Cutaneous Tuberculosis

On this page
  1. Direct answer
  2. What you must remember
  3. Mapping a lesion to its mechanism
  4. The Indian reality
  5. Frequently asked questions
  6. Related topics

Direct answer

A slowly enlarging plaque with apple-jelly (translucent, yellow-brown) nodules on diascopy over the face or neck of a patient in TB-endemic India is lupus vulgaris — the commonest form of cutaneous tuberculosis in India, arising haematogenously in a sensitised host with long-term squamous carcinoma risk. The spectrum spans exogenous inoculation (primary TB chancre in the non-immune, tuberculosis verrucosa cutis in the sensitised), endogenous spread (scrofuloderma from an underlying lymph node, orificial tuberculosis of mucocutaneous junctions in advanced disease, miliary and gummatous forms), and the paucibacillary immunological tuberculids — papulonecrotic tuberculid and erythema induratum of Bazin. Diagnosis rests on biopsy with caseating granulomas plus AFB, supported by NAAT/CBNAAT and culture per National TB Elimination Programme algorithms; treatment is standard antitubercular therapy.

What you must remember

  • Classification logic: route (exogenous inoculation versus endogenous spread) and host immunity (anergic hosts get multibacillary disease, sensitised hosts get paucibacillary) predict every form — learn the grid, not the list.
  • Lupus vulgaris: soft, brown-red plaque with apple-jelly nodules on diascopy, face and neck predilection, decades-long course, scarring and a recognised progression to squamous cell carcinoma — the commonest form in India.
  • Scrofuloderma: bluish, undermined sinus tracts and puckered scarring over a caseating lymph node — usually cervical; the commonest form in some paediatric Indian series.
  • Tuberculosis verrucosa cutis: warty, hyperkeratotic plaque at an inoculation site in a sensitised host (butchers, pathologists — the prosector's wart); TB chancre is its non-immune counterpart, an ulcer with regional nodes.
  • Orificial and miliary forms: autoinoculation at mucocutaneous orifices and haematogenous dissemination both signal poor immunity — search for pulmonary and other foci.
  • Tuberculids: papulonecrotic tuberculid (necrotic papules on extensor surfaces) and erythema induratum of Bazin (tender nodules on calves of young women, lobular panniculitis with vasculitis) — strongly positive tuberculin, lesions themselves culture-negative, responding to ATT.
  • Diagnosis: biopsy for caseating granulomas and AFB (organisms sparse in paucibacillary forms), NAAT/CBNAAT on tissue, culture with line-probe assay for resistance; tuberculin and IGRA are supportive, not diagnostic.
  • Treatment: daily antitubercular therapy per NTEP with the same regimen as pulmonary disease; response is judged clinically and lesions must be notified like any TB case.

Mapping a lesion to its mechanism

Three patients illustrate the grid. The first: a 45-year-old woman with a fifteen-year plaque over the cheek that shows apple-jelly nodules on pressed-glass diascopy — lupus vulgaris, haematogenous seeding in a sensitised host; biopsy for granulomas, chest imaging, NAAT on tissue, ATT, and long-term surveillance of any scar that ulcerates or thickens because squamous carcinoma is the feared late complication. The second: an 8-year-old with a discharging sinus above a matted cervical node and puckered surrounding skin — scrofuloderma, direct extension; aspirate the node for NAAT and test for HIV, then treat. The third: a young woman with recurrent tender calf nodules that ulcerate — erythema induratum of Bazin, a tuberculid: search for an active focus, expect the lesion itself to be culture-negative, and treat as tuberculosis. The warty plaque on a butcher's hand completes the set — tuberculosis verrucosa cutis, inoculation in an already-sensitised worker.

The skill being examined is the mapping: morphology plus host immunity predicts bacillary load, which predicts the yield of AFB staining and the risk of missing the diagnosis on smear alone.

The Indian reality

India carries the world's largest TB burden, and cutaneous disease is both under-recognised and over-treated: the two errors are steroid creams smothering lupus vulgaris into atypical plaques, and months of empirical ATT handed out for nonspecific granulomatous dermatoses without biopsy or NAAT. The corrective discipline: every chronic, progressive, scarring or ulcerating skin lesion in this country earns a biopsy and mycobacterial testing before the label; CBNAAT and line-probe assays are available free under the National TB Elimination Programme, so "no access" is no longer an excuse; and every treated case is notified. Two local contrasts worth quoting: sarcoidosis, the great mimicker, shows non-caseating granulomas and negative mycobacterial studies — the sarcoid-versus-TB decision is a genuinely Indian examination dilemma; and leishmaniasis and deep mycoses in the differential of chronic plaques explain why tissue must travel to mycology as well as bacteriology.

Frequently asked questions

Which is the commonest form of cutaneous tuberculosis in India?

Lupus vulgaris in most Indian series — a chronic facial plaque with apple-jelly nodules on diascopy and late malignant potential.

What does apple-jelly appearance on diascopy indicate?

Translucent yellow-brown lupus vulgaris granulations revealed by pressing a glass slide — a bedside sign of tubercular granuloma.

What are tuberculids?

Immunological reactions to haematogenous mycobacterial antigen — papulonecrotic tuberculid and erythema induratum of Bazin — culture-negative lesions with strong tuberculin responses that settle on ATT.

How is cutaneous tuberculosis confirmed?

Biopsy showing caseating granulomas with AFB plus NAAT/CBNAAT and culture on tissue; tuberculin and IGRA only support the diagnosis.

Where does erythema induratum of Bazin occur?

Tender, sometimes ulcerating nodules on the posterior calves of young women — a lobular panniculitis with vasculitis treated as tuberculosis.

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