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๐ CLINICAL LEPROSY - Dermatology Resident Study Note
Chapter 2.1 - Jopling's Handbook of Leprosy (6th Ed.)
Authors: Kabir Sardana, Premanshu Bhushan, Ananta Khurana
1. INTRODUCTION & MICROBIOLOGY
| Feature | Detail |
|---|---|
| Causative organism | Mycobacterium leprae |
| Discovery | G.A. Hansen, Norway, 1873 (published 1874) |
| Significance | Oldest known bacterium pathogenic to humans |
| Related species | M. lepromatosis - diverged from common ancestor after massive gene inactivation |
| Laboratory growth | Footpads of mice (Shepard); optimal inoculum ~10ยณ bacilli (<10โถ required) |
| Disseminated animal model | Rees, 1966 - thymectomized + irradiated mice |
| Incubation period | 3-5 years (range: 2 months - 10 years) |
| Target cell | Schwann cell of peripheral nerves |
| Route of nerve infection | Colonization of epineurial vessels โ endoneurial infection |
| Susceptibility | Only ~5% of exposed individuals develop clinical disease |
Nerve anatomy (relevant to leprosy):
NERVE STRUCTURE
โโโ Epineurium (outer coat - loose connective tissue, first colonized)
โโโ Perineurium (multilayered, encloses fascicles)
โโโ Fascicle = axons + Schwann cells
โโโ Endoneurium (fine layer around Schwann cells and axons - site of infection)
๐ Clinical Pearl: The predilection for cool areas of the body explains why earlobes, nose tip, dorsum of hands/feet, and peripheral nerves at bony prominences are preferentially affected.
2. CLASSIFICATION OF LEPROSY
Why Classify? (7 Reasons)
- Estimate immunological status and stability
- Assess infectivity
- Predict prognosis and likelihood of complications/reactions
- Guide treatment (drugs + duration)
- Uniform nomenclature for scientific discourse
- Correlate clinical and histological features
- Explain host-parasite relationship
Historical Classification Timeline
| Year | Classification | Key Terms Introduced |
|---|---|---|
| 1848 | Danielssen & Boeck | Nodular vs Anesthetic |
| 1895 | Hansen & Looft | Tuberous vs Maculoanesthetic |
| 1931 | Manila | Cutaneous / Neural / Mixed |
| 1938 | Cairo | Lepromatous (for cutaneous) |
| 1946 | Pan-American | Tuberculoid; "Uncharacteristic" |
| 1948 | Havana | "Indeterminate" introduced |
| 1952 | WHO Expert Committee | 4 groups: L, B, T, I |
| 1953 | Madrid | 2 stable poles (TT, LL) + 2 unstable (I, B) |
| 1955 | Indian Classification | 6 types: T, B, L, I, MA, P |
| 1966 | Ridley-Jopling | TT, BT, BB, BL, LL (immunological basis) |
| 1981 | New IAL | 5 groups: I, T, B, L, P (merged MA into T) |
| 1982 | WHO operational | PB (โค5 lesions) vs MB (โฅ6 lesions) |
The Ridley-Jopling Classification (Most Important)
Basis: 4 parameters - Clinical + Histological + Bacteriological (SSS) + Immunological (Lepromin)
HIGH CMI โโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโ LOW CMI
TT BT BB BL LL
(Tuberculoid) (BT) (Mid-border) (BL) (Lepromatous)
STABLE UNSTABLE UNSTABLE UNSTABLE STABLE
- TT & LL: Immunologically stable poles
- BT, BB, BL: Unstable - may upgrade (toward TT) or downgrade (toward LL)
WHO Operational Classification (Field Use)
| Feature | PB (Paucibacillary) | MB (Multibacillary) |
|---|---|---|
| Skin lesions | 1-5 | โฅ6 |
| Peripheral nerves involved | 0 or 1 | >1 |
| Skin smear | Negative at all sites | Positive at any site |
โ ๏ธ Note (NLEP India 2009): If ANY one feature is MB, classify as MB.
3. LEPROSY SPECTRUM - CLINICAL FEATURES IN DETAIL
3A. INDETERMINATE LEPROSY
- Earliest clinically apparent lesion
- One or a few hypopigmented macules - faint, ill-defined
- No granuloma on histology; no bacilli; no immunological response yet
- May spontaneously heal (especially in children)
- Common sites: gluteal region, back, arms
๐ Clinical Pearl: Indeterminate leprosy is a diagnosis of exclusion. The skin smear is negative, lepromin may be weakly positive or negative. It can evolve to any type depending on immune response.
3B. TUBERCULOID LEPROSY (TT)
| Parameter | TT Features |
|---|---|
| Lesion number | 1-3 (very few) |
| Morphology | Macule or plaque |
| Border | Well-defined, raised, outer edge sloping inward |
| Surface | Dry, scaly, hairless |
| Sensation | Completely anesthetic |
| Color | Hypopigmented (in dark skin); erythematous (in pale skin) |
| Distribution | Asymmetrical |
| AFB (SSS) | Negative (0) |
| Lepromin test | Strongly positive (Mitsuda โฅ5mm) |
| CMI | High |
Nerve involvement: Single nerve trunk enlarged near the skin lesion. The nerve supplying the patch is characteristically enlarged.
๐ Clinical Pearl: In TT, "the nerve that supplies the patch is always enlarged" - this is pathognomonic. Test sensation WITH the lesion in bright light, and always palpate the relevant nerve.
3C. BORDERLINE LEPROSY (BT, BB, BL)
Most common type globally (often misclassified as TT)
Key differences across the borderline spectrum:
| Feature | BT | BB | BL |
|---|---|---|---|
| Lesion number | Few - many | Many | Many - numerous |
| Border definition | Well-defined mostly | Irregular, "punched out" | Ill-defined |
| Surface | Dry, may scale | Intermediate | Shiny, smooth |
| Anesthesia | Moderate | Partial | Mild |
| AFB (SSS) | Scanty/absent | Always present | Numerous (small globi) |
| Lepromin | Positive | Negative | Negative |
| Satellite lesions | May be present | Classic feature | May be present |
The "Swiss cheese" or "punched-out" lesion: Classic BB pattern - hypopigmented center with a raised, reddish outer ring and an "immune zone" appearing between center and outer ring.
Important clinical points for borderline leprosy:
- Immunological instability - can upgrade or downgrade
- Nerve damage is most severe and most frequent in borderline spectrum
- Polyneuritic phase may precede skin lesions
- Asymmetric nerve involvement is typical (e.g., left facial palsy + right ulnar thickening + left lateral popliteal nerve)
Geographic pattern: BT predominates in Africans; BL predominates in Asians and Europeans (genetic difference in CMI expression).
๐ Clinical Pearl: Borderline leprosy has the HIGHEST risk of lepra reactions and nerve damage. A patient with multiple asymmetrically enlarged nerves and satellite lesions = BT/BB.
3D. LEPROMATOUS LEPROSY (LL)
| Subtype | Description |
|---|---|
| LLs (subpolar LL) | Down-graded from borderline; most common form |
| LLp (polar LL) | Primary LL; inherent immune defect; rarer |
Prodromal symptoms (before skin lesions):
- Nasal symptoms: Stuffiness, crust formation, blood-stained discharge
- Bilateral ankle/leg edema: Worst at day-end, disappears overnight; late stages = "woody hard"
Skin lesions:
- Multiple, bilaterally symmetrical
- Macules appear first โ papules โ nodules
- Color: Erythematous (pale skin); coppery or faint hypopigmented (dark skin)
- Edges: Indefinite (no immune response to create contrast)
- Sensation: Lost late in LL (unlike TT where it is lost early)
Advanced LL features (Leonine facies complex):
HEAD-TO-TOE ADVANCED LL CHANGES
โโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโ
โ FACE: Leonine facies โ
โ Superciliary + ciliary madarosis โ
โ Thickened ear lobes โ
โ Saddle nose (septal perforation) โ
โ Collapsed nose โ
โ "Stern" leprous stare โ
โ VOICE: Hoarseness (laryngeal involvement)โ
โ TEETH: Upper incisor loosening/loss โ
โ LIMBS: "Glove and stocking" anesthesia โ
โ Ichthyosis (thighs, legs) โ
โ Shortening of digits (trauma) โ
โ LEGS: Bilateral symmetrical edema โ
โโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโ
๐ Clinical Pearl: In LL, "macules are best seen in bright sunlight with oblique rays" and become more prominent with heat/exercise. SSS from ear lobes is the highest-yield site in LL.
4. COMPARISON TABLE: ALL TYPES
| Feature | TT | BT | BB | BL | LL |
|---|---|---|---|---|---|
| Lesions | 1-3 | Few-many | Many | Many | Innumerable |
| Edges | Sharp | Partly sharp | Irregular | Fading | Indefinite |
| Surface | Dry/scaly | Dry | Intermediate | Shiny | Shiny |
| Anesthesia | Complete | Moderate | Partial | Slight | Very late |
| AFB (BI) | 0 | 0-1 | 1-2 | 3-4 | 5-6 |
| Lepromin | +++++ | +++ | - | - | - |
| CMI | High | Moderate | Borderline | Low | Absent |
| Stability | Stable | Unstable | Unstable | Unstable | Stable |
| Reactions | Type 1 (rare) | Type 1 | Type 1 | Type 1+ENL | ENL |
| Granuloma | Compact, epithelioid | Epithelioid | Loose | Macro-foam | Foam cells |
| Globi | Absent | Absent | Rare | Small | Large |
5. NERVE INVOLVEMENT
Commonly Affected Nerves (in order of frequency):
| Nerve | Site of Palpation | Deficit |
|---|---|---|
| Ulnar | Behind medial epicondyle | Claw hand (4th-5th digits), loss of sensation medial 1.5 fingers |
| Common peroneal | Head of fibula | Foot drop, loss of sensation dorsum foot |
| Posterior tibial | Behind medial malleolus | Plantar anesthesia, intrinsic muscle loss (claw toes) |
| Radial cutaneous | Dorsum of wrist | Sensory loss dorsum hand |
| Median | Carpal tunnel | Thenar wasting, sensory loss lateral 3.5 fingers |
| Facial (VII) | Parotid region | Lagophthalmos (orbicularis weakness) |
| Trigeminal (V) | - | Corneal anesthesia |
| Greater auricular | Over SCM | Enlarged (especially in BT/BB) |
| Radial nerve | Spiral groove | Wrist drop |
Pure neuritic leprosy (PNL): ~18% of cases. No skin lesions, only nerve involvement. Commonest in India.
๐ Clinical Pearl: "The 4 thickened nerves of leprosy" - Greater auricular, Ulnar, Common peroneal, Posterior tibial. The greater auricular nerve is visible and palpable in the neck. Any visible nerve in the body (without cause) = leprosy till proven otherwise.
6. OCULAR LEPROSY
| Mechanism | Lesion |
|---|---|
| V nerve (corneal anesthesia) | Exposure keratitis, corneal ulcer |
| VII nerve (lagophthalmos) | Lagophthalmos โ ectropion โ exposure keratitis โ corneal ulcer |
| Direct bacillary infiltration | Miliary lepromata (corneal), iritis, iris atrophy |
| Reaction | Acute iritis, scleritis (ENL) |
Ocular complications by spectrum:
| Complication | Spectrum |
|---|---|
| Lagophthalmos | Whole spectrum |
| Corneal hypoaesthesia | Whole spectrum |
| Acute iritis + scleritis | MB leprosy |
| Chronic iritis + iris atrophy | MB leprosy |
| Cataract | Whole spectrum |
Superficial punctate keratitis (LL specific): Milky haze in upper cornea with tiny white spots ("grains of chalk") = miliary lepromata. Pannus starts at superior lateral limbus (unlike trachoma, which is upper central).
๐ Clinical Pearl: Leprous iritis is characteristically "miotic and fixed" - due to direct invasion of iris by bacilli with fibrosis. The classic "leprous pea" is a small, round, yellowish, gelatinous nodule at sclerocorneal junction (3 and 9 o'clock).
7. LEPRA REACTIONS
These are acute inflammatory episodes interrupting the chronic course of leprosy. They represent the MOST COMMON cause of nerve damage.
Type 1 Reaction (Reversal Reaction / T1R)
| Feature | Detail |
|---|---|
| Immunological basis | Delayed hypersensitivity (Type IV) - sudden CMI upregulation |
| Occurs in | Borderline spectrum (BT, BB, BL) ONLY |
| Timing | Any time - during/after treatment |
| Skin features | Existing lesions become erythematous, oedematous, tender |
| New lesions | May appear |
| Nerve features | Acute neuritis - pain, tenderness, rapid loss of function |
| Systemic features | Absent (no fever usually) |
| Treatment | Prednisolone (standard WHO regimen 40mg/day tapered) |
Upgrading vs Downgrading T1R:
- Upgrading (reversal): On treatment, moves toward TT pole
- Downgrading: Without treatment, moves toward LL pole (usually silent)
Type 2 Reaction - Erythema Nodosum Leprosum (ENL)
| Feature | Detail |
|---|---|
| Immunological basis | Immune complex disease (Type III) - Arthus-type |
| Occurs in | MB leprosy (BL, LL) |
| Timing | Usually after starting treatment (or spontaneously in untreated) |
| Skin features | Crops of painful, tender, erythematous nodules on extensor surfaces |
| Systemic features | Fever, malaise, arthralgia, lymphadenopathy, hepatosplenomegaly |
| Nerve features | Acute neuritis (less severe than T1R) |
| Other organ involvement | Iridocyclitis, orchitis, epididymitis, arthritis, dactylitis, glomerulonephritis |
| Treatment | Thalidomide (drug of choice, except in women of childbearing age); steroids; clofazimine |
Lucio Reaction (Third Reaction)
- Occurs in diffuse lepromatous leprosy (Lucio leprosy / Lazarine leprosy)
- Pathological: Ischemic necrosis due to endothelial proliferation + bacilli in endothelium
- Lesions: Purpuric, polygonal, geographic ulcers on limbs
- Serious - can be fatal
8. DEFORMITIES AND COMPLICATIONS
Mechanism of Deformity:
M. leprae โ Nerve damage โ Anesthesia + Paralysis
โ
Repeated trauma/burns (unrecognized)
โ
Infection โ Osteomyelitis
โ
Bone resorption โ Shortening / Loss of digits
Common Deformities:
| Deformity | Nerve | Mechanism |
|---|---|---|
| Claw hand (4th, 5th digit) | Ulnar | Intrinsic minus hand |
| Complete claw hand | Ulnar + Median | All intrinsics lost |
| Wrist drop | Radial | Extensor weakness |
| Foot drop | Common peroneal | Dorsiflexion weakness |
| Claw toes | Posterior tibial | Intrinsic foot muscle loss |
| Lagophthalmos | Facial (VII) | Orbicularis weakness |
| Saddle nose | Direct - nasal cartilage/bone | Septal destruction by bacilli |
| Shortening of digits | All sensory nerves | Repeated trauma + resorption |
| Plantar ulcer | Posterior tibial | Anesthesia + pressure |
9. DIAGNOSIS
Cardinal Signs of Leprosy (WHO):
- Hypopigmented/erythematous skin lesion(s) with definite loss of sensation
- Involvement/thickening of peripheral nerve with sensory loss ยฑ weakness
- Positive skin smear (AFB on slit-skin smear)
Diagnosis = 1 or more cardinal signs present
Slit-Skin Smear (SSS):
- Sites: Both earlobes, lesional skin (2-4 sites)
- Stain: Ziehl-Neelsen (ZN)
- Scoring: Bacteriological Index (BI) = log scale 0-6
| BI Score | Bacilli per field |
|---|---|
| 0 | No AFB in 100 oil-immersion fields |
| 1+ | 1-10 AFB per 100 fields |
| 2+ | 1-10 per 10 fields |
| 3+ | 1-10 per field |
| 4+ | 10-100 per field |
| 5+ | 100-1000 per field |
| 6+ | >1000 per field (globi seen) |
Morphological Index (MI): % of uniformly stained (solid) bacilli = measure of bacterial viability
Lepromin Test (Mitsuda Test):
- 0.1 mL of heat-killed M. leprae injected intradermally
- Early reaction (Fernandez): 48 hrs - DTH (not diagnostic)
- Late reaction (Mitsuda): 3-4 weeks - granuloma formation (measures CMI)
- Interpretation:
- Positive (โฅ5mm induration): TT/BT, normal individuals
- Negative: BB/BL/LL
- NOT a diagnostic test - measures immune status only
10. HISTOPATHOLOGY OVERVIEW
| Type | Histology |
|---|---|
| TT | Compact epithelioid granulomas with Langhan's giant cells; nerve destruction; no bacilli |
| BT | Epithelioid granulomas, less compact; bacilli scanty |
| BB | Loose epithelioid granulomas; "naked granuloma" (lymphocytes absent from center) |
| BL | Macrophages with foamy change; inflammatory infiltrate; subepidermal free zone |
| LL | Foamy (Virchow) cells; "grenz zone" (subepidermal free zone); abundant bacilli; globi |
| Indeterminate | Non-specific infiltrate around nerves/vessels; no granuloma |
๐ Clinical Pearl: The "grenz zone" (Unna's grenz zone) = a clear zone of normal collagen between the epidermis and the cellular infiltrate in LL. Pathognomonic of lepromatous leprosy.
11. TREATMENT OVERVIEW (MDT - WHO)
| Regimen | Drugs | Duration |
|---|---|---|
| PB MDT | Rifampicin 600mg once/month + Dapsone 100mg/day | 6 months |
| MB MDT | Rifampicin 600mg once/month + Dapsone 100mg/day + Clofazimine 50mg/day + 300mg once/month | 12 months |
Note: Release from treatment (RFT) after completing MDT - patient is considered cured regardless of BI.
12. CLINICAL PEARLS SUMMARY
| # | Pearl |
|---|---|
| 1 | The TARGET CELL of M. leprae is the Schwann cell |
| 2 | M. leprae grows best at cool temperatures (27-33ยฐC) - explains body distribution |
| 3 | Lepromin test is NOT diagnostic - it measures immunological status |
| 4 | Pure neuritic leprosy is common in India (~18%) - diagnosis by nerve biopsy |
| 5 | Borderline leprosy = MOST COMMON globally + MOST NERVE DAMAGE |
| 6 | T1R reactions = borderline spectrum; ENL = MB spectrum |
| 7 | Thalidomide is DOC for ENL (NEVER in women of childbearing age - teratogenic) |
| 8 | Grenz zone = hallmark of LL histology |
| 9 | Saddle nose = septal destruction in LL; the nasal septum is destroyed before the nasal bones |
| 10 | "Active" bacillus assessment = Morphological Index (not Bacteriological Index) |
| 11 | SSS site with highest yield in LL = earlobes (bilateral) |
| 12 | Lucio reaction = distinct from ENL; occurs only in diffuse non-nodular LL |
| 13 | Madarosis (outer third of eyebrows first) = superciliary madarosis = classic LL sign |
| 14 | Clofazimine in MDT has largely abolished chronic ENL-associated iritis |
| 15 | Trident hand: loss of index, middle, ring = median + ulnar combined palsy |
13. CLINICAL CORRELATION
How to approach a new patient clinically:
STEP 1: Count and examine lesions
- โค5 lesions, well-defined, anesthetic โ PB/tuberculoid end
-
5 lesions, shiny, poorly defined โ MB/lepromatous end
STEP 2: Examine nerves (always bilateral, systematic)
- Palpate: Greater auricular, ulnar, radial cutaneous, median, radial, common peroneal, posterior tibial
STEP 3: Test sensation
- Light touch (cotton wool), pinprick, temperature (warm/cold tubes)
STEP 4: Perform SSS
- Sites: Both earlobes + lesional skin
STEP 5: Classify and treat appropriately with WHO MDT
14. DIAGRAM: THE LEPROSY SPECTRUM
RESISTANCE: HIGH โโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโโบ LOW
TT BT BB BL LL
โ โ โ โ โ
LESIONS: 1-3 4-10 Many Many Countless
EDGES: Sharp Semidef. Punched Fading Indefinite
SSS (BI): 0 0-1 1-2 3-4 5-6
LEPROMIN: +++ ++ - - -
REACTION: - T1R rare T1R T1+ENL ENL
STABLE: โ โ โ โ โ
15. VIVA QUESTIONS WITH ANSWERS
Q1. What is the target cell of M. leprae and what determines the type of leprosy that develops?
A: The target cell is the Schwann cell of peripheral nerves. The type of leprosy depends on the host's cell-mediated immunity (CMI). High CMI โ tuberculoid; absent CMI โ lepromatous. The bacilli colonize epineurial vessels first, then invade endoneurium.
Q2. What are the four parameters of Ridley-Jopling classification?
A: 1. Clinical features, 2. Histological features, 3. Bacteriological features (SSS/BI), 4. Immunological features (lepromin test).
Q3. What is the significance of pure neuritic leprosy (PNL)?
A: PNL has no skin lesions - only peripheral nerve involvement. It accounts for ~18% of cases (especially in India). Diagnosis requires nerve biopsy (sural nerve most commonly). It is classified as MB for treatment purposes.
Q4. Why does M. leprae prefer peripheral nerves and cooler body areas?
A: M. leprae has a unique tropism for Schwann cells. Its optimal growth temperature is 27-33ยฐC, lower than core body temperature. This explains involvement of earlobes, nasal mucosa, cornea, dorsum of hands/feet, and peripheral nerve trunks at superficial bony prominences (ulnar at elbow, common peroneal at fibular head, posterior tibial at medial malleolus).
Q5. How do Type 1 and Type 2 lepra reactions differ immunologically and clinically?
| Feature | T1R (Reversal) | T2R (ENL) |
|---|---|---|
| Type of hypersensitivity | Type IV (cellular) | Type III (immune complex) |
| Spectrum affected | Borderline (BT, BB, BL) | MB (BL, LL) |
| Skin lesions | Existing lesions inflamed | New tender nodules |
| Systemic symptoms | Absent/mild | Fever, malaise, arthralgia |
| Nerve damage | Severe, acute | Less severe |
| Treatment | Prednisolone | Thalidomide / steroids |
Q6. What is the grenz zone and where is it found?
A: The grenz zone (Unna's zone) is a subepidermal clear zone of normal collagen between the epidermis and the inflammatory cell infiltrate. It is characteristic of lepromatous leprosy (LL) on histopathology.
Q7. A patient has left facial nerve palsy, right ulnar nerve thickening, and left lateral popliteal nerve enlargement. What type of leprosy is this and what is its significance?
A: This pattern of asymmetric multiple nerve involvement is characteristic of borderline leprosy (BB/BT). The significance: borderline patients have highest risk of lepra reactions, severe nerve damage, and crippling deformities. They require MB-MDT and close monitoring.
Q8. What is the Mitsuda reaction and what does a positive result indicate?
A: The Mitsuda reaction (late lepromin test) is read at 3-4 weeks. A positive reaction (โฅ5mm) indicates a well-developed granulomatous CMI response against M. leprae. It is positive in TT, BT, and normal individuals. It is NOT diagnostic of leprosy but helps classify the position in the spectrum and assess prognosis.
Q9. What are the early features of lepromatous leprosy before skin lesions appear?
A: Two prodromal features: (1) Nasal symptoms - stuffiness, crusting, blood-stained discharge (due to nasal mucosal infiltration); (2) Bilateral ankle edema - due to autonomic nerve involvement and capillary endothelium damage; worst at end of day.
Q10. What is Lucio leprosy and how is Lucio reaction different from ENL?
A: Lucio leprosy (diffuse non-nodular LL) is a rare form of primary LL with diffuse skin infiltration without discrete nodules. Lucio reaction is a necrotizing vasculitis caused by M. leprae invading endothelial cells โ vascular occlusion โ ischemic necrosis. It presents as polygonal/geographic purpuric ulcers, mainly on limbs. Unlike ENL (immune complex), Lucio reaction is a primary vasculitis and can be fatal. Not included in standard WHO classification.
Q11. Explain madarosis in leprosy. Which type shows it earliest?
A: Madarosis = loss of eyebrows/eyelashes. In leprosy, it begins with outer third of eyebrows (superciliary madarosis) followed by eyelashes (ciliary madarosis). It is seen in lepromatous leprosy (LL) due to direct bacillary infiltration of the hair follicles and autonomic nerve damage. The "stern leprous stare" is due to orbicularis weakness with levator overaction.
Q12. What determines whether borderline leprosy upgrades or downgrades?
A: Treatment initiates immunological upgrading (reversal reaction toward TT). Without treatment, borderline patients tend to downgrade silently toward LL. The genetic and immunological status of the patient determines the speed and direction of shift. Downgrading reactions are usually silent; upgrading reactions present as T1R.
16. MCQ WITH ANSWERS
MCQ 1. M. leprae was discovered by:
- A) Armauer Hansen
- B) Gerhard Hansen
- C) Robert Koch
- D) Louis Pasteur
Answer: B - Gerhard (Georg Armauer) Hansen, Norway, 1873. (Published 1874 - making it the oldest known bacterium pathogenic to humans)
MCQ 2. The target cell of M. leprae is:
- A) Macrophage
- B) Dendritic cell
- C) Schwann cell โ
- D) Endothelial cell
Answer: C. M. leprae has a specific tropism for Schwann cells. Macrophages are the predominant histiocyte in lesions but are not the primary target of infection.
MCQ 3. Which classification of leprosy uses four parameters - clinical, histological, bacteriological, and immunological?
- A) Madrid classification
- B) WHO operational
- C) Indian (IAL)
- D) Ridley-Jopling โ
Answer: D. The Ridley-Jopling system is the most scientific and research-oriented classification.
MCQ 4. The most stable types in the Ridley-Jopling spectrum are:
- A) TT and BT
- B) TT and LL โ
- C) LL and BL
- D) BT and BL
Answer: B. TT (tuberculoid pole) and LL (lepromatous pole) are immunologically stable. Borderline types (BT, BB, BL) are unstable.
MCQ 5. Which nerve is palpated behind the medial epicondyle?
- A) Median nerve
- B) Radial cutaneous nerve
- C) Ulnar nerve โ
- D) Common peroneal nerve
Answer: C. The ulnar nerve is felt in the ulnar groove behind the medial epicondyle. Its thickening is one of the earliest signs of borderline leprosy.
MCQ 6. A BI of 5+ on slit-skin smear means:
- A) 1-10 AFB per 10 fields
- B) 10-100 AFB per field
- C) 100-1000 AFB per field โ
- D) >1000 AFB per field
Answer: C. BI 5+ = 100-1000 bacilli per oil-immersion field. BI 6+ = >1000/field (globi).
MCQ 7. Type 1 lepra reaction occurs in:
- A) LL only
- B) MB leprosy (BL + LL)
- C) Borderline spectrum (BT, BB, BL) โ
- D) All types
Answer: C. Type 1 (reversal) reaction is restricted to borderline leprosy. It represents a shift in CMI. TT and LL are stable and do not exhibit T1R.
MCQ 8. The drug of choice for ENL is:
- A) Dapsone
- B) Rifampicin
- C) Prednisolone
- D) Thalidomide โ
Answer: D. Thalidomide is the DOC for ENL. It inhibits TNF-alpha production. Contraindicated in women of childbearing age due to teratogenicity.
MCQ 9. The "grenz zone" in leprosy histology is characteristic of:
- A) Tuberculoid leprosy
- B) Borderline tuberculoid
- C) Lepromatous leprosy โ
- D) Pure neuritic leprosy
Answer: C. Grenz zone = clear subepidermal zone of normal collagen, pathognomonic of LL. The overlying epidermis is thinned (unlike TT where it is thickened).
MCQ 10. Lucio reaction occurs in:
- A) BT leprosy
- B) BB leprosy
- C) BL leprosy
- D) Diffuse lepromatous leprosy โ
Answer: D. Lucio reaction is specific to diffuse (non-nodular) lepromatous leprosy. It represents necrotizing endothelial vasculitis with vascular occlusion.
MCQ 11. Pure neuritic leprosy is most common in:
- A) Africa
- B) South America
- C) India โ
- D) Southeast Asia
Answer: C. Pure neuritic leprosy accounts for ~18% of cases and is most common in India.
MCQ 12. The Mitsuda reaction is read at:
- A) 24-48 hours
- B) 48-72 hours
- C) 1 week
- D) 3-4 weeks โ
Answer: D. Mitsuda (late lepromin) = 3-4 weeks (measures granuloma formation). Fernandez (early reaction) = 48 hours.
MCQ 13. Which of the following is an early prodromal symptom of lepromatous leprosy?
- A) Anesthetic patch on back
- B) Nasal stuffiness and bilateral ankle edema โ
- C) Thickened ulnar nerve
- D) Lagophthalmos
Answer: B. Nasal symptoms and bilateral ankle edema may precede skin lesions of LL by months to years.
MCQ 14. According to NLEP India (2009), a patient with 4 skin lesions, 2 nerve trunks involved, and negative SSS is classified as:
- A) PB
- B) MB โ
- C) Indeterminate
- D) Cannot classify
Answer: B. Although skin lesions (4) and SSS (negative) suggest PB, the patient has >1 nerve involved, which makes them MB. If ANY one feature is MB, classify as MB (NLEP 2009 criteria).
MCQ 15. The immunological basis of Type 2 reaction (ENL) is:
- A) Type I hypersensitivity (IgE-mediated)
- B) Type II (cytotoxic)
- C) Type III (immune complex) โ
- D) Type IV (delayed type)
Answer: C. ENL is an Arthus-type immune complex (Type III) reaction involving complement activation, neutrophil influx, and TNF-alpha release.
๐ธ ILLUSTRATIVE IMAGES (Reference Images)
Leprosy spectrum images can be found at:
- CDC Clinical Overview of Leprosy - with spectrum photographs
- JAAD 2024 - Ridley-Jopling Leprosy Review
(Spectrum photos from CDC show: TT dark lesions on trunk; BT wide lesions; BL multiple nodular lesions on chest; LL numerous facial nodules)
๐ SOURCES
-
Primary Source: Jopling's Handbook of Leprosy, 6th Edition (2020). Chapter 2.1: Clinical Leprosy. Authors: Kabir Sardana, Premanshu Bhushan, Ananta Khurana. CRC Press/Taylor & Francis.
-
Supporting Review: Makhakhe L. "Leprosy review." S Afr Fam Pract 2021;63(1) [PMID: 34797098]
-
Immunopathogenesis: Silva MJA et al. "An update on leprosy immunopathogenesis: systematic review." Front Immunol 2024 [PMID: 39308868]
-
Neurological complications: Calderone A et al. "The Neurological Impact of Leprosy: Manifestations and Treatment Approaches." Neurol Int 2024 [PMID: 39585070]
-
Diagnostic tests review: Frรณes LAR Jr et al. "Laboratory and functional tests in leprosy diagnosis: a practical guide for clinical decision-making." An Bras Dermatol 2026 [PMID: 41863863]
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Clinical overview: CDC Hansen's Disease (Leprosy) Clinical Overview - cdc.gov
-
AI Diagnostic Aid review: Fernandes JRN et al. "Artificial Intelligence on Diagnostic Aid of Leprosy." J Clin Med 2023 [PMID: 38202187]
โ ๏ธ Recent Evidence Note (2024-2026): A 2024 systematic review on leprosy immunopathogenesis [PMID: 39308868] provides updated insights into innate and adaptive immunity in leprae infection that complement Ridley-Jopling concepts. A 2026 review [PMID: 41863863] provides a practical guide for laboratory testing in leprosy that updates the classic SSS/lepromin approach with molecular diagnostics (PCR, serology) - worth reviewing for modern practice.
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