I have a case of leprosy in my dermatology practical exam prepare me extensively with questions and answers that examiner can ask
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A leprosy long case can be examined from several angles:
-
Case presentation
- How to introduce the patient and summarize findings
- Provisional diagnosis and clinical classification
-
Lesion examination
- Morphology, distribution, sensory impairment, hair loss, dryness, anhidrosis
- Differential diagnoses of hypopigmented or erythematous anesthetic patches/plaques
-
Peripheral nerve examination
- Which nerves to palpate, technique, tenderness, thickening
- Motor, sensory, autonomic deficits and deformities
-
Classification
- Ridley-Jopling spectrum
- WHO paucibacillary versus multibacillary operational classification
- Clinical features of TT, BT, BB, BL, LL, and pure neuritic leprosy
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Investigations
- Slit-skin smear: sites, technique, bacteriological index, morphological index
- Skin biopsy and histopathology
- Lepromin test, including why it is not a diagnostic test
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Treatment
- WHO multidrug therapy for PB and MB disease
- Counseling, adherence, contact screening, adverse effects
- Management of nerve function impairment and disability prevention
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Reactions and emergencies
- Type 1 reversal reaction
- Type 2 reaction or erythema nodosum leprosum
- Lucio phenomenon
- Acute neuritis and when steroids are indicated
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Complications and rehabilitation
- Grade of disability, ulcers, claw hand, foot drop, lagophthalmos
- Eye, hand, and foot care
- Reconstructive procedures and physiotherapy principles
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Epidemiology and public health
- Transmission, infectivity, incubation period, stigma
- Contact prophylaxis and prevention
High-yield practical principle: leprosy is diagnosed clinically when at least one cardinal sign is present: definite sensory loss in a pale or reddish skin lesion, thickened peripheral nerve with sensory or motor loss, or demonstration of acid-fast bacilli in a slit-skin smear.
Which area should I turn into an extensive examiner-style viva with model answers first?
- Full long-case viva, from introduction through treatment
- Classification and clinical features
- Nerve examination, deformities, and disability grading
- Reactions, treatment, and difficult examiner questions
Give me a complete leprosy long-case viva
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Searching the Web
WHO leprosy guidelines multidrug therapy 2026 contacts post exposure prophylaxis
Searching PubMed
leprosy AND treatment
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Searching Images
clinical leprosy hypopigmented anesthetic patch peripheral nerve thickening examination
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https://www.who.int/news-room/fact-sheets/detail/leprosy
Complete Leprosy Long-Case Viva
Use this as a spoken examination framework. Adapt the lesion count, nerves involved, and deformities to the actual patient in front of you.
1. How to Present the Case
Q. Please present the case.
Model answer
This is a ___-year-old [man/woman] with complaints of ___ hypopigmented/reddish skin patches or plaques over ___ for ___ duration, associated with reduced sensation, dryness, loss of sweating, tingling, or weakness of the affected part.On cutaneous examination, there are ___ well-defined/ill-defined, hypopigmented/erythematous, dry, scaly/non-scaly, hypoesthetic/anesthetic patches or plaques over ___. Hair growth and sweating are reduced/absent over the lesions.Peripheral nerve examination shows thickening, with or without tenderness, of the ___ nerve, associated with sensory and/or motor impairment in its distribution. There is/there is no visible deformity, trophic ulcer, or eye involvement.Therefore, this is a case of Hansen disease (leprosy), clinically most consistent with ___ [borderline tuberculoid, borderline lepromatous, etc.], operationally classified as ___ [paucibacillary or multibacillary] leprosy, with/without a lepra reaction and with/without grade ___ disability.
Do not call it "tuberculoid leprosy" solely from one hypopigmented patch. First establish the cardinal signs, assess all nerves and lesions, then classify.
A. Basic Questions
Q. What is leprosy?
Answer:
Leprosy, or Hansen disease, is a chronic granulomatous infectious disease caused principally by Mycobacterium leprae, and more rarely M. lepromatosis. It predominantly affects the skin, peripheral nerves, mucosa of the upper respiratory tract, and eyes. The major clinical consequence is peripheral neuropathy causing sensory loss, weakness, deformity, and trophic ulcers.
Leprosy, or Hansen disease, is a chronic granulomatous infectious disease caused principally by Mycobacterium leprae, and more rarely M. lepromatosis. It predominantly affects the skin, peripheral nerves, mucosa of the upper respiratory tract, and eyes. The major clinical consequence is peripheral neuropathy causing sensory loss, weakness, deformity, and trophic ulcers.
Q. What are the cardinal signs of leprosy?
Answer: Diagnosis is made when at least one of these is present:
- Definite sensory loss in a pale or reddish skin lesion.
- Thickened/enlarged peripheral nerve with loss of sensation and/or weakness of muscles supplied by that nerve.
- Demonstration of acid-fast bacilli in a slit-skin smear.
This is the WHO clinical basis of diagnosis, summarized in the WHO leprosy fact sheet.
Q. Why is sensory testing so important?
Answer:
Many disorders cause hypopigmented or erythematous lesions, but definite impairment of sensation within a lesion strongly supports leprosy. It reflects involvement of cutaneous nerve fibers by M. leprae. Loss of temperature sensation usually appears first, followed by light touch, pain, and finally deep pressure.
Many disorders cause hypopigmented or erythematous lesions, but definite impairment of sensation within a lesion strongly supports leprosy. It reflects involvement of cutaneous nerve fibers by M. leprae. Loss of temperature sensation usually appears first, followed by light touch, pain, and finally deep pressure.
Q. Why are the lesions dry and hairless?
Answer:
Involvement of autonomic nerve fibers causes anhidrosis and xerosis. Damage to skin appendages causes reduced or absent hair growth. These changes support neuropathic involvement.
Involvement of autonomic nerve fibers causes anhidrosis and xerosis. Damage to skin appendages causes reduced or absent hair growth. These changes support neuropathic involvement.
Q. Which sensory modalities do you test?
Answer:
Test and compare with normal adjacent skin:
Test and compare with normal adjacent skin:
- Temperature, using warm and cool test tubes if available.
- Light touch, with cotton wool.
- Pain, using a sterile blunt/sharp pin carefully.
- Deep pressure if needed.
Test from normal skin toward the lesion, ask the patient to close their eyes, and compare corresponding sites on both sides. Avoid repeatedly testing the exact same point because the patient may guess.
Q. Does every hypopigmented patch with reduced sensation mean leprosy?
Answer:
No. Sensory loss must be definite, reproducible, and interpreted with the morphology of the lesion and nerve examination. Differential diagnoses include tinea versicolor, pityriasis alba, vitiligo, post-inflammatory hypopigmentation, nevus depigmentosus, psoriasis, sarcoidosis, cutaneous tuberculosis, and peripheral neuropathies. None typically produces the characteristic combination of an anesthetic lesion and thickened peripheral nerve.
No. Sensory loss must be definite, reproducible, and interpreted with the morphology of the lesion and nerve examination. Differential diagnoses include tinea versicolor, pityriasis alba, vitiligo, post-inflammatory hypopigmentation, nevus depigmentosus, psoriasis, sarcoidosis, cutaneous tuberculosis, and peripheral neuropathies. None typically produces the characteristic combination of an anesthetic lesion and thickened peripheral nerve.
B. Organism, Transmission, and Pathogenesis
Q. Describe Mycobacterium leprae.
Answer:
- Slender, acid-fast bacillus.
- Obligate intracellular pathogen with predilection for macrophages and Schwann cells.
- Cannot be cultured on ordinary artificial culture media.
- Multiplies very slowly, with a long incubation period.
- Prefers cooler tissues, hence predilection for skin, superficial peripheral nerves, earlobes, nose, hands, feet, and testes.
Q. How is leprosy transmitted?
Answer:
The main route is prolonged close exposure to untreated multibacillary disease, principally via nasal and oral droplets. Rarely, damaged skin may contribute. Most exposed persons do not develop disease because host cell-mediated immunity and genetic susceptibility determine disease expression.
The main route is prolonged close exposure to untreated multibacillary disease, principally via nasal and oral droplets. Rarely, damaged skin may contribute. Most exposed persons do not develop disease because host cell-mediated immunity and genetic susceptibility determine disease expression.
Q. What is the incubation period?
Answer:
Usually several years. It is commonly around 2 to 5 years in paucibacillary disease and often 5 years or longer in multibacillary disease, but may be much longer.
Usually several years. It is commonly around 2 to 5 years in paucibacillary disease and often 5 years or longer in multibacillary disease, but may be much longer.
Q. Is it highly infectious?
Answer:
No. Transmission generally requires close and prolonged contact with an untreated infectious multibacillary patient. After starting effective MDT, infectivity falls rapidly. The patient should be reassured that leprosy is curable and ordinary social contact should not lead to stigma or isolation.
No. Transmission generally requires close and prolonged contact with an untreated infectious multibacillary patient. After starting effective MDT, infectivity falls rapidly. The patient should be reassured that leprosy is curable and ordinary social contact should not lead to stigma or isolation.
Q. Explain the pathogenesis of nerve damage.
Answer:
M. leprae infects Schwann cells. Nerve injury results from:
M. leprae infects Schwann cells. Nerve injury results from:
- Direct bacillary involvement of Schwann cells.
- Granulomatous inflammation and edema within rigid nerve fascicles.
- Immune-mediated injury, especially during lepra reactions.
- Chronic fibrosis and axonal loss.
The outcome is sensory, motor, and autonomic dysfunction. Loss of protective sensation leads to repeated unnoticed trauma, fissures, burns, ulcers, infection, and deformity.
Q. Why do different forms of leprosy occur?
Answer:
They reflect the host immune response.
They reflect the host immune response.
- Tuberculoid pole: strong cell-mediated Th1-predominant immunity, low bacillary load, localized disease.
- Lepromatous pole: weak cell-mediated immunity with Th2-predominant response, high bacillary load, widespread symmetric disease.
- Borderline forms are immunologically unstable and lie between these poles.
The clinical-immunologic spectrum is shown in Dermatology, 2-Volume Set, 5e, p. 1562.
C. Examination of Skin Lesions
Q. How do you describe a leprosy lesion?
Answer:
Describe:
Describe:
- Number
- Site and distribution
- Symmetry
- Morphology: macule, patch, plaque, papule, nodule, diffuse infiltration
- Color: hypopigmented, erythematous, copper-colored
- Margin: well-defined or ill-defined
- Surface: dry, scaly, infiltrated, shiny, ulcerated
- Hair and sweating over the lesion
- Sensory impairment
- Whether lesions are tender, edematous, or inflamed, suggesting a reaction
Q. What are typical lesions in tuberculoid leprosy?
Answer:
- One or few lesions
- Large, asymmetrical, dry hypopigmented or erythematous patches/plaques
- Sharply defined, often raised, active margins
- Marked sensory loss and anhidrosis
- Hair loss may occur
- Early, asymmetrical nerve thickening
- Smear generally negative
Q. What are typical lesions in lepromatous leprosy?
Answer:
- Numerous, bilaterally symmetrical lesions
- Ill-defined macules, papules, plaques, nodules, or diffuse infiltration
- Sensory loss may be late and diffuse
- Symmetrical polyneuropathy
- Face, ears, trunk, and extensor limbs may be involved
- Madarosis, nasal involvement, and testicular involvement can occur
- Slit-skin smear is usually strongly positive
Q. What does “glove and stocking anesthesia” suggest?
Answer:
It suggests diffuse symmetrical peripheral neuropathy, seen particularly in multibacillary disease such as borderline lepromatous and lepromatous leprosy. It is not the pattern of a localized tuberculoid lesion.
It suggests diffuse symmetrical peripheral neuropathy, seen particularly in multibacillary disease such as borderline lepromatous and lepromatous leprosy. It is not the pattern of a localized tuberculoid lesion.
Q. What is a satellite lesion?
Answer:
A small lesion close to a larger primary lesion, often seen in borderline tuberculoid disease. It supports the borderline nature of the disease.
A small lesion close to a larger primary lesion, often seen in borderline tuberculoid disease. It supports the borderline nature of the disease.
Q. What is a histoid lesion?
Answer:
Histoid leprosy is a variant of multibacillary leprosy. It presents with firm, shiny, dome-shaped papules or nodules over apparently normal skin, often with a high bacillary load. It may occur in relapse, particularly after inadequate therapy or dapsone monotherapy, but can also occur de novo.
Histoid leprosy is a variant of multibacillary leprosy. It presents with firm, shiny, dome-shaped papules or nodules over apparently normal skin, often with a high bacillary load. It may occur in relapse, particularly after inadequate therapy or dapsone monotherapy, but can also occur de novo.
Q. What is diffuse lepromatous leprosy?
Answer:
It is a diffuse infiltrative form of multibacillary leprosy, often without discrete nodules initially. The skin becomes diffusely shiny and infiltrated, especially on the face and limbs. It may be associated with Lucio phenomenon.
It is a diffuse infiltrative form of multibacillary leprosy, often without discrete nodules initially. The skin becomes diffusely shiny and infiltrated, especially on the face and limbs. It may be associated with Lucio phenomenon.
D. Peripheral Nerve Examination
Q. Which nerves are commonly examined in leprosy?
Answer:
| Nerve | Where to examine | Important deficit |
|---|---|---|
| Great auricular | Over sternocleidomastoid, near ear | Sensory loss over lower auricle/angle of jaw |
| Ulnar | Behind medial epicondyle | Clawing of ring/little fingers, interossei weakness |
| Median | At wrist/forearm | Thenar weakness, impaired thumb opposition |
| Radial cutaneous | Near wrist | Dorsal radial hand sensory loss |
| Common peroneal | Behind neck of fibula | Foot drop |
| Posterior tibial | Behind medial malleolus | Sole sensory loss, intrinsic foot weakness |
| Facial nerve | Facial movements | Lagophthalmos |
| Trigeminal nerve | Corneal sensation | Corneal anesthesia and injury |
Superficial nerves such as the ulnar, common peroneal, posterior tibial, great auricular, and facial nerve are particularly important. Andrews' Diseases of the Skin, p. 399, notes that the ulnar nerve may be palpably enlarged several centimeters above the medial epicondyle.
Q. How do you palpate a peripheral nerve?
Answer:
- Explain the procedure and ensure the limb is relaxed.
- Compare both sides.
- Use the pulp of the index and middle fingers, not the fingertip.
- Roll the nerve gently against an underlying firm structure.
- Note:
- Thickening
- Consistency: soft, firm, hard, beaded
- Tenderness
- Mobility
- Temperature, if inflamed
- Correlate with sensory and motor function of that nerve.
Never press harshly. The goal is to identify thickening and tenderness, not to cause pain.
Q. What is the significance of a tender nerve?
Answer:
Tenderness suggests active neuritis, often during a lepra reaction. It is an urgent finding because untreated neuritis can cause irreversible sensory and motor loss. Assess weakness, new sensory loss, pain, and nerve function immediately.
Tenderness suggests active neuritis, often during a lepra reaction. It is an urgent finding because untreated neuritis can cause irreversible sensory and motor loss. Assess weakness, new sensory loss, pain, and nerve function immediately.
Q. How do you examine the ulnar nerve?
Answer:
Flex the patient's elbow slightly. Palpate in the ulnar groove behind the medial epicondyle and trace proximally. Compare sides. Then test:
Flex the patient's elbow slightly. Palpate in the ulnar groove behind the medial epicondyle and trace proximally. Compare sides. Then test:
- Sensation over the little finger and ulnar side of the hand.
- Abduction/adduction of fingers, especially little-finger abduction.
- Card test or paper test for interossei.
- Froment sign, if indicated.
- Look for wasting of interossei, hollowing of first web space, and ulnar clawing.
Q. How do you examine the common peroneal nerve?
Answer:
Palpate posterior to the neck of fibula. Test:
Palpate posterior to the neck of fibula. Test:
- Dorsiflexion of ankle.
- Extension of great toe.
- Eversion of foot.
- Sensation over dorsum of foot and first web space.
Weakness produces foot drop and a high-stepping gait.
Q. How do you examine posterior tibial nerve involvement?
Answer:
Palpate behind the medial malleolus. Test sensation over the sole using cotton wool and pinprick. Loss of protective sensation predisposes to plantar callosities, fissures, and trophic ulcers.
Palpate behind the medial malleolus. Test sensation over the sole using cotton wool and pinprick. Loss of protective sensation predisposes to plantar callosities, fissures, and trophic ulcers.
Q. Why is the posterior tibial nerve clinically important?
Answer:
Even without obvious weakness, sensory loss over the sole permits repeated trauma and pressure injury. This can lead to chronic plantar ulcers, osteomyelitis, resorption of bones, and eventual shortening of digits.
Even without obvious weakness, sensory loss over the sole permits repeated trauma and pressure injury. This can lead to chronic plantar ulcers, osteomyelitis, resorption of bones, and eventual shortening of digits.
E. Motor Examination and Deformities
Q. What motor deformities can occur?
Answer:
| Nerve affected | Deformity/clinical effect |
|---|---|
| Ulnar nerve | Clawing of ring and little fingers, interosseous wasting |
| Median nerve | Thenar wasting, impaired opposition, “thumb-in-palm” tendency |
| Ulnar + median nerves | Complete claw hand |
| Common peroneal nerve | Foot drop |
| Posterior tibial nerve | Intrinsic foot weakness and plantar sensory loss |
| Facial nerve | Lagophthalmos, exposure keratitis |
| Trigeminal nerve | Corneal anesthesia and corneal ulceration |
Q. Explain claw hand in leprosy.
Answer:
Ulnar nerve palsy paralyzes the interossei and medial lumbricals. The extensor digitorum hyperextends the metacarpophalangeal joints, while flexor digitorum profundus and superficialis flex the interphalangeal joints. This produces clawing, most prominent in the ring and little fingers.
Ulnar nerve palsy paralyzes the interossei and medial lumbricals. The extensor digitorum hyperextends the metacarpophalangeal joints, while flexor digitorum profundus and superficialis flex the interphalangeal joints. This produces clawing, most prominent in the ring and little fingers.
Q. What is the difference between mobile and fixed claw hand?
Answer:
In a mobile claw hand, passive correction of the fingers is possible and deformity may be amenable to tendon transfer after disease has become inactive and nerve function is stable. In a fixed claw hand, joint contractures have developed, requiring physiotherapy, splinting, and sometimes release before reconstruction.
In a mobile claw hand, passive correction of the fingers is possible and deformity may be amenable to tendon transfer after disease has become inactive and nerve function is stable. In a fixed claw hand, joint contractures have developed, requiring physiotherapy, splinting, and sometimes release before reconstruction.
Q. What is lagophthalmos and why is it dangerous?
Answer:
Lagophthalmos is incomplete eyelid closure due to facial nerve paralysis. It causes exposure of the cornea, dryness, keratitis, ulceration, scarring, and potential blindness. Test by asking the patient to close the eyes gently and then tightly, while observing for incomplete closure.
Lagophthalmos is incomplete eyelid closure due to facial nerve paralysis. It causes exposure of the cornea, dryness, keratitis, ulceration, scarring, and potential blindness. Test by asking the patient to close the eyes gently and then tightly, while observing for incomplete closure.
Q. What is a trophic ulcer?
Answer:
It is a chronic ulcer due to loss of protective sensation and autonomic dysfunction. It commonly occurs at pressure points such as the heel, metatarsal heads, and lateral border of the foot. It is usually painless because of anesthesia.
It is a chronic ulcer due to loss of protective sensation and autonomic dysfunction. It commonly occurs at pressure points such as the heel, metatarsal heads, and lateral border of the foot. It is usually painless because of anesthesia.
Q. How do you manage a plantar trophic ulcer?
Answer:
- Rest and pressure off-loading.
- Debridement of callus and necrotic tissue.
- Appropriate wound care and culture-directed antibiotics if secondarily infected.
- Assess for osteomyelitis if deep or chronic.
- Protective footwear or custom microcellular rubber footwear after healing.
- Daily inspection of anesthetic feet.
- Treat the underlying leprosy and active neuritis/reaction where present.
F. Classification
Q. Describe the Ridley-Jopling classification.
Answer:
It is an immunological and histopathological classification:
It is an immunological and histopathological classification:
- Indeterminate leprosy
- Tuberculoid leprosy (TT)
- Borderline tuberculoid leprosy (BT)
- Mid-borderline or borderline-borderline leprosy (BB)
- Borderline lepromatous leprosy (BL)
- Lepromatous leprosy (LL)
It represents a spectrum from strong cell-mediated immunity at the tuberculoid pole to poor cell-mediated immunity at the lepromatous pole.
Q. Differentiate tuberculoid and lepromatous leprosy.
| Feature | Tuberculoid leprosy | Lepromatous leprosy |
|---|---|---|
| Cell-mediated immunity | Strong | Poor/absent |
| Bacillary load | Very low | Very high |
| Lesions | Few, asymmetric, sharply defined | Numerous, symmetric, ill-defined |
| Sensory loss | Early and marked in lesions | Late, diffuse, symmetrical |
| Nerve involvement | Asymmetrical, early, marked | Symmetrical, diffuse, later |
| Slit-skin smear | Usually negative | Strongly positive |
| Lepromin test | Positive | Negative |
| Infectivity | Low | High if untreated |
| Histology | Well-formed granulomas | Foamy macrophages packed with bacilli |
Q. What is the WHO operational classification?
Answer:
It is a practical classification for treatment.
It is a practical classification for treatment.
- Paucibacillary (PB): 1 to 5 skin lesions, without bacilli demonstrated on slit-skin smear.
- Multibacillary (MB): more than 5 lesions, nerve involvement, or any positive slit-skin smear.
Always follow the current national program's operational definition if it differs locally. WHO describes PB and MB classification and treatment in its current fact sheet.
Q. Is a patient with one lesion and a positive smear PB or MB?
Answer:
Multibacillary, because any demonstrated bacilli on slit-skin smear classify the patient as MB.
Multibacillary, because any demonstrated bacilli on slit-skin smear classify the patient as MB.
Q. Is pure neuritic leprosy PB or MB?
Answer:
Operationally, it is generally treated as multibacillary disease because nerve involvement is present and classification by lesion count is not reliable.
Operationally, it is generally treated as multibacillary disease because nerve involvement is present and classification by lesion count is not reliable.
Q. What is indeterminate leprosy?
Answer:
It is an early, unstable form with one or a few ill-defined hypopigmented macules and mild or doubtful sensory loss. Nerve thickening is often absent or minimal, and smear is generally negative. It may resolve spontaneously or evolve toward a more definite form.
It is an early, unstable form with one or a few ill-defined hypopigmented macules and mild or doubtful sensory loss. Nerve thickening is often absent or minimal, and smear is generally negative. It may resolve spontaneously or evolve toward a more definite form.
G. Investigations
Q. Is leprosy a clinical diagnosis?
Answer:
Yes. In most settings, diagnosis is primarily clinical based on cardinal signs. Investigations support diagnosis, classify disease, and help in difficult or atypical cases.
Yes. In most settings, diagnosis is primarily clinical based on cardinal signs. Investigations support diagnosis, classify disease, and help in difficult or atypical cases.
Q. What investigations will you order?
Answer:
- Slit-skin smear for acid-fast bacilli.
- Skin biopsy for histopathology and Fite-Faraco staining.
- Nerve function assessment: sensory testing and voluntary muscle testing.
- Nerve biopsy only in selected difficult cases, particularly suspected pure neuritic leprosy when diagnosis remains uncertain.
- PCR where available, especially in diagnostically difficult cases.
- Baseline investigations before therapy as locally indicated:
- CBC
- Liver function tests
- Renal function tests
- G6PD testing where dapsone risk is a concern
- Pregnancy testing when thalidomide is being considered
Q. Describe slit-skin smear technique.
Answer:
After cleaning the site, pinch the skin to reduce bleeding, make a small incision with a sterile blade, scrape the dermal tissue from the incision, spread it evenly on a slide, air-dry, fix, and stain for acid-fast bacilli, usually with modified Ziehl-Neelsen or Fite-Faraco technique.
After cleaning the site, pinch the skin to reduce bleeding, make a small incision with a sterile blade, scrape the dermal tissue from the incision, spread it evenly on a slide, air-dry, fix, and stain for acid-fast bacilli, usually with modified Ziehl-Neelsen or Fite-Faraco technique.
Sites may include both earlobes, active lesion margins, elbows, knees, and other cool sites. The exact standardized sites vary by national program.
Q. What is bacteriological index?
Answer:
The bacteriological index, or BI, is a logarithmic estimate of bacillary density in slit-skin smears. It ranges from 0 to 6+.
The bacteriological index, or BI, is a logarithmic estimate of bacillary density in slit-skin smears. It ranges from 0 to 6+.
- 0: no bacilli seen.
- Increasing grades indicate increasing bacillary density.
- 6+: very large numbers of bacilli in each microscopic field.
It is especially useful in multibacillary disease and follow-up, though it declines slowly even after effective treatment.
Q. What is morphological index?
Answer:
The morphological index is the proportion of uniformly staining, apparently solid bacilli among all bacilli in a smear. It historically reflects viable bacilli. It falls rapidly with effective treatment but is less commonly used routinely now.
The morphological index is the proportion of uniformly staining, apparently solid bacilli among all bacilli in a smear. It historically reflects viable bacilli. It falls rapidly with effective treatment but is less commonly used routinely now.
Q. What are skin-biopsy findings in tuberculoid leprosy?
Answer:
Well-formed epithelioid-cell granulomas with Langhans giant cells and dense lymphocytic infiltration, often involving dermal nerves and adnexal structures. Bacilli are scanty or absent.
Well-formed epithelioid-cell granulomas with Langhans giant cells and dense lymphocytic infiltration, often involving dermal nerves and adnexal structures. Bacilli are scanty or absent.
Q. What are skin-biopsy findings in lepromatous leprosy?
Answer:
Diffuse dermal infiltrate of foamy macrophages, called Virchow cells or lepra cells, packed with acid-fast bacilli. A clear subepidermal grenz zone is characteristic. Bacilli can occur in clumps called globi.
Diffuse dermal infiltrate of foamy macrophages, called Virchow cells or lepra cells, packed with acid-fast bacilli. A clear subepidermal grenz zone is characteristic. Bacilli can occur in clumps called globi.
Andrews' Diseases of the Skin, p. 401.
Q. What is the lepromin test?
Answer:
It is an intradermal test using killed M. leprae antigen. It assesses host cell-mediated immunity and helps with prognostic or classification purposes. It is usually positive in tuberculoid disease and negative in lepromatous disease.
It is an intradermal test using killed M. leprae antigen. It assesses host cell-mediated immunity and helps with prognostic or classification purposes. It is usually positive in tuberculoid disease and negative in lepromatous disease.
Q. Is lepromin test diagnostic of leprosy?
Answer:
No. It cannot diagnose active leprosy because healthy individuals in endemic areas may be positive, and some patients with leprosy may be negative. It is not used to decide whether an individual has leprosy.
No. It cannot diagnose active leprosy because healthy individuals in endemic areas may be positive, and some patients with leprosy may be negative. It is not used to decide whether an individual has leprosy.
H. Lepra Reactions
Q. What are lepra reactions?
Answer:
They are acute immunological inflammatory episodes occurring before, during, or after MDT. They are not evidence of treatment failure. They are major causes of new nerve damage and disability, so prompt recognition and treatment are essential.
They are acute immunological inflammatory episodes occurring before, during, or after MDT. They are not evidence of treatment failure. They are major causes of new nerve damage and disability, so prompt recognition and treatment are essential.
Q. Name the types of lepra reaction.
Answer:
- Type 1 reaction, also called reversal reaction.
- Type 2 reaction, also called erythema nodosum leprosum or ENL.
- Lucio phenomenon, a severe necrotizing vasculopathic reaction in diffuse lepromatous leprosy.
Q. What is Type 1 lepra reaction?
Answer:
Type 1 reaction is a cell-mediated immune reaction occurring mainly in borderline disease, namely BT, BB, and BL. Existing lesions become acutely red, swollen, warm, and sometimes tender. New edema and acute neuritis may occur. Systemic symptoms are usually absent or mild.
Type 1 reaction is a cell-mediated immune reaction occurring mainly in borderline disease, namely BT, BB, and BL. Existing lesions become acutely red, swollen, warm, and sometimes tender. New edema and acute neuritis may occur. Systemic symptoms are usually absent or mild.
The key danger is acute nerve function impairment.
Q. What are the clinical features of Type 1 reaction?
Answer:
- Sudden erythema, edema, and tenderness of pre-existing lesions
- New lesions may appear because previously subclinical lesions become inflamed
- Tender thickened nerves
- New sensory loss
- New weakness, such as clawing, foot drop, or lagophthalmos
- Edema of hands, feet, or face
- Usually no high fever or widespread painful nodules
Q. What is Type 2 reaction or ENL?
Answer:
ENL is an immune-complex-mediated systemic inflammatory reaction occurring mainly in BL and LL disease with high bacillary load. It presents with crops of painful erythematous papules or nodules, often accompanied by fever and systemic involvement.
ENL is an immune-complex-mediated systemic inflammatory reaction occurring mainly in BL and LL disease with high bacillary load. It presents with crops of painful erythematous papules or nodules, often accompanied by fever and systemic involvement.
Q. What are the features of ENL?
Answer:
- Recurrent crops of tender erythematous nodules
- Fever, malaise, arthralgia, and myalgia
- Neuritis
- Edema
- Iritis or uveitis
- Orchitis
- Lymphadenitis
- Dactylitis
- Nephritis
- Rarely, systemic organ involvement
Q. Differentiate Type 1 reaction from ENL.
| Feature | Type 1 reaction | Type 2 reaction, ENL |
|---|---|---|
| Mechanism | Cell-mediated immunity | Immune-complex-mediated inflammation |
| Usual spectrum | Borderline: BT, BB, BL | BL and LL |
| Skin lesions | Existing lesions become red, swollen, tender | New crops of painful erythematous papules/nodules |
| Systemic symptoms | Usually absent/mild | Common: fever, arthralgia, malaise |
| Neuritis | Common and dangerous | May occur |
| Eye/testis involvement | Less typical | Commoner, especially iritis and orchitis |
| Main treatment | Corticosteroids if neuritis/severe reaction | NSAIDs for mild disease; corticosteroids and/or thalidomide for severe recurrent ENL where permitted |
Q. What factors can precipitate lepra reactions?
Answer:
MDT initiation, intercurrent infection, pregnancy and puerperium, vaccination, stress, trauma, and hormonal changes. Reactions may also occur after treatment completion.
MDT initiation, intercurrent infection, pregnancy and puerperium, vaccination, stress, trauma, and hormonal changes. Reactions may also occur after treatment completion.
Q. What is Lucio phenomenon?
Answer:
Lucio phenomenon is a severe necrotizing vasculopathy seen in diffuse lepromatous leprosy. It presents with painful purpuric lesions that develop central necrosis and ulceration, typically on the limbs. It requires urgent specialist care, MDT, wound care, treatment of secondary infection, and management of systemic complications.
Lucio phenomenon is a severe necrotizing vasculopathy seen in diffuse lepromatous leprosy. It presents with painful purpuric lesions that develop central necrosis and ulceration, typically on the limbs. It requires urgent specialist care, MDT, wound care, treatment of secondary infection, and management of systemic complications.
Q. If a patient develops a reaction during MDT, should MDT be stopped?
Answer:
No. Continue MDT unless there is a specific drug toxicity or contraindication. Treat the reaction simultaneously. Stopping MDT risks incomplete cure and resistance, and does not treat the immune reaction.
No. Continue MDT unless there is a specific drug toxicity or contraindication. Treat the reaction simultaneously. Stopping MDT risks incomplete cure and resistance, and does not treat the immune reaction.
I. Treatment
Q. What is the principle of treatment?
Answer:
Leprosy is curable with multidrug therapy. Treatment aims to kill bacilli, prevent transmission, stop progression, treat reactions and neuritis promptly, and prevent disability through rehabilitation and self-care.
Leprosy is curable with multidrug therapy. Treatment aims to kill bacilli, prevent transmission, stop progression, treat reactions and neuritis promptly, and prevent disability through rehabilitation and self-care.
Q. What is WHO MDT for adults?
Answer:
WHO recommends the same three drugs for both PB and MB disease:
WHO recommends the same three drugs for both PB and MB disease:
| Drug | Monthly supervised dose | Daily self-administered dose |
|---|---|---|
| Rifampicin | 600 mg once monthly | None |
| Clofazimine | 300 mg once monthly | 50 mg daily |
| Dapsone | 100 mg once monthly | 100 mg daily |
- PB leprosy: 6 months.
- MB leprosy: 12 months.
Use the weight-based pediatric packs and local/national protocol for children. The WHO guidance confirms three-drug MDT with 6 months for PB and 12 months for MB disease.
Q. Why is MDT used rather than one drug?
Answer:
Combination therapy rapidly kills bacilli, reduces infectivity, shortens treatment, and reduces the development of drug resistance. Dapsone monotherapy is obsolete because resistance developed.
Combination therapy rapidly kills bacilli, reduces infectivity, shortens treatment, and reduces the development of drug resistance. Dapsone monotherapy is obsolete because resistance developed.
Q. What are important adverse effects of rifampicin?
Answer:
- Orange-red discoloration of urine, tears, sweat, and other secretions
- Hepatotoxicity
- Flu-like syndrome, especially with intermittent exposure
- Thrombocytopenia, rarely
- Potent enzyme induction leading to drug interactions, including reduced efficacy of oral contraceptives and some antiretroviral/anticoagulant medicines
Q. What are important adverse effects of dapsone?
Answer:
- Hemolysis, especially in G6PD deficiency
- Methemoglobinemia
- Dapsone hypersensitivity syndrome: fever, rash, hepatitis, lymphadenopathy, eosinophilia
- Agranulocytosis, rarely
- Peripheral neuropathy, rarely
Q. What are important adverse effects of clofazimine?
Answer:
- Red-brown to black discoloration of skin
- Ichthyosis and dryness
- Gastrointestinal intolerance
- Abdominal pain or enteropathy, rarely severe with high cumulative dose
Counsel about pigmentation before starting treatment because it affects adherence.
Q. What is the treatment of acute neuritis or severe Type 1 reaction?
Answer:
This is urgent. Continue MDT and begin systemic corticosteroids, commonly prednisolone, with the dose and taper individualized to severity, nerve function impairment, diabetes, infection risk, and local protocol. Reassess sensory and motor nerve function frequently. If there is nerve abscess, severe compressive neuropathy, or failure despite appropriate medical management, refer for specialist evaluation and possible decompression.
This is urgent. Continue MDT and begin systemic corticosteroids, commonly prednisolone, with the dose and taper individualized to severity, nerve function impairment, diabetes, infection risk, and local protocol. Reassess sensory and motor nerve function frequently. If there is nerve abscess, severe compressive neuropathy, or failure despite appropriate medical management, refer for specialist evaluation and possible decompression.
Q. How is ENL treated?
Answer:
- Mild ENL: NSAIDs, rest, symptomatic treatment, while continuing MDT.
- Moderate or severe ENL, neuritis, iritis, orchitis, or systemic involvement: systemic corticosteroids.
- Severe recurrent ENL: thalidomide can be very effective but is strictly contraindicated in pregnancy because of profound teratogenicity. It requires controlled prescribing and reliable pregnancy prevention where used.
- Clofazimine at anti-inflammatory doses may be used in selected recurrent cases, under specialist supervision.
Q. Is thalidomide used in Type 1 reaction?
Answer:
No. Its principal role is severe recurrent ENL, not routine Type 1 reaction. It is absolutely contraindicated in pregnancy.
No. Its principal role is severe recurrent ENL, not routine Type 1 reaction. It is absolutely contraindicated in pregnancy.
Q. When should you refer urgently?
Answer:
- New weakness or sensory loss
- Painful tender nerve
- Foot drop, clawing, or lagophthalmos
- Red eye, eye pain, photophobia, diminished vision, or corneal anesthesia
- Severe ENL with systemic involvement
- Orchitis
- Deep infected plantar ulcer or suspected osteomyelitis
- Suspected drug hypersensitivity, severe anemia, hepatitis, or severe dapsone reaction
J. Disability Grading
Q. What is WHO disability grading?
Answer:
| Grade | Eye | Hand/foot |
|---|---|---|
| Grade 0 | No anesthesia or visible damage | No anesthesia or visible damage |
| Grade 1 | No visible damage, but impaired corneal sensation or reduced vision not due to visible damage | Anesthesia present, but no visible deformity/damage |
| Grade 2 | Visible eye damage, lagophthalmos, severe visual impairment | Visible deformity or damage, such as claw hand, foot drop, trophic ulcer, absorption, or amputation |
The overall grade is the highest grade found in either eye, either hand, or either foot.
Q. Give examples of grade 2 disability.
Answer:
- Claw hand
- Foot drop
- Trophic ulcer
- Absorption of fingers or toes
- Lagophthalmos
- Corneal opacity
- Severe visual impairment due to leprosy
Q. Why is disability grading important?
Answer:
It documents baseline disease burden, identifies rehabilitation needs, permits monitoring, guides referral, and has public-health significance. New grade 2 disability indicates late detection and risk of permanent impairment.
It documents baseline disease burden, identifies rehabilitation needs, permits monitoring, guides referral, and has public-health significance. New grade 2 disability indicates late detection and risk of permanent impairment.
K. Eye, Nose, Testes, and Systemic Examination
Q. What eye examination will you perform?
Answer:
- Inspect eyebrows and eyelashes for madarosis.
- Test facial nerve by asking the patient to close eyes gently and tightly.
- Look for lagophthalmos.
- Test corneal sensation carefully with a fine cotton wisp, if appropriate.
- Look for conjunctival injection, corneal opacity, ulceration, or exposure keratitis.
- Ask about pain, redness, photophobia, blurring of vision, and watering.
- Refer urgently if there is red eye, eye pain, photophobia, or visual loss.
Q. What is madarosis?
Answer:
Loss of eyebrows and/or eyelashes. Bilateral loss of the lateral eyebrows is classically associated with lepromatous disease, although it is not specific.
Loss of eyebrows and/or eyelashes. Bilateral loss of the lateral eyebrows is classically associated with lepromatous disease, although it is not specific.
Q. What nasal features occur in leprosy?
Answer:
Chronic nasal stuffiness, epistaxis, crusting, septal perforation, and collapse of the nasal bridge in advanced disease. Nasal mucosal infiltration is particularly associated with multibacillary disease.
Chronic nasal stuffiness, epistaxis, crusting, septal perforation, and collapse of the nasal bridge in advanced disease. Nasal mucosal infiltration is particularly associated with multibacillary disease.
Q. What testicular features occur?
Answer:
Infiltration or recurrent orchitis in lepromatous disease may cause testicular atrophy, infertility, and hypogonadism. Ask about pain, swelling, reduced libido, and infertility where clinically appropriate.
Infiltration or recurrent orchitis in lepromatous disease may cause testicular atrophy, infertility, and hypogonadism. Ask about pain, swelling, reduced libido, and infertility where clinically appropriate.
L. Differential Diagnosis
Q. What is the differential diagnosis of a hypopigmented anesthetic patch?
Answer:
The strongest differential is leprosy itself when sensory loss is definite. Other causes of hypopigmented lesions include:
The strongest differential is leprosy itself when sensory loss is definite. Other causes of hypopigmented lesions include:
| Condition | Distinguishing feature |
|---|---|
| Tinea versicolor | Fine branny scale, no definite sensory loss or nerve thickening |
| Pityriasis alba | Mild ill-defined hypopigmentation, usually face of children, normal sensation |
| Vitiligo | Chalk-white depigmentation, normal texture and sensation |
| Post-inflammatory hypopigmentation | History of preceding dermatitis/injury, normal nerve examination |
| Nevus depigmentosus | Congenital or early-onset stable patch, normal sensation |
| Cutaneous tuberculosis | Plaques/nodules but not characteristic anesthesia with nerve thickening |
| Sarcoidosis | Papules/plaques, no peripheral nerve thickening pattern |
| Peripheral neuropathy | Sensory loss follows neuropathic distribution, usually no characteristic skin patch |
Q. What is the differential diagnosis of thickened peripheral nerves?
Answer:
Leprosy is an important cause in endemic settings. Other possibilities include hereditary neuropathies such as Charcot-Marie-Tooth disease, neurofibromatosis, amyloidosis, chronic inflammatory demyelinating polyradiculoneuropathy, nerve tumors, and localized traumatic or compressive neuropathies. Correlate with skin lesions, sensory loss, epidemiology, and slit-skin smear/biopsy.
Leprosy is an important cause in endemic settings. Other possibilities include hereditary neuropathies such as Charcot-Marie-Tooth disease, neurofibromatosis, amyloidosis, chronic inflammatory demyelinating polyradiculoneuropathy, nerve tumors, and localized traumatic or compressive neuropathies. Correlate with skin lesions, sensory loss, epidemiology, and slit-skin smear/biopsy.
Q. How do you differentiate leprosy from vitiligo?
Answer:
Vitiligo produces complete depigmentation, often with leukotrichia, but sensation, sweating, and peripheral nerves are normal. Leprosy lesions are often hypopigmented rather than completely depigmented, may be dry and hairless, show sensory impairment, and may be associated with thickened nerves.
Vitiligo produces complete depigmentation, often with leukotrichia, but sensation, sweating, and peripheral nerves are normal. Leprosy lesions are often hypopigmented rather than completely depigmented, may be dry and hairless, show sensory impairment, and may be associated with thickened nerves.
M. Epidemiology, Prevention, and Counseling
Q. How will you counsel this patient?
Answer:
- Explain that leprosy is curable.
- Explain that early and regular MDT prevents disability and reduces infectivity.
- Reassure the patient that casual contact does not justify isolation or discrimination.
- Explain possible drug adverse effects, especially clofazimine pigmentation and rifampicin discoloration of body fluids.
- Stress that lepra reactions can occur despite treatment and do not mean treatment failure.
- Teach daily self-examination of anesthetic hands and feet.
- Advise avoidance of burns, cuts, hot surfaces, barefoot walking, and repetitive pressure.
- Provide protective footwear and splints where needed.
- Encourage family and close contacts to attend screening.
Q. What is contact screening?
Answer:
Household, neighborhood, and social contacts should be examined for skin lesions and nerve involvement. WHO recommends contact screening with single-dose rifampicin post-exposure prophylaxis for eligible contacts after excluding leprosy and tuberculosis, according to local program rules. See the WHO prevention recommendation.
Household, neighborhood, and social contacts should be examined for skin lesions and nerve involvement. WHO recommends contact screening with single-dose rifampicin post-exposure prophylaxis for eligible contacts after excluding leprosy and tuberculosis, according to local program rules. See the WHO prevention recommendation.
Q. What is SDR-PEP?
Answer:
SDR-PEP means single-dose rifampicin post-exposure prophylaxis. It is given to eligible contacts after clinical screening and exclusion of active leprosy and tuberculosis, as part of a contact-tracing program. It does not replace ongoing surveillance and early case detection.
SDR-PEP means single-dose rifampicin post-exposure prophylaxis. It is given to eligible contacts after clinical screening and exclusion of active leprosy and tuberculosis, as part of a contact-tracing program. It does not replace ongoing surveillance and early case detection.
Q. Can leprosy recur after adequate MDT?
Answer:
Yes, although relapse is uncommon. Consider relapse when new lesions or progressive nerve impairment occur after a period of clinical stability, particularly with rising bacillary index or evidence of drug resistance. Distinguish it from lepra reaction, which is acute and inflammatory. A 2025 systematic review reported that relapse remains an important follow-up issue, especially in multibacillary disease (PMID 41082563).
Yes, although relapse is uncommon. Consider relapse when new lesions or progressive nerve impairment occur after a period of clinical stability, particularly with rising bacillary index or evidence of drug resistance. Distinguish it from lepra reaction, which is acute and inflammatory. A 2025 systematic review reported that relapse remains an important follow-up issue, especially in multibacillary disease (PMID 41082563).
N. Rapid-Fire Examiner Questions
Q. Why are earlobes commonly involved?
Answer: They are cooler body sites and favor bacillary survival.
Q. Why are nerves thickened?
Answer: Bacillary invasion, granulomatous inflammation, edema, fibrosis, and enlargement of nerve fascicles.
Q. Why is the ulnar nerve commonly involved?
Answer: It is superficial at the elbow and is relatively cooler, making it vulnerable to infiltration and inflammation.
Q. Which nerves are assessed for eye complications?
Answer: Facial nerve for eyelid closure and trigeminal nerve for corneal sensation.
Q. What is the commonest cause of deformity in leprosy?
Answer: Peripheral nerve damage, especially during unrecognized or untreated reactions.
Q. What is silent neuropathy?
Answer: New nerve function impairment without pain or tenderness. It is dangerous because it may be missed unless sensory and motor testing are performed routinely.
Q. Can a patient develop reaction after completing MDT?
Answer: Yes. Reactions can occur before, during, or after completion of MDT.
Q. Is a positive slit-skin smear required to diagnose leprosy?
Answer: No. A clinical cardinal sign is sufficient. Smears are often negative in paucibacillary disease.
Q. What is the commonest form in children?
Answer: Paucibacillary forms are common, but any form can occur. A child case indicates ongoing community transmission and requires careful contact evaluation.
Q. What is the significance of leprosy in a child?
Answer: It suggests recent transmission in the community and is an important public-health indicator.
Q. What is mononeuritis multiplex in leprosy?
Answer: Asymmetric involvement of multiple individual peripheral nerves, often characteristic of tuberculoid or borderline disease.
Q. Does healing of lesions mean nerve function will recover?
Answer: Not necessarily. Skin lesions can improve while nerve damage persists or progresses. Nerve function must be independently assessed.
Q. Why should you not test sensation over ulcerated skin alone?
Answer: Ulceration itself alters local sensation and creates unreliable findings. Test intact adjacent skin in the relevant nerve territory.
Q. What is the most dangerous error in managing leprosy?
Answer: Missing acute neuritis or eye involvement, because delayed treatment can result in irreversible paralysis or blindness.
O. Final Examiner-Level Summary
This patient has Hansen disease, diagnosed clinically by the presence of ___ cardinal sign(s): ___ . The morphology, distribution of lesions, nerve involvement, smear status, and lesion count suggest ___ type on the Ridley-Jopling spectrum and ___ operational class for MDT.I would document sensory and motor nerve function, disability grade, and eye involvement; perform slit-skin smear and/or biopsy where indicated; begin WHO MDT; screen contacts; provide self-care and disability-prevention counseling; and actively look for lepra reaction, acute neuritis, ulcers, and ocular disease.The immediate priority is to prevent irreversible nerve damage, especially if there is tenderness, recent sensory loss, weakness, foot drop, clawing, or lagophthalmos.
The core practical message is simple: recognize the cardinal sign, examine every relevant peripheral nerve, document disability, classify correctly for MDT, and never miss neuritis or eye involvement.
Why does ot happen that generally spouse of a leprosy patient doesn’t have clinical signs and symptoms of leprosy when they are the one living closest
Reading File
Searching the Web
WHO leprosy household contacts risk immunity most contacts do not develop disease
Searching PubMed
leprosy AND household contacts
Finding Sources
Finding Sources
Living closest to a patient raises a spouse's risk, but exposure does not automatically cause clinical leprosy. Most exposed people never develop disease.
Why this happens
-
Most people have effective natural immunity
- M. leprae has low infectivity.
- In most people, cell-mediated immunity contains or clears infection before it produces skin lesions or nerve damage.
- Only a small proportion of exposed people develop clinical disease.
-
Leprosy depends on host susceptibility, not exposure alone
- Genetic factors influence susceptibility and the type of immune response.
- Strong cell-mediated immunity tends to control bacilli, while poor cell-mediated immunity permits multibacillary disease.
- Thus, two people living in the same home can have very different outcomes.
-
The index patient may not have been highly infectious
- Transmission is mainly associated with untreated multibacillary leprosy, in which bacilli may be shed from nasal/oral secretions.
- Paucibacillary disease carries much lower transmission potential.
- Once effective multidrug therapy starts, infectivity falls rapidly.
-
Clinical disease has a very long incubation period
- Leprosy may take years to become clinically evident.
- A spouse could be uninfected, have controlled infection, or rarely develop signs later. Absence of disease now does not prove there was never exposure.
-
Exposure is not limited to the spouse
- The apparent patient may have acquired infection years earlier from another close contact or community exposure, not necessarily from their spouse.
- In endemic settings, exposure can occur outside the home as well.
-
“Infection” and “disease” are different
- A person may be exposed, and perhaps transiently infected, but never develop the clinical features needed for a diagnosis: anesthetic skin lesion, thickened nerve with deficit, or a positive slit-skin smear.
A good viva answer is:
“Household contacts, including spouses, are at increased risk, particularly when the patient has untreated multibacillary disease. However, leprosy is not highly infectious, and development of clinical disease depends mainly on prolonged exposure plus host genetic and cell-mediated immune susceptibility. Most contacts mount an effective immune response and never develop clinical leprosy. Also, the incubation period is long, and the patient may have acquired infection from a source other than the spouse.”
This aligns with Harrison’s Principles of Internal Medicine, which notes that the important risk factors are duration and intensity of close contact, especially with multibacillary disease, together with host genetic susceptibility (Harrison’s Principles of Internal Medicine, 22e, p. 1449). Goldman-Cecil Medicine similarly states that M. leprae is not highly transmissible despite prolonged close contact being a risk factor.
Practical point: the spouse should still undergo contact screening for skin lesions and sensory/motor nerve impairment. WHO recommends screening household, neighborhood, and social contacts, with eligible contacts offered single-dose rifampicin post-exposure prophylaxis under local program protocols, as described in the WHO leprosy guidance.
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