Cutaneous Tuberculosis

Cutaneous tuberculosis (TB) is a heterogeneous group of skin infections caused by Mycobacterium tuberculosis (and rarely M. bovis or attenuated BCG), classified by the route of infection and the host's immune status. Though only ~1–2% of all TB, it is a recurring NEET PG favourite for its classic morphology — the apple-jelly nodule of lupus vulgaris, scrofuloderma over lymph nodes, and the immunological "tuberculids."

Definition & classification

Cutaneous TB is a chronic granulomatous skin disease. Lesions are classified by how the organism reaches the skin (exogenous vs endogenous) and whether bacilli are demonstrable (true TB = multibacillary/paucibacillary with organisms; tuberculids = hypersensitivity reaction, organisms usually absent but PCR may be positive).

A practical, exam-oriented classification rests on the host's prior sensitisation and immune competence:

Type	Route / mechanism	Mantoux	Bacillary load	Classic clinical picture
Tuberculous chancre (primary inoculation)	Exogenous, no prior immunity	Negative → becomes positive	Multibacillary	Painless ulcer + regional lymphadenopathy (cutaneous "primary complex")
TB verrucosa cutis (TBVC)	Exogenous re-infection in sensitised host	Strongly positive	Paucibacillary	Warty verrucous plaque on hand/foot ("prosector's wart")
Lupus vulgaris	Endogenous (haematogenous/lymphatic) or exogenous, high immunity	Strongly positive	Paucibacillary	Reddish-brown plaque with apple-jelly nodules, head & neck
Scrofuloderma	Contiguous spread from node/bone/joint	Positive	Multibacillary	Cold abscess → undermined ulcers + bridging scars over neck
Orificial (TB cutis orificialis)	Autoinoculation, low immunity	Often negative (anergy)	Multibacillary	Painful punched-out ulcers at mucocutaneous junctions
Acute miliary TB of skin	Haematogenous in severe immunosuppression	Negative (anergy)	Multibacillary	Crops of papulovesicles/purpura, very ill patient
Metastatic TB abscess (gumma)	Haematogenous in malnourished/immunosuppressed	Variable	Multibacillary	Fluctuant subcutaneous cold abscess(es)

High-yield: The two multibacillary, low-immunity forms — orificial TB and acute miliary TB — typically show a negative Mantoux (anergy) and carry a poor prognosis. The paucibacillary, high-immunity forms — lupus vulgaris and TBVC — show a strongly positive Mantoux. This Mantoux–bacillary-load inverse relationship is repeatedly tested.

Tuberculids

Tuberculids are symmetrical eruptions thought to be an id (hypersensitivity) reaction to M. tuberculosis antigens in a person with moderate-to-high immunity and a focus of TB elsewhere. Mantoux is strongly positive; organisms are scanty/absent on smear and culture, though PCR may detect mycobacterial DNA. They resolve with anti-tubercular therapy (ATT) — a key diagnostic clue.

Tuberculid	Morphology	Site	Histology hallmark
Lichen scrofulosorum	Tiny grouped follicular/perifollicular lichenoid papules, asymptomatic	Trunk (often with underlying nodal/bone TB, common in children)	Superficial dermal tuberculoid granulomas around follicles/ducts
Papulonecrotic tuberculid	Crops of dusky papules with central necrosis → varioliform scars	Extensor limbs, buttocks	Wedge-shaped dermal necrosis + leucocytoclastic/granulomatous vasculitis
Erythema induratum of Bazin (nodular vasculitis)	Tender erythematous nodules that ulcerate	Calves (posterior legs) of young women	Lobular panniculitis with vasculitis

High-yield: Lichen scrofulosorum — grouped lichenoid papules on the trunk of a child with lymph-node/bone TB. Papulonecrotic tuberculid — necrotic papules on extensors healing with varioliform (pock-like) scars. Erythema induratum of Bazin — ulcerating nodules on the calves of young women (lobular panniculitis). These three eponymic/site associations are the most asked tuberculid facts.

Etiology & pathophysiology

The causative organism is Mycobacterium tuberculosis (acid-fast bacillus, Ziehl–Neelsen / auramine positive). M. bovis and the BCG strain cause similar disease, the latter as a vaccination complication (BCG-itis, regional lymphadenitis, or rarely lupus vulgaris at the vaccination site).

The clinical form is governed by an interplay of:

1. Route — exogenous inoculation (chancre, TBVC), contiguous spread (scrofuloderma), haematogenous/lymphatic dissemination (lupus vulgaris, miliary, gumma), or autoinoculation from one's own secretions (orificial).
2. Host cell-mediated immunity (CMI) — a robust Th1/delayed-type hypersensitivity response produces tightly organised tuberculoid granulomas, few bacilli, and a strongly positive Mantoux (lupus vulgaris, TBVC, tuberculids). Poor CMI gives multibacillary, poorly formed granulomas, anergy, and severe disease (orificial, miliary).

Pathogenesis flow: bacillary entry → uptake by dermal macrophages → antigen presentation → CMI (Th1, IFN-γ, TNF-α) → epithelioid + Langhans giant cell granuloma formation → caseation necrosis (variable) → fibrosis/scarring or progressive tissue destruction depending on immune balance.

High-yield: The classic histology of cutaneous TB is the tuberculoid granuloma — central caseous necrosis surrounded by epithelioid histiocytes and Langhans giant cells, with a peripheral lymphocyte cuff. Lupus vulgaris characteristically shows granulomas with little or no caseation; scrofuloderma shows massive caseation.

Clinical features (form by form)

Lupus vulgaris — the most common form in many series. A slowly extending, reddish-brown to apple-jelly–coloured plaque, predilection for the head and neck (in India also buttocks/limbs). Characteristic central scarring with peripheral active extension; new nodules can appear within old scars (a hallmark of its chronicity). Long-standing lesions risk malignant transformation.

High-yield: On diascopy (pressing a glass slide on the lesion to empty cutaneous blood), lupus vulgaris reveals "apple-jelly" nodules — translucent yellowish-brown granulomas. This is the single most frequently asked clinical sign of cutaneous TB.

TB verrucosa cutis — asymptomatic, slowly growing verrucous/warty plaque with an irregular border, usually on the hand, knee or foot (sites of trauma in sensitised individuals, e.g. butchers, pathologists — "prosector's wart", or "anatomist's wart"). No regional lymphadenopathy. Heals with scarring.

Scrofuloderma — overlies an infected lymph node (cervical/supraclavicular), bone or joint. Begins as a firm subcutaneous nodule → cold abscess → breakdown into undermined, ragged ulcers and sinuses discharging caseous material → heals with characteristic puckered, bridging ("rope-like") scars. Most common form in children in some Indian studies.

Tuberculous chancre — at a site of inoculation (minor trauma), a painless brownish papule/nodule → shallow ulcer with undermined edge + regional lymphadenopathy ("primary cutaneous complex"), in a non-sensitised host (children).

Orificial TB — painful, soft, punched-out ulcers with a "swollen" yellowish base at mucocutaneous junctions (mouth, anus, genitalia) due to autoinoculation from advanced pulmonary, intestinal or GU TB. Marker of poor prognosis.

Acute miliary TB of skin — crops of bluish papules, vesicles, pustules or purpuric lesions in an acutely ill, often immunosuppressed (HIV, infants) patient with disseminated TB.

Metastatic tuberculous abscess (gumma) — single or multiple non-tender fluctuant subcutaneous nodules that break down into abscesses/sinuses, in malnourished or immunosuppressed hosts.

Diagnosis & investigation of choice

Diagnosis combines morphology, tuberculin (Mantoux) testing, histopathology, and microbiological/molecular confirmation.

Diagnostic approach (stepwise):

Clinical morphology + diascopy → Mantoux/IGRA → Skin biopsy for histopathology (granuloma) → ZN stain & culture (gold standard) ± PCR/GeneXpert → screen for systemic focus (CXR, nodal/bone imaging) → therapeutic trial of ATT if confirmation difficult.

• Mantoux test (tuberculin/PPD): read at 48–72 hours; ≥10 mm induration is positive in the immunocompetent (≥5 mm if immunocompromised). Strongly positive in lupus vulgaris, TBVC and tuberculids; negative (anergic) in orificial and miliary forms.
• Histopathology: tuberculoid granuloma (epithelioid cells, Langhans giant cells, caseation, lymphocytes). The investigation that establishes the tissue diagnosis in paucibacillary forms.
• AFB demonstration: ZN stain of tissue/discharge — positive mainly in multibacillary forms (scrofuloderma, orificial, miliary). Often negative in lupus vulgaris/TBVC.
• Culture (Lowenstein–Jensen / liquid BACTEC MGIT) = the definitive / gold-standard confirmation but slow (weeks) and low-yield in paucibacillary disease.
• NAAT (PCR / CBNAAT–GeneXpert MTB/RIF): rapid, detects DNA even when smear/culture negative, and gives rifampicin-resistance status — increasingly the practical investigation of choice, especially in paucibacillary lesions and tuberculids.
• IGRA (QuantiFERON-TB Gold / T-SPOT): confirms TB infection, not affected by prior BCG; useful where Mantoux is equivocal.

High-yield: Culture remains the gold standard for confirmation, but for rapid diagnosis with paucibacillary lesions and in tuberculids, PCR/CBNAAT is the most useful test. Histopathology is the key initial confirmatory investigation for lupus vulgaris and TBVC where bacilli are scant.

Management / drug of choice

Cutaneous TB is treated with standard multidrug anti-tubercular therapy (ATT) identical in principle to systemic TB, as per RNTCP/NTEP and WHO regimens.

• Intensive phase (2 months): HRZE — isoniazid (H), rifampicin (R), pyrazinamide (Z), ethambutol (E).
• Continuation phase (4 months): HR — isoniazid + rifampicin.

Total 6 months for most forms; extended (9–12 months) may be needed for extensive lupus vulgaris, bone/joint-related scrofuloderma, or poor response. Adjunctive surgery (excision of small lupus vulgaris plaques, drainage of cold abscesses, node excision) is occasionally used. Pyridoxine (vitamin B6) is given to prevent isoniazid neuropathy.

Drug	Key adverse effect (most tested)
Isoniazid (H)	Peripheral neuropathy (prevent with pyridoxine), hepatitis
Rifampicin (R)	Hepatitis, orange-red secretions, drug interactions (enzyme inducer)
Pyrazinamide (Z)	Hyperuricaemia/arthralgia, hepatotoxic
Ethambutol (E)	Retrobulbar (optic) neuritis — dose-related, reversible

High-yield: A good response to ATT is itself diagnostically supportive — tuberculids (especially lichen scrofulosorum) clear within a few weeks of starting ATT, confirming their tuberculous aetiology.

Complications

• Squamous cell carcinoma arising in long-standing lupus vulgaris scars ("lupus carcinoma") — the most important late complication; basal cell carcinoma is less common.
• Disfiguring scarring & contractures, destruction of cartilage/nose ("lupus" tissue destruction historically), ectropion.
• Lymphoedema from chronic lymphatic involvement.
• Secondary bacterial infection of ulcers.
• Underlying systemic TB (pulmonary, nodal, skeletal) — must always be sought, as cutaneous lesions may be the visible tip of disseminated disease.

High-yield: SCC is the classic malignancy complicating chronic lupus vulgaris — any new growth/ulceration/induration in a long-standing plaque warrants biopsy.

Key differentials

Cutaneous TB form	Important differentials
Lupus vulgaris	Sarcoidosis (lupus pernio), discoid lupus erythematosus, leishmaniasis, lupoid leprosy, deep mycoses, tertiary syphilis
TB verrucosa cutis	Chromoblastomycosis, blastomycosis, verruca vulgaris, hypertrophic lichen planus, SCC
Scrofuloderma	Atypical mycobacterial infection, actinomycosis, sporotrichosis, hidradenitis suppurativa, lymphoma
Orificial TB	Aphthous/major ulcers, SCC, syphilitic ulcer, Crohn's orofacial disease
Erythema induratum (Bazin)	Erythema nodosum, polyarteritis nodosa, pancreatic panniculitis, nodular vasculitis of other cause
Papulonecrotic tuberculid	PLEVA (Mucha–Habermann), prurigo, secondary syphilis, vasculitis

High-yield: Lupus vulgaris vs lupus pernio (sarcoid): apple-jelly nodules on diascopy + caseating granuloma + positive Mantoux favour TB; non-caseating "naked" granulomas + raised ACE + violaceous nose/ear plaques favour sarcoidosis. Erythema nodosum vs erythema induratum: EN = tender nodules on shins (anterior), septal panniculitis, does NOT ulcerate; EIB = calves (posterior), lobular panniculitis with vasculitis, ulcerates.

Mnemonics & memory hooks

• Multibacillary forms (organisms plenty, immunity low, Mantoux often negative): "SOM-A" — Scrofuloderma, Orificial, Miliary, Abscess (gumma) + tuberculous chancre.
• Paucibacillary / high-immunity, Mantoux strongly positive: Lupus vulgaris, TBVC, and the tuberculids.
• Tuberculids on the calf of a young woman = Erythema induratum of Bazin ("Bazin = Back of leg").
• ATT regimen: "RIPE" for 2 months, then RI (rifampicin + isoniazid) for 4 months.

Recently asked / exam angle

NEET PG and INI-CET have repeatedly tested cutaneous TB through pattern-recognition and one-liner association MCQs:

• "Apple-jelly nodules on diascopy" → Lupus vulgaris (single most common stem).
• Classification by route of infection / immune status — match the form to exogenous vs endogenous spread and to Mantoux positivity (the multibacillary-anergic vs paucibacillary-reactive dichotomy).
• "Prosector's/anatomist's wart" in a pathologist or butcher → TB verrucosa cutis.
• Bridging/cord-like scars over cold abscess of cervical nodes → Scrofuloderma.
• Grouped lichenoid follicular papules on the trunk of a child with nodal TB → Lichen scrofulosorum, clears rapidly with ATT.
• Necrotic papules on extensors healing with varioliform scars → Papulonecrotic tuberculid.
• Ulcerating tender nodules on the calf of a young woman → Erythema induratum of Bazin (lobular panniculitis with vasculitis).
• SCC arising in a long-standing facial plaque → complication of lupus vulgaris.
• Investigation of choice / gold standard — culture is gold standard; CBNAAT/PCR for rapid/paucibacillary; histology for tissue confirmation.
• Histology image of caseating granuloma with Langhans giant cells mapped to cutaneous TB.

Rapid revision

1. Cutaneous TB is classified by route of infection and host immunity; commonest forms in India are lupus vulgaris and scrofuloderma.
2. Apple-jelly nodules on diascopy = lupus vulgaris; head & neck plaque with central scarring + peripheral extension.
3. Lupus vulgaris histology — granulomas with minimal caseation; scrofuloderma — massive caseation with cold abscess and bridging scars.
4. TB verrucosa cutis = warty plaque from exogenous re-infection in a sensitised host = "prosector's wart."
5. Orificial and acute miliary TB are multibacillary, low-immunity forms with a negative (anergic) Mantoux and poor prognosis.
6. Tuberculids are hypersensitivity reactions — strongly positive Mantoux, scanty organisms, resolve with ATT.
7. Lichen scrofulosorum = grouped follicular lichenoid papules on the trunk of a child with nodal TB.
8. Papulonecrotic tuberculid = necrotic papules on extensors → varioliform scars.
9. Erythema induratum of Bazin = ulcerating nodules on the calves of young women; lobular panniculitis with vasculitis (contrast with septal, shin-based, non-ulcerating erythema nodosum).
10. Culture = gold standard; CBNAAT/PCR for rapid and paucibacillary confirmation; Mantoux read at 48–72 h, ≥10 mm positive.
11. Treatment = standard ATT — 2 months HRZE + 4 months HR; extend for extensive/skeletal disease; give pyridoxine.
12. Squamous cell carcinoma is the classic malignant complication of chronic lupus vulgaris; ethambutol's hallmark toxicity is optic neuritis.