfringolysin O) cause membrane lysis, myonecrosis, intravascular haemolysis and profound cardiac depression.
• This mechanism explains why protein-synthesis inhibitors (clindamycin, linezolid) are added to switch off toxin production.

10.5  Clinical Features

10.5.1  Early Clinical Features — the diagnostic window

• Pain out of proportion to physical findings — the single most important early clue. Severe, unrelenting pain in a limb with unimpressive overlying erythema. [FAVORITE EXAM QUESTION]
• Systemic toxicity out of proportion — fever, tachycardia, hypotension, confusion, in a patient whose skin "just looks like cellulitis".
• Woody, tense induration extending beyond the visible erythema; oedema beyond the margin of erythema.
• Rapid progression — advancing margins over hours, not days; failure to respond to appropriate antibiotics in 24–48 h.
• Absence of lymphangitis and lymphadenopathy (spread is along fascia, not lymphatics).

10.5.2  Late/Established Features

• Skin anaesthesia — loss of sensation over the affected skin due to destruction of cutaneous nerves; an ominous and near-pathognomonic sign. [VERY HIGH-YIELD]
• Bullae — initially serous, becoming haemorrhagic/violaceous.
• Ecchymosis and dusky discolouration, progressing to frank skin necrosis, sloughing and gangrene.
• Crepitus — subcutaneous gas; present in only ~30% but highly specific; suggests anaerobes or clostridia.
• Foul-smelling "dishwater" or "dirty dishwater" discharge — thin, greyish, non-purulent exudate.
• Systemic toxicity — high fever or hypothermia, tachycardia, hypotension, oliguria, altered sensorium, disseminated intravascular coagulation, multi-organ dysfunction; features of toxic shock syndrome (diffuse macular erythroderma, late desquamation).

HARD SIGNS DEMANDING IMMEDIATE SURGICAL EXPLORATION ▪  Pain out of proportion  |  Skin anaesthesia  |  Haemorrhagic bullae ▪  Crepitus / gas on radiograph  |  Skin necrosis or ecchymosis  |  "Dishwater" discharge ▪  Rapid progression despite antibiotics  |  Systemic toxicity, hypotension, organ failure ▪  Presence of any of these = theatre, not a scanner.

10.6  LRINEC Score

The Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC) uses six routine blood parameters to stratify risk in patients with a soft-tissue infection. [COMMON MCQ]

LRINEC score
Parameter		Value		Points
C-reactive protein (mg/L)		≥150		4
Total leukocyte count (per mm³)		15,000–25,000		1
		>25,000		2
Haemoglobin (g/dL)		11–13.5		1
		<11		2
Serum sodium (mmol/L)		<135		2
Serum creatinine (mg/dL)		>1.6		2
Serum glucose (mg/dL)		>180		1
Maximum score		—		13
LRINEC risk stratification
Score	Risk Category		Probability of NSTI
≤5	Low risk		<50%
6–7	Intermediate risk		50–75%
≥8	High risk		>75%

10.6.1  Limitations of LRINEC — must be known

• Poor sensitivity (~60–70% in validation studies) — a low score does NOT exclude necrotising fasciitis. Up to 1 in 10 proven cases score ≤5. [VERY HIGH-YIELD]
• Originally derived retrospectively in a single centre; subsequent prospective validations have shown much weaker performance.
• Confounded by pre-existing anaemia, renal failure, diabetes and any severe infection — CRP and glucose are non-specific.
• Performs poorly in children, immunocompromised patients, and Vibrio/clostridial infections.
• May be low in early disease — the exact time when the score would be most useful.
• Use it to raise suspicion, never to rule out. Clinical judgement and surgical exploration override the score.

10.7  Investigations

10.7.1  Laboratory Findings

• Leukocytosis with left shift (or leukopenia in overwhelming sepsis); CRP markedly raised (>150 mg/L).
• Hyponatraemia (Na <135 mmol/L) — a classic and useful associated finding.
• Raised creatinine and urea (acute kidney injury), hyperglycaemia, metabolic acidosis with raised lactate.
• Raised creatine kinase and lactate dehydrogenase — indicate muscle involvement (myonecrosis). [IMPORTANT]
• Hypoalbuminaemia, hypocalcaemia (fat saponification), coagulopathy/DIC (low platelets, raised INR, low fibrinogen, raised D-dimer).
• Blood cultures — positive in ~60% of Type II (streptococcal) infections; take before antibiotics but never delay therapy.
• Anaemia (haemolysis in clostridial infection).

10.7.2  Imaging

• Plain radiograph: subcutaneous gas is highly specific but present in a minority; also excludes foreign body.
• CT with contrast (most practical): fascial thickening and non-enhancement of fascia (the key sign), fluid tracking along deep fascial planes >3 mm, soft-tissue gas, fat stranding, oedema, abscess. Fast and widely available.
• MRI (most sensitive): T2/STIR hyperintensity of the deep fascia with thickening >3 mm, and — most importantly — non-enhancement of necrotic fascia on post-gadolinium T1 indicating devitalised tissue; distinguishes necrotising from non-necrotising infection and defines depth (fasciitis vs myositis). Limitation: time-consuming; must never delay theatre. [VERY HIGH-YIELD]
• Ultrasound: bedside; shows fascial fluid, subcutaneous thickening and gas artefact; operator-dependent.

10.7.3  Bedside Exploration ("Finger Test")

• Under local anaesthesia, a 2–3 cm incision is made down to the deep fascia at the suspected site.
• Positive findings: lack of bleeding, greyish necrotic fascia, thin foul "dishwater" fluid, and — the hallmark — the tissue planes separate with minimal finger pressure ("positive finger test") because fascial adherence has been destroyed. [FAVORITE EXAM QUESTION]
• A positive test mandates immediate transfer to theatre for formal debridement.
• Rapid, requires no imaging, and can be performed at the bedside or in the emergency department.

10.7.4  Frozen-Section Biopsy

• A deep incisional biopsy including fascia sent for urgent frozen section.
• Histology: necrosis of superficial fascia, thrombosis of blood vessels, dense polymorph infiltration of the deep dermis and fascia, and microorganisms within the destroyed fascia, with relative sparing of muscle in pure fasciitis.
• Useful in equivocal early cases, but must never delay definitive surgery when clinical suspicion is high.

10.8  Differential Diagnosis

• Severe cellulitis / erysipelas — pain proportionate, no anaesthesia, no crepitus, responds to antibiotics.
• Abscess / pyomyositis — localised collection, less systemic toxicity.
• Clostridial myonecrosis — muscle rather than fascia; crepitus more prominent; more rapid.
• Deep-vein thrombosis, compartment syndrome, acute limb ischaemia — compartment syndrome shares "pain out of proportion"; measure compartment pressures.
• Pyoderma gangrenosum, calciphylaxis, warfarin/heparin skin necrosis, vasculitis — surgery is harmful in pyoderma gangrenosum (pathergy), so exclude it in atypical, culture-negative ulcers. [IMPORTANT]
• Toxic shock syndrome without NSTI, erythema multiforme/TEN, acute gout, snake-bite envenomation with local necrosis (relevant in India).

10.9  Management

Necrotising Fasciitis — Emergency Pathway

SUSPECT: pain out of proportion, systemic toxicity, rapid progression, bullae, crepitus, anaesthesia ↓ RESUSCITATE — large-bore IV access, aggressive fluids, blood cultures, lactate, cross-match ↓ BROAD-SPECTRUM IV ANTIBIOTICS + CLINDAMYCIN within 1 hour (do not wait for results) ↓ CALL SURGEON / ICU IMMEDIATELY — imaging ONLY if it does not delay theatre ↓ BEDSIDE FINGER TEST if diagnosis uncertain → positive = go to theatre ↓ URGENT RADICAL DEBRIDEMENT — excise all necrotic tissue to bleeding, adherent margins; take tissue for Gram stain/culture ↓ RE-EXPLORE (planned "second look") at 12–24 h, and repeat every 24–48 h until no further necrosis ↓ ICU SUPPORT — vasopressors, ventilation, renal replacement, glycaemic control, nutrition; consider IVIG in streptococcal TSS ↓ DE-ESCALATE antibiotics on culture; RECONSTRUCT (skin graft/flap) once infection controlled; rehabilitation

10.9.1  Immediate Surgical Exploration

• Time to first debridement is the strongest modifiable predictor of survival — ideally within 6–12 hours of presentation. [VERY HIGH-YIELD]
• Generous incisions over the affected area; excise ALL necrotic skin, fat and fascia back to healthy, bleeding, adherent tissue.
• Send deep tissue for Gram stain, aerobic/anaerobic culture and histology.
• Leave wounds open — no primary closure; dressings or negative-pressure wound therapy once necrosis is controlled.
• Fournier gangrene: consider diverting colostomy for faecal contamination and suprapubic catheter for urinary diversion; testes are usually spared (separate blood supply from the aorta) and can be preserved in thigh pouches.
• Cervicofacial disease: secure the airway early (low threshold for tracheostomy) and exclude mediastinal extension.
• Amputation may be life-saving in extensive limb disease.

10.9.2  Serial Debridement

• Planned re-exploration at 12–24 hours is mandatory, and repeated every 24–48 hours until the wound is stable.
• A median of 3 debridements is typical; underestimating the extent at first operation is the commonest error.
• Fewer than two debridements is a marker of inadequate source control and is associated with higher mortality.

10.9.3  Empirical Broad-Spectrum Antibiotics

• Must cover Gram-positives (including MRSA), Gram-negatives and anaerobes; give within 1 hour of recognition.
• Regimen: Piperacillin–tazobactam 4.5 g IV 6-hourly OR meropenem 1 g IV 8-hourly PLUS Vancomycin/teicoplanin/linezolid (MRSA cover) PLUS Clindamycin 600–900 mg IV 8-hourly (toxin suppression).
• Add doxycycline + ceftriaxone/ceftazidime for suspected Vibrio vulnificus (sea-water exposure, cirrhosis); ciprofloxacin for Aeromonas.
• De-escalate to targeted therapy on culture; continue until debridement is complete, the patient is clinically stable and afebrile for 48–72 h (typically 10–14 days or longer).

10.9.4  Clindamycin for Toxin Suppression

• Clindamycin is added to (never substituted for) a β-lactam in all suspected streptococcal/clostridial NSTI. [VERY HIGH-YIELD]
• Mechanism 1 — inhibits bacterial protein synthesis (50S ribosome) → shuts off exotoxin/superantigen production.
• Mechanism 2 — efficacy is not affected by inoculum size or growth phase, overcoming the "Eagle effect": penicillins act on the cell wall and lose efficacy against stationary-phase organisms at a high bacterial load, which is exactly the situation in necrotising infection. [FAVORITE EXAM QUESTION]
• Mechanism 3 — suppresses M-protein synthesis (enhancing phagocytosis) and modulates TNF-α production.
• Linezolid is an alternative protein-synthesis inhibitor with similar antitoxin effect plus MRSA activity.
• Continue clindamycin until the patient is haemodynamically stable and source control is achieved (usually 48–72 h beyond).

10.9.5  Intravenous Immunoglobulin (IVIG)

• Rationale: pooled IgG contains neutralising antibodies against streptococcal superantigens (SpeA/B/C), blocking T-cell activation and the cytokine storm.
• Considered in streptococcal toxic shock syndrome with necrotising fasciitis and in refractory shock; typical dose 1 g/kg on day 1 then 0.5 g/kg on days 2 and 3 (regimens vary; 2 g/kg single dose also used).
• Evidence is observational and from underpowered trials — benefit is plausible but not definitively proven; expensive and not routinely available. Adjunct only, never a substitute for surgery. [IMPORTANT]

10.9.6  Hyperbaric Oxygen Therapy

• Rationale: raises tissue oxygen tension → bactericidal to anaerobes, inhibits clostridial alpha-toxin production, enhances neutrophil oxidative killing and antibiotic activity, promotes angiogenesis and fibroblast function.
• Best evidence is in clostridial myonecrosis (gas gangrene); data in polymicrobial necrotising fasciitis are conflicting.
• Must never delay surgery, resuscitation or antibiotics; limited availability, and unsafe in haemodynamically unstable ventilated patients.
• Contraindications include untreated pneumothorax and certain chemotherapy agents (bleomycin, cisplatin, doxorubicin).

10.9.7  Intensive Care Support

• Sepsis bundle: early fluid resuscitation, vasopressors (noradrenaline first line), lactate clearance, and source control.
• Mechanical ventilation for ARDS; renal replacement therapy for acute kidney injury (common with myoglobinuria and toxin injury).
• Correction of coagulopathy and DIC; transfusion support; glycaemic control (insulin infusion in diabetics); analgesia and sedation.
• Nutritional support is critical — these patients are profoundly catabolic with huge protein losses from open wounds; early enteral feeding with high protein/calorie targets.
• Venous thromboembolism prophylaxis, stress-ulcer prophylaxis, physiotherapy and early rehabilitation.
• Tetanus prophylaxis in contaminated traumatic wounds.

10.10  Complications

• Septic shock, streptococcal/staphylococcal toxic shock syndrome, DIC, multi-organ dysfunction.
• Acute kidney injury, ARDS, myocardial depression.
• Extensive tissue loss requiring amputation or major reconstruction; scarring and contractures.
• Fournier gangrene: faecal/urinary fistula, testicular loss (rare), sexual dysfunction, permanent stoma.
• Cervicofacial: descending necrotising mediastinitis, airway obstruction, jugular vein thrombosis, empyema.
• Secondary nosocomial infection, critical-illness neuromyopathy, malnutrition, prolonged rehabilitation, psychological morbidity and PTSD.

10.11  Mortality Predictors

• Delay to first debridement (>12–24 hours) — the strongest modifiable predictor. [VERY HIGH-YIELD]
• Age >60 years; diabetes mellitus, cirrhosis, chronic kidney disease, malignancy, immunosuppression.
• Truncal, perineal or cervicofacial site (worse than limb disease, which can be amputated).
• Shock/hypotension at presentation, need for vasopressors, high lactate, acute kidney injury.
• Bacteraemia; Vibrio vulnificus or clostridial infection; polymicrobial infection in an immunocompromised host.
• Extensive body-surface involvement; fewer than two debridements; WBC >30,000/mm³, creatinine >2 mg/dL, hyponatraemia.
• Scoring: LRINEC (diagnostic), APACHE II, SOFA and the Fournier Gangrene Severity Index (FGSI ≥9 predicts high mortality) for prognosis.

10.12  Prognosis

• Overall mortality 20–40%; approaches 100% without surgery.
• Streptococcal NSTI with toxic shock syndrome: mortality 30–70%; Vibrio vulnificus NSTI in cirrhosis: >50%.
• Fournier gangrene: mortality typically 20–40%, higher with anorectal source and FGSI ≥9.
• Survivors face prolonged hospitalisation, multiple reconstructive procedures, functional impairment and significant psychological sequelae.

 

SECTION 11  |  Clostridial Myonecrosis (Gas Gangrene)

Clostridial myonecrosis is a fulminant, toxin-mediated necrosis of skeletal muscle caused by Clostridium species, characterised by gas in tissues, profound systemic toxicity and rapid progression to death without immediate surgery. [VERY HIGH-YIELD]

11.1  Traumatic Gas Gangrene

• Accounts for ~70% of cases; caused predominantly by Clostridium perfringens type A.
• Follows deep, contaminated, devitalised wounds — road traffic accidents, crush and blast injuries, compound fractures, agricultural injuries with soil contamination (a major Indian scenario), war wounds, criminal/septic abortion, intramuscular injections, bowel or biliary surgery.
• Anaerobic, devitalised muscle with a low redox potential is the essential substrate — clostridial spores germinate only in this environment. [IMPORTANT]
• Incubation is short: usually less than 24 hours (range 6 hours to 3 days).

11.2  Spontaneous (Non-traumatic) Gas Gangrene

• Caused predominantly by Clostridium septicum — which is aerotolerant and can therefore infect normal, well-perfused muscle after haematogenous seeding from the gut. [VERY HIGH-YIELD]
• Strongly associated with colonic malignancy (especially caecal carcinoma), colonic polyps, diverticular disease, neutropenic enterocolitis (typhlitis), haematological malignancy, chemotherapy-induced neutropenia and diabetes mellitus.
• Any patient with spontaneous C. septicum infection must undergo colonoscopy/CT colonography to exclude occult colonic carcinoma — a favourite examination point. [FAVORITE EXAM QUESTION]
• Typically presents with atraumatic limb or trunk pain progressing over hours in a systemically toxic patient.

11.3  Organisms and Toxins

• Clostridium perfringens — Gram-positive, spore-forming, obligate anaerobe; "boxcar-shaped" bacilli; non-motile; produces a double zone of haemolysis on blood agar; Nagler reaction positive (lecithinase neutralised by antitoxin on egg-yolk agar); stormy clot fermentation in litmus milk.
• Clostridium septicum — motile, aerotolerant; spontaneous gas gangrene; colonic malignancy association.
• Others: C. novyi, C. histolyticum, C. sordellii (associated with obstetric infection, medical abortion and injection drug use — profound leukaemoid reaction, haemoconcentration and refractory shock without fever).

11.3.1  Alpha Toxin — the central virulence factor

• C. perfringens alpha toxin is a PHOSPHOLIPASE C (lecithinase) — the principal lethal and necrotising toxin. [VERY HIGH-YIELD]
• Hydrolyses lecithin (phosphatidylcholine) and sphingomyelin in cell membranes → lysis of myocytes, endothelium, platelets and erythrocytes.
• Causes massive intravascular haemolysis (classic tea/port-wine coloured plasma, jaundice, haemoglobinuria), platelet aggregation and microvascular thrombosis (worsening ischaemia and toxin trapping), and direct myocardial suppression with bradycardia and hypotension.
• Suppresses neutrophil chemotaxis and function — the classic histological finding is muscle necrosis with abundant Gram-positive bacilli but strikingly FEW inflammatory cells. [COMMON MCQ]
• Theta toxin (perfringolysin O) — a cholesterol-dependent cytolysin causing further cell lysis and vascular leukostasis.
• Saccharolytic and proteolytic enzymes ferment muscle glycogen → hydrogen and carbon dioxide → tissue gas and crepitus.

11.4  Clinical Features

• Sudden, severe, rapidly increasing pain at the wound site — the earliest symptom, out of proportion to appearances.
• Tense oedema and a sense of heaviness; the wound may exude thin, brownish, serosanguinous, sweetish/foul-smelling discharge.
• Skin: initially pale and tense → bronze/dusky discolouration ("bronzed appearance") → haemorrhagic bullae → frank gangrene with a marbled appearance.
• Crepitus from tissue gas (more prominent than in necrotising fasciitis, though absent early and in C. septicum).
• Muscle findings at surgery: dark red/reddish-brown or greyish, non-contractile ("does not twitch on stimulation"), does not bleed on cutting, and later becomes friable and black. [VERY HIGH-YIELD]
• Systemic toxicity is disproportionately severe: profound tachycardia OUT OF PROPORTION TO A ONLY MODEST FEVER, sweating, pallor, agitation, then "toxic delirium", hypotension, oliguria and multi-organ failure. [FAVORITE EXAM QUESTION]
• Massive haemolysis — jaundice, haemoglobinuria, dark plasma, acute kidney injury, DIC.
• Progression is measured in hours — the margin may advance several centimetres per hour.

11.5  Investigations

11.5.1  Radiological Gas

• Plain radiograph: gas dissecting ALONG MUSCLE BUNDLES in a linear/feathery pattern — the hallmark of myonecrosis (in necrotising fasciitis gas lies in the fascial planes). [VERY HIGH-YIELD]
• CT is more sensitive: intramuscular gas, muscle oedema and non-enhancement, fascial fluid, and the extent of proximal spread.
• MRI shows muscle T2 hyperintensity with non-enhancement; must not delay surgery.
• Remember that gas may be absent early or in C. septicum infection — its absence does not exclude gas gangrene, and gas may also arise from other gas-forming organisms (E. coli, Klebsiella, anaerobic streptococci), open wounds and subcutaneous emphysema.

11.5.2  Smear and Culture

• Gram stain of wound exudate is the fastest and most useful test: large, "boxcar-shaped" Gram-positive bacilli with BLUNT ENDS, few or NO inflammatory cells (leukocyte-poor), and absent spores in tissue. [VERY HIGH-YIELD]
• Anaerobic culture on blood agar — C. perfringens shows a double zone of β-haemolysis; Nagler reaction (lecithinase activity on egg-yolk agar inhibited by specific antitoxin) confirms; stormy clot in litmus milk; Robertson cooked meat medium for enrichment.
• Blood cultures — bacteraemia common in spontaneous disease.
• Laboratory: leukocytosis (or leukaemoid reaction), haemolytic anaemia with spherocytes, raised bilirubin and LDH, haemoglobinuria, markedly raised creatine kinase, acute kidney injury, metabolic acidosis, DIC, hypocalcaemia.
• Histology (frozen section): coagulative myonecrosis with Gram-positive rods and scanty neutrophils.

11.6  Treatment

11.6.1  Surgical Treatment — the priority

• Immediate, radical surgical debridement of all necrotic muscle is the single life-saving intervention. [VERY HIGH-YIELD]
• Excise until healthy, bleeding, contractile muscle is reached; decompress fascial compartments; leave wounds wide open.
• Amputation (often open/guillotine) is frequently required for extensive limb involvement and should not be delayed in a deteriorating patient.
• Planned re-exploration every 12–24 hours until progression stops.
• Remove foreign bodies, stabilise fractures, and address the source (bowel resection or hysterectomy in uterine gas gangrene; colonoscopy after recovery for C. septicum).

11.6.2  Antibiotics

• Regimen of choice: high-dose Penicillin G (benzylpenicillin) 3–4 million units IV 4-hourly PLUS Clindamycin 900 mg IV 8-hourly. [VERY HIGH-YIELD]
• Clindamycin is essential — it inhibits alpha-toxin and theta-toxin synthesis, is unaffected by inoculum size (overcoming the Eagle effect that limits penicillin at high bacterial density), and has shown survival benefit in experimental models.
• Penicillin allergy: clindamycin + metronidazole, or a carbapenem, or chloramphenicol.
• Add broad-spectrum cover (piperacillin–tazobactam or meropenem ± vancomycin) until polymicrobial infection is excluded.
• Duration: continue until debridement is complete and the patient is stable, usually 10–14 days.
• Antitoxin (polyvalent gas gangrene antiserum) is NO LONGER recommended — unproven efficacy and high risk of anaphylaxis/serum sickness. [IMPORTANT]

11.6.3  Hyperbaric Oxygen

• Clostridial myonecrosis is the strongest indication for hyperbaric oxygen among the soft-tissue infections.
• Typical regimen: 3 ATA for 90 minutes, three sessions in the first 24 hours, then twice daily.
• Mechanism: bactericidal to obligate anaerobes, halts alpha-toxin production, demarcates viable from non-viable tissue (may allow more conservative debridement), enhances neutrophil killing.
• Order of priority remains: resuscitation → antibiotics → SURGERY → hyperbaric oxygen. Never transfer an unstable patient for HBOT before debridement.

11.6.4  Supportive Care

• Aggressive fluid resuscitation, vasopressors, transfusion for haemolytic anaemia, correction of DIC.
• Renal support for haemoglobinuric acute kidney injury; monitor potassium and acid–base status.
• Tetanus prophylaxis (contaminated wound) and nutritional support; analgesia; ICU care.

Gas gangrene versus necrotising fasciitis
Feature	Clostridial Myonecrosis	Necrotising Fasciitis
Primary tissue	Muscle	Superficial and deep fascia (muscle spared early)
Organism	C. perfringens, C. septicum	Polymicrobial (Type I) or S. pyogenes (Type II)
Onset after injury	Very rapid — <24 h	Usually 1–4 days
Crepitus/gas	Marked, along muscle bundles	Variable (~30%), along fascial planes
Discharge	Thin, brown, serosanguinous, sweetish odour	"Dishwater", foul-smelling
Skin colour	Bronze/marbled with haemorrhagic bullae	Dusky, ecchymotic, bullous
Muscle at surgery	Non-contractile, non-bleeding, dark	Usually viable early
Gram stain	Boxcar bacilli with FEW leukocytes	Mixed organisms with many neutrophils
Haemolysis	Marked (alpha toxin)	Uncommon
Fever vs pulse	Tachycardia out of proportion to fever	High fever with tachycardia
Hyperbaric oxygen	Best evidence	Adjunct, conflicting evidence
Antibiotics	Penicillin + clindamycin	Broad-spectrum + MRSA cover + clindamycin

11.7  Prognosis

• Mortality 20–30% with prompt treatment; >50% for truncal disease and nearly 100% if untreated.
• Spontaneous C. septicum gas gangrene carries a worse prognosis (mortality up to 70%) because of delayed recognition and underlying malignancy/neutropenia.
• Poor prognostic markers: delay to surgery, trunk/abdominal involvement, shock, haemolysis and renal failure, age, diabetes, immunosuppression, bacteraemia.
• Survivors need reconstruction, prosthetic rehabilitation after amputation and — for C. septicum — colonic evaluation for occult malignancy.

 

SECTION 12  |  Pyomyositis and Infectious Myositis

Pyomyositis is a primary bacterial infection of skeletal muscle producing intramuscular abscess, arising from haematogenous seeding rather than contiguous spread. It is common in tropical countries — India is an endemic region — and is an important differential for a febrile child or young adult with limb pain and no obvious focus. [VERY HIGH-YIELD]

12.1  Types

• Tropical pyomyositis ("myositis tropicans") — occurs in healthy children and young adults in hot humid climates; often follows blunt trauma or vigorous exercise; India, Africa, Southeast Asia, Pacific Islands.
• Temperate-climate pyomyositis — occurs almost exclusively in immunocompromised hosts (HIV — the leading association in temperate zones, diabetes mellitus, malignancy, cirrhosis, chronic kidney disease, corticosteroids, injection drug use); older patients; more often multifocal.
• Primary pyomyositis — haematogenous infection of otherwise normal muscle (the classic form).
• Secondary pyomyositis — direct extension from adjacent osteomyelitis, septic arthritis, penetrating trauma, injection or surgery.
• Streptococcal myositis — fulminant S. pyogenes invasion of muscle with toxic shock; distinct from pyomyositis, mortality up to 80–100%.
• Bacterial myositis — diffuse infective myositis without abscess (streptococcal, clostridial or Gram-negative).
• Psoas abscess and iliacus abscess — see 12.8.

12.2  Etiology

• Staphylococcus aureus — responsible for 75–90% of tropical pyomyositis; MRSA increasingly reported, often PVL-positive. [FAVORITE EXAM QUESTION]
• Streptococcus pyogenes (Group A) — second commonest; also Groups B, C, G (GBS in diabetics and the elderly).
• Streptococcus pneumoniae, Escherichia coli, Klebsiella, Salmonella (in sickle-cell disease and enteric fever — relevant in India), Pseudomonas, Yersinia, Aeromonas.
• Anaerobes; Mycobacterium tuberculosis (tuberculous pyomyositis and cold psoas abscess — an important Indian differential); Nocardia, Cryptococcus and Candida in the immunosuppressed.
• Consider melioidosis (Burkholderia pseudomallei) in patients from endemic areas of coastal/eastern India with diabetes, which classically causes multifocal abscesses.

12.3  Risk Factors

• Blunt muscle trauma or strenuous exercise — creates a locus of injured muscle for seeding during transient bacteraemia. [IMPORTANT]
• HIV infection (the dominant risk factor in non-tropical settings), diabetes mellitus, malignancy, chemotherapy, corticosteroids, transplantation.
• Injection drug use; malnutrition, vitamin A deficiency, anaemia and parasitic infestation (proposed contributors in tropical disease).
• Concurrent skin infection or transient bacteraemia; sickle-cell disease; chronic kidney and liver disease.
• Hot humid climate, young age, male predominance (~2:1).

12.4  Stages of Pyomyositis

Three stages of pyomyositis — a classic examination question
Stage	Timing	Features and Management
Stage 1 — Invasive	Week 1 (days 1–14)	Diffuse crampy muscle ache, low-grade fever, "woody" firm induration without fluctuance; NO pus yet; only ~2% present here. Treated with antibiotics alone — no drainage needed
Stage 2 — Suppurative	Weeks 2–3	>90% present at this stage. Fever, exquisite localised tenderness, swelling; pus is now present; muscle aspiration is positive. Requires DRAINAGE + antibiotics
Stage 3 — Late / Septicaemic	After week 3	Fluctuant abscess with systemic toxicity, bacteraemia, septic shock, metastatic abscesses, endocarditis, acute kidney injury. High mortality; urgent drainage + IV antibiotics + ICU support

12.5  Clinical Features

• Fever with localised muscle pain, cramping and tenderness — most often the thigh (quadriceps — commonest single muscle), gluteal muscles, iliopsoas, calf, trunk and shoulder girdle.
• Woody, firm, indurated swelling with characteristically NORMAL overlying skin in the early stage — a key discriminator from cellulitis. [VERY HIGH-YIELD]
• Antalgic gait, refusal to bear weight or "pseudo-paralysis" in children; limb held in a position of comfort.
• Fluctuance appears late (deep muscles may never fluctuate).
• Solitary abscess in ~60–75%; multifocal in 15–40% (more common in the immunocompromised) — always examine all muscle groups. [IMPORTANT]
• Later: swinging fever, rigors, systemic toxicity, sepsis.

12.6  Investigations

• Blood cultures — positive in only ~5–30% in tropical disease but up to 30–50% in temperate/immunocompromised patients; always take before antibiotics.
• Leukocytosis with neutrophilia, raised ESR and CRP; eosinophilia may be present in tropical cases (associated parasitic infestation).
• Creatine kinase is characteristically NORMAL or only mildly raised — a valuable negative finding that distinguishes pyomyositis from rhabdomyolysis and viral/inflammatory myositis. [FAVORITE EXAM QUESTION]
• Blood glucose/HbA1c and HIV serology in every adult with pyomyositis.
• Ultrasound — first-line and bedside: hypoechoic/heterogeneous intramuscular collection with muscle bulking, internal debris and hyperaemic rim; guides aspiration; limited for deep muscles (psoas).
• CT with contrast — shows muscle enlargement with a low-attenuation centre and rim enhancement, gas, and is best for iliopsoas and deep pelvic/paraspinal muscles; guides percutaneous drainage.
• MRI is the INVESTIGATION OF CHOICE — most sensitive, detects stage 1 disease before pus forms (diffuse muscle T2/STIR hyperintensity with enlargement), defines abscess extent, and shows adjacent osteomyelitis or septic arthritis. [VERY HIGH-YIELD]
• Aspirate/pus for Gram stain, aerobic and anaerobic culture, AFB stain, GeneXpert MTB/RIF and fungal studies — tuberculosis must be actively excluded in India.
• Plain radiograph — usually normal; may show soft-tissue swelling, gas, or coexisting bone changes.

12.7  Differential Diagnosis

• Cellulitis (skin involved), deep-vein thrombosis, haematoma, muscle strain/contusion, myositis ossificans.
• Osteomyelitis and septic arthritis (may coexist), transient synovitis, acute osteomyelitis of the femur in a child with a limp.
• Rhabdomyolysis (CK massively raised), viral myositis, autoimmune inflammatory myopathies (symmetrical proximal weakness, raised CK).
• Soft-tissue sarcoma, lymphoma, muscle metastasis; tuberculous cold abscess; hydatid cyst of muscle; cysticercosis (relevant in India).
• Necrotising fasciitis — pain out of proportion, systemic toxicity, skin changes.

12.8  Psoas and Iliacus Abscess

• Primary psoas abscess — haematogenous, S. aureus in >80%; common in young patients in tropical countries, injection drug users and diabetics.
• Secondary psoas abscess — spread from adjacent structures: Crohn disease, appendicitis, diverticulitis, colorectal carcinoma, vertebral osteomyelitis/discitis, pyelonephritis, and — critically in India — tuberculous spondylitis (Pott disease) with a "cold" psoas abscess tracking beneath the inguinal ligament. Organisms are gut flora or M. tuberculosis. [VERY HIGH-YIELD]
• Classic triad (present in <30%): fever, back/flank pain, and limp; also weight loss, abdominal or hip pain radiating to the thigh, and a flexed hip.
• Positive psoas sign — pain on passive extension of the hip; the patient lies with the hip flexed and externally rotated.
• CT abdomen/pelvis with contrast is the investigation of choice; MRI is preferred where spinal or tuberculous disease is suspected.
• Management: image-guided percutaneous catheter drainage plus antibiotics is first line; open/laparoscopic drainage for multiloculated collections, failure of percutaneous drainage, or when the primary bowel source needs surgery. Antitubercular therapy for tuberculous abscess (per NTEP regimens), with drainage for large or compressive collections.

12.9  Treatment

12.9.1  Drainage

• Stage 1: antibiotics alone — no collection to drain; response is usually rapid.
• Stage 2 and 3: drainage is mandatory — ultrasound- or CT-guided percutaneous aspiration/catheter drainage is preferred for accessible, unilocular collections. [IMPORTANT]
• Open surgical drainage for large, multiloculated or deep abscesses, failure of percutaneous drainage, necrotic muscle, or when a necrotising infection cannot be excluded.
• Send all material for culture, AFB and fungal studies; leave a drain in large cavities and repeat imaging if fever persists.

12.9.2  Antibiotics

• Empirical cover must target S. aureus: IV cloxacillin/flucloxacillin or cefazolin; add vancomycin/teicoplanin/linezolid/clindamycin where MRSA is prevalent — standard practice in most Indian hospitals.
• Immunocompromised, diabetic or secondary/psoas abscess: broaden to cover Gram-negatives and anaerobes (piperacillin–tazobactam, or a carbapenem in severe disease; add metronidazole with a narrow agent).
• De-escalate on culture results.
• Duration: IV therapy until clinically improved and afebrile (usually 2–3 weeks), then oral to complete 3–6 weeks total; longer if osteomyelitis, multifocal disease or immunocompromise. [IMPORTANT]
• Antitubercular therapy for confirmed tuberculous pyomyositis (NTEP-standard 2HRZE/4HRE with extension per site and response).

12.10  Complications

• Sepsis and septic shock; metastatic abscesses (lung, brain, kidney, liver).
• Osteomyelitis and septic arthritis by contiguous spread; infective endocarditis.
• Compartment syndrome, rhabdomyolysis and acute kidney injury.
• Muscle fibrosis, scarring, contracture and permanent functional loss; deep-vein thrombosis.
• Recurrence; acute respiratory distress syndrome and multi-organ failure in stage 3.

12.11  Prognosis

• Excellent with early diagnosis and drainage — mortality <1–5% in immunocompetent tropical pyomyositis.
• Mortality rises to 10–20% or more with delayed presentation, stage 3 disease, immunocompromise, multifocal involvement or bacteraemia.
• Full functional recovery is usual after adequate drainage; residual weakness follows extensive necrosis.

 

SECTION 13  |  Bite-Wound and Inoculation Infections

Bite wounds inoculate the oral flora of the biter and the skin flora of the victim into deep tissue. In India, animal bites are a major public-health problem: millions of animal-bite cases are reported annually and rabies remains endemic, so every mammalian bite requires simultaneous assessment for bacterial infection, tetanus and rabies. [VERY HIGH-YIELD]

13.1  Types of Bite and Inoculation Injury

Bite wound and likely organism
Bite / Injury	Key Organisms and Features
Dog bite	Commonest bite worldwide and in India (~80–90% of bites). Crush + laceration injury. Pasteurella canis, P. multocida, Capnocytophaga canimorsus, S. aureus, streptococci, anaerobes. Infection rate ~5–20%
Cat bite	Deep puncture wounds that seal over → highest infection rate (~30–50%). Pasteurella multocida (>75%) — infection within 12–24 hours; risk of septic arthritis and osteomyelitis. Also Bartonella henselae (cat-scratch disease)
Human bite	Eikenella corrodens, viridans streptococci, S. aureus, Prevotella, Fusobacterium, Peptostreptococcus. Consider HBV, HCV and HIV transmission risk
Clenched-fist injury ("fight bite")	The most serious human bite. Laceration over the 3rd/4th metacarpophalangeal joint from striking a tooth. Tooth penetrates the extensor tendon and joint capsule; when the fist opens, contaminated tissue is drawn proximally, sealing bacteria inside the joint. High risk of septic arthritis, extensor tendon injury, osteomyelitis. [FAVORITE EXAM QUESTION]
Monkey bite	Major in Indian urban temple/tourist settings. Bacterial flora as for other primates plus Herpes B virus (Macacine herpesvirus 1) from macaques — rare but potentially fatal encephalomyelitis; rabies prophylaxis is mandatory (Category III)
Rat bite	Streptobacillus moniliformis (rat-bite fever/Haverhill fever — fever, migratory polyarthritis, maculopapular rash on palms and soles) and Spirillum minus (sodoku — relapsing fever, indurated ulcer at the site, regional lymphadenopathy, no arthritis)
Pig bite	Polymicrobial: Pasteurella aerogenes, Actinobacillus suis, Streptococcus suis, Flavobacterium, anaerobes; often deep and heavily contaminated
Fish and marine-animal injury	Vibrio vulnificus, Aeromonas, Erysipelothrix rhusiopathiae, Mycobacterium marinum, Streptococcus iniae; catfish/stingray envenomation adds toxin injury
Soil-contaminated wound	Clostridium tetani, Clostridium perfringens, Enterobacterales, Nocardia, environmental fungi; agricultural injuries in India
Injection-site infection	S. aureus (including MRSA), streptococci, oral flora (needle-licking), Clostridium spp. (skin-popping); abscess, cellulitis, septic thrombophlebitis, endocarditis
ORGANISM SPOTTERS ▪  Pasteurella multocida — small Gram-negative coccobacillus; cellulitis within 12–24 h of a cat bite; drug of choice amoxicillin–clavulanate; resistant to flucloxacillin, cephalexin and clindamycin — a key exam trap. [VERY HIGH-YIELD] ▪  Capnocytophaga canimorsus — fastidious Gram-negative rod from dog saliva; causes fulminant sepsis, purpura fulminans and DIC in asplenic, alcoholic and cirrhotic patients. ▪  Eikenella corrodens — human bite/clenched-fist injury; resistant to clindamycin, flucloxacillin, metronidazole and first-generation cephalosporins; sensitive to penicillin/amoxicillin–clavulanate. ▪  Streptobacillus moniliformis — rat-bite fever with rash on palms/soles and polyarthritis. ▪  Spirillum minus — sodoku: relapsing fever with local ulceration and NO arthritis.

13.2  Wound Assessment

• History: biting animal and its vaccination/behaviour, provoked or unprovoked, time since bite, geographical location, first-aid given, patient comorbidity (asplenia, cirrhosis, diabetes, immunosuppression), tetanus and rabies immunisation status, allergies.
• Examination: site, type (puncture, laceration, avulsion, crush), depth, contamination, devitalised tissue, foreign body (tooth fragment), and signs of established infection.
• Photograph and document the wound; measure and map lesions.
• Baseline bloods and radiograph where indicated; X-ray for suspected fracture, retained tooth or air in a joint.

13.2.1  Neurovascular Examination

• Assess distal sensation, two-point discrimination, motor power of each nerve (median, ulnar, radial in hand injuries), capillary refill and pulses before local anaesthesia.
• Document findings meticulously — bite injuries are frequently medicolegal.
• Suspect arterial injury with expanding haematoma, pulsatile bleeding or absent pulses.

13.2.2  Joint and Tendon Involvement

• Examine the hand in the position in which it was injured — with the fist clenched — because tendon and capsular defects retract and are missed in the extended position. [VERY HIGH-YIELD]
• Test the full range of active and passive movement and tendon function individually.
• Any wound overlying a joint must be assumed to have penetrated the joint until proved otherwise; explore in theatre.
• Radiograph for air within the joint, fracture or retained tooth fragment; MRI/ultrasound if uncertain.

13.3  Wound Management

13.3.1  Irrigation

• Copious irrigation with normal saline (at least 250 mL–1 L per wound) under moderate pressure using a syringe and splash guard — the single most effective measure to reduce infection and, for rabies, to reduce viral load. [VERY HIGH-YIELD]
• For possible rabies exposure, wash the wound with soap and running water for at least 15 minutes, then apply a virucidal agent (povidone-iodine or 70% alcohol).
• Do not inject irrigation fluid under pressure into puncture wounds (risks deep dissemination); do not use hydrogen peroxide or strong antiseptics on tissue.

13.3.2  Debridement

• Excise devitalised, crushed and necrotic tissue and remove foreign material (tooth fragments, hair, dirt).
• Be conservative on the face (cosmesis and good blood supply) and more aggressive on the extremities.
• Do not debride tissue that could be reconstructed without surgical planning; involve plastic/hand surgery for complex wounds.

13.3.3  Culture

• Do not culture fresh, clinically uninfected bite wounds — the yield is unhelpful and does not predict later infection. [COMMON MCQ]
• Do culture clinically infected wounds, wounds in immunocompromised or asplenic patients, wounds failing therapy, and deep/operative specimens.
• Request aerobic and anaerobic culture and inform the laboratory of the bite source (fastidious organisms need special media and longer incubation).

13.3.4  Primary versus Delayed Closure

• Primary closure is acceptable for: fresh (<12 h; <24 h on the face) facial and scalp wounds (excellent vascularity and cosmetic priority), clean wounds after thorough irrigation and debridement in low-risk patients.
• DO NOT close primarily: [VERY HIGH-YIELD]
  • All cat bites and puncture wounds
  • All hand and foot bites
  • Clenched-fist injuries
  • Wounds presenting >12–24 hours after injury
  • Clinically infected wounds
  • Crush injuries with devitalised tissue
  • Wounds in immunocompromised, asplenic, diabetic or vasculopathic patients
• Use loose approximation, adhesive strips, or delayed primary closure at 3–5 days; large defects may need delayed grafting or flap cover.

13.3.5  Prophylactic Antibiotics

Amoxicillin–clavulanate is the drug of choice for prophylaxis and treatment of all mammalian bites because it covers Pasteurella, Eikenella, staphylococci, streptococci and anaerobes. Prophylaxis is given for 3–5 days. [VERY HIGH-YIELD]

Indications for prophylaxis

• All cat bites and all human bites (including clenched-fist injuries).
• Bites of the hand, foot, face, genitalia, or overlying a joint, bone, tendon or prosthesis.
• Puncture wounds, deep or crush injuries, wounds requiring debridement or closure.
• Immunocompromised, asplenic, cirrhotic or diabetic patients, and those with prosthetic joints or valves.
• Presentation delayed >8–12 hours, or wounds with associated oedema/venous or lymphatic compromise.

Alternatives in penicillin allergy

• Doxycycline, or a fluoroquinolone (ciprofloxacin/levofloxacin) or cotrimoxazole PLUS metronidazole or clindamycin for anaerobic cover.
• In children: cotrimoxazole + clindamycin, or azithromycin.
• Avoid monotherapy with flucloxacillin, first-generation cephalosporins, clindamycin, erythromycin or aminoglycosides — these miss Pasteurella and/or Eikenella. [IMPORTANT]

13.3.6  Treatment of Established Infection

• Mild, superficial: oral amoxicillin–clavulanate 625 mg TDS for 7–14 days with review at 24–48 hours.
• Moderate/severe, hand involvement, systemic features, failed orals: admit; IV ampicillin–sulbactam, piperacillin–tazobactam, ceftriaxone + metronidazole, or ertapenem; add vancomycin/teicoplanin if MRSA is likely.
• Elevate and immobilise the limb (splint the hand in the position of function); analgesia.
• Surgical exploration and washout for clenched-fist injuries, suspected joint or tendon-sheath involvement, abscess and necrotising infection.
• Duration: 7–14 days for soft-tissue infection; 3 weeks for septic arthritis; 4–6 weeks for osteomyelitis.

13.4  Tetanus Prophylaxis

Tetanus prophylaxis for wound management
Immunisation History	Clean Minor Wound	All Other (Tetanus-prone) Wounds
≥3 doses, last dose <5 years ago	No Td needed	No Td needed
≥3 doses, last dose 5–10 years ago	No Td needed	Td/Tdap booster
≥3 doses, last dose >10 years ago	Td/Tdap booster	Td/Tdap booster
<3 doses or unknown	Td/Tdap — begin/complete the primary series	Td/Tdap PLUS human tetanus immunoglobulin (TIG) 250–500 IU IM at a separate site with a separate syringe

• Tetanus-prone wounds: contaminated with soil, dust, saliva or faeces; puncture wounds; avulsions; crush injuries; burns; frostbite; wounds with devitalised tissue; wounds >6 hours old; missile injuries.
• India: primary immunisation is delivered under the Universal Immunisation Programme (pentavalent at 6, 10, 14 weeks; DPT boosters at 16–24 months and 5–6 years; Td at 10 and 16 years); Td is given to pregnant women (Td1, Td2 or a booster) as part of maternal and neonatal tetanus elimination. [IMPORTANT]

13.5  Rabies Risk Assessment

Rabies is 100% fatal but 100% preventable. India follows WHO categories and the National Rabies Control Programme; the intradermal route (updated Thai Red Cross regimen) is widely used to reduce cost. [VERY HIGH-YIELD]

WHO categories of rabies exposure and post-exposure prophylaxis
Category	Type of Contact	Post-Exposure Prophylaxis
I	Touching or feeding animals; licks on intact skin	None (wash the area); no vaccine required
II	Nibbling of uncovered skin; minor scratches or abrasions WITHOUT bleeding	Wound washing + anti-rabies VACCINE
III	Single or multiple transdermal bites or scratches, licks on broken skin, contamination of mucous membranes with saliva, contact with bats, and all bites of the head, neck, face, hands and genitalia	Wound washing + VACCINE + RABIES IMMUNOGLOBULIN (RIG) infiltrated into and around the wound

• Wound care first: wash with soap and running water for ≥15 minutes, then apply povidone-iodine or 70% alcohol. Do not suture immediately where possible; if suturing is unavoidable, infiltrate RIG first and place loose sutures.
• Vaccine (cell-culture: PCEC, PVRV, PDEV): intramuscular Essen regimen (days 0, 3, 7, 14, 28) or Zagreb 2-1-1 (days 0, 7, 21); intradermal updated Thai Red Cross regimen — 0.1 mL at 2 sites on days 0, 3, 7 and 28 (widely used in India). Give into the deltoid (anterolateral thigh in infants) — never the gluteal region. [IMPORTANT]
• Rabies immunoglobulin (Category III only): human RIG 20 IU/kg or equine RIG 40 IU/kg, infiltrated as much as anatomically feasible into and around all wounds; any remainder need not be given intramuscularly at a distant site (current WHO advice). Never inject RIG through the same syringe or at the same site as the vaccine.
• Previously fully vaccinated patients need only 2 booster doses (days 0 and 3) and no RIG.
• Observe the dog/cat for 10 days where possible ("10-day observation rule") — if the animal remains healthy, prophylaxis may be discontinued after the initial doses; bats, monkeys and wild animals are always treated as Category III.
• Pregnancy, infancy, lactation and immunosuppression are not contraindications to rabies PEP.

13.6  Complications of Bite Wounds

• Local: cellulitis, abscess, lymphangitis, septic arthritis, osteomyelitis, flexor tenosynovitis, tendon rupture, necrotising fasciitis.
• Systemic: bacteraemia and sepsis, endocarditis, meningitis, fulminant Capnocytophaga sepsis with purpura fulminans in asplenic patients.
• Specific syndromes: rat-bite fever, cat-scratch disease, tularaemia, rabies, Herpes B encephalomyelitis (macaque bites), tetanus.
• Blood-borne virus transmission (HBV, HCV, HIV) after human bites — assess and offer post-exposure prophylaxis and serological follow-up.
• Functional and cosmetic: scarring, disfigurement (especially facial dog bites in children), joint stiffness, contracture, nerve injury, amputation.
• Psychological: post-traumatic stress and animal phobia, particularly in children.

BITE WOUNDS — INSTANT RECALL ▪  Highest infection rate — cat bite (deep punctures, Pasteurella multocida). ▪  Most commonly infected bite overall by volume — dog bite (most frequent bite). ▪  Most serious human bite — clenched-fist injury over the 3rd/4th MCP joint. ▪  Drug of choice for all mammalian bites — amoxicillin–clavulanate. ▪  Never close primarily — cat bites, hand/foot bites, punctures, clenched-fist injuries, wounds >12–24 h old. ▪  Category III exposure needs — vaccine + rabies immunoglobulin infiltrated into the wound. ▪  Asplenic patient bitten by a dog — think Capnocytophaga canimorsus.

 

SECTION 14  |  Diabetic Foot Infection

Diabetic foot infection (DFI) is infection of the soft tissues or bone below the malleoli in a person with diabetes mellitus. It is the commonest cause of non-traumatic lower-limb amputation and, in India — home to one of the world's largest diabetic populations — a leading cause of prolonged hospitalisation and disability. A lifetime risk of foot ulceration of 19–34% and a 5-year mortality after major amputation exceeding that of many cancers make this a high-stakes topic. [VERY HIGH-YIELD]

THE "DIABETIC FOOT TRIAD" ▪  Neuropathy — removes the protective warning of pain, alters foot architecture, and dries the skin. ▪  Peripheral arterial disease (ischaemia) — impairs healing and antibiotic delivery. ▪  Immunopathy — hyperglycaemia impairs neutrophil chemotaxis, phagocytosis and oxidative killing. ▪  Superimposed repetitive trauma converts this vulnerable foot into an ulcer, and ulceration is the portal for infection. >80% of diabetic amputations are preceded by a foot ulcer.

14.1  Classification of the Diabetic Foot

14.1.1  Pathophysiological Classification

Neuropathic versus ischaemic versus neuroischaemic foot
Feature	Neuropathic	Ischaemic
Frequency	~35%	~15% (neuroischaemic ~50% and rising)
Foot temperature	Warm	Cold
Pulses	Bounding / present	Absent or feeble
Sensation	Absent (glove-and-stocking loss)	Usually preserved (painful)
Pain	Painless ulcer	Painful ulcer, rest pain, claudication
Skin	Dry, fissured (autonomic denervation), warm	Thin, shiny, hairless, atrophic, cool
Ulcer site	Pressure points — plantar metatarsal heads, heel, under callus	Margins — toe tips, heel, lateral border, between toes
Ulcer edge	Punched out with surrounding callus	Irregular, no callus, necrotic base
Deformity	Claw toes, high arch, Charcot foot	Usually absent
ABI	Normal or high (calcified vessels)	<0.9 (or non-compressible >1.3)
Treatment emphasis	Off-loading	Revascularisation

• Neuroischaemic foot — features of both; now the commonest pattern in clinical practice and carries the worst prognosis. Ischaemia limits healing while neuropathy removes pain, so presentation is late.

14.1.2  Wagner (Meggitt–Wagner) Grading

Wagner classification of diabetic foot ulcers
Grade	Description
Grade 0	No open lesion — intact skin, may have deformity, callus or cellulitis ("foot at risk")
Grade 1	Superficial ulcer — partial or full thickness, not through fascia
Grade 2	Deep ulcer extending to tendon, capsule or bone, without abscess or osteomyelitis
Grade 3	Deep ulcer with abscess, osteomyelitis or joint sepsis
Grade 4	Localised gangrene — forefoot or heel
Grade 5	Gangrene of the whole foot — requires major amputation

• Limitation: grades depth and gangrene only — does not account for ischaemia or infection independently, which is why the University of Texas and IWGDF systems were developed. [IMPORTANT]

14.1.3  University of Texas Classification

A two-dimensional grid that adds ischaemia and infection to depth — a better predictor of amputation than Wagner. [COMMON MCQ]

University of Texas diabetic-foot classification
Stage ↓ / Grade →	0 (Pre/post-ulcerative)	I (Superficial)	II (To tendon/capsule)	III (To bone/joint)
A — Clean wound	A0	A1	A2	A3
B — Infection	B0	B1	B2	B3
C — Ischaemia	C0	C1	C2	C3
D — Infection + ischaemia	D0	D1	D2	D3 — worst prognosis

• Amputation risk rises progressively with both increasing grade (depth) and stage (infection/ischaemia); stage D grade 3 has the highest amputation rate.

14.1.4  PEDIS Classification

• Developed by the International Working Group on the Diabetic Foot (IWGDF) primarily for research standardisation; each element graded 1–4.
• P — Perfusion (1 = no PAD; 2 = PAD without critical ischaemia; 3 = critical limb ischaemia)
• E — Extent/size (wound area in cm²)
• D — Depth/tissue loss (superficial → fascia/muscle/tendon → bone/joint)
• I — Infection (1 = none; 2 = mild/superficial; 3 = moderate/deep; 4 = severe with systemic response)
• S — Sensation (1 = no loss of protective sensation; 2 = loss present)

14.1.5  IWGDF/IDSA Severity Classification of Infection

IWGDF/IDSA classification of diabetic foot infection severity
Severity (PEDIS grade)	Clinical Definition
Uninfected (PEDIS 1)	No systemic or local signs of infection
Mild (PEDIS 2)	≥2 signs of inflammation (purulence, erythema, pain, tenderness, warmth, induration) with erythema ≤2 cm around the ulcer and infection limited to skin and subcutaneous tissue; no systemic signs
Moderate (PEDIS 3)	Local infection with erythema >2 cm, OR involving structures deeper than skin/subcutis (abscess, osteomyelitis, septic arthritis, fasciitis); no systemic inflammatory response
Severe (PEDIS 4)	Local infection with systemic inflammatory response syndrome (SIRS) — ≥2 of: temperature >38°C or <36°C, pulse >90/min, respiratory rate >20/min or PaCO₂ <32 mmHg, WBC >12,000 or <4,000/mm³ or >10% bands
Add "(O)"	Appended to moderate or severe when osteomyelitis is present (IWGDF 2019/2023)

• Severity drives disposition: mild → outpatient oral therapy; moderate → often admission and IV therapy with surgical review; severe → immediate admission, IV antibiotics, urgent surgical assessment and vascular review. [VERY HIGH-YIELD]

14.2  Pathogenesis

Pathogenesis of the Diabetic Foot Ulcer and Infection

CHRONIC HYPERGLYCAEMIA ↓ Sensory neuropathy → loss of protective sensation  |  Motor neuropathy → intrinsic muscle wasting, claw toes, prominent metatarsal heads  |  Autonomic neuropathy → dry fissured skin, arteriovenous shunting ↓ PERIPHERAL ARTERIAL DISEASE — infrapopliteal, distal, diffuse, calcified ↓ Abnormal foot pressures + REPETITIVE UNNOTICED TRAUMA + callus formation ↓ Subcutaneous haemorrhage beneath callus → skin breakdown → FOOT ULCER ↓ Bacterial colonisation → invasion; impaired neutrophil function and poor tissue perfusion ↓ Spread along tendon sheaths and fascial compartments of the foot ↓ DEEP ABSCESS  |  NECROTISING INFECTION  |  OSTEOMYELITIS  |  GANGRENE ↓ AMPUTATION  ←  unless off-loading, debridement, antibiotics and revascularisation intervene

14.2.1  Neuropathy

• Sensory: distal symmetrical "glove-and-stocking" loss of pain, temperature and vibration → loss of protective sensation (LOPS); the patient does not feel a stone in the shoe or a burn.
• Motor: wasting of intrinsic foot muscles → clawing of the toes, prominent metatarsal heads, pes cavus → abnormally high plantar pressures.
• Autonomic: loss of sweating → dry, cracked, fissured skin providing a portal for bacteria; arteriovenous shunting → a warm, well-perfused-looking but functionally ischaemic foot with distended dorsal veins; also contributes to Charcot neuroarthropathy via increased bone blood flow and osteoclastic resorption.

14.2.2  Peripheral Arterial Disease

• In diabetes it is characteristically distal, diffuse and bilateral, affecting the tibial and peroneal (infrapopliteal) arteries while often sparing the foot arteries — which makes distal bypass and angioplasty feasible. [IMPORTANT]
• Medial arterial calcification (Mönckeberg sclerosis) makes vessels non-compressible → falsely elevated ankle–brachial index, so toe pressures and TcPO₂ are needed.
• Ischaemia impairs oxygen delivery, leukocyte function, antibiotic penetration and wound healing.

14.2.3  Repetitive Trauma

• Ill-fitting footwear, barefoot walking (culturally common in India — temple visits, household use), foreign bodies in the shoe, thermal injury (hot water, heaters, walking on hot sand), improper nail cutting and "bathroom surgery" on corns.
• Callus acts as a foreign body concentrating pressure → subcutaneous haemorrhage → ulceration.
• Limited joint mobility and foot deformity concentrate plantar pressure at the metatarsal heads.

14.3  Microbiology

• Mild, acute, previously untreated infection: usually monomicrobial aerobic Gram-positive cocci — S. aureus and β-haemolytic streptococci.
• Chronic, previously treated, deep or severe infection: POLYMICROBIAL — Gram-positives plus Enterobacterales (E. coli, Klebsiella, Proteus), Pseudomonas aeruginosa and anaerobes (Bacteroides, Peptostreptococcus).
• Pseudomonas is over-represented in India and other warm climates, particularly with wet dressings, foot soaking and macerated wounds. [IMPORTANT]
• MRSA is frequent in patients with prior hospitalisation or antibiotic exposure; Indian tertiary-centre series report high MRSA and high ESBL/carbapenem-resistant Enterobacterales rates — local antibiograms must guide empirical therapy.
• Anaerobes with necrotic, gangrenous or foul-smelling wounds.

14.4  Assessment

14.4.1  Ulcer Assessment

• Record site, size (length × width × depth in cm), shape, edge, base (granulation, slough, necrosis, exposed tendon/bone), exudate and odour; photograph and trace at each visit.
• Debride callus and slough before assessing depth — the true extent of an ulcer is always greater than it appears. [VERY HIGH-YIELD]
• Probe the wound with a sterile blunt metal probe for sinuses, undermining and bone.
• Assess for signs of infection (the classic signs are blunted by neuropathy and ischaemia — a high index of suspicion is required), and for crepitus, bullae, fluctuance and rapid progression suggesting necrotising infection.
• Examine the whole foot including interdigital spaces (tinea, maceration), nails, heel and the contralateral foot.
• Look for Charcot deformity, and always inspect footwear.

14.4.2  Probe-to-Bone Test

• Technique: a sterile, blunt-tipped, sterile metal probe is gently advanced through the ulcer; the test is positive if a hard, gritty structure (bone) is felt without intervening soft tissue. [VERY HIGH-YIELD]
• Interpretation depends on pre-test probability: in a high-risk population (deep/chronic ulcers in hospital) a positive test has a high positive predictive value (~85–95%) for osteomyelitis; in low-risk outpatients a negative test is more useful for ruling it out (high negative predictive value).
• Simple, cheap, bedside and reproducible — combine it with an elevated ESR (>70 mm/h) and a plain radiograph for a practical diagnostic strategy. [COMMON MCQ]
• A positive test should prompt bone imaging and consideration of bone biopsy.

14.4.3  Deep-Tissue Sampling

• Superficial wound swabs are unreliable — they grow colonising flora and mislead therapy. [VERY HIGH-YIELD]
• Preferred specimens: curettage of the ulcer base after debridement, deep-tissue biopsy, aspirate of purulent collections, or intra-operative tissue.
• Send for aerobic and anaerobic culture with sensitivity; add fungal and mycobacterial studies in chronic non-healing wounds (India).
• Take specimens before starting antibiotics where feasible.

14.4.4  Osteomyelitis Assessment

• Suspect diabetic foot osteomyelitis (DFO) when: the ulcer is >2 cm² in area or >3 mm deep, has been present >2 weeks, overlies a bony prominence, probe-to-bone is positive, there is a "sausage toe" (diffusely swollen, red toe), the ESR is >70 mm/h, or the ulcer fails to heal despite adequate off-loading and perfusion. [VERY HIGH-YIELD]
• Plain radiograph first (repeat in 2–4 weeks if initially normal — bone changes lag by 2–3 weeks).
• MRI is the imaging modality of choice (sensitivity ~90%, specificity ~80%).
• Bone biopsy with histology and culture is the gold standard — indicated where the diagnosis is uncertain, in culture-discordant cases, or to guide prolonged therapy.

14.4.5  Vascular Assessment

• Ankle–brachial index (ABI): highest ankle systolic pressure ÷ highest brachial systolic pressure. Normal 0.9–1.3; 0.4–0.9 = PAD; <0.4 = critical limb ischaemia; >1.3 = non-compressible calcified vessels (unreliable — common in diabetes). [COMMON MCQ]
• Toe pressure and toe–brachial index (TBI): digital vessels are usually spared from medial calcification, so toe pressure is more reliable in diabetes. Toe pressure >30 mmHg (ideally >50 mmHg) is generally needed for ulcer healing; TBI <0.7 is abnormal.
• Transcutaneous oxygen pressure (TcPO₂): measures skin oxygenation. >40 mmHg predicts healing; <25–30 mmHg indicates critical ischaemia and poor healing, and is an indication for revascularisation.
• Also: palpation of dorsalis pedis and posterior tibial pulses, Doppler waveform analysis (triphasic → monophasic), duplex ultrasound, CT/MR angiography and digital subtraction angiography (gold standard before intervention).

14.5  Investigations

• Blood: full blood count, ESR and CRP (ESR >70 mm/h supports osteomyelitis), blood glucose, HbA1c, renal and liver function, albumin (nutrition), electrolytes; blood cultures if systemically unwell; procalcitonin where available.
• Plain radiography — first-line for all infected diabetic foot wounds: looks for osteolysis, cortical erosion, periosteal reaction, sequestrum, soft-tissue gas, foreign body and Charcot changes; poor sensitivity early (bone loss of 30–50% needed).
• MRI — modality of choice for osteomyelitis, deep abscess and the extent of soft-tissue infection: marrow low signal on T1, high on T2/STIR with post-gadolinium enhancement.
• CT — bone detail, sequestrum, gas, foreign body; when MRI is contraindicated.
• Nuclear imaging — three-phase technetium-99m bone scan is sensitive but non-specific; labelled-leukocyte (Tc-99m HMPAO or In-111) scan combined with sulphur-colloid marrow imaging, or FDG-PET/CT, helps distinguish osteomyelitis from Charcot neuroarthropathy when MRI is equivocal or contraindicated. [IMPORTANT]
• Bone biopsy — histopathology plus culture; the reference standard for DFO.

14.6  Differential Diagnosis — Charcot Neuroarthropathy

The single most important differential of a hot, red, swollen diabetic foot is acute Charcot neuroarthropathy, because the treatments are opposite: infection needs debridement and antibiotics, whereas Charcot needs immediate immobilisation and total-contact casting. [FAVORITE EXAM QUESTION]

Diabetic foot infection versus acute Charcot neuroarthropathy
Feature	Infection / Osteomyelitis	Acute Charcot Foot
Skin break/ulcer	Usually present (portal of entry)	Typically absent — skin intact
Site	Related to the ulcer	Midfoot (tarsometatarsal/Lisfranc) most common
Elevation test	Erythema persists on elevating the leg	Erythema FADES on elevating the leg for 5–10 min (vasomotor)
Temperature difference	Variable	Affected foot 2–8°C warmer than the other
Systemic signs / fever	May be present	Absent
ESR / CRP / WBC	Raised (ESR often >70 mm/h)	Normal or mildly raised
Radiograph	Osteolysis, cortical erosion, periosteal reaction, sequestrum	Fragmentation, dislocation, subluxation, "rocker-bottom" deformity
MRI	Marrow oedema centred on the ulcer/cortical break, sinus tract, soft-tissue collection	Marrow oedema in multiple periarticular bones, subchondral cysts, no sinus tract
Treatment	Debridement + antibiotics ± revascularisation	Total-contact cast, off-loading, non-weight-bearing (NO antibiotics)

• Eichenholtz staging of Charcot: Stage 0 (inflammation, normal X-ray), Stage 1 (fragmentation/development), Stage 2 (coalescence), Stage 3 (consolidation/reconstruction).
• Other differentials: gout, septic arthritis, DVT, cellulitis, sarcoma, and the two may coexist — the hardest scenario, usually requiring MRI ± bone biopsy.

14.7  Management

Diabetic Foot Infection — Management Algorithm

Diabetic foot ulcer with suspected infection ↓ CLASSIFY: IWGDF/IDSA severity (mild / moderate / severe)  +  assess PERFUSION  +  assess for OSTEOMYELITIS ↓ DEBRIDE callus and necrotic tissue → take DEEP TISSUE specimen (never a superficial swab) ↓ MILD → oral antibiotic (Gram-positive cover) 1–2 weeks, outpatient, off-load, review 48–72 h ↓ MODERATE → admit or close outpatient care; broad-spectrum antibiotic 1–3 weeks; imaging; surgical review ↓ SEVERE / limb-threatening → ADMIT, resuscitate, IV broad-spectrum antibiotics, URGENT SURGICAL DRAINAGE / DEBRIDEMENT ↓ ASSESS PERFUSION — ABI, toe pressure, TcPO₂ → if ischaemic, URGENT VASCULAR REVIEW for REVASCULARISATION ↓ OSTEOMYELITIS? → bone biopsy/MRI → resection of infected bone ± 6 weeks antibiotics (or 3 weeks if bone resected) ↓ OFF-LOADING (total contact cast) + GLYCAEMIC CONTROL + NUTRITION + wound care ↓ Healing → PREVENTION: therapeutic footwear, education, podiatry surveillance, annual screening

14.7.1  Empirical Antibiotics

Empirical antibiotic therapy in diabetic foot infection
Severity	Empirical Regimen
Mild (oral, 1–2 weeks)	Target Gram-positive cocci: cephalexin, cloxacillin, amoxicillin–clavulanate; if MRSA likely — cotrimoxazole, doxycycline, clindamycin or linezolid
Moderate (oral or IV, 1–3 weeks)	Broad cover: amoxicillin–clavulanate, or ceftriaxone + metronidazole, or ampicillin–sulbactam; add MRSA cover if risk factors
Severe (IV, 2–4 weeks)	Piperacillin–tazobactam or a carbapenem (meropenem/imipenem) or cefoperazone–sulbactam, PLUS vancomycin/teicoplanin/linezolid/daptomycin for MRSA; add clindamycin if necrotising infection is suspected
Pseudomonas risk (macerated wound, warm climate, water exposure, prior antibiotics)	Add antipseudomonal cover — piperacillin–tazobactam, ceftazidime, cefepime, meropenem or ciprofloxacin
Osteomyelitis	6 weeks if bone is retained; 2–3 weeks if all infected bone is resected; ≤5 days if the infected bone is completely amputated with clean margins

• Antibiotics are never a substitute for drainage, debridement and revascularisation. [VERY HIGH-YIELD]
• Do not treat clinically uninfected ulcers with antibiotics — this drives resistance without improving healing. [IMPORTANT]
• De-escalate to culture-directed therapy as soon as reliable deep-tissue results are available; oral step-down with agents of good bioavailability (fluoroquinolones, linezolid, clindamycin, cotrimoxazole, rifampicin in combination) shortens hospital stay.

14.7.2  Debridement and Drainage

• Sharp surgical debridement is the cornerstone — remove callus, slough, necrotic tissue and infected bone until healthy bleeding tissue is reached; repeat as needed.
• Urgent (same-day) surgery is required for: abscess, necrotising fasciitis, gas in tissues, compartment syndrome of the foot, wet gangrene and severe systemic sepsis.
• Adjunctive methods: enzymatic, larval (maggot), hydrosurgical and autolytic debridement — not substitutes for sharp debridement in infected wounds.
• Do not debride an ischaemic, dry-gangrenous digit before assessing perfusion — revascularise first, then debride (except in wet gangrene/sepsis, where drainage is immediate).

14.7.3  Revascularisation

• Indicated in critical limb-threatening ischaemia: rest pain, non-healing ulcer, gangrene, ABI <0.5, ankle pressure <50–70 mmHg, toe pressure <30 mmHg, or TcPO₂ <25–30 mmHg. [VERY HIGH-YIELD]
• Endovascular angioplasty ± stenting — first line for most infrapopliteal disease; repeatable, low morbidity.
• Distal bypass surgery (femoro-distal or popliteal-to-pedal, ideally with autologous vein) — for long occlusions or failed endovascular therapy; durable results.
• Perform urgent drainage of pus first, then revascularise, then perform definitive reconstructive debridement.
• Adjuncts: antiplatelet therapy, high-intensity statin, blood-pressure control, smoking cessation, supervised exercise.

14.7.4  Off-loading

• Off-loading is the single most important intervention for healing a NEUROPATHIC PLANTAR ULCER — without it, no other treatment will work. [VERY HIGH-YIELD]
• Total contact cast (TCC) is the gold standard for a non-infected, non-ischaemic plantar forefoot ulcer — heals ~90% within 6–8 weeks by redistributing pressure and enforcing adherence.
• Removable cast walker / instant TCC (a removable walker rendered irremovable) — nearly as effective and preferable when frequent wound inspection is needed (i.e. in infected wounds, where a TCC is relatively contraindicated).
• Other modalities: half-shoes, felted foam, custom insoles, crutches and wheelchair, bed rest.
• Callus must be debrided at every visit — leaving callus negates off-loading.
• Long-term: therapeutic footwear with custom-moulded insoles reduces re-ulceration by ~50%.

14.7.5  Glycaemic and Metabolic Control

• Optimise glycaemia — insulin is usually required during acute infection; sepsis and infection cause marked insulin resistance.
• Targets: individualised, but aim for near-normal glucose during healing (HbA1c <7–8% long term).
• Correct anaemia, hypoalbuminaemia and vitamin/protein deficiency; provide high-protein nutritional support; treat oedema and heart failure; stop smoking; treat dyslipidaemia and hypertension.
• Screen for and manage diabetic nephropathy and retinopathy — the presence of one microvascular complication predicts others.

14.7.6  Multidisciplinary Foot Care

• A multidisciplinary diabetic foot team reduces major amputation rates by 40–80% — one of the best-evidenced interventions in this field. [VERY HIGH-YIELD]
• Team: diabetologist/physician, vascular surgeon, orthopaedic/podiatric surgeon, podiatrist, microbiologist, radiologist, diabetes nurse educator, orthotist and plastic surgeon.
• Function: rapid-access foot clinic, standardised assessment and classification, urgent pathways for the infected or ischaemic foot, and structured follow-up.
• India: increasingly established at tertiary centres; primary prevention through the National Programme for Prevention and Control of Non-Communicable Diseases (NP-NCD) and Health & Wellness Centres under Ayushman Bharat is central to reducing the burden.

14.7.7  Adjunctive Wound Therapies

• Negative-pressure wound therapy (NPWT/VAC) — for large post-debridement or post-amputation wounds; promotes granulation and reduces oedema and exudate. Contraindicated over exposed vessels or untreated osteomyelitis/necrotic tissue.
• Moist wound healing with appropriate dressings (hydrogels, alginates, foams); avoid soaking the foot.
• Topical/systemic adjuncts with limited evidence: hyperbaric oxygen (may reduce major amputation in selected ischaemic wounds), growth factors (PDGF/becaplermin), bioengineered skin substitutes, platelet-rich plasma.
• Amputation is not a failure but a therapeutic decision when the foot is unsalvageable — see below.

14.7.8  Indications for Amputation

• Life-threatening sepsis not controlled by drainage and antibiotics (urgent guillotine amputation).
• Extensive/spreading gangrene or necrotising infection, or extensive tissue loss beyond reconstruction.
• Unreconstructable critical limb ischaemia with rest pain or non-healing tissue loss.
• Intractable rest pain in a non-revascularisable limb; non-functional, deformed limb where amputation gives better function than salvage.
• Extensive osteomyelitis destroying the foot architecture; chronic non-healing ulcer with failed maximal therapy.
• Levels: digital/ray → transmetatarsal → Lisfranc/Chopart → below-knee (BKA) → above-knee (AKA); preserve length wherever healing potential allows (BKA has far better prosthetic rehabilitation than AKA).

14.8  Recurrence Prevention

• Recurrence is the rule, not the exception: ~40% within 1 year and ~65% within 5 years — these patients are "in remission", not cured. [IMPORTANT]
• Annual (or more frequent) foot screening for every diabetic: 10-g Semmes–Weinstein monofilament at defined plantar sites, 128-Hz tuning-fork vibration, biothesiometer, ankle reflexes, pulses and ABI, and inspection for deformity/callus.
• Patient education: daily foot inspection (with a mirror or a family member), never walk barefoot — including indoors and at temples, check inside footwear before wearing, test bath-water temperature by hand, avoid heaters and hot-water bottles on the feet, moisturise but not between toes, cut nails straight across, seek help within 24 hours for any new lesion.
• Therapeutic footwear and custom insoles; regular podiatric callus debridement; treatment of fungal nail and skin infection; prophylactic surgery for deformity (Achilles tendon lengthening, exostectomy, digital arthroplasty) in selected patients.
• Structured follow-up stratified by risk category; smoking cessation; glycaemic, lipid and blood-pressure control.

14.9  Prognosis

• Healing of a neuropathic ulcer with adequate off-loading: 80–90% within 20 weeks; ischaemic ulcers heal far less reliably without revascularisation.
• Around 15–25% of diabetic foot ulcers ultimately lead to amputation.
• 5-year mortality after a diabetic foot ulcer is ~30%, and after major amputation is 50–70% — comparable to or worse than many common cancers; death is usually cardiovascular. [VERY HIGH-YIELD]
• Poor prognostic factors: peripheral arterial disease, osteomyelitis, deep infection, renal failure/dialysis, poor glycaemic control, delayed presentation, previous amputation and low socio-economic status.
• Multidisciplinary care, early referral and off-loading are the strongest modifiable determinants of outcome.

 

SECTION 15  |  Osteomyelitis

15.1  Definition

Osteomyelitis is inflammation of bone and its marrow cavity caused by an infecting organism, leading to progressive inflammatory destruction of bone, necrosis (sequestrum) and new bone formation (involucrum). [IMPORTANT]

15.2  Classification

15.2.1  By Duration

Acute versus chronic osteomyelitis
Feature	Acute	Chronic
Duration	Days to <2 weeks (some define <6 weeks)	>6 weeks / months–years
Onset	Rapid, systemic upset, high fever	Insidious, low-grade or afebrile
Pain	Severe, constant, throbbing	Dull, intermittent, may be minimal
Sequestrum	Absent	Present — the defining feature
Involucrum	Absent	Present
Sinus tract	Absent	Present, discharging pus
Radiograph	Normal for 10–14 days; then soft-tissue swelling, periosteal reaction	Sequestrum, involucrum, cloaca, sclerosis, cavities, deformity
ESR/CRP	Markedly raised	Variable, often only mildly raised
Blood culture	Positive in ~50% (haematogenous)	Usually negative
Treatment	Antibiotics ± drainage; may cure without surgery	Surgery is essential — antibiotics alone will not cure
Cure	Usually complete	Relapse common; "arrest" rather than cure

• Subacute osteomyelitis — insidious, mild symptoms, few systemic features, normal or mildly raised inflammatory markers; the classic form is Brodie abscess.

15.2.2  By Route of Infection (Waldvogel classification)

• Haematogenous osteomyelitis — blood-borne seeding; commonest in children (metaphysis of long bones) and in adults as vertebral osteomyelitis; usually monomicrobial.
• Contiguous-focus osteomyelitis — spread from adjacent soft-tissue infection, ulcer, sinusitis, dental sepsis, or after open fracture/surgery; often polymicrobial.
• Osteomyelitis associated with vascular insufficiency — the diabetic/ischaemic foot; polymicrobial, poor healing.
• Post-traumatic — open fractures (Gustilo–Anderson type III highest risk), penetrating injury.
• Postoperative / implant-associated — internal fixation, arthroplasty, spinal instrumentation; biofilm-mediated.

15.2.3  Cierny–Mader Classification

The most useful surgical staging system: anatomical type (1–4) combined with physiological host class (A/B/C) to give 12 clinical stages that guide treatment and predict outcome. [VERY HIGH-YIELD]

Cierny–Mader classification — anatomical types
Type	Description
Type I — Medullary	Endosteal disease only (e.g. haematogenous osteomyelitis, infected intramedullary nail). Treated by intramedullary reaming
Type II — Superficial	Cortical surface infection from a contiguous soft-tissue focus; requires soft-tissue coverage
Type III — Localised	Full-thickness cortical sequestration and cavitation, but the bone remains stable after debridement
Type IV — Diffuse	Circumferential/through-and-through disease; bone is UNSTABLE before or after debridement — requires resection and reconstruction/stabilisation
Cierny–Mader physiological host classes
Class	Description
A host	Normal immune, metabolic and vascular status — best outcome
B host	Compromised: B(s) systemic (diabetes, malnutrition, renal/hepatic failure, malignancy, immunosuppression, smoking, extremes of age), B(l) local (chronic lymphoedema, venous stasis, major vessel disease, arteritis, extensive scarring, radiation fibrosis), or B(ls) both
C host	Treatment (morbidity of curative therapy) is worse than the disease — palliation or suppression only

15.2.4  Special Anatomical Forms

• Vertebral osteomyelitis (spondylodiscitis) — see 15.4.
• Diabetic foot osteomyelitis — see Section 14.
• Discitis — infection of the intervertebral disc; in children the disc is vascularised so primary discitis occurs; in adults it is usually secondary to vertebral osteomyelitis.
• Spondylodiscitis — combined vertebral body and disc involvement (the usual adult pattern).
• Calcaneal osteomyelitis — heel puncture wounds ("through-shoe" nail injuries → Pseudomonas aeruginosa), pressure sores, diabetic heel ulcers; difficult to eradicate because of poor soft-tissue cover.
• Culture-negative osteomyelitis — occurs with prior antibiotics, fastidious/slow-growing organisms (tuberculosis, Brucella, fungi, Kingella kingae in children), or inadequate sampling. Approach: stop antibiotics for ≥2 weeks and re-biopsy, extend culture incubation, request AFB/fungal cultures, GeneXpert MTB/RIF, Brucella serology and 16S rRNA PCR. [IMPORTANT]

15.3  Pathological Terms — must be defined precisely

Pathological terminology in chronic osteomyelitis
Term	Definition
Sequestrum	A fragment of DEAD, avascular, necrotic bone separated from living bone. Appears dense/sclerotic and whiter than surrounding bone on radiograph (because it is not resorbed and surrounding living bone becomes osteopenic). Harbours biofilm; antibiotics cannot penetrate it; it MUST be surgically removed (sequestrectomy) — the reason antibiotics alone cannot cure chronic osteomyelitis. [VERY HIGH-YIELD]
Involucrum	A sheath of NEW LIVING BONE laid down by the elevated periosteum around the sequestrum — the body's attempt to contain the infection and maintain continuity
Cloaca	An opening/defect in the involucrum through which pus and sequestra discharge from the medullary cavity to the surface
Sinus tract	An epithelialised tract from the infected bone through the soft tissues to the skin, discharging pus intermittently
Brodie abscess	A localised subacute intraosseous abscess, classically in the metaphysis of the distal tibia in adolescents; presents with insidious localised pain, often worse at night, with few systemic features; radiograph shows a well-defined lucent lesion with a surrounding rim of reactive sclerosis; MRI shows the "penumbra sign". Treated by curettage plus antibiotics. [FAVORITE EXAM QUESTION]

15.4  Special Settings

15.4.1  Osteomyelitis in Sickle-Cell Disease

• Salmonella species are classically the commonest cause of osteomyelitis in sickle-cell disease (S. typhimurium, S. enteritidis, S. paratyphi), though S. aureus remains the commonest cause of osteomyelitis overall, including in some sickle-cell series. [FAVORITE EXAM QUESTION]
• Mechanism: bowel-wall microinfarction allows Salmonella translocation, while infarcted bone provides a nidus; functional asplenia impairs clearance of encapsulated organisms.
• Typically diaphyseal and often multifocal/symmetrical, unlike the metaphyseal single-site disease of other children.
• Key clinical problem: distinguishing osteomyelitis from a bone-infarction (vaso-occlusive) crisis — both cause fever, bone pain and raised inflammatory markers. Favouring infection: swinging fever >38.5°C persisting >2 days, focal fluctuant swelling, positive blood culture, marked leukocytosis, and MRI showing an abscess, sinus tract or cortical destruction. MRI ± bone aspiration/biopsy is often required. [VERY HIGH-YIELD]
• Treatment: empirical cover for both Salmonella and S. aureus (e.g. ceftriaxone + cloxacillin, or ciprofloxacin-based therapy in adults), 4–6 weeks, plus drainage of abscesses; supportive sickle-cell care (hydration, analgesia, oxygen, transfusion as indicated).

15.4.2  Osteomyelitis in Injection Drug Users

• Organisms: S. aureus (including MRSA) commonest; also Pseudomonas aeruginosa, Serratia, Candida, streptococci and oral anaerobes (needle-licking).
• Characteristic sites: vertebrae (especially lumbar), sacroiliac joint, sternoclavicular joint, pubic symphysis and costochondral junctions — the "axial/fibrocartilaginous" pattern. [COMMON MCQ]
• Frequently accompanied by infective endocarditis (right-sided, tricuspid), septic pulmonary emboli, septic thrombophlebitis and epidural abscess — always echocardiograph and take blood cultures.
• Screen for HIV, hepatitis B and hepatitis C; anticipate poor adherence — consider long-acting or supervised regimens and address addiction (opioid substitution therapy).

15.4.3  Vertebral Osteomyelitis and Spondylodiscitis

• Route: haematogenous seeding of the vertebral end-plate via the segmental arteries, spreading to the adjacent disc and next vertebra; lumbar > thoracic > cervical.
• Sources: urinary tract infection and instrumentation, skin/soft-tissue infection, endocarditis, IV catheters, injection drug use, spinal surgery.
• Organisms: S. aureus (~50%), coagulase-negative staphylococci (post-instrumentation), streptococci, Enterobacterales (especially after UTI), Pseudomonas; and — critically in India — Mycobacterium tuberculosis (Pott disease) and Brucella (Brucellar spondylitis, classically lower lumbar). [VERY HIGH-YIELD]
• Clinical features: insidious, unremitting back pain that is worse at night and at rest and not relieved by lying down, focal spinal tenderness and paraspinal spasm; fever in only ~50%; neurological deficit in 15–30% (radiculopathy, cord compression, cauda equina).
• Red flags demanding urgent MRI: new severe back pain with fever, neurological deficit, bacteraemia (particularly S. aureus), immunosuppression, IV drug use, recent spinal procedure, malignancy.
• Investigations: ESR and CRP (raised in >90% — useful for monitoring), blood cultures ×2–3 sets (positive in ~50–70%), MRI with contrast is the imaging of choice (T1 low, T2/STIR high signal in vertebral bodies with disc involvement and end-plate erosion), CT-guided biopsy for culture and histology if blood cultures are negative, transoesophageal echocardiography if S. aureus or streptococcal bacteraemia.
• Pyogenic vs tuberculous spondylitis: pyogenic disease destroys the disc early, is usually one motion segment, and progresses over weeks; tuberculous spondylitis relatively SPARES the disc until late, involves multiple/contiguous levels with anterior vertebral body destruction, large paravertebral "cold" abscesses, subligamentous spread, gibbus deformity, and progresses over months. [FAVORITE EXAM QUESTION]
• Treatment: 6 weeks of targeted IV/oral antibiotics is standard for pyogenic disease (extended to 12 weeks in undrained abscess, implant retention or slow response); antitubercular therapy under NTEP for Pott disease (intensive phase HRZE followed by continuation — typically 9–12 months for spinal TB, with drug-susceptibility-guided modification). Bracing and analgesia; surgery for cord compression/neurological deficit, spinal instability, large abscess, failure of medical therapy, or the need for tissue diagnosis — decompression, debridement and instrumented fusion.

15.5  Etiology by Age and Setting

Likely organisms by age and clinical setting
Setting	Likely Organisms
Neonates (<2 months)	S. aureus, Group B Streptococcus, E. coli and other Gram-negatives; may be multifocal with adjacent septic arthritis
Children >2 months	S. aureus (commonest overall), Streptococcus pyogenes, S. pneumoniae, Kingella kingae (a common culture-negative cause in <4 years; requires PCR/blood-culture bottles), H. influenzae type b (unimmunised)
Adults	S. aureus (commonest at every age), coagulase-negative staphylococci (implants), streptococci, Enterobacterales, Pseudomonas
Sickle-cell disease	Salmonella spp. (classic association) and S. aureus
Injection drug use	S. aureus (MRSA), Pseudomonas, Serratia, Candida
Diabetic foot / vascular insufficiency	Polymicrobial — S. aureus, streptococci, Enterobacterales, Pseudomonas, anaerobes
Prosthetic joint / implant	Coagulase-negative staphylococci (S. epidermidis), S. aureus, Cutibacterium acnes (shoulder), enterococci
Puncture wound through footwear	Pseudomonas aeruginosa — classic
Human/animal bite	Eikenella corrodens, Pasteurella multocida, anaerobes
Endemic/India-specific	Mycobacterium tuberculosis (spine, hip, knee), Brucella (occupational, unpasteurised milk), melioidosis (B. pseudomallei), fungal (Candida, Aspergillus, mucormycosis in uncontrolled diabetes)

15.6  Pathogenesis

Pathogenesis of Acute Haematogenous Osteomyelitis (Child)

Transient bacteraemia (from skin, throat, gut) ± minor blunt trauma to bone ↓ Bacteria lodge in the METAPHYSIS — sluggish blood flow in hairpin sinusoidal loops, absent phagocytic lining cells, fenestrated capillaries ↓ Acute inflammation, exudate and INTRAOSSEOUS PRESSURE RISE within the rigid bone → severe pain ↓ Vascular thrombosis and ischaemia → BONE NECROSIS ↓ Pus tracks through Volkmann and Haversian canals to the SUBPERIOSTEAL space → periosteal elevation (further devascularising cortex) ↓ Dead bone separates = SEQUESTRUM;  elevated periosteum lays down new bone = INVOLUCRUM;  opening in involucrum = CLOACA ↓ Rupture through periosteum → soft-tissue abscess → SINUS TRACT to skin ↓ CHRONIC OSTEOMYELITIS with biofilm on dead bone — antibiotics alone cannot cure

• Age-related anatomy explains the pattern of spread: [VERY HIGH-YIELD]
  • Infants (<1 year): transphyseal vessels cross the growth plate → epiphyseal and joint involvement, with septic arthritis common.
  • Children (1 year–physeal closure): the physis acts as a barrier, so infection stays metaphyseal and spreads subperiosteally; joint involvement occurs only where the metaphysis is intracapsular — hip, shoulder, elbow, ankle.
  • Adults (after physeal closure): vessels re-cross the closed physis, so epiphyseal, subchondral and joint spread returns; vertebral involvement predominates.
• Biofilm is the central mechanism of chronicity: sessile bacteria encased in an extracellular polysaccharide matrix on dead bone or implants are metabolically dormant, up to 1000× less susceptible to antibiotics, and shielded from immune cells — hence the absolute requirement for surgical removal of dead bone and implants. [VERY HIGH-YIELD]
• S. aureus virulence: adhesins (MSCRAMMs binding fibronectin, collagen and bone sialoprotein), intracellular persistence within osteoblasts and osteocytes, small-colony variants causing relapse, and induction of RANKL-mediated osteoclastic bone resorption.

15.7  Pathology

• Acute: marrow oedema, dense neutrophil infiltration, vascular congestion and thrombosis, bone necrosis, subperiosteal abscess.
• Chronic: sequestrum surrounded by granulation tissue, involucrum, chronic inflammatory infiltrate (lymphocytes, plasma cells, macrophages), fibrosis, reactive sclerosis and marrow replacement.
• Tuberculous osteomyelitis: caseating epithelioid granulomas with Langhans giant cells, AFB on Ziehl–Neelsen stain, relative disc sparing in spinal disease.
• Chronic recurrent multifocal osteomyelitis (CRMO) is a sterile autoinflammatory mimic in children — culture-negative, multifocal, relapsing; treated with NSAIDs/bisphosphonates, not antibiotics.

15.8  Clinical Features

Acute osteomyelitis

• Children: abrupt fever, malaise and irritability; severe localised bone pain and exquisite metaphyseal tenderness; refusal to use the limb (pseudoparalysis) or to bear weight; overlying warmth, swelling and erythema appear later; commonest sites — distal femur and proximal tibia (around the knee).
• Neonates: may be strikingly afebrile with only reduced limb movement, irritability and poor feeding; often multifocal with adjacent septic arthritis.
• Adults: more insidious; localised pain and tenderness, low-grade fever; vertebral disease presents as unremitting back pain.
• Look for the source (skin infection, dental sepsis, UTI, IV line, injection use) and for endocarditis.

Chronic osteomyelitis

• Longstanding dull bone pain with intermittent flares, discharging sinus with intermittent extrusion of small sequestra, local swelling, thickened deformed bone.
• Scarred, adherent, pigmented skin; limb shortening, angular deformity or pathological fracture in children whose physis was damaged.
• Systemic upset minimal between flares; anaemia of chronic disease and amyloidosis (AA) in long-neglected cases.

15.9  Investigations

15.9.1  Inflammatory Markers

• CRP rises within 6 hours, peaks at ~48 h and normalises in ~1 week with treatment — the best marker for MONITORING response. [VERY HIGH-YIELD]
• ESR rises over 3–5 days and takes 3–4 weeks to normalise — useful for long-term follow-up; ESR >70 mm/h supports osteomyelitis in the diabetic foot.
• Leukocytosis is often absent in adults and in chronic disease — normal white cell count does not exclude osteomyelitis.
• Procalcitonin has limited sensitivity in bone and joint infection.

15.9.2  Blood Culture

• Positive in ~50% of acute haematogenous osteomyelitis in children — take at least two sets before antibiotics.
• A positive blood culture with typical imaging may obviate bone biopsy.
• Usually negative in chronic and contiguous-focus disease.

15.9.3  Plain Radiography

• Normal for the first 10–14 days — a normal radiograph NEVER excludes acute osteomyelitis. [VERY HIGH-YIELD]
• Earliest change: deep soft-tissue swelling with loss of fat planes (3–5 days).
• Then: periosteal reaction/new bone (10–14 days), osteopenia and lytic destruction (requires 30–50% bone loss), cortical erosion.
• Chronic disease: sequestrum (dense sclerotic fragment), involucrum, cloaca, cavitation, sclerosis, deformity, pathological fracture.
• Always the first investigation — cheap, available, excludes fracture and tumour.

15.9.4  CT

• Best modality for cortical detail — sequestrum, cloaca, gas, foreign bodies and bony sinus tracts; useful in surgical planning.
• Guides percutaneous bone biopsy and drainage.
• Inferior to MRI for marrow and soft-tissue assessment; degraded by metal implants (though less so with metal-artefact-reduction protocols).

15.9.5  MRI

• Investigation of choice — sensitivity 90–100%, specificity 80–90%; positive within 3–5 days of onset. [VERY HIGH-YIELD]
• Findings: marrow oedema — low signal on T1, high signal on T2/STIR — with post-gadolinium enhancement; cortical destruction, subperiosteal and soft-tissue abscess, sinus tracts, joint effusion.
• "Penumbra sign" — a rim of high T1 signal around an abscess cavity, characteristic of Brodie abscess/subacute osteomyelitis.
• Essential for the spine (cord compression, epidural abscess) and for the diabetic foot.
• Limitations: cost/availability, metal artefact, cannot always distinguish infection from Charcot arthropathy, tumour or fracture; post-operative changes persist for months.

15.9.6  Nuclear Imaging

• Three-phase Tc-99m MDP bone scan — highly sensitive from 24–48 hours but non-specific (positive in fracture, tumour, surgery, Charcot); useful when MRI is contraindicated or multifocal disease is suspected.
• Labelled-leukocyte scan (Tc-99m HMPAO-WBC or In-111) — better specificity for infection; combined with Tc-99m sulphur-colloid marrow imaging it distinguishes infection from marrow-displacing processes (a mismatch indicates infection).
• Gallium-67 — useful in vertebral osteomyelitis (leukocyte scans perform poorly in the spine).
• FDG-PET/CT — the most accurate nuclear technique, excellent for chronic osteomyelitis, spinal infection and implant-associated infection; less affected by metal artefact.

15.9.7  Bone Biopsy and Histopathology

• Bone biopsy with culture and histopathology is the GOLD STANDARD for diagnosis and for guiding targeted therapy. [VERY HIGH-YIELD]
• Indications: negative blood cultures, chronic osteomyelitis, diabetic foot osteomyelitis, suspected tuberculosis/fungal/Brucella infection, atypical presentation, and when prolonged therapy is planned.
• Sinus-tract swabs correlate poorly with deep bone cultures (except for S. aureus) and must not be used to direct therapy. [COMMON MCQ]
• Whenever safe, withhold antibiotics for ≥2 weeks (48 hours minimum) before biopsy to improve yield.
• Send for aerobic, anaerobic, mycobacterial and fungal culture; Gram and Ziehl–Neelsen stains; GeneXpert MTB/RIF; and histopathology; consider 16S rRNA PCR in culture-negative cases.
• Histology: neutrophils and necrotic bone in acute disease; lymphoplasmacytic infiltrate, fibrosis and sequestra in chronic disease; caseating granulomas in tuberculosis.

15.10  Differential Diagnosis

• Ewing sarcoma — the classic mimic in a child: fever, raised ESR, bone pain, "onion-skin" lamellated periosteal reaction, diaphyseal, systemic upset; biopsy is mandatory before assuming infection. [FAVORITE EXAM QUESTION]
• Osteosarcoma — metaphyseal, "sunburst" periosteal reaction, Codman triangle.
• Langerhans cell histiocytosis (eosinophilic granuloma), leukaemia/lymphoma, bone metastases, osteoid osteoma (night pain relieved by NSAIDs).
• Septic arthritis, transient synovitis (child with a limp), rheumatic fever, juvenile idiopathic arthritis, reactive arthritis.
• Bone infarction/sickle-cell crisis, Charcot neuroarthropathy, gout, stress fracture, cellulitis, deep soft-tissue abscess.
• CRMO/chronic non-bacterial osteomyelitis and SAPHO syndrome — sterile, relapsing, multifocal.
• India-specific: tuberculous osteomyelitis, brucellosis, mycetoma (Madura foot — Actinomadura/Madurella, with triad of swelling, sinuses and grains), fungal osteomyelitis.

15.11  Treatment

Osteomyelitis — Diagnostic and Management Pathway

Bone pain + fever ± sinus/ulcer  →  Suspect osteomyelitis ↓ FBC, CRP, ESR, BLOOD CULTURES ×2  +  PLAIN RADIOGRAPH ↓ Radiograph normal or equivocal → MRI (investigation of choice)  [Bone scan/FDG-PET if MRI contraindicated] ↓ Obtain MICROBIOLOGICAL DIAGNOSIS — blood culture, or BONE BIOPSY/aspirate (never a sinus swab) ↓ ACUTE haematogenous → empirical IV antibiotics → targeted therapy; drain subperiosteal/soft-tissue abscess ↓ CHRONIC / sequestrum / implant / dead bone → SURGERY IS ESSENTIAL ↓ SURGERY: sequestrectomy + saucerisation + debridement to bleeding bone + dead-space management + soft-tissue cover ± stabilisation ↓ Targeted antibiotics — 4–6 weeks (longer for implant/TB); ORAL SWITCH once stable (OVIVA evidence) ↓ Monitor CRP/ESR; treat host factors (glycaemia, nutrition, smoking, vascular supply); rehabilitate ↓ Persistent/relapsing disease → re-debride, exclude TB/fungus/resistant organism, consider CHRONIC SUPPRESSIVE THERAPY

15.11.1  Medical Treatment

• Empirical therapy (after cultures): anti-staphylococcal agent — cloxacillin/flucloxacillin or cefazolin; vancomycin/teicoplanin/linezolid/daptomycin where MRSA is likely (standard empirical practice in most Indian hospitals). Add Gram-negative cover (ceftriaxone/piperacillin–tazobactam) in neonates, the elderly, diabetics, immunocompromised patients and post-urinary-sepsis vertebral disease.
• Targeted therapy on culture: MSSA → cloxacillin or cefazolin; MRSA → vancomycin, teicoplanin, daptomycin or linezolid; streptococci → penicillin/ceftriaxone; Enterobacterales → cephalosporin/carbapenem per sensitivity; Pseudomonas → ceftazidime/cefepime/piperacillin–tazobactam/meropenem ± ciprofloxacin; Salmonella → ceftriaxone or ciprofloxacin.
• Rifampicin should be added (never used alone) for staphylococcal implant-associated or biofilm infection because of its unique activity against adherent, stationary-phase organisms; combine with a fluoroquinolone or other companion drug. [VERY HIGH-YIELD]
• Oral agents with excellent bone penetration: fluoroquinolones, clindamycin, linezolid, cotrimoxazole, rifampicin, fusidic acid.
• Oral therapy is non-inferior to intravenous therapy after the first week in bone and joint infection (OVIVA trial, 2019) — a major practice change and a favourite examination point. [COMMON MCQ]
• Tuberculous osteomyelitis: antitubercular therapy under NTEP — intensive phase HRZE followed by continuation phase, typically 9–12 months for spinal and other skeletal TB, with drug-susceptibility testing (GeneXpert MTB/RIF on tissue) and Nikshay notification.
• Adjuncts: analgesia, splintage in the acute phase, nutritional support, glycaemic control, smoking cessation, correction of anaemia, and treatment of the primary source.

15.11.2  Surgical Indications

• Presence of a sequestrum or any dead bone (antibiotics cannot penetrate).
• Abscess — subperiosteal, intraosseous, soft-tissue or epidural — requiring drainage.
• Failure of appropriate antibiotic therapy after 24–48 hours in acute disease (persistent fever, rising CRP).
• Chronic osteomyelitis with sinus tract, cavity or involucrum.
• Infected implant or prosthesis (biofilm) — debridement ± removal.
• Spinal disease with neurological deficit, instability, epidural abscess or large paravertebral abscess.
• Need for tissue diagnosis where cultures are negative and tuberculosis/tumour is possible.
• Pathological fracture, non-union, deformity, or malignant transformation.
• Surgical principles: radical debridement to bleeding bone ("paprika sign"), sequestrectomy, saucerisation, dead-space management (antibiotic-impregnated PMMA beads or spacers, calcium sulphate carriers, muscle flaps, Masquelet induced-membrane technique), stable skeletal fixation (external fixator or Ilizarov bone transport for segmental defects), and adequate soft-tissue coverage (local or free flap).

15.11.3  Duration of Therapy

Duration of antimicrobial therapy
Situation	Duration
Acute haematogenous osteomyelitis (children)	3–4 weeks total (IV until clinically improved and CRP falling — often 3–7 days — then oral)
Acute osteomyelitis (adults)	4–6 weeks from the last major debridement
Chronic osteomyelitis	≥6 weeks after adequate surgical debridement; longer if debridement incomplete
Vertebral osteomyelitis (pyogenic)	6 weeks; 12 weeks if undrained abscess, implant retention or slow response
Diabetic foot osteomyelitis	6 weeks if bone retained; 2–3 weeks if infected bone resected; ≤5 days if completely amputated
Implant-associated infection with retention	3 months (hip/other) to 6 months (knee), rifampicin-based for staphylococci
Skeletal tuberculosis	9–12 months (NTEP-based regimen)

15.11.4  Chronic Suppressive Therapy

• Indications: infected implant that cannot be removed, a Cierny–Mader class C host, unresectable disease, patient refusal of or unfitness for surgery, relapse after maximal therapy.
• Agents: oral cotrimoxazole, doxycycline, clindamycin, linezolid (beware of prolonged-use myelosuppression, neuropathy and lactic acidosis), amoxicillin or a cephalosporin, chosen on sensitivity and tolerability.
• Aim is control of symptoms and prevention of systemic sepsis rather than cure; continue long term (often indefinitely) with regular monitoring of blood counts, renal and liver function, and periodic reassessment for surgical candidacy. [IMPORTANT]

15.12  Complications

• Local: chronic osteomyelitis, recurrent sinus, pathological fracture, non-union, bone loss and deformity, limb-length discrepancy and growth arrest (physeal damage in children), joint stiffness and ankylosis.
• Contiguous spread: septic arthritis (especially with intracapsular metaphyses — hip, shoulder, elbow, ankle), soft-tissue abscess, epidural abscess with paraplegia in spinal disease.
• Systemic: bacteraemia and sepsis, infective endocarditis, metastatic abscesses, deep-vein thrombosis and septic pulmonary emboli.
• Long term: secondary (AA) amyloidosis in chronic neglected disease, anaemia of chronic disease, avascular necrosis, chronic pain and disability.
• Malignant transformation of a chronic sinus — see below.

15.12.1  Malignant Transformation of a Chronic Sinus

• Marjolin ulcer — squamous cell carcinoma arising in a long-standing chronic osteomyelitis sinus tract or scar, typically after a latency of 20–30 years. [FAVORITE EXAM QUESTION]
• Incidence roughly 0.2–1.7% of chronic osteomyelitis cases.
• Warning features: change in the character or volume of discharge, foul odour, new pain in a previously painless sinus, bleeding, everted/heaped-up margins, exuberant granulation tissue, rapid enlargement and new inguinal lymphadenopathy.
• Any suspicious chronic sinus must be biopsied — do not attribute new changes to "just chronic infection".
• Behaviour is more aggressive than ordinary SCC, with a higher rate of lymph-node metastasis; treatment is wide excision, often amputation, with nodal assessment.
• Rarely, other malignancies (fibrosarcoma, basal cell carcinoma, lymphoma) arise in chronic sinuses.

15.13  Prognosis

• Acute haematogenous osteomyelitis treated within 3–5 days: cure rates >90% with minimal sequelae.
• Delayed treatment beyond 5–7 days markedly increases the risk of chronicity, growth disturbance and joint destruction.
• Chronic osteomyelitis: "arrest" rather than cure — recurrence in 20–30%, and relapse can occur years later; outcomes correlate closely with Cierny–Mader stage (Type I/A host best; Type IV/B host worst).
• Adverse prognostic factors: inadequate debridement, retained implant or dead bone, poor soft-tissue cover, peripheral vascular disease, diabetes, malnutrition, smoking, immunosuppression and MRSA/multidrug-resistant organisms.
• Adequate surgery with soft-tissue cover and targeted antibiotics achieves long-term remission in 80–90% of well-selected patients.

 

SECTION 16  |  Septic Arthritis

16.1  Definition

Septic (pyogenic/suppurative) arthritis is infection of the synovial joint space by pyogenic organisms, producing an acute purulent effusion with rapid enzymatic destruction of articular cartilage.

Simple explanation: bacteria multiply inside a closed joint; pus, bacterial toxins and host neutrophil enzymes digest cartilage within days. It is a surgical emergency — cartilage loss begins within 48–72 hours and is irreversible. [VERY HIGH-YIELD]

SEPTIC ARTHRITIS IS A JOINT EMERGENCY ▪  Any acutely hot, swollen, painful joint with restricted movement is septic arthritis until proved otherwise. ▪  Delay beyond 24–48 hours markedly increases risk of permanent cartilage destruction and secondary osteoarthritis. ▪  Mortality of native-joint septic arthritis remains 7–15%, rising to ~30% in polyarticular disease and the elderly. ▪  Never give antibiotics before aspirating the joint (unless the patient is in septic shock) — cultures become negative within hours.

16.2  Types of Joint and Periarticular Infection

Native-joint infection

• Infection of a normal or previously diseased natural joint.
• Commonest form; monoarticular in 80–90%.
• Knee is the most frequently involved joint in adults (~50%), followed by hip, shoulder, ankle, wrist and elbow.
• Hip is the commonest joint in infants and young children — presents with the limb held in flexion, abduction and external rotation. [COMMON MCQ]

Gonococcal arthritis

Caused by Neisseria gonorrhoeae; classically affects young, sexually active adults and is the commonest cause of septic arthritis in this group in Western data. It is comparatively uncommon in Indian practice, where Staphylococcus aureus dominates. [IMPORTANT]

• Disseminated gonococcal infection (DGI) has two overlapping presentations:
• Arthritis–dermatitis syndrome (bacteraemic form) — migratory polyarthralgia, tenosynovitis (especially of wrist/hand extensors) and scanty painless pustular or haemorrhagic skin lesions on the distal limbs. Synovial fluid culture is usually negative; blood culture may be positive.
• Purulent monoarthritis (localised form) — a single frankly septic joint, usually knee; synovial fluid culture positive in ~50%.
• The triad of tenosynovitis + dermatitis + migratory polyarthralgia is the classic examination answer for DGI. [FAVORITE EXAM QUESTION]
• Responds dramatically to therapy; joint destruction is uncommon.
• Associated with terminal complement (C5–C9) deficiency in patients with recurrent neisserial infection — check CH50. [COMMON MCQ]

Polyarticular septic arthritis

• Two or more joints involved; accounts for 10–20% of cases.
• Strongly associated with rheumatoid arthritis, connective tissue disease, immunosuppression, overwhelming sepsis and infective endocarditis.
• Carries far higher mortality (~30–50%) than monoarticular disease because it reflects bacteraemic seeding.
• In a patient with rheumatoid arthritis, superimposed sepsis is frequently mistaken for a disease flare — a single joint disproportionately inflamed in an otherwise controlled RA must be aspirated. [VERY HIGH-YIELD]

Prosthetic-joint infection

Infection of an implanted arthroplasty; biofilm-mediated, indolent, and managed by fundamentally different principles from native-joint infection. Discussed fully in Section 17.

Sternoclavicular joint infection

• Uncommon; disproportionately seen in injection drug users, patients with indwelling central venous catheters and haemodialysis patients.
• Organisms: S. aureus most common; Pseudomonas aeruginosa classically in injection drug users.
• Presents with anterior chest wall pain and swelling; may be mistaken for cardiac pain.
• CT or MRI is mandatory — the joint is deep and complications (retrosternal abscess, mediastinitis, chest-wall abscess) are frequent.
• Often needs en-bloc resection, not simple drainage.

Sacroiliac joint infection

• Typically unilateral; affects young adults, injection drug users and pregnant/postpartum women.
• Presents with fever, buttock or low back pain radiating to the thigh, and a painful limp; hip movement is preserved but SI stress tests are positive.
• FABER (Patrick) test and direct SI compression reproduce pain.
• Plain films are normal early — MRI is the investigation of choice; CT-guided aspiration establishes the organism.
• Usually responds to antibiotics alone; drainage reserved for abscess.

Septic bursitis

• Infection of a superficial bursa — olecranon and prepatellar bursae account for the great majority.
• Mechanism: direct inoculation through overlying skin after trauma or repeated pressure (occupational — the classic Indian equivalents are floor-scrubbing, mopping and prolonged kneeling; "housemaid knee", "student elbow").
• S. aureus causes 80–90%.
• Key discriminator from septic arthritis: in bursitis the swelling is superficial and clearly demarcated over the bursa, and passive joint movement is preserved and relatively painless; in septic arthritis all movement is agonising. [VERY HIGH-YIELD]
• Diagnosis: bursal aspiration for cell count, Gram stain, culture and crystals.
• Treatment: aspiration (may need repeating) plus antistaphylococcal antibiotics for 2–3 weeks; surgical bursectomy for refractory or recurrent disease.

Infectious tenosynovitis

• Infection within a tendon sheath — most importantly the flexor tendon sheaths of the hand (see also Section 9).
• Kanavel four cardinal signs: flexed resting posture of the digit, fusiform (sausage) swelling, tenderness along the tendon sheath, and severe pain on passive extension. [FAVORITE EXAM QUESTION]
• Organisms: S. aureus, streptococci; Pasteurella after cat bite; Eikenella after clenched-fist injury.
• Chronic granulomatous tenosynovitis — think tuberculosis (very relevant in India), atypical mycobacteria (M. marinum in fish-tank/fish-handling exposure) and fungi.
• Requires urgent surgical drainage and sheath irrigation — delay leads to tendon necrosis and permanent stiffness.

16.3  Aetiology

Organisms causing native-joint septic arthritis
Group / Setting	Organisms
Overall commonest	Staphylococcus aureus — 40–60% of all cases, and the commonest at every age in India
Streptococci	Streptococcus pyogenes, groups B, C and G; S. pneumoniae — second commonest group
Young sexually active adults	Neisseria gonorrhoeae
Neonates	Group B Streptococcus, S. aureus, Gram-negative bacilli, Candida
Children <5 years	S. aureus, Kingella kingae, group A Streptococcus, S. pneumoniae; Haemophilus influenzae type b now rare after Hib vaccination
Elderly, diabetic, urosepsis	Gram-negative bacilli — E. coli, Klebsiella, Proteus
Injection drug users	S. aureus (including MRSA), Pseudomonas aeruginosa, Serratia — with axial joint predilection
Sickle-cell disease	Salmonella species and S. aureus
Immunocompromised / HIV	S. aureus, Gram-negatives, Mycobacterium tuberculosis, atypical mycobacteria, fungi
Bite / trauma	Pasteurella multocida, Eikenella corrodens, anaerobes
Chronic monoarthritis in India	Mycobacterium tuberculosis — always in the differential; also Brucella (occupational/raw milk) and fungi
TUBERCULAR ARTHRITIS — THE INDIAN CAVEAT ▪  India carries the world’s largest tuberculosis burden; osteoarticular TB accounts for 1–3% of all TB and about 10–15% of extrapulmonary TB. ▪  Presents as chronic monoarthritis with insidious pain, swelling, night sweats, weight loss and marked muscle wasting — not the acute hot joint of pyogenic arthritis. ▪  Commonest sites: spine (Pott disease) > hip > knee. ▪  Synovial fluid: lymphocyte-predominant, high protein, low glucose; AFB smear positive in only ~20%, culture in ~80%; synovial biopsy with histopathology and CBNAAT gives the highest yield. ▪  Treated under NTEP with standard ATT for 12 months for osteoarticular disease. [VERY HIGH-YIELD]

16.4  Risk Factors

Host factors

• Age >80 years or <5 years.
• Rheumatoid arthritis — the single strongest predisposing joint disease (damaged synovium, immunosuppressive therapy).
• Osteoarthritis, gout, pseudogout, Charcot joint — any pre-existing joint damage.
• Diabetes mellitus, chronic kidney disease, cirrhosis, malignancy.
• HIV infection and other immunodeficiency; corticosteroids, anti-TNF biologics, DMARDs, chemotherapy.
• Injection drug use, alcohol dependence, malnutrition.
• Haemophilia and repeated haemarthrosis; sickle-cell disease.

Local and procedural factors

• Prosthetic joint or orthopaedic implant.
• Recent intra-articular corticosteroid injection, arthroscopy or joint surgery — a very common Indian scenario is repeated unsterile intra-articular injection for knee osteoarthritis by unqualified practitioners. [IMPORTANT]
• Penetrating trauma, animal or human bite over a joint, thorn or splinter injury.
• Overlying skin infection — cellulitis, ulcer, psoriasis, eczema.
• Adjacent osteomyelitis (especially in children, where metaphysis is intracapsular at the hip, shoulder, elbow and ankle).

16.5  Pathogenesis

Pathogenesis of septic arthritis

Bacterial entry — haematogenous (commonest) | direct inoculation | contiguous spread from osteomyelitis or cellulitis ↓ Synovium is highly vascular and lacks a basement membrane — organisms readily enter the joint space ↓ Bacterial adhesins (S. aureus MSCRAMMs) bind collagen, fibronectin and bone sialoprotein on cartilage ↓ Acute synovitis: massive neutrophil influx into a closed space ↓ Release of neutrophil elastase, collagenase, host matrix metalloproteinases and bacterial toxins ↓ Degradation of proteoglycan first (within 48 h), then collagen of articular cartilage ↓ Rising intra-articular pressure → impaired synovial blood flow → cartilage and epiphyseal ischaemia ↓ Chondrolysis, subchondral bone erosion, pannus formation ↓ Fibrous or bony ankylosis, secondary osteoarthritis, joint destruction

WHY THE HIP IS SPECIAL IN CHILDREN ▪  The femoral neck metaphysis lies inside the hip capsule, so metaphyseal osteomyelitis decompresses directly into the joint. ▪  The same applies at the proximal humerus, radial neck and distal fibula. ▪  Raised intracapsular pressure compresses the retinacular vessels supplying the femoral head → avascular necrosis and later coxa magna/coxa vara. ▪  This is why paediatric hip sepsis requires emergency arthrotomy and decompression, not just aspiration. [VERY HIGH-YIELD]

16.6  Clinical Features

Typical presentation

• Acute monoarthritis — pain, swelling, warmth, erythema and severe restriction of both active and passive movement, evolving over hours to a few days.
• The joint is held in the position of maximum capsular volume (hip: flexion, abduction, external rotation; knee: 15–30° flexion; shoulder: adduction and internal rotation) to minimise intra-articular pressure. [COMMON MCQ]
• Fever in only ~60%; rigors in ~20%. Absence of fever never excludes septic arthritis. [IMPORTANT]
• Refusal to weight-bear, pseudoparalysis of a limb in infants, or an irritable non-moving limb in a neonate.
• Effusion is demonstrable in superficial joints (patellar tap, bulge sign); deep joints (hip, sacroiliac, sternoclavicular, shoulder) may show only pain on movement.

Atypical and difficult presentations

• Elderly and immunosuppressed — afebrile, minimally inflamed joint with only confusion or functional decline.
• Rheumatoid arthritis — sepsis masquerading as a flare; steroids blunt the inflammatory response.
• Infants — irritability, poor feeding, pseudoparalysis, pain on nappy change (hip).
• Deep joints — hip and sacroiliac sepsis may present only with limp, groin, buttock or referred knee pain. [IMPORTANT]
• Post-injection sepsis — pain that worsens rather than improves 48–72 hours after intra-articular steroid.

KOCHER CRITERIA — SEPTIC ARTHRITIS VS TRANSIENT SYNOVITIS OF THE HIP IN CHILDREN ▪  Non-weight-bearing on the affected side ▪  Temperature >38.5°C ▪  ESR >40 mm/h ▪  Peripheral WBC >12,000/mm³ ▪  Probability of septic arthritis: 1 criterion ~3%, 2 ~40%, 3 ~93%, 4 ~99%. CRP >20 mg/L is an additional independent predictor. [FAVORITE EXAM QUESTION]

16.7  Investigations

Synovial fluid analysis — the definitive investigation

Arthrocentesis before antibiotics is the single most important step. Aspirate through healthy, non-cellulitic skin; for the hip and other deep joints use image guidance. Send fluid for cell count with differential, Gram stain, culture and sensitivity, crystal examination under polarised light, and — where indicated — AFB smear/culture, CBNAAT and fungal studies. [VERY HIGH-YIELD]

Synovial fluid interpretation
Parameter	Normal	Inflammatory	Septic
Appearance	Clear, straw	Translucent, yellow	Turbid, purulent, may be blood-stained
Viscosity	High	Reduced	Very low
WBC/mm³	<200	2,000–50,000	>50,000 (often >100,000)
Neutrophils	<25%	>50%	>75–90%
Glucose	Near serum	Slightly low	<50% of serum / very low
Protein	Low	Raised	Markedly raised
Lactate	Low	Variable	High (>10 mmol/L suggests sepsis)
Crystals	Absent	May be present	May coexist — crystals do NOT exclude infection
CRITICAL CAVEATS IN SYNOVIAL FLUID INTERPRETATION ▪  A WBC count <50,000/mm³ does not exclude septic arthritis — early infection, partially treated infection, immunosuppression, gonococcal disease and prosthetic joints all show lower counts. ▪  Crystals and infection can coexist. Finding urate or CPPD crystals never rules out sepsis; if the clinical picture is septic, treat as septic. [VERY HIGH-YIELD] ▪  Counts >100,000/mm³ with >90% neutrophils are highly suggestive but can occur in crystal arthritis and acute rheumatoid flares. ▪  Never delay aspiration for imaging in a superficial joint.

Gram stain

• Rapid, cheap and guides the first antibiotic dose.
• Sensitivity: ~50–75% for Gram-positive organisms, ~40–50% for Gram-negatives, and <25% for gonococci.
• A negative Gram stain has no exclusion value. [IMPORTANT]

Culture

• Synovial fluid culture is positive in 70–90% of non-gonococcal cases when taken before antibiotics.
• Inoculating fluid directly into blood-culture bottles at the bedside significantly increases yield.
• Yield falls sharply after even one antibiotic dose — hence aspirate first.
• Request prolonged incubation if Kingella, Brucella or anaerobes are suspected; mycobacterial and fungal cultures need specific media and up to 6 weeks.

Blood culture

• Two sets from separate sites before antibiotics.
• Positive in ~50% of non-gonococcal septic arthritis, and may be the only positive culture in up to 10%.
• Persistent S. aureus bacteraemia mandates echocardiography to exclude infective endocarditis and a search for metastatic foci (spine, other joints). [IMPORTANT]

NAAT for gonorrhoea

• Because gonococcal cultures are fastidious and frequently negative, nucleic acid amplification testing (NAAT) is the diagnostic mainstay.
• Test synovial fluid plus urogenital, rectal and pharyngeal specimens — the mucosal site is far more often positive than the joint. [COMMON MCQ]
• Still send culture where possible, since only culture provides antimicrobial susceptibility in an era of rising cephalosporin resistance.
• Screen for co-existing HIV, syphilis, hepatitis B and Chlamydia, and treat partners — notifiable under Indian STI/RTI control programme guidance.

Blood and inflammatory markers

• Leucocytosis with neutrophilia (may be absent in the elderly).
• ESR and CRP raised in >90%; CRP is the better marker for monitoring response — a failure to fall by day 5–7 suggests inadequate drainage or wrong antibiotic.
• Procalcitonin supports a bacterial cause but does not replace aspiration.
• Serum urate is unhelpful acutely (may be normal in acute gout and raised in sepsis).
• Add blood glucose/HbA1c, renal and liver function, and HIV testing where risk factors exist.

Imaging

Imaging in septic arthritis
Modality	Role and findings
Plain radiograph	Baseline; normal early. Shows soft-tissue swelling, joint space widening (effusion), then joint space narrowing, erosions and periarticular osteopenia after 7–14 days. Essential to exclude fracture, tumour and pre-existing arthritis.
Ultrasound	First-line for deep joints (hip, shoulder, sacroiliac); detects effusion and guides aspiration. Cannot distinguish septic from sterile effusion.
MRI	Most sensitive; shows effusion, synovial thickening and enhancement, marrow oedema, and detects coexisting osteomyelitis or abscess. Investigation of choice for sacroiliac, sternoclavicular and spinal joints.
CT	Useful for sternoclavicular and sacroiliac joints, bone destruction and guided aspiration.
Radionuclide scan	High sensitivity, poor specificity; reserved for multifocal or occult disease.

16.8  Differential Diagnosis

Differential diagnosis of the acute hot joint
Condition	Discriminating features
Gout	Male, first MTP joint (podagra), recurrent self-limiting attacks, tophi, precipitated by alcohol/diuretics. Synovial fluid: needle-shaped, negatively birefringent monosodium urate crystals. Fluid can still be purulent — always culture.
Pseudogout (CPPD)	Elderly, knee and wrist, chondrocalcinosis on radiograph. Fluid: rhomboid, weakly positively birefringent calcium pyrophosphate crystals.
Reactive arthritis	Asymmetrical oligoarthritis of lower limbs 1–4 weeks after enteric or genitourinary infection; conjunctivitis, urethritis, keratoderma blennorrhagicum, circinate balanitis; HLA-B27 positive; sterile synovial fluid.
Rheumatoid arthritis	Symmetrical small-joint polyarthritis, morning stiffness >1 h, RF/anti-CCP positive. Beware superimposed sepsis in a single disproportionately inflamed joint.
Haemarthrosis	Trauma, haemophilia or anticoagulation; frankly bloody aspirate with fat globules if intra-articular fracture; normal WBC for the degree of blood.
Transient synovitis	Children 3–8 years, mild pain, low or no fever, normal inflammatory markers, weight-bears; use Kocher criteria.
Acute rheumatic fever	Migratory large-joint polyarthritis after streptococcal pharyngitis; carditis, chorea, raised ASO; dramatic response to salicylates. Still important in India.
Osteomyelitis / cellulitis	Point bone tenderness or skin involvement with preserved passive joint movement.
Tubercular arthritis	Chronic monoarthritis, cold abscess, marked wasting, lymphocytic fluid.
Charcot arthropathy	Painless or disproportionately painless gross joint destruction in a neuropathic diabetic foot.
THE RULE THAT SAVES JOINTS ▪  When you cannot distinguish crystal arthritis from sepsis, treat as sepsis until cultures are final. ▪  Untreated gout damages nothing in 48 hours; untreated sepsis destroys the joint. [VERY HIGH-YIELD]

16.9  Management

Management algorithm — acute hot joint

Acute hot, swollen, painful joint ↓ Urgent joint aspiration before antibiotics (image-guided if deep) + 2 sets of blood cultures ↓ Send: cell count & differential | Gram stain | culture | crystals | (AFB/CBNAAT if indicated) ↓ Start empirical IV antibiotics immediately after aspiration ↓ Drain the joint — repeated needle aspiration OR arthroscopic OR open drainage ↓ Rationalise antibiotics on culture and sensitivity | Splint briefly, then early passive mobilisation ↓ Monitor clinical response + CRP | Repeat aspiration if effusion reaccumulates ↓ No improvement by 48–72 h → re-image, re-drain, reconsider organism and diagnosis

Empirical antibiotic therapy

Start intravenously immediately after aspiration. Choice is guided by Gram stain, age, comorbidity and local resistance patterns — an important consideration in India, where community MRSA prevalence in S. aureus SSTI isolates is substantial and Gram-negative resistance is high. [IMPORTANT]

Empirical antibiotic choice in native-joint septic arthritis
Clinical setting	Empirical regimen
Gram-positive cocci on smear	IV cloxacillin/flucloxacillin 2 g 6-hourly, or cefazolin 2 g 8-hourly
MRSA suspected or prevalent	IV vancomycin (target trough 15–20 mg/L) or teicoplanin; alternatives — daptomycin, linezolid
Gram-negative bacilli on smear	IV ceftriaxone 2 g daily, or cefepime/piperacillin–tazobactam if Pseudomonas possible
No organism seen, healthy adult	IV cloxacillin (or vancomycin where MRSA is likely) + ceftriaxone
Elderly, diabetic, urosepsis, immunosuppressed	Vancomycin + ceftriaxone or piperacillin–tazobactam
Injection drug user	Vancomycin + antipseudomonal agent (piperacillin–tazobactam or cefepime)
Suspected gonococcal	IV ceftriaxone 1 g daily plus a single dose of azithromycin 1 g orally; switch to oral after clinical response
Post-bite or penetrating trauma	IV amoxicillin–clavulanate or ampicillin–sulbactam
Neonate	IV cloxacillin (or vancomycin) + gentamicin or cefotaxime

• Rationalise to a narrow-spectrum agent as soon as sensitivities are available — core antimicrobial stewardship practice.
• Intravenous therapy for the first 2 weeks, then oral step-down with an agent of good bioavailability and bone/joint penetration (e.g. linezolid, clindamycin, fluoroquinolone plus rifampicin as appropriate).
• Intra-articular antibiotics are contraindicated — they cause chemical synovitis and add nothing to systemic therapy. [FAVORITE EXAM QUESTION]

Joint drainage

Antibiotics alone are inadequate: pus under pressure must be evacuated. Selecting the method is a common examination and viva theme.

Repeated needle aspiration

• Appropriate for accessible superficial joints (knee, ankle, wrist, elbow, small joints) with fluid that aspirates freely.
• Aspirate to dryness daily (or more often) until the effusion stops reaccumulating and cell counts fall.
• Advantages: no anaesthesia, bedside, repeatable, allows serial monitoring of the fluid.
• Change to surgical drainage if effusion persists beyond 5–7 days, becomes loculated, or the patient fails to improve.

Arthroscopic drainage

• Preferred surgical method for the knee and shoulder; increasingly used for ankle, elbow, wrist and hip.
• Permits direct visualisation, lysis of adhesions, debridement of fibrinous loculations and copious lavage with a tourniquet-free, minimally invasive approach.
• Lower morbidity, less postoperative pain, faster rehabilitation and shorter stay than arthrotomy.
• Allows a second-look procedure if needed.

Open surgical drainage (arthrotomy)

• Indications: [VERY HIGH-YIELD]
• Hip sepsis — particularly in infants and children (emergency arthrotomy)
• Joints inaccessible to needle or scope (sacroiliac, sternoclavicular, some shoulders)
• Thick pus, loculation or extensive fibrin that cannot be evacuated arthroscopically
• Failure of aspiration or arthroscopic lavage after 5–7 days
• Coexisting osteomyelitis or periarticular abscess needing debridement
• Prosthetic-joint infection, foreign body or penetrating injury with retained material
• Delayed presentation with established joint destruction

Adjunctive measures

• Splint in a position of function for 24–48 hours for analgesia, then begin early passive and active-assisted mobilisation — prolonged immobilisation causes stiffness and adhesions. [IMPORTANT]
• Adequate analgesia; NSAIDs are permissible once sepsis is being treated.
• Physiotherapy for muscle strength and range of motion; avoid weight-bearing on an infected weight-bearing joint until inflammation settles.
• Correct the underlying condition — glycaemic control, nutrition, treat the source (skin ulcer, urinary sepsis, endocarditis).
• Consider short adjunctive dexamethasone in paediatric septic arthritis: trial evidence suggests reduced residual dysfunction, though it is not universal practice.
• Manage the entry portal — treat tinea pedis, ulcers and injection sites to prevent recurrence.

Duration of treatment

Duration of antibiotic therapy
Organism / setting	Total duration
Neisseria gonorrhoeae	7–14 days
Streptococcus species	2–3 weeks
Staphylococcus aureus	3–4 weeks (longer if bacteraemic or endocarditis)
Gram-negative bacilli	3–4 weeks
Associated osteomyelitis	6 weeks or more
Prosthetic-joint infection	3 months (hip) to 6 months (knee) — see Section 17
Tubercular arthritis	12 months of ATT under NTEP

16.10  Complications

• Articular cartilage destruction and secondary osteoarthritis — the commonest long-term sequel.
• Fibrous or bony ankylosis, joint contracture and permanent stiffness.
• Osteomyelitis of adjacent bone; chronic infection.
• Avascular necrosis of the femoral head, growth-plate injury, limb-length discrepancy and deformity in children.
• Pathological dislocation (especially paediatric hip), joint instability.
• Periarticular abscess, sinus formation, spread to adjacent bursa or tendon sheath.
• Bacteraemia, septic shock, metastatic abscesses, infective endocarditis.
• Recurrence or relapse; treatment-related complications (vancomycin nephrotoxicity, C. difficile colitis).
• Long-term functional disability and loss of livelihood — a major socioeconomic burden in manual workers.

16.11  Prognosis

• Overall mortality 7–15%; up to 30–50% in polyarticular sepsis, the elderly and those with bacteraemia.
• Permanent joint dysfunction in 25–50% of survivors.
• Poor prognostic factors: [VERY HIGH-YIELD]
• Delay in diagnosis and drainage beyond 24–48 hours
• Age >65 years or infancy
• Pre-existing joint disease, especially rheumatoid arthritis
• Hip or shoulder involvement; polyarticular disease
• Immunosuppression, diabetes, chronic kidney disease
• S. aureus (especially MRSA) or Gram-negative infection
• Positive blood cultures / persistent bacteraemia
• Synovial fluid still culture-positive after 7 days of therapy
• Prompt aspiration, early drainage and appropriate antibiotics give good functional recovery in the majority.

SEPTIC ARTHRITIS — RAPID VIVA ▪  Commonest organism overall — Staphylococcus aureus. ▪  Commonest joint in adults — knee; in infants — hip. ▪  Investigation of choice — synovial fluid aspiration before antibiotics. ▪  Synovial WBC suggesting sepsis — >50,000/mm³ with >75% neutrophils. ▪  Do crystals rule out infection? — No. ▪  Position of the septic hip — flexion, abduction, external rotation. ▪  Criteria differentiating septic arthritis from transient synovitis — Kocher criteria. ▪  Classic triad of disseminated gonococcal infection — tenosynovitis, dermatitis, migratory polyarthralgia. ▪  Are intra-articular antibiotics used? — Never. ▪  Absolute indication for emergency arthrotomy — septic arthritis of the hip in a child.

 

SECTION 17  |  Prosthetic-Joint and Orthopaedic-Device Infection

17.1  Definition and Burden

Prosthetic-joint infection (PJI) is infection involving the implant and the surrounding bone–implant interface, characterised by biofilm formation on the prosthesis, which renders the organism phenotypically tolerant to antibiotics and to host defences.

• Incidence: 1–2% after primary hip or knee arthroplasty, and 3–5% or more after revision surgery.
• Absolute numbers are rising steeply in India with the rapid expansion of joint replacement surgery.
• It is the most feared complication of arthroplasty — cost, repeated surgery, prolonged antibiotics and frequently permanent functional loss.
• The same principles apply to internal fixation devices, spinal instrumentation and external fixator pins.

17.2  Classification by Time of Onset

Classification of prosthetic-joint infection
Type	Onset	Source and organisms	Typical presentation
Early	<3 months of surgery	Intraoperative or perioperative wound contamination; virulent organisms — S. aureus, Gram-negative bacilli, group B streptococci, enterococci	Acute wound pain, erythema, dehiscence, purulent or persistent discharge, fever, haematoma
Delayed (low-grade)	3–24 months	Intraoperative contamination with low-virulence organisms — coagulase-negative staphylococci (S. epidermidis), Cutibacterium acnes, enterococci	Persistent or new implant pain, early loosening; often afebrile with minimal signs — the most difficult to diagnose
Late haematogenous	>24 months	Blood-borne seeding from a distant focus — skin, dental, urinary, respiratory, gastrointestinal; S. aureus, streptococci, Gram-negatives	Sudden pain in a previously well-functioning joint, with features of the primary infection elsewhere
TIME OF ONSET PREDICTS THE ORGANISM AND THE OPERATION ▪  Early + virulent organism + well-fixed implant → debridement with implant retention may succeed. ▪  Delayed + low-virulence + loosening → almost always needs implant removal (revision). ▪  Late haematogenous → find and eradicate the distant source, or the new prosthesis will be reinfected too. [VERY HIGH-YIELD] ▪  Cutibacterium acnes is the classic organism of indolent shoulder arthroplasty infection and needs prolonged (14-day) anaerobic culture — otherwise reported as "culture-negative". [COMMON MCQ]

17.3  Biofilm Pathogenesis

Biofilm pathogenesis on an implant

Implant surface immediately coated with host proteins — fibronectin, fibrinogen, collagen, albumin ("conditioning film") ↓ Bacterial adhesion via adhesins/MSCRAMMs to the conditioned surface ↓ Irreversible attachment and microcolony formation ↓ Secretion of extracellular polymeric substance (glycocalyx / slime) — polysaccharide, protein, extracellular DNA ↓ Mature three-dimensional biofilm with water channels and nutrient gradients ↓ Deep bacteria enter a metabolically dormant, slow-growing "persister" state ↓ Antibiotic tolerance (up to 1000-fold), impaired antibody and phagocyte penetration ↓ Periodic dispersion of planktonic cells → relapse, chronic infection, implant loosening

Why biofilm changes everything

• Standard MIC-based susceptibility testing reflects planktonic bacteria and grossly overestimates in-vivo efficacy.
• Only a few agents have useful anti-biofilm activity: rifampicin for staphylococci and fluoroquinolones for Gram-negative bacilli. [VERY HIGH-YIELD]
• Rifampicin must never be used alone — resistance emerges rapidly by a single-step rpoB mutation; always combine (with a fluoroquinolone, cotrimoxazole, doxycycline, fusidic acid or linezolid).
• Rifampicin should be added only after the wound is dry and the bacterial load has been surgically reduced, to prevent resistance.
• A foreign body reduces the infecting inoculum needed for S. aureus infection by a factor of about 10⁴ — hence infections occur with trivial contamination.
• Cure without removing the implant is possible only when the biofilm is immature (early infection) and surgically debulked.

17.4  Risk Factors

• Patient: obesity, diabetes mellitus (particularly HbA1c >8%), rheumatoid arthritis, immunosuppression, malnutrition, chronic kidney disease, cirrhosis, malignancy, smoking, injection drug use, active infection elsewhere, prior PJI or revision surgery, S. aureus nasal carriage.
• Operative: prolonged operative time (>2.5 h), revision or complex surgery, poor theatre discipline, inadequate laminar flow, breach of asepsis, blood transfusion, wound haematoma.
• Postoperative: persistent wound drainage (>5 days), superficial wound infection, dehiscence, distant infection or bacteraemia (especially S. aureus).

17.5  Clinical Features

• Pain is the cardinal symptom — new, persistent or worsening pain in a prosthetic joint is infection until excluded. [IMPORTANT]
• Early infection: local heat, erythema, wound dehiscence, persistent wound drainage beyond 5–7 days, purulent discharge, fever.
• Delayed infection: chronic dull pain, especially start-up pain and rest pain, early implant loosening, no fever.
• Late haematogenous: abrupt onset of pain and effusion in a previously silent joint plus systemic sepsis.
• A sinus tract communicating with the prosthesis is pathognomonic and by itself confirms PJI. [FAVORITE EXAM QUESTION]
• Aseptic loosening is the main mimic — pain typically activity-related and improves with rest, with normal inflammatory markers.

17.6  Diagnostic Criteria

MSIS / IDSA DEFINITION OF PROSTHETIC-JOINT INFECTION ▪  Major criteria (either one confirms PJI): ▪  A sinus tract communicating with the prosthesis, or ▪  Two positive periprosthetic cultures with phenotypically identical organisms. ▪  Minor criteria (supportive, combination required): ▪  Raised ESR and CRP ▪  Raised synovial fluid leucocyte count or ++ change on leucocyte esterase strip ▪  Raised synovial neutrophil percentage (PMN%) ▪  Positive histology of periprosthetic tissue ▪  A single positive culture ▪  Raised synovial alpha-defensin (where available)

ESR and CRP

• First-line screening tests; performed together.
• Usual thresholds for chronic PJI: ESR >30 mm/h and CRP >10 mg/L.
• High negative predictive value — both normal makes chronic PJI unlikely.
• Poorly useful in the early postoperative period, when both are physiologically elevated: CRP normally peaks at 2–3 days and falls by day 7–14, so a secondary rise or failure to fall is the meaningful signal. [IMPORTANT]
• Falsely elevated in inflammatory arthritis and other infections; C. acnes infections may have normal markers.

Synovial fluid leucocyte count

Joint aspiration is the key preoperative test. Thresholds are much lower than in native-joint sepsis because a low-grade biofilm infection provokes a smaller inflammatory response. [VERY HIGH-YIELD]

Synovial fluid thresholds in prosthetic-joint infection
Setting	Leucocyte count	Neutrophil %
Chronic (>6 weeks post-op)	>3,000 cells/µL	>65–80%
Acute (<6 weeks post-op)	>10,000 cells/µL	>90%
Native septic arthritis (for contrast)	>50,000 cells/µL	>75–90%

• Withhold antibiotics for at least 2 weeks before aspiration wherever safe, to maximise culture yield.
• Also send fluid for crystals — pseudogout and gout can occur in prosthetic joints.
• Alpha-defensin and leucocyte esterase are useful adjuncts with high specificity, and retain accuracy despite prior antibiotics.

Culture

• Obtain a minimum of 3–6 separate periprosthetic tissue samples with fresh instruments for each; swabs are inadequate and should not be used. [IMPORTANT]
• Two or more samples growing the same organism confirms infection; a single growth of a skin commensal usually indicates contamination.
• Incubate for 14 days to recover C. acnes and other fastidious slow growers.
• Culture-negative PJI (7–15%) — usually due to prior antibiotics, fastidious organisms, inadequate sampling or mycobacteria/fungi. Send AFB and fungal cultures, and consider molecular testing (16S rRNA PCR, metagenomic sequencing).
• In India, also consider tubercular prosthetic infection in culture-negative cases with granulomatous histology.

Histopathology

• Frozen or permanent section of periprosthetic membrane.
• Criterion: >5 neutrophils per high-power field in at least 5 separate HPFs (×400) indicates acute inflammation consistent with infection.
• High specificity; useful intraoperatively to decide between one-stage and two-stage revision.
• Note that neutrophils are counted — not lymphocytes or plasma cells, which suggest an aseptic lymphocyte-dominated reaction (e.g. metal-on-metal wear debris).

Implant sonication

• The explanted prosthesis is placed in Ringer solution and subjected to low-energy ultrasound, which dislodges adherent biofilm bacteria; the sonicate fluid is then cultured quantitatively.
• Significantly more sensitive than conventional periprosthetic tissue culture, especially after recent antibiotics.
• Threshold commonly used: >50 CFU/mL of sonicate fluid.
• The single best test to demonstrate biofilm organisms — a favourite examination point. [FAVORITE EXAM QUESTION]

Imaging

• Plain radiographs — serial films show periprosthetic lucency >2 mm, implant migration, subsidence, periosteal reaction and osteolysis; normal early.
• Nuclear imaging — triple-phase bone scan is sensitive but non-specific (positive up to 1 year after surgery); labelled-leucocyte scan combined with bone marrow imaging is the most accurate nuclear technique.
• CT/MRI — limited by metal artefact, but metal-artefact-reduction sequences demonstrate abscess, sinus tracts and osteolysis.
• Sinography/fistulography may map a sinus tract.

17.7  Management

Treatment requires combined surgical and antimicrobial therapy, planned jointly by orthopaedic surgeon, microbiologist and infectious disease physician. The surgical option is chosen from four strategies. [VERY HIGH-YIELD]

Choosing the surgical strategy in prosthetic-joint infection

Confirmed prosthetic-joint infection ↓ Symptoms <3 weeks (or <3 months post-op) + well-fixed implant + intact soft tissues + susceptible organism? ↓ YES → DAIR — debridement, antibiotics and implant retention (exchange modular parts) ↓ NO → implant loose, chronic symptoms, sinus tract, resistant organism or poor soft tissue ↓ Good soft tissues, known susceptible organism, adequate bone stock → one-stage revision ↓ Difficult organism, poor soft tissues, sinus, bone loss, unknown organism → two-stage revision (gold standard) ↓ Unfit for major surgery, repeated failures, non-functional limb → resection arthroplasty / arthrodesis / amputation ± long-term suppressive antibiotics

Debridement, antibiotics and implant retention (DAIR)

• Indications: duration of symptoms <3 weeks, early postoperative or acute haematogenous infection, well-fixed prosthesis, healthy soft-tissue envelope, no sinus tract, and an organism susceptible to a biofilm-active agent.
• Procedure: open (preferably not arthroscopic) radical debridement, synovectomy, copious lavage, and exchange of all modular components (liner, head) to break the biofilm.
• Antibiotics: 2 weeks IV followed by prolonged oral therapy — total 3 months for hip, 6 months for knee; add rifampicin combination therapy for staphylococci and a fluoroquinolone for Gram-negatives.
• Success rate 60–80% in well-selected cases, but falls sharply if the symptom duration criterion is breached.
• Advantages: preserves bone stock and function, single operation, lower morbidity.

One-stage (direct exchange) revision

• Removal of the infected prosthesis, radical debridement, and immediate reimplantation of a new prosthesis in the same sitting, usually with antibiotic-loaded cement.
• Indications: known organism with predictable susceptibility, healthy soft tissues without sinus, adequate bone stock, and a medically fit patient.
• Contraindications: unknown or multidrug-resistant organism, fungal infection, sinus tract, severe bone loss, poor soft-tissue cover, systemic sepsis.
• Followed by 3 months of targeted antibiotics.
• Success 80–90% in selected patients; advantages are a single anaesthetic, shorter hospital stay, lower cost and better function — relevant considerations in resource-limited Indian practice.

Two-stage revision — the gold standard

• Stage 1: removal of all implants, cement and infected tissue; radical debridement; insertion of an antibiotic-impregnated cement spacer (commonly gentamicin/vancomycin), maintaining joint space, soft-tissue tension and some function.
• Interval: organism-directed IV then oral antibiotics for 6 weeks, followed by an antibiotic-free window of 2–6 weeks with repeat ESR/CRP and aspiration to confirm eradication.
• Stage 2: reimplantation of the definitive prosthesis once infection is proved eradicated; further tissue samples taken at reimplantation.
• Highest eradication rate — 85–95%; the standard for chronic PJI, resistant organisms, fungal infection and sinus tracts.
• Disadvantages: two major operations, prolonged disability, bone loss, cost, and inferior final function compared with one-stage revision.

Resection arthroplasty, arthrodesis and amputation

• Resection (excision) arthroplasty — permanent removal of the prosthesis without reimplantation (Girdlestone procedure at the hip). Reserved for repeated failures, non-ambulatory patients, uncontrolled infection or unreconstructable bone loss. Gives pain relief and infection control at the cost of shortening, instability and poor function.
• Arthrodesis — mainly for the knee after failed revision; provides a stable painless limb.
• Amputation — last resort for life-threatening uncontrolled sepsis, massive bone and soft-tissue loss, or a useless painful limb.

Chronic suppressive antibiotic therapy

• Long-term oral antibiotics without implant removal, aiming to control rather than eradicate infection.
• Indications: patient unfit for or refusing revision surgery, well-fixed implant, susceptible organism amenable to a well-tolerated oral agent, and no systemic sepsis.
• Typical agents: cotrimoxazole, doxycycline, linezolid (watch for cytopenias and neuropathy on prolonged use), amoxicillin, or a fluoroquinolone for Gram-negatives.
• Continued for years or indefinitely, with monitoring for toxicity and resistance.
• Not curative — relapse is expected if therapy stops. [IMPORTANT]

17.8  Prevention

• Preoperative optimisation — glycaemic control, weight reduction, nutrition, smoking cessation, treatment of dental, skin and urinary infection.
• Screening and decolonisation of nasal S. aureus carriers with mupirocin plus chlorhexidine body wash.
• Chlorhexidine–alcohol skin preparation and appropriate hair removal (clippers, not razors).
• Surgical antibiotic prophylaxis with cefazolin (or vancomycin where MRSA prevalence is high) within 60 minutes of incision, redosed for long procedures, discontinued within 24 hours.
• Laminar-flow theatre, body exhaust suits, minimal theatre traffic, meticulous asepsis and short operative time.
• Antibiotic-loaded cement in high-risk patients.
• Prompt treatment of distant infection and bacteraemia in any patient with an implant.
• Routine antibiotic prophylaxis before dental procedures is no longer recommended for prosthetic joints except in selected high-risk patients — a frequently tested change in guidance. [COMMON MCQ]

17.9  Prognosis

• Eradication rates: DAIR 60–80%, one-stage revision 80–90%, two-stage revision 85–95%.
• Poor prognostic factors: [VERY HIGH-YIELD]
• Symptom duration >3 weeks before debridement
• Loose implant or sinus tract
• MRSA, small-colony variants, enterococci, multidrug-resistant Gram-negatives and fungi
• Rheumatoid arthritis, diabetes, immunosuppression, poor soft-tissue envelope
• Previous revision surgery for infection; polymicrobial infection
• Inability to use rifampicin (resistance or intolerance)
• PJI mortality at 1 year is significant in the elderly (up to 5–8%), and functional outcome after two-stage revision is usually inferior to the original arthroplasty.
• Long-term follow-up is mandatory — late relapse can occur years after apparently successful treatment.

PROSTHETIC-JOINT INFECTION — RAPID VIVA ▪  Commonest organisms — coagulase-negative staphylococci and S. aureus. ▪  Organism of indolent shoulder arthroplasty infection — Cutibacterium acnes (needs 14-day culture). ▪  Pathognomonic sign of PJI — sinus tract communicating with the prosthesis. ▪  Synovial WBC threshold in chronic PJI — >3,000/µL with >65–80% neutrophils. ▪  Histology criterion — >5 neutrophils/HPF in 5 fields. ▪  Most sensitive test for biofilm organisms — implant sonication culture. ▪  Anti-biofilm agents — rifampicin (staphylococci) and fluoroquinolones (Gram-negatives). ▪  Why is rifampicin never used alone? — rapid emergence of resistance. ▪  Gold-standard surgery for chronic PJI — two-stage revision. ▪  Duration of antibiotics after DAIR — 3 months (hip), 6 months (knee).

 

SECTION 18  |  Master Comparison Tables

All high-yield differentiating tables for this chapter, consolidated for rapid pre-examination revision.

18.1  Classification of Skin and Soft-Tissue Infections

Basis	Categories
Anatomical depth	Epidermal || Dermal || Follicular || Subcutaneous || Fascial || Muscular
Clinical morphology	Purulent || Non-purulent || Necrotising || Toxin-mediated
Severity	Mild || Moderate || Severe || Complicated SSTI || ABSSSI
Acquisition	Community-acquired || Healthcare-associated || Postoperative || Post-traumatic || Bite-related || Water-related || Immunocompromised host

18.2  Common Organisms by Anatomical Site

Site / Layer	Usual organisms
Epidermis	S. aureus, S. pyogenes (impetigo); Corynebacterium minutissimum (erythrasma)
Dermis	S. pyogenes (erysipelas, ecthyma)
Hair follicle	S. aureus; Pseudomonas aeruginosa (hot-tub folliculitis)
Subcutaneous tissue	S. aureus (abscess), S. pyogenes and streptococci (cellulitis)
Fascia	Type I polymicrobial (anaerobes + Enterobacterales); Type II S. pyogenes ± S. aureus; Type III Vibrio vulnificus, Aeromonas
Muscle	S. aureus (pyomyositis); Clostridium perfringens, C. septicum (myonecrosis)
Bone	S. aureus overall; Salmonella in sickle-cell disease; M. tuberculosis in India
Joint	S. aureus; N. gonorrhoeae in young adults; coagulase-negative staphylococci and C. acnes in prostheses

18.3  Purulent versus Non-Purulent SSTI

Feature	Purulent	Non-purulent
Examples	Furuncle, carbuncle, abscess	Cellulitis, erysipelas, necrotising infection
Usual organism	S. aureus (including CA-MRSA)	Streptococci (β-haemolytic)
Primary treatment	Incision and drainage	Antibiotics
Antibiotics	Adjunctive — for systemic features, size >2 cm, multiple lesions, immunosuppression	Essential — the mainstay
MRSA cover	Usually required empirically	Only if risk factors or systemic toxicity
Culture	Pus for Gram stain and culture	Usually low yield; blood culture if systemic

18.4  Cellulitis versus Erysipelas

Feature	Cellulitis	Erysipelas
Depth	Deep dermis + subcutaneous fat	Upper dermis + superficial lymphatics
Organism	S. aureus and streptococci	Almost always S. pyogenes
Margin	Ill-defined, flat, indistinct	Sharply demarcated, raised, palpable edge
Colour	Pink to dull red	Fiery red, shiny ("peau d’orange")
Onset	Gradual, over days	Abrupt, with high fever and rigors
Common site	Lower limb	Lower limb; face (butterfly pattern)
Systemic upset	Variable	Prominent and early
Blistering / lymphangitis	Occasional	Common
Treatment	Antistaphylococcal + antistreptococcal cover	Penicillin is the drug of choice

18.5  Cellulitis Mimics ("Pseudocellulitis")

Mimic	Discriminating features
Deep-vein thrombosis	Calf tenderness, swelling without sharp erythema, risk factors; Doppler ultrasound
Stasis dermatitis	Bilateral, chronic, itchy rather than painful, afebrile, varicose veins, haemosiderin staining
Lipodermatosclerosis	Chronic induration with "inverted champagne bottle" leg, venous insufficiency
Contact dermatitis	Itch dominates, sharply follows contact pattern, vesicles, no fever
Gout	Joint-centred, exquisite tenderness, podagra, tophi, crystals in aspirate
Erythema nodosum	Tender nodules over shins, bilateral, no warmth spreading, TB/sarcoid/drug association
Necrotising infection	Pain out of proportion, systemic toxicity, bullae, crepitus, skin anaesthesia
Others	Insect bite reaction, drug eruption, panniculitis, calciphylaxis, carcinoma erysipeloides
KEY DISCRIMINATOR ▪  Bilateral lower-limb "cellulitis" is almost never cellulitis — think stasis dermatitis. [VERY HIGH-YIELD]

18.6  Non-Bullous versus Bullous Impetigo

Feature	Non-bullous	Bullous
Frequency	~70% — commoner	~30%
Organism	S. aureus > S. pyogenes	S. aureus (phage group II) only
Mechanism	Direct invasion of broken skin	Exfoliative toxin A/B cleaving desmoglein-1
Lesion	Vesicopustule → honey-coloured (golden) crust	Flaccid bulla → collarette of scale, shallow erosion
Site	Face — perioral and perinasal; limbs	Trunk, axillae, groin, nappy area; neonates
Preceding skin break	Usually present	Not required — intact skin
Nikolsky sign	Negative	May be positive around lesions
Complication	Post-streptococcal glomerulonephritis	May progress to SSSS in infants

18.7  Folliculitis, Furuncle and Carbuncle

Feature	Folliculitis	Furuncle	Carbuncle
Extent	Follicular ostium only	Whole follicle + perifollicular dermis	Several adjacent follicles coalescing
Depth	Superficial	Deep, single	Deep, multiloculated
Appearance	Small perifollicular pustule	Tender red nodule with central pustule	Large indurated plaque with multiple draining sinuses (cribriform)
Site	Any hair-bearing area	Face, neck, axilla, buttock	Nape of neck, back, thigh
Systemic upset	None	Minimal	Fever, malaise, bacteraemia
Association	Shaving, occlusion, hot tubs	Diabetes, obesity, nasal carriage	Diabetes mellitus — strongly
Treatment	Topical antiseptic/antibiotic	Warm compress ± I&D	Surgical drainage/deroofing + systemic antibiotics

18.8  Necrotising Fasciitis versus Cellulitis

Feature	Cellulitis	Necrotising fasciitis
Pain	Proportionate to signs	Out of proportion to findings
Progression	Hours to days, gradual	Rapid — extends hourly
Skin	Erythema, warmth	Dusky/violaceous, bullae, ecchymosis, necrosis
Sensation	Normal or hyperaesthetic	Anaesthesia over the lesion
Crepitus	Absent	May be present
Systemic toxicity	Mild to moderate	Severe — shock, organ failure, confusion
Tissue feel	Soft, tender	Woody-hard induration beyond the erythema
Response to antibiotics	Improves in 48 h	Deteriorates despite antibiotics
Investigations	Modest CRP/WBC	High LRINEC, CK raised, acidosis, renal failure
Treatment	Antibiotics	Immediate surgical exploration and debridement

18.9  Types of Necrotising Soft-Tissue Infection

Type	Microbiology	Typical setting
Type I	Polymicrobial — anaerobes + Enterobacterales + streptococci	Diabetes, elderly, postoperative, perineum (Fournier gangrene), abdominal wall
Type II	Monomicrobial — group A Streptococcus ± S. aureus	Healthy young adults; limbs; trauma, varicella, NSAID use; toxic shock syndrome
Type III	Marine Gram-negatives — Vibrio vulnificus, Aeromonas hydrophila	Seawater exposure, raw shellfish, cirrhosis / iron overload; haemorrhagic bullae
Type IV	Fungal — Candida, Mucorales	Immunocompromised, burns, penetrating trauma
Clostridial myonecrosis	C. perfringens, C. septicum	Trauma with soil contamination; spontaneous form with colonic malignancy
Synergistic necrotising cellulitis	Mixed aerobe–anaerobe	Perineum and lower limb in diabetics; foul discharge
Streptococcal myositis	Group A Streptococcus	Rare, fulminant muscle necrosis, very high mortality

18.10  LRINEC Score and Its Limitations

Parameter		Value	Points
CRP (mg/L)		≥150	4
Total WBC (/mm³)		15,000–25,000 || >25,000	1 || 2
Haemoglobin (g/dL)		11–13.5 || <11	1 || 2
Sodium (mmol/L)		<135	2
Creatinine (mg/dL)		>1.6	2
Glucose (mg/dL)		>180	1
Score	Risk of necrotising infection
≤5	Low risk (<50%)
6–7	Intermediate risk (50–75%)
≥8	High risk (>75%)
LIMITATIONS OF LRINEC ▪  Derived retrospectively; sensitivity as low as 60–80% in validation studies. ▪  A low score never excludes necrotising fasciitis — up to 1 in 10 proven cases score ≤5. ▪  Less reliable in children, in immunocompromised patients and in Type II streptococcal disease. ▪  Confounded by diabetes, chronic kidney disease and anaemia, all of which raise the score independently. ▪  It is an adjunct only — the decision to operate is clinical. [VERY HIGH-YIELD]

18.11  Gas Gangrene versus Necrotising Fasciitis

Feature	Clostridial myonecrosis	Necrotising fasciitis
Primary tissue	Muscle	Fascia (muscle usually spared)
Organism	C. perfringens, C. septicum	Polymicrobial or group A Streptococcus
Incubation	Very short — 6–24 hours	1–4 days
Discharge	Thin, brown, sweetish odour	Foul "dishwater" pus (Type I)
Crepitus / gas	Marked, early	Variable, later (Type I)
Gram stain	Large Gram-positive boxcar bacilli with few neutrophils	Mixed flora or chains of cocci
Muscle at surgery	Non-contractile, non-bleeding, brick-red to black	Viable, but fascia necrotic with easy blunt separation
Haemolysis	Marked (alpha toxin)	Uncommon
Adjunct	Hyperbaric oxygen has a defined role	IVIG for streptococcal toxic shock

18.12  Bite Wound and Likely Organism

Bite / exposure	Characteristic organism
Dog bite	Pasteurella canis, Capnocytophaga canimorsus (fulminant sepsis in asplenia/cirrhosis), staphylococci, anaerobes
Cat bite	Pasteurella multocida — rapid onset within 12–24 h; deep puncture; Bartonella henselae (cat-scratch disease)
Human bite / clenched-fist	Eikenella corrodens, viridans streptococci, S. aureus, anaerobes; risk of HIV, HBV, HCV
Monkey bite	Herpes B virus (Macacine herpesvirus 1) — fatal encephalitis; plus bacterial flora and rabies
Rat bite	Streptobacillus moniliformis (Haverhill fever) and Spirillum minus (sodoku)
Pig bite	Pasteurella aerogenes, Actinobacillus, anaerobes
Fish / marine injury	Vibrio vulnificus, Aeromonas hydrophila, Mycobacterium marinum, Erysipelothrix rhusiopathiae
Soil-contaminated wound	Clostridium tetani, C. perfringens, Bacillus, Enterobacterales, fungi
Injection-site (drug use)	S. aureus (MRSA), streptococci, anaerobes, Clostridium botulinum/tetani, Pseudomonas

18.13  Bite-Wound Prophylaxis Indications

Consideration	Details
Antibiotic prophylaxis indicated	All cat and human bites || Hand, foot, face and genital bites || Deep puncture wounds || Wounds needing surgical repair || Crush injury with devitalised tissue || Bites over or near a joint, bone or prosthesis || Immunocompromised, asplenic, cirrhotic, diabetic patients || Presentation delayed >8–12 hours || Wounds with oedema or venous/lymphatic compromise
Drug of choice	Amoxicillin–clavulanate for 3–5 days (prophylaxis) or 7–14 days (established infection)
Penicillin allergy	Doxycycline, or a fluoroquinolone/cotrimoxazole plus metronidazole or clindamycin
Avoid	Cephalexin, cloxacillin, clindamycin or erythromycin alone — poor activity against Pasteurella and Eikenella [COMMON MCQ]
Wound closure	Generally delayed primary closure; face may be closed primarily after copious irrigation; never close clenched-fist or cat-bite punctures
Tetanus	Toxoid if >5 years since last dose; toxoid + human tetanus immunoglobulin if unimmunised or uncertain
Rabies	Category II → vaccine; Category III (transdermal bite, mucosal contact, bat exposure) → vaccine + rabies immunoglobulin infiltrated into the wound

18.14  Wagner Classification of Diabetic Foot Ulcer

Grade	Description
Grade 0	No open lesion; intact skin with bony deformity or callus ("foot at risk")
Grade 1	Superficial ulcer, full thickness, not involving deeper tissue
Grade 2	Deeper ulcer reaching tendon, capsule or bone, without abscess or osteomyelitis
Grade 3	Deep ulcer with abscess, osteomyelitis or joint sepsis
Grade 4	Localised gangrene — forefoot or heel
Grade 5	Gangrene of the entire foot — requires major amputation

18.15  University of Texas Diabetic-Foot Classification

Stage \ Grade	0 — pre/post-ulcer	I — superficial	II — to tendon/capsule	III — to bone/joint
A — Clean	A0	A1	A2	A3
B — Infected	B0	B1	B2	B3
C — Ischaemic	C0	C1	C2	C3
D — Infected + ischaemic	D0	D1	D2	D3
WHY UT IS BETTER THAN WAGNER ▪  Wagner grades depth only; the University of Texas system grades depth (0–III) and stages infection and ischaemia (A–D). ▪  Risk of amputation rises with both increasing grade and advancing stage — stage D3 has the worst outcome. [VERY HIGH-YIELD]

18.16  IWGDF/IDSA Diabetic-Foot Infection Severity

PEDIS grade / IDSA severity	Clinical features
1 — Uninfected	No purulence or signs of inflammation
2 — Mild	≥2 signs of inflammation; cellulitis ≤2 cm around ulcer; limited to skin and subcutaneous tissue; no systemic features
3 — Moderate	Cellulitis >2 cm, or lymphangitis, spread beneath fascia, deep-tissue abscess, gangrene, or involvement of muscle, tendon, joint or bone; systemically well
4 — Severe	Any foot infection with systemic inflammatory response — temperature >38°C or <36°C, pulse >90/min, respiratory rate >20/min, WBC >12,000 or <4,000/mm³
Add "(O)"	Appended to grade 3 or 4 when osteomyelitis is present
PEDIS ACRONYM ▪  Perfusion — Extent/size — Depth/tissue loss — Infection — Sensation. [COMMON MCQ]

18.17  Osteomyelitis Classifications

System	Categories
By duration	Acute || Subacute (Brodie abscess) || Chronic
By pathogenesis (Waldvogel)	Haematogenous || Contiguous focus || Associated with vascular insufficiency
By setting	Post-traumatic || Postoperative || Implant-associated || Vertebral || Diabetic foot
Cierny–Mader — anatomical type	I Medullary || II Superficial || III Localised (full-thickness, stable) || IV Diffuse (unstable, needs reconstruction)
Cierny–Mader — host class	A Normal host || B Compromised (Bs systemic, Bl local, Bls both) || C Treatment worse than disease

18.18  Acute versus Chronic Osteomyelitis

Feature	Acute	Chronic
Duration	Days to <2 weeks	>6 weeks / relapsing
Onset	Sudden, febrile, toxic	Insidious, low-grade or afebrile
Pain	Severe, constant, localised	Dull, intermittent
Hallmark	Bone marrow inflammation and pus	Sequestrum, involucrum, cloaca, sinus tract
Radiograph	Normal for 10–14 days; soft-tissue swelling only	Sclerosis, sequestrum, periosteal new bone, cavities
MRI	Marrow oedema — early positive	Sequestrum, sinus, abscess, cortical destruction
Blood culture	Positive in ~50%	Usually negative — bone biopsy essential
Treatment	Antibiotics alone often curative (4–6 weeks)	Surgical debridement mandatory + prolonged antibiotics
Cure rate	High (>90% in children)	Lower; relapse common even years later

18.19  Native-Joint versus Prosthetic-Joint Infection

Feature	Native joint	Prosthetic joint
Organism	S. aureus, streptococci, N. gonorrhoeae	Coagulase-negative staphylococci, S. aureus, C. acnes
Pathogenesis	Acute suppuration in synovium	Biofilm on implant surface
Presentation	Acute hot swollen joint, fever	Often indolent — persistent pain, loosening, afebrile
Synovial WBC threshold	>50,000/mm³	>3,000/µL (chronic); >10,000/µL (acute)
Neutrophil %	>75–90%	>65–80% (chronic)
Key extra tests	Gram stain, crystals, NAAT for gonococcus	Sonication culture, alpha-defensin, histology >5 PMN/HPF
Culture incubation	Standard	14 days (for C. acnes)
Antibiotic duration	2–4 weeks	3 months (hip) – 6 months (knee)
Biofilm-active drugs	Not required	Rifampicin (staphylococci); fluoroquinolone (Gram-negatives)
Definitive treatment	Drainage + antibiotics	DAIR / one-stage / two-stage revision

18.20  MRSA-Active Antimicrobial Agents

Agent	Route	Key practical points
Vancomycin	IV	Reference agent for severe MRSA; trough 15–20 mg/L; nephrotoxicity, "red man" syndrome (infusion-rate related); poor lung penetration
Teicoplanin	IV/IM	Once daily, less nephrotoxic; widely used in India
Linezolid	IV/Oral	100% oral bioavailability, excellent tissue and bone penetration; myelosuppression, optic and peripheral neuropathy, serotonin syndrome with SSRIs; avoid >28 days
Clindamycin	IV/Oral	Good tissue penetration, suppresses toxin production; check D-test for inducible resistance; C. difficile risk
Cotrimoxazole	Oral	Cheap, effective for CA-MRSA SSTI; weak antistreptococcal activity; hyperkalaemia, rash
Doxycycline / minocycline	Oral	Useful for mild CA-MRSA SSTI; avoid in children <8 years and pregnancy
Daptomycin	IV	Bactericidal; inactivated by pulmonary surfactant — never for pneumonia; monitor CPK for myopathy
Ceftaroline	IV	Anti-MRSA cephalosporin; useful in complicated SSTI
Tigecycline	IV	Broad spectrum; poor bloodstream levels; higher all-cause mortality signal — reserve
Mupirocin (topical)	Topical	Nasal decolonisation of S. aureus carriers
Newer agents	IV	Dalbavancin, oritavancin, telavancin, tedizolid — long half-life options where available

 

SECTION 19  |  Important Diagrams, Figures and Algorithms

All figures required for this chapter, consolidated. Each entry states exactly what the labelled figure must show and why it is examined.

��  Figure 1 — Anatomical depth of skin and soft-tissue infections Vertical cross-section of skin labelling epidermis, dermis, hair follicle, subcutaneous fat, superficial and deep fascia and muscle, with the corresponding infection annotated at each level: impetigo (epidermis), erysipelas (upper dermis + lymphatics), ecthyma (dermis), folliculitis/furuncle/carbuncle (follicle), cellulitis and abscess (subcutis), necrotising fasciitis (fascia), pyomyositis and myonecrosis (muscle). The single most useful orientation figure for the whole chapter. [ Insert labelled figure here ]

��  Figure 2 — Cellulitis assessment algorithm Flow diagram from "erythematous painful limb" through exclusion of pseudocellulitis and necrotising infection, severity grading (Eron/CREST class I–IV), decision on outpatient oral versus inpatient intravenous therapy, MRSA risk assessment, and criteria for imaging and blood culture. [ Insert labelled figure here ]

��  Figure 3 — Purulent abscess management algorithm Pathway from fluctuant lesion → bedside ultrasound → incision and drainage → decision node for adjunctive antibiotics (lesion >2 cm, multiple lesions, systemic features, immunosuppression, failure of I&D, extremes of age) → culture → MRSA cover → recurrent abscess pathway with decolonisation. [ Insert labelled figure here ]

��  Figure 4 — Necrotising fasciitis emergency pathway Time-critical pathway: clinical suspicion (pain out of proportion, systemic toxicity, hard woody induration) → resuscitation and broad-spectrum antibiotics with clindamycin → do not delay for imaging → immediate surgical exploration with finger test → radical debridement → planned re-look at 24 h → serial debridement → ICU support, IVIG for streptococcal TSS → reconstruction. [ Insert labelled figure here ]

��  Figure 5 — Diabetic-foot infection management algorithm From ulcer assessment through PEDIS/IDSA severity grading, vascular assessment (ABI, toe pressure, TcPO2), probe-to-bone and imaging for osteomyelitis, deep-tissue culture, empirical then culture-directed antibiotics, debridement and drainage, revascularisation, off-loading, glycaemic control and multidisciplinary follow-up, with amputation indications. [ Insert labelled figure here ]

��  Figure 6 — Probe-to-bone test Line drawing of a sterile blunt metal probe inserted into a diabetic foot ulcer contacting hard, gritty bone. Annotate: positive test in a high-prevalence setting has high positive predictive value for osteomyelitis; negative test in a low-prevalence setting has high negative predictive value. Cheap, bedside and highly examinable. [ Insert labelled figure here ]

��  Figure 7 — Osteomyelitis diagnostic pathway Algorithm from suspicion → inflammatory markers and blood cultures → plain radiograph (normal for 10–14 days) → MRI as the imaging modality of choice → bone biopsy for microbiology and histopathology (the gold standard) → targeted antibiotics ± surgical debridement, with the caveat that sinus tract swabs must not be used to guide therapy. [ Insert labelled figure here ]

��  Figure 8 — Septic arthritis management algorithm Acute hot joint → urgent aspiration before antibiotics + blood cultures → synovial cell count, Gram stain, culture, crystals → empirical intravenous antibiotics → drainage decision (repeated aspiration vs arthroscopic vs open arthrotomy) → de-escalation on sensitivities → early mobilisation → reassessment at 48–72 h if no response. [ Insert labelled figure here ]

��  Figure 9 — Prosthetic-joint infection management algorithm Confirmed PJI → classify by onset (early/delayed/late haematogenous) → assess implant fixation, soft tissues, organism and symptom duration → DAIR vs one-stage revision vs two-stage revision vs resection arthroplasty/suppression, with the antibiotic duration for each limb of the algorithm. [ Insert labelled figure here ]

��  Figure 10 — Bite-wound management pathway From bite presentation → wound assessment and neurovascular/tendon/joint examination → copious irrigation and debridement → radiograph for fracture or retained tooth → culture if infected → decision on primary versus delayed closure → prophylactic versus therapeutic antibiotics → tetanus prophylaxis → rabies category assessment and post-exposure prophylaxis → follow-up at 24–48 h. [ Insert labelled figure here ]

��  Figure 11 — Biofilm formation on an orthopaedic implant Five-stage sequence: conditioning film of host proteins → reversible then irreversible bacterial adhesion → microcolony formation → mature biofilm with extracellular polymeric matrix and persister cells → dispersion of planktonic bacteria. Annotate antibiotic tolerance and the role of rifampicin and fluoroquinolones. [ Insert labelled figure here ]

��  Figure 12 — Pathological anatomy of chronic osteomyelitis Longitudinal section of a long bone labelling sequestrum (dead avascular bone), involucrum (new subperiosteal bone), cloaca (opening in the involucrum), sinus tract to the skin surface and the surrounding infected granulation tissue. Essential for both written answers and viva. [ Insert labelled figure here ]

 

SECTION 20  |  Important Clinical Photographs

Superficial and epidermal infections

• Non-bullous impetigo — perioral and perinasal vesicopustules with honey-coloured golden crusts on an erythematous base in a child.
• Bullous impetigo — flaccid, thin-walled bullae with clear then turbid fluid on the trunk or nappy area, some ruptured leaving a collarette of scale and shallow erosion.
• Ecthyma — punched-out ulcer with a thick adherent greyish-yellow crust and raised violaceous indurated margin on the shin, healing with scarring.
• Erythrasma — well-demarcated red-brown finely scaly patch in the groin or axilla, with the classic coral-red fluorescence under Wood lamp.
• Pitted keratolysis — multiple shallow crater-like pits coalescing on the weight-bearing surface of a macerated malodorous sole (common in Indian farmers and soldiers in occlusive footwear).

Follicular and purulent infections

• Folliculitis — crops of small perifollicular pustules each pierced by a hair, on the thigh, beard area or trunk.
• Furuncle (boil) — solitary tender erythematous nodule with a central necrotic pustular punctum on the neck or buttock.
• Carbuncle — large indurated dusky plaque on the nape of the neck discharging pus from multiple points (cribriform / "sieve-like" appearance) in a diabetic patient.
• Cutaneous abscess — fluctuant tender erythematous swelling with central pointing, before and after incision and drainage.

Non-purulent and spreading infections

• Cellulitis — diffuse, ill-defined, warm erythema and oedema of the lower leg with an indistinct advancing margin; mark the border with a skin pencil to monitor progression.
• Erysipelas — fiery-red, shiny, oedematous plaque with a sharply demarcated, raised, palpable edge on the cheek (butterfly distribution) or shin.
• Orbital cellulitis — unilateral eyelid swelling with proptosis, chemosis, restricted and painful eye movements and reduced visual acuity — contrast with preseptal cellulitis, where the globe is normal.
• Staphylococcal scalded skin syndrome — infant with diffuse tender erythema, perioral radial fissuring and crusting, superficial sheet-like desquamation and positive Nikolsky sign, with mucosae spared.

Necrotising and deep infections

• Necrotising fasciitis — dusky violaceous discoloration with haemorrhagic bullae, skin necrosis and ill-defined borders, extending beyond the visible erythema; and the intraoperative photograph showing grey necrotic fascia with "dishwater" fluid and loss of resistance to blunt finger dissection.
• Fournier gangrene — necrosis of the scrotal, perineal and lower abdominal wall skin with crepitus and foul discharge, typically in an elderly diabetic man.
• Gas gangrene (clostridial myonecrosis) — tense oedematous limb with bronze-brown discoloration, tense bullae, and thin serosanguinous discharge with a sweetish odour; intraoperative view of non-contractile, non-bleeding brick-red muscle.
• Haemorrhagic bullae of Vibrio vulnificus infection — tense violaceous haemorrhagic bullae on the leg of a patient with cirrhosis after seawater exposure or raw shellfish ingestion.
• Clenched-fist injury ("fight bite") — small innocuous-looking laceration over the third or fourth metacarpophalangeal joint with surrounding swelling — always deeper than it appears.
• Acute paronychia — tender erythematous swelling of the nail fold with visible pus tracking beneath the eponychium.

Diabetic foot, bone and joint

• Neuropathic diabetic foot ulcer — punched-out ulcer with surrounding callus over a plantar pressure point (metatarsal head), in a warm, dry, well-perfused foot with bounding pulses.
• Ischaemic/neuroischaemic ulcer — painful ulcer on the toe tip or heel margin with a cold, pulseless, hairless, shiny foot and gangrenous toes.
• Charcot foot — grossly swollen, warm, erythematous, deformed midfoot with "rocker-bottom" collapse of the arch, disproportionately painless.
• Chronic osteomyelitis with discharging sinus — sinus opening over the tibia with surrounding puckered scarring and seropurulent discharge; watch for Marjolin ulcer (everted malignant edges) in a long-standing sinus.
• Septic arthritis — grossly swollen, red, warm knee held in slight flexion, with the aspirate photograph showing frankly turbid purulent synovial fluid.

 

SECTION 21  |  Important Radiology Images

Plain radiography

• Soft-tissue gas — linear or feathery lucencies dissecting along fascial planes and muscle bundles in gas gangrene or Type I necrotising fasciitis. Highly specific, but present in only about half of cases — absence never excludes the diagnosis. [VERY HIGH-YIELD]
• Acute osteomyelitis — earliest change is deep soft-tissue swelling with loss of fat planes; bone changes (lytic destruction, periosteal reaction) appear only after 10–14 days and ~30–50% loss of bone mineral.
• Chronic osteomyelitis — sequestrum (dense sclerotic detached fragment) lying within a lucent cavity, surrounded by involucrum (new periosteal bone) with a cloaca.
• Brodie abscess — well-defined lucent metaphyseal lesion with a surrounding rim of reactive sclerosis, classically in the proximal tibia of an adolescent.
• Diabetic foot osteomyelitis — cortical erosion, periosteal reaction and destruction of the metatarsal head or phalanx beneath an ulcer.
• Charcot neuroarthropathy — fragmentation, dislocation, debris and midfoot collapse with preserved bone density — the key contrast with osteomyelitis.
• Septic arthritis — early joint-space widening from effusion, then rapid uniform joint-space loss with subchondral erosion on serial films.
• Prosthetic-joint infection — periprosthetic lucency >2 mm, implant migration or subsidence, focal osteolysis and periosteal new bone on serial radiographs.

Ultrasound

• Cutaneous abscess — anechoic or hypoechoic collection with posterior acoustic enhancement, internal debris and the "squish sign" on probe compression; distinguishes drainable pus from phlegmon.
• Necrotising fasciitis — thickened fascia with fluid tracking >4 mm along the deep fascial plane and subcutaneous air producing dirty shadowing.
• Septic arthritis / hip effusion in a child — anechoic joint effusion with capsular distension; guides aspiration.

CT

• Psoas abscess — enlarged psoas muscle containing a low-attenuation collection with rim enhancement, with or without gas; look for adjacent vertebral destruction suggesting tubercular (Pott) origin.
• Necrotising soft-tissue infection — fascial thickening, fat stranding, non-enhancing fascia and gas tracking along fascial planes.
• Fournier gangrene — perineal and scrotal wall thickening with subcutaneous gas.
• Sternoclavicular and sacroiliac joint infection — bone erosion, joint-space widening and adjacent soft-tissue or retrosternal abscess.

MRI

• Pyomyositis — enlarged muscle, hyperintense on T2/STIR with rim-enhancing intramuscular abscess on post-gadolinium T1; distinguishes early diffuse (stage 1) from suppurative (stage 2) disease.
• Osteomyelitis — low signal on T1, high signal on T2/STIR marrow oedema with post-contrast enhancement; the investigation of choice, positive within 3–5 days.
• Diabetic foot — differentiates osteomyelitis (confluent marrow T1 hypointensity) from Charcot foot (subchondral, periarticular changes with deformity), and demonstrates deep abscess and sinus tracts.
• Vertebral osteomyelitis/discitis — disc-space narrowing with T2 hyperintensity, endplate erosion of two contiguous vertebrae and paravertebral or epidural abscess; in tubercular spondylitis the disc is relatively preserved with large paravertebral cold abscess and subligamentous spread.
• Necrotising fasciitis — thick (>3 mm) hyperintense deep fascial signal on T2/STIR with non-enhancement of necrotic fascia; sensitive but must never delay surgery.
• Sacroiliitis — unilateral bone marrow oedema, joint-space fluid and capsular enhancement.

Nuclear imaging

• Three-phase bone scan — increased uptake in all three phases in osteomyelitis; sensitive but non-specific, and remains positive up to a year after surgery.
• Labelled-leucocyte scan with bone marrow imaging — the most accurate nuclear technique for prosthetic-joint and diabetic-foot infection.
• FDG-PET/CT — high sensitivity for chronic and vertebral osteomyelitis and for implant infection; useful where MRI is contraindicated.

 

SECTION 22  |  Important Microbiology and Histopathology Slides

Gram stain and smear

• Staphylococcus aureus — Gram-positive cocci in grape-like clusters with abundant neutrophils; on blood agar, golden-yellow beta-haemolytic colonies; coagulase and catalase positive. Why it matters: the commonest organism in every part of this chapter.
• Streptococcus pyogenes — Gram-positive cocci in chains; beta-haemolytic, bacitracin-sensitive, PYR positive, Lancefield group A. Why it matters: erysipelas, Type II necrotising fasciitis, streptococcal toxic shock.
• Clostridium perfringens — large, brick-shaped ("boxcar") Gram-positive bacilli with characteristically scanty neutrophils in wound exudate; double-zone haemolysis on blood agar; Nagler reaction positive (lecithinase/alpha toxin neutralised by antitoxin). Why it matters: the classic examination smear of gas gangrene. [FAVORITE EXAM QUESTION]
• Vibrio vulnificus — curved Gram-negative bacilli; grows on TCBS; from bulla fluid or blood in a cirrhotic patient with seawater exposure.
• Pasteurella multocida — small Gram-negative coccobacilli from a cat-bite wound; bipolar staining.
• Neisseria gonorrhoeae — Gram-negative intracellular diplococci within neutrophils; oxidase positive; grows on Thayer–Martin medium.
• Polymicrobial "dishwater" pus of Type I necrotising fasciitis — mixed Gram-positive cocci, Gram-negative bacilli and Gram-variable anaerobes together.
• Mycobacterium tuberculosis — acid-fast bacilli on Ziehl–Neelsen stain from synovial fluid, bone or cold abscess aspirate; confirm with CBNAAT/NAAT, which also detects rifampicin resistance under NTEP. [VERY HIGH-YIELD]

Histopathology

• Necrotising fasciitis — frozen section showing fascial necrosis, dense neutrophilic infiltration, thrombosis of nutrient vessels (fascial thrombosis) and microorganisms within the fascial plane, with relative sparing of muscle.
• Clostridial myonecrosis — coagulative muscle necrosis with gas spaces, abundant bacilli and a striking paucity of inflammatory cells (leucocytes are lysed by alpha toxin).
• Acute osteomyelitis — marrow packed with neutrophils, congested vessels, bone trabecular necrosis and early osteoclastic resorption.
• Chronic osteomyelitis — dead bone with empty osteocyte lacunae (sequestrum), surrounding fibrosis, plasma-cell and lymphocyte infiltration, and reactive new bone formation.
• Tubercular osteomyelitis/arthritis — epithelioid cell granulomas with Langhans giant cells and central caseous necrosis.
• Prosthetic-joint infection — periprosthetic membrane with >5 neutrophils per high-power field in at least 5 fields (×400); lymphocyte-rich infiltrates instead suggest an aseptic wear-particle reaction. [COMMON MCQ]
• Marjolin ulcer — well-differentiated squamous cell carcinoma arising in the wall of a chronic osteomyelitis sinus.

Special microbiological techniques

• Implant sonication culture — explanted prosthesis in Ringer solution, low-energy ultrasound dislodges biofilm, quantitative culture of sonicate fluid (>50 CFU/mL significant). More sensitive than tissue culture, especially after antibiotics.
• Deep-tissue / bone biopsy culture — the gold standard in osteomyelitis and diabetic foot infection; superficial and sinus-tract swabs correlate poorly with bone pathogens and must not guide therapy. [VERY HIGH-YIELD]
• Prolonged 14-day incubation — required to recover Cutibacterium acnes in shoulder arthroplasty infection.
• D-test (double-disc diffusion) — detects inducible clindamycin resistance in erythromycin-resistant S. aureus; a positive D-shaped zone contraindicates clindamycin.
• PVL gene and SCCmec typing — characterises community-associated MRSA in recurrent furunculosis and severe necrotising SSTI.
• 16S rRNA PCR and metagenomic sequencing — for culture-negative osteomyelitis and prosthetic-joint infection.

 

SECTION 23  |  Rapid Revision — High-Yield One-Liners

SKIN AND SOFT-TISSUE INFECTIONS ▪  Commonest organism in SSTI overall — Staphylococcus aureus. ▪  Honey-coloured golden crust — non-bullous impetigo. ▪  Impetigo complication that antibiotics do not prevent — post-streptococcal glomerulonephritis. ▪  Toxin in bullous impetigo and SSSS — exfoliative toxin A/B cleaving desmoglein-1. ▪  Nikolsky positive, mucosa spared, cleavage in granular layer — SSSS; mucosa involved with full-thickness necrosis — toxic epidermal necrolysis. ▪  Ulcerated impetigo extending into dermis and healing with a scar — ecthyma. ▪  Carbuncle site and association — nape of neck, diabetes mellitus. ▪  Hot-tub folliculitis organism — Pseudomonas aeruginosa. ▪  Treatment of an abscess — incision and drainage (ubi pus, ibi evacua). ▪  Erysipelas — sharply demarcated raised edge, S. pyogenes, penicillin. ▪  Bilateral lower-limb "cellulitis" — think stasis dermatitis, not infection. ▪  Coral-red Wood lamp fluorescence — erythrasma (Corynebacterium minutissimum).

NECROTISING AND MUSCLE INFECTIONS ▪  Single most important early clue to necrotising fasciitis — pain out of proportion to physical findings. ▪  Type II necrotising fasciitis organism — group A Streptococcus. ▪  Necrotising fasciitis of the perineum — Fournier gangrene. ▪  Marine Gram-negative necrotising infection in a cirrhotic — Vibrio vulnificus. ▪  Antibiotic added specifically to switch off exotoxin production — clindamycin (Eagle effect). ▪  Definitive treatment of necrotising fasciitis — immediate radical surgical debridement; imaging must never delay it. ▪  Spontaneous gas gangrene organism and its sinister association — Clostridium septicum with colonic carcinoma. [VERY HIGH-YIELD] ▪  C. perfringens major lethal toxin — alpha toxin (lecithinase/phospholipase C). ▪  Commonest organism of tropical pyomyositis — S. aureus; commonest muscle — quadriceps. ▪  Investigation of choice for pyomyositis and psoas abscess — MRI (CT for psoas).

BITES, DIABETIC FOOT AND BONE ▪  Cat bite organism with rapid onset — Pasteurella multocida. ▪  Clenched-fist injury organism — Eikenella corrodens. ▪  Fulminant sepsis after dog bite in an asplenic patient — Capnocytophaga canimorsus. ▪  Drug of choice for bite-wound prophylaxis — amoxicillin–clavulanate. ▪  Category III rabies exposure — vaccine + immunoglobulin infiltrated into the wound. ▪  Commonest cause of non-traumatic lower-limb amputation — diabetic foot infection. ▪  Bedside test for diabetic foot osteomyelitis — probe-to-bone test. ▪  Investigation of choice for osteomyelitis — MRI; gold standard for diagnosis — bone biopsy with culture and histopathology. ▪  Plain radiograph in acute osteomyelitis is normal for — 10–14 days. ▪  Dead bone in chronic osteomyelitis — sequestrum; new surrounding bone — involucrum; its opening — cloaca. ▪  Subacute localised osteomyelitis in the metaphysis — Brodie abscess. ▪  Osteomyelitis organism in sickle-cell disease — Salmonella. ▪  Malignancy in a chronic osteomyelitis sinus — Marjolin ulcer (squamous cell carcinoma).

JOINTS AND IMPLANTS ▪  Commonest organism in native septic arthritis — S. aureus; commonest joint in adults — knee; in infants — hip. ▪  Investigation of choice — synovial fluid aspiration before antibiotics. ▪  Synovial WBC suggesting native-joint sepsis — >50,000/mm³ with >75% neutrophils. ▪  Crystals in the aspirate — do not exclude infection. ▪  Criteria for septic arthritis versus transient synovitis in a child — Kocher criteria. ▪  Triad of disseminated gonococcal infection — tenosynovitis, dermatitis, migratory polyarthralgia. ▪  Kanavel signs — flexor tendon sheath infection. ▪  Emergency arthrotomy is mandatory in — septic arthritis of the hip in a child. ▪  Intra-articular antibiotics — never used. ▪  Organism of indolent shoulder prosthesis infection — Cutibacterium acnes (14-day culture). ▪  Pathognomonic of prosthetic-joint infection — sinus tract communicating with the prosthesis. ▪  Most sensitive test for biofilm organisms — implant sonication. ▪  Anti-biofilm agents — rifampicin (staphylococci) and fluoroquinolones (Gram-negatives); never rifampicin alone. ▪  Gold-standard surgery for chronic prosthetic-joint infection — two-stage revision.

INDIAN PUBLIC-HEALTH AND STEWARDSHIP ANCHORS ▪  Osteoarticular and spinal tuberculosis is treated under the National TB Elimination Programme (NTEP) with 12 months of ATT; CBNAAT is the first-line molecular test and also reports rifampicin resistance. ▪  Rabies post-exposure prophylaxis follows National Rabies Control Programme categories; India accounts for a large share of global rabies deaths, and dog bite is the commonest exposure. ▪  Tetanus prophylaxis for every contaminated wound; immunisation status is recorded under the Universal Immunisation Programme. ▪  Diabetes prevalence makes diabetic foot infection the single largest driver of admission and amputation in Indian SSTI practice; multidisciplinary foot clinics and footwear/off-loading education are the cornerstone of prevention. ▪  Empirical MRSA and carbapenem use must follow local antibiograms and the National Action Plan on Antimicrobial Resistance (NAP-AMR) and ICMR treatment guidelines — de-escalate on culture, document indication and duration.

 

End of Part 2 — Bacterial Infections of the Skin, Soft Tissues and Bones

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