1. Differential diagnosis & management of Inguinal Bubo 2. Discuss leprosy- Clinical, bacteriological, histological, immunological features 3. (A) Esthiomene (B) HAART 4. Role of counselling in management of STI 5. (A) Newer drugs in leprosy (B) Vaccines in leprosy 6. Deformities in leprosy and their management 7. (A) Congenital Syphilis (B) Non treponemal serological test in syphilis 8. Discuss herpes genitalis 9. (A) Nerve biopsy in leprosy (B) Clofazimine 10. (A) ENL (B) OHL (Oral Hairy Leukoplakia) in 10marks format for 3rd yr dermatology post graduate theory examination

Reading File

Given the scale and complexity of this request (10 exam topics for a 3rd year dermatology PG theory exam), I'll use parallel subagents to research all topics simultaneously from the medical library, then compile comprehensive answers.

general-purpose

You are a medical research agent. Search the medical textbook library database for content on these 5 topics related to STI/Dermatology for a 3rd year postgraduate dermatology theory exam. For each topic, find and read the relevant textbook sections. TOPICS TO RESEARCH: 1. Inguinal Bubo - differential diagnosis and management (LGV, chancroid, plague, filariasis, etc.) 2. Leprosy - complete discussion: clinical features, bacteriological features, histological features, immunological features (Ridley-Jopling classification, types, reactions) 3. (A) Esthiomene - definition, causes, clinical features, management; (B) HAART - highly active antiretroviral therapy in HIV/STI context 4. Role of counselling in management of STI 5. (A) Newer drugs in leprosy (B) Vaccines in leprosy INSTRUCTIONS: - Use query_library_db to search headings_fts and paragraphs_fts for each topic - Read relevant file sections using read_file with appropriate offsets - Extract detailed, exam-relevant information - Return comprehensive notes for each topic with all clinical details, classifications, treatment regimens, drug names, doses where available Start with these searches: ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'inguinal bubo' ORDER BY rank LIMIT 5 ``` ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'leprosy clinical features' ORDER BY rank LIMIT 5 ``` ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'esthiomene' ORDER BY rank LIMIT 5 ``` ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'counselling STI sexually transmitted' ORDER BY rank LIMIT 5 ``` ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'newer drugs leprosy vaccines' ORDER BY rank LIMIT 5 ``` Then read the relevant file sections and compile detailed notes. Return all findings as structured notes per topic.

general-purpose

You are a medical research agent. Search the medical textbook library database for content on these 5 topics related to STI/Dermatology for a 3rd year postgraduate dermatology theory exam. For each topic, find and read the relevant textbook sections. TOPICS TO RESEARCH: 6. Deformities in leprosy and their management (claw hand, foot drop, lagophthalmos, saddle nose, etc.) 7. (A) Congenital Syphilis - features, diagnosis, management; (B) Non-treponemal serological tests in syphilis (VDRL, RPR) 8. Herpes genitalis - etiology, clinical features, diagnosis, management, complications 9. (A) Nerve biopsy in leprosy - indications, technique, findings; (B) Clofazimine - pharmacology, mechanism, uses, side effects 10. (A) ENL (Erythema Nodosum Leprosum) - features, management; (B) OHL (Oral Hairy Leukoplakia) - features, diagnosis, management INSTRUCTIONS: - Use query_library_db to search headings_fts and paragraphs_fts for each topic - Read relevant file sections using read_file with appropriate offsets - Extract detailed, exam-relevant information - Return comprehensive notes for each topic with all clinical details, classifications, treatment regimens Start with these searches: ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'leprosy deformities management' ORDER BY rank LIMIT 5 ``` ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'congenital syphilis' ORDER BY rank LIMIT 5 ``` ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'herpes genitalis genital herpes' ORDER BY rank LIMIT 5 ``` ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'nerve biopsy leprosy clofazimine' ORDER BY rank LIMIT 5 ``` ```sql SELECT title, book_title, '/textbooks/' || block_file_path AS file_path, line_number, para_line_ranges, para_count FROM headings_fts WHERE headings_fts MATCH 'erythema nodosum leprosum ENL oral hairy leukoplakia' ORDER BY rank LIMIT 5 ``` Then read the relevant file sections and compile detailed notes. Return all findings as structured notes per topic.

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Both subagents have completed their research. Now I'll compile all 10 answers in full 10-mark PG exam format.

Can you continue from where it stopped

All research is complete. Now compiling all 10 answers in full 10-mark PG exam format.---

3rd Year Dermatology PG Theory Examination

Model Answers (10 Marks Each)

Q1. Differential Diagnosis & Management of Inguinal Bubo

Definition

An inguinal bubo is an enlarged, tender lymph node (or group of nodes) in the inguinal region resulting from inflammatory or neoplastic processes draining from the lower limb, perineum, genitalia, or anal region.

Differential Diagnosis

A. STI-Related (Infective) Causes

Disease	Causative Agent	Character of Bubo
Lymphogranuloma Venereum (LGV)	Chlamydia trachomatis L1, L2, L3	Matted, multi-locular; groove sign (pathognomonic); fluctuant; may rupture
Chancroid	Haemophilus ducreyi	Unilocular, tender, fluctuant, overlying erythema; ruptures forming "kissing ulcers"
Primary Syphilis	Treponema pallidum	Non-tender, rubbery, discrete, bilateral (satellite bubo) - "Bubo of steel"
Herpes Genitalis	HSV-2 (mainly)	Tender, bilateral, does not suppurate
Donovanosis (Granuloma Inguinale)	Klebsiella granulomatis	Pseudo-bubo (subcutaneous granuloma, not true lymphadenopathy) in inguinal region

B. Non-STI Infective Causes

Bubonic Plague - Yersinia pestis; extremely tender, rapidly suppurating; systemic toxaemia; flea bite history
Tuberculosis - cold abscess; matted, non-tender; central caseation; sinuses
Filariasis - Wuchereria bancrofti; recurrent lymphangitis, lymphoedema; tropical background
Cat-scratch disease - Bartonella henselae; scratch history; self-limiting
Pyogenic lymphadenitis - secondary to infected wounds of lower limb, cellulitis

C. Non-Infective Causes

Lymphoma (Hodgkin's/Non-Hodgkin's) - rubbery, non-tender, progressive
Metastatic carcinoma - hard, fixed, irregular (from vulva, penis, rectum, lower limb)
Reactive lymphadenopathy

Distinguishing Features: Groove Sign of LGV

The inguinal ligament (Poupart's ligament) divides the enlarged nodes above and below, creating a pathognomonic groove - present in ~20% of LGV cases.

Management

General Principles

Syndromic management when laboratory confirmation unavailable
Treat both partners simultaneously
Aspiration preferred over incision and drainage (I&D causes sinus formation)
Screen for other STIs (HIV, Syphilis, HBV)

Specific Treatment

LGV:

First line: Doxycycline 100 mg BD x 21 days
Alternative: Azithromycin 1 g weekly x 3 weeks OR Erythromycin 500 mg QID x 21 days
Pregnancy: Erythromycin 500 mg QID x 21 days

Chancroid:

Azithromycin 1 g single dose OR
Ceftriaxone 250 mg IM single dose OR
Ciprofloxacin 500 mg BD x 3 days OR
Erythromycin 500 mg TDS x 7 days

Syphilis (with bubo):

Benzathine Penicillin G 2.4 MU IM single dose

Plague:

Streptomycin 1 g IM BD OR Doxycycline 100 mg BD x 10 days
Strict isolation, notifiable disease

Bubo Aspiration Technique

Insert needle from healthy adjacent skin at an angle
Aspirate pus (avoids fistula formation)
Never cruciate incision (leads to chronic discharging sinus)

Partner Management

LGV: trace contacts within 30 days of symptom onset
Chancroid: trace within 10 days
Syphilis: trace within 3 months (primary), 6 months (secondary)

Q2. Leprosy - Clinical, Bacteriological, Histological, Immunological Features

Introduction

Leprosy (Hansen's Disease) is a chronic granulomatous infection caused by Mycobacterium leprae, an obligate intracellular bacillus affecting skin, peripheral nerves, mucous membranes, and eyes. It is classified by the Ridley-Jopling (R-J) spectrum and WHO classification.

Causative Organism - Bacteriological Features

Mycobacterium leprae:

Gram-positive, acid-fast bacillus (Ziehl-Neelsen stain - red against blue background)
Obligate intracellular; cannot be cultured on artificial media
Doubling time: 12-13 days (slowest of all bacteria)
Optimum growth temperature: 27-30°C (explains predilection for cooler body parts - skin, peripheral nerves, anterior eye, testes, nasal mucosa)
Viable bacilli stain solid; dead bacilli appear fragmented/granular (Morphological Index - MI)
Bacteriological Index (BI): logarithmic scale 1+ to 6+ (Ridley's log scale)

BI Score	Bacilli per field
1+	1-10 in 100 fields
2+	1-10 in 10 fields
3+	1-10 in average field
4+	10-100 per average field
5+	100-1000 per average field
6+	>1000 per average field

Ridley-Jopling Classification

1. Tuberculoid Leprosy (TT)

Clinical:

1-3 well-defined, hypopigmented/erythematous macules or plaques
Sharply defined edges, raised borders
Completely anaesthetic, anhidrotic, alopecic
Nerve involvement: single, thickened, asymmetric
Self-healing in many

Bacteriological: BI = 0 (paucibacillary); AFB absent on slit-skin smear

Histological:

Well-formed epithelioid cell granulomas
Langhans giant cells present
Dense lymphocytic infiltration
Granulomas erode and destroy sub-epidermal zone (no Grenz zone)
Nerves: perineural granuloma, obliterated nerve architecture

Immunological:

Strong cell-mediated immunity (CMI) - Th1 response
Lepromin test (Mitsuda reaction): strongly positive (>10 mm at 28 days)
High IL-2, IFN-γ, IL-12
Low/absent anti-PGL-1 antibodies
CD4:CD8 ratio HIGH in lesions

2. Borderline Tuberculoid (BT)

Clinical:

Multiple plaques (3-10), less well-defined
Satellite lesions around main plaque (characteristic)
Impaired sensation (less complete than TT)
Multiple nerve trunks involved

Bacteriological: BI = 0-1+ (paucibacillary)

Histological:

Epithelioid granulomas with fewer Langhans cells
Narrow Grenz zone beginning to appear
Nerve twigs infiltrated but architecture partially preserved

Immunological: Lepromin test: mildly positive; moderate CMI

3. Borderline Borderline (BB) - Mid-borderline (Unstable)

Clinical:

Many lesions; "Swiss cheese" appearance (punched-out areas of normal skin within lesions)
Dimorphic lesions - annular lesions with irregular inner and outer edges
Moderate sensory loss
Symmetric distribution

Bacteriological: BI = 3+ (multibacillary)

Histological:

Epithelioid cells without Langhans cells
Prominent Grenz zone
"Naked" lymphocytes

Immunological: Lepromin test: negative; unstable - shifts toward TT (upgrading) or LL (downgrading) with reactions

4. Borderline Lepromatous (BL)

Clinical:

Numerous lesions; some with defined edges, some vague
Sloping inner edge, sharp outer edge of lesions
Papules, nodules, plaques
Moderate sensory loss

Bacteriological: BI = 4-5+ (multibacillary)

Histological:

Macrophages replacing epithelioid cells
Grenz zone prominent
Nerve involvement with "onion-peel" perineural fibrosis (pathognomonic)
Some foamy macrophages beginning to appear

Immunological: Lepromin test: negative; predominantly humoral (Th2) response

5. Lepromatous Leprosy (LL)

Clinical:

Diffuse infiltration; symmetrical lesions
Early: vague hypopigmented macules, loss of lateral eyebrows (madarosis - first sign)
Late: leonine facies, pendulous earlobes, gynaecomastia
Diffuse nasal involvement → saddle nose deformity
Bilateral, symmetrical nerve thickening
Stocking-glove anaesthesia (glove and stocking pattern)
Corneal anaesthesia, lagophthalmos, iritis

Bacteriological: BI = 5-6+ (heavily multibacillary); globi (packets of bacilli within macrophages)

Histological:

Foamy (lipid-laden) macrophages (Virchow cells/lepra cells) filled with bacilli
Dense subepidermal Grenz zone (Unna's clear zone)
No lymphocytes, no giant cells
Bacilli in endothelial cells, smooth muscle
"Lepra cells" with globi on Wade-Fite stain

Immunological:

Absent CMI (complete anergy)
Lepromin test: negative
HIGH anti-PGL-1 antibodies (can be used for diagnosis)
High IL-4, IL-5, IL-10 (Th2 dominance)
CD4:CD8 ratio LOW in lesions
Polyclonal hypergammaglobulinaemia
False-positive VDRL, RF, ANA

WHO Classification

Type	Skin Lesions	Smear	Regimen
Paucibacillary (PB)	1-5	Negative	6 months MDT
Multibacillary (MB)	>5	Positive/Negative	12 months MDT

Leprosy Reactions (Immunological Basis)

Type 1 (Reversal Reaction) - Delayed Hypersensitivity (Type IV)

Occurs in borderline types (BT, BB, BL)
Sudden upgrading of CMI
EXISTING lesions become inflamed (erythematous, oedematous, tender)
Acute neuritis - most damaging
No systemic features
Treat with Prednisolone 40-60 mg/day, taper over 6 months

Type 2 (ENL - Erythema Nodosum Leprosum) - Immune Complex (Type III)

Occurs in BL and LL
NEW erythematous tender nodules, mainly on face and extensor limbs
Systemic features: fever, malaise, iridocyclitis, orchitis, arthritis, neuritis
Treat with Thalidomide 100-300 mg/day (males) or Prednisolone; Clofazimine for recurrent ENL

MDT Regimens (WHO)

PB (6 months):

Rifampicin 600 mg once monthly (supervised)
Dapsone 100 mg daily (self-administered)

MB (12 months):

Rifampicin 600 mg once monthly (supervised)
Clofazimine 300 mg once monthly (supervised) + 50 mg daily
Dapsone 100 mg daily

Q3. (A) Esthiomene (B) HAART

A. Esthiomene

Definition

Esthiomene (from Greek: "eating away") is the chronic, progressive, destructive ulceration and lymphoedema of the female external genitalia, historically associated with tertiary LGV (Lymphogranuloma Venereum). The term means "that which eats away."

Causes

LGV (C. trachomatis L1-L3) - most common classical cause
Donovanosis (Klebsiella granulomatis)
Filariasis (Wuchereria bancrofti)
TB of the vulva (rare)
Crohn's disease (metastatic)

Pathogenesis (in LGV)

Tertiary stage of LGV (years after primary infection)
Chronic lymphatic obstruction → elephantiasis of vulva
Progressive fibrosis, ulceration, and scarring
Rectovaginal fistulae, anorectal strictures (more common in women due to lymphatic drainage pattern)

Clinical Features

Gross, brawny oedema of the vulva and labia (elephantiasis vulvae)
Polypoid hypertrophic lymphoedematous tissue ("lymphorrhoids" - perianal polypoid masses)
Chronic indolent ulcers with undermined edges
Anorectal stricture: crampy pain, ribbon-like stools, constipation
Rectovaginal/vesicovaginal fistulae
Risk of squamous cell carcinoma (long-standing esthiomene)

Management

Medical:

Doxycycline 100 mg BD x 21 days (minimum); prolonged courses needed
Azithromycin 1 g weekly x 3+ weeks
Treat underlying filarial infection if applicable

Surgical:

Excision of lymphoedematous tissue
Dilatation of anorectal strictures
Fistula repair
Skin grafting as needed

B. HAART (Highly Active Antiretroviral Therapy)

Definition

HAART refers to combination antiretroviral therapy (cART) using at least 3 antiretroviral agents from 2 or more drug classes, designed to suppress HIV replication to undetectable levels (<50 copies/mL).

Drug Classes and Mechanisms

Class	Mechanism	Examples
NRTIs (Nucleoside/Nucleotide Reverse Transcriptase Inhibitors)	Competitive inhibition + chain termination of reverse transcriptase	Tenofovir (TDF/TAF), Zidovudine (AZT), Lamivudine (3TC), Emtricitabine (FTC), Abacavir (ABC)
NNRTIs (Non-nucleoside RTIs)	Non-competitive binding to RT (different site)	Efavirenz (EFV), Nevirapine (NVP), Rilpivirine, Doravirine
PIs (Protease Inhibitors)	Block HIV protease, preventing viral maturation	Lopinavir/r, Darunavir/r, Atazanavir
INSTIs (Integrase Strand Transfer Inhibitors)	Block integration of viral DNA into host genome	Dolutegravir (DTG), Raltegravir, Bictegravir
Entry/Fusion Inhibitors	Block CCR5 co-receptor (Maraviroc) or gp41 fusion (Enfuvirtide)	Maraviroc, Enfuvirtide

Preferred First-Line Regimen (WHO/NACO India)

TDF + 3TC (or FTC) + DTG (Tenofovir + Lamivudine + Dolutegravir)

High barrier to resistance (DTG)
Single daily pill available
Well tolerated

Goals of HAART

Viral suppression: HIV RNA <50 copies/mL
CD4 count recovery (>500 cells/mm³)
Prevention of AIDS-defining illnesses
Prevention of transmission (U=U: Undetectable = Untransmittable)
Normalization of life expectancy

HAART in STI Context

When to start: Immediately in all HIV-positive patients regardless of CD4 count
IRIS (Immune Reconstitution Inflammatory Syndrome): Paradoxical worsening of OIs (e.g., worsening of TB, CMV, Kaposi's) after HAART initiation - due to restored immune response
OHL (Oral Hairy Leukoplakia) improves/resolves with HAART
Molluscum contagiosum, Kaposi's sarcoma resolve with immune recovery

Side Effects of Key Drugs

Tenofovir: nephrotoxicity, Fanconi syndrome, bone mineral density loss
Efavirenz: CNS effects (vivid dreams, depression), teratogenic
Dolutegravir: weight gain, neural tube defects (peri-conception - use with caution)
Zidovudine: bone marrow suppression, myopathy
Lopinavir/r: dyslipidaemia, GI intolerance, lipodystrophy

Q4. Role of Counselling in Management of STI

Introduction

Counselling is the process of helping individuals understand their health condition, cope with it, and adopt health-seeking behaviour. In STI management, it is an integral component that goes beyond prescribing medication - it addresses behaviour, partner notification, and prevention.

Goals of STI Counselling

Reduce stigma and facilitate disclosure
Promote testing and treatment compliance
Ensure partner treatment (prevent re-infection)
Encourage behaviour change (condom use, partner reduction)
Prevent complications (PID, infertility, congenital infection)
Address psychosocial issues (anxiety, depression, relationship strain)

Types of Counselling in STI

1. Pre-Test Counselling

Explain nature and purpose of the test
Discuss window period (especially for HIV - 3-4 weeks for 4th generation Ag/Ab assay)
Discuss implications of positive and negative results
Obtain informed consent
Risk assessment (sexual history, risk behaviours)
Dispel myths and address confidentiality concerns

2. Post-Test Counselling

If Positive:

Break news sensitively (in private, non-judgmental)
Explain diagnosis, treatment, and prognosis
Discuss partner notification (voluntary or assisted)
Address immediate emotional needs (denial, anger, fear)
Reinforce treatment adherence
Discuss safer sex practices, condom demonstration
Plan follow-up

If Negative:

Explain window period - may need repeat testing
Reinforce continued safe sex practices
Address risk reduction strategies
Not a "clearance certificate"

3. Partner Notification and Contact Tracing

STI	Look-back Period
Primary Syphilis	3 months
Secondary Syphilis	6 months
Early Latent Syphilis	1 year
Gonorrhoea	2 months
Chlamydia	6 months
LGV	30 days before symptoms

Methods:

Patient referral: Patient informs partners themselves
Provider referral: Healthcare provider notifies
Contract referral: Patient agrees to notify within a set time, provider follows up

4. Behaviour Change Communication (BCC)

Condom promotion and correct usage counselling
Reduction of concurrent partners
Avoidance of commercial sex / needle sharing
Prompt treatment of STIs reduces HIV risk

5. Specific Counselling Situations

HIV/AIDS Counselling (ICTC - Integrated Counselling and Testing Centre):

SA-ICTC (Standalone): in district hospitals
F-ICTC (Facility-based): integrated in ANC/TB clinics
Mobile ICTC: outreach
PPTCT (Prevention of Parent-to-Child Transmission): ANC counselling for HIV+ mothers

Syphilis: Counsel about treatment duration, need to avoid sexual contact until treated, re-infection risk

Herpes: Counsel about lifelong nature, asymptomatic shedding, antiviral suppression for frequent recurrences and partners

HPV/Warts: Counsel that warts may recur, HPV may persist, Pap smear surveillance for partners, vaccination

Leprosy Counselling (special emphasis):

Reassure that leprosy is curable with MDT
Dispel myths about heredity and curse
Explain importance of completing 6/12 months MDT
Counsel on self-care of anaesthetic limbs (daily inspection, soaking, oiling)
Prevent disability by recognizing reaction symptoms early
Socially rehabilitate - employment, family reintegration
Stigma reduction in community

6. Components of Effective STI Counselling (5 C's)

Consent - informed, voluntary
Confidentiality - protected health information
Counselling - adequate pre/post test
Correct results - quality-assured testing
Connections - to care, treatment, and support services

Documentation and Follow-up

Record counselling in confidential register
Schedule follow-up: test of cure (gonorrhoea 1 week, syphilis 3/6/12 months VDRL)
Evaluate for treatment response and re-counselling needs

Q5. (A) Newer Drugs in Leprosy (B) Vaccines in Leprosy

A. Newer Drugs in Leprosy

Background

With the rare emergence of M. leprae resistance to standard MDT agents (especially Dapsone, Rifampicin), newer drugs have been investigated. These also form the basis of alternative MDT (A-MDT) regimens.

1. Fluoroquinolones

Ofloxacin

Mechanism: Inhibits DNA gyrase (topoisomerase II) and topoisomerase IV
Bactericidal against M. leprae
Dose: 400 mg/day
Used in Rifampicin-resistant leprosy or Dapsone intolerance
SE: GI upset, photosensitivity, tendinopathy

Moxifloxacin

Newer 8-methoxyfluoroquinolone
Most potent fluoroquinolone against M. leprae
Dose: 400 mg/day
Faster bacterial killing compared to Ofloxacin
Used in newer MDR regimens

Sparfloxacin

400 mg/day; phototoxicity more common

2. Minocycline

Semi-synthetic tetracycline
Mechanism: Inhibits bacterial protein synthesis (30S subunit)
Dose: 100 mg/day
Unique among tetracyclines in being bactericidal against M. leprae
Used when Rifampicin, Dapsone, or Clofazimine contraindicated
Avoids Clofazimine's skin pigmentation

3. Clarithromycin

Macrolide; inhibits 50S ribosomal subunit
Dose: 500 mg/day
Bactericidal activity against M. leprae in mouse footpad studies
Used in alternative regimens

4. Rifapentine

Long-acting rifamycin (structurally related to Rifampicin)
Longer half-life allows less frequent dosing
Potentially useful in intermittent regimens

ROM Regimen (Single-Dose for Single Lesion PB Leprosy)

Rifampicin 600 mg + Ofloxacin 400 mg + Minocycline 100 mg - single dose

WHO-recommended for single skin lesion PB leprosy (field conditions)
Cure rate comparable to 6-month PB MDT
Advantage: Single supervised dose, no compliance issues

MDR Leprosy Regimen (WHO 2018)

For proven Rifampicin-resistant leprosy:

6 months: Clarithromycin 500 mg/day + Moxifloxacin 400 mg/day + Minocycline 100 mg/day
18 months: Moxifloxacin 400 mg/day + Minocycline 100 mg/day (or Clofazimine 50 mg/day)

Drugs for Reactions (Newer Approaches)

Thalidomide:

Mechanism: TNF-alpha inhibition + immunomodulation
Highly effective for ENL (Type 2 reaction)
Dose: 100-300 mg/day
STRICT CONTRAINDICATION: Teratogenic (phocomelia) - cannot use in women of childbearing age
Sedation, peripheral neuropathy are adverse effects

Pentoxifylline:

TNF-alpha inhibitor; alternative to Thalidomide for ENL
Dose: 400 mg TDS

Anti-TNF agents (experimental):

Infliximab, Etanercept investigated for severe refractory ENL

B. Vaccines in Leprosy

1. BCG (Bacillus Calmette-Guerin) - Most Evidence

Type: Live attenuated Mycobacterium bovis
Protection rate: 20-80% (highly variable by geography; ~34% in India, up to 80% in some trials)
Mechanism: Cross-reactive immunity between BCG and M. leprae (both are mycobacteria sharing antigens, especially PGL-1)
BCG also protects against tuberculoid end of spectrum more than lepromatous
Recommendation: Part of India's National Immunization Programme (given at birth)

2. MIP (Mycobacterium indicus pranii) Vaccine - Licensed in India

Formerly called: ICRC bacillus (Indian Cancer Research Centre)
Type: Heat-killed, non-pathogenic mycobacterium with cross-reactive antigens
Developed by: JALMA, Agra (ICMR)
Trials: TLMI (Trial of Leprosy in Mesodermal Immunostimulant) - large RCT in India
Protection: ~65% protective efficacy in contacts of leprosy patients
Additional benefit: Accelerates bacterial clearance in MB patients when used adjuvant to MDT
Dose: 2 intradermal injections (0.1 mL each) at 0 and 6 months
Licensed by DCGI in India as an immunotherapeutic adjunct for leprosy
Currently available under NLEP for contacts in endemic areas

3. BCG + Killed M. leprae Vaccine

Combination of BCG with heat-killed M. leprae extracted from armadillo tissue
Superior protection to BCG alone in some studies
Limited by supply of M. leprae (armadillo-sourced)

4. BCG + MLSA (M. leprae Soluble Antigen)

Combination vaccine studied in Malawi and other endemic regions
Mixed results

5. Chemoprophylaxis as "Vaccine Equivalent"

Single-Dose Rifampicin (SDR) Prophylaxis:

Given to household and social contacts of newly diagnosed leprosy patients
Dose: Adults 600 mg; Children (2-15 years) 300 mg; <2 years 150 mg
COLEP Trial (Bangladesh): 57% reduction in leprosy incidence in contacts at 2 years
WHO-recommended (2016 guidelines): SDR post-exposure prophylaxis (SDR-PEP) for contacts in hyperendemic areas
Not suitable for those already on MDT, TB treatment, or contacts with signs of leprosy

Summary Table: Vaccines

Vaccine	Type	Efficacy	Status
BCG	Live attenuated	20-80% variable	National programme
MIP (ICRC)	Killed	~65%	Licensed in India
BCG + killed M. leprae	Combined	Higher than BCG alone	Research/limited use
SDR Rifampicin (PEP)	Chemoprophylaxis	~57% at 2 years	WHO-recommended

Q6. Deformities in Leprosy and Their Management

Introduction

Deformities in leprosy result from nerve damage (neuritis), repeated trauma to anaesthetic limbs, muscle weakness/paralysis, and progressive bone resorption. Prevention and early intervention are more important than late surgical correction.

WHO Disability Grading (2016)

Grade	Eyes	Hands	Feet
0	No problem	No problem	No problem
1	Anaesthesia present, no visible problem	Anaesthesia present, no visible problem	Anaesthesia present, no visible problem
2	Visible problem: lagophthalmos, iridocyclitis, corneal opacity	Visible problem: claw hand, absorption, contracture, wound	Visible problem: claw foot, absorption, contracture, wound

Nerves Commonly Affected and Resultant Deformities

Nerve	Site of Damage	Deformity
Ulnar nerve	Elbow	Claw hand (ring and little fingers) - "Ulnar claw"
Median nerve	Wrist/forearm	Thenar wasting, claw index/middle fingers, Ape thumb deformity
Combined ulnar + median	Forearm	Complete claw hand ("main-en-griffe")
Radial nerve	Spiral groove	Wrist drop
Common peroneal (lateral popliteal)	Fibula neck	Foot drop
Posterior tibial	Ankle	Clawing of toes, plantar anaesthesia, plantar ulcers
Facial nerve	Zygomatic arch	Lagophthalmos (inability to close eye)
Greater auricular nerve	Neck	Thickened nerve visible
Supraorbital nerve	Forehead	Loss of forehead sensation

Specific Deformities

1. Claw Hand (Main-en-griffe)

Cause: Intrinsic muscle paralysis (lumbrical and interossei) due to ulnar/median nerve damage
Features: Hyperextension at MCPs, flexion at IPJs of affected fingers
Ulnar claw: Ring and little fingers (ulnar 2 fingers)
Median claw: Index and middle fingers
Combined: All 4 fingers clawed ("complete claw")
Prevention: Passive stretching exercises, cocking-up splint prevents fixed contracture

Surgery:

Fowler's operation: Extensor digitorum communis (EDC) re-routing to lumbrical position
Brand's operation: Transfer of FDS (flexor digitorum superficialis) to replace intrinsic muscles
Bunnel's lasso procedure: Dynamic tenodesis
Correction of MCP hyperextension by capsulodesis

2. Foot Drop

Cause: Lateral popliteal (common peroneal) nerve palsy
Features: Inability to dorsiflex and evert foot; high-stepping gait; equinovarus deformity
Prevention: Foot drop splint (plastic AFO - ankle-foot orthosis), physical therapy

Surgery:

Tibialis posterior transfer (through interosseous membrane to dorsum of foot) - most common
Peroneal bypass using plantaris tendon

3. Plantar Ulcers (Trophic Ulcers)

Cause: Anaesthesia of sole (posterior tibial nerve) + trauma + repeated pressure
Features: Usually under metatarsal heads; painless; punched-out; secondary infection leads to osteomyelitis, bone absorption
Management:
- Rest, offloading with Total Contact Cast (TCC) or Scotchcast boot
- Wound debridement
- Antibiotics for secondary infection
- Microcellular rubber (MCR) footwear with moulded insoles
- Patient education: daily foot inspection, soaking and oiling, avoidance of barefoot walking

4. Lagophthalmos (Inability to Close Eye)

Cause: Facial nerve (zygomatic branch) palsy
Consequences: Corneal exposure → desiccation → ulceration → blindness
Management:
- Protective spectacles/goggles
- Artificial tears (methyl cellulose eye drops) QID
- Eye pad at night
- Tarsorrhaphy (lateral suturing of eyelids) - temporary or permanent
- Lateral fascial sling procedure
- Gold weight implant in upper eyelid (gravity-assisted closure)

5. Saddle Nose Deformity

Cause: Destruction of nasal cartilage and bone by granulomatous infiltration (LL)
Also due to septal perforation and nasal mucosal atrophy
Surgery: Rhinoplasty with cartilage graft (rib/ear cartilage) or silastic implant

6. Absorption of Digits (Autoamputation)

Cause: Repeated trauma, trophic ulcers, osteomyelitis in anaesthetic fingers/toes
Progressive resorption of phalanges → "pencil-tip" tapering
Prevention: Self-care regimen (soaking hands in water 20 min, applying oil, wearing protective gloves)
Amputation may be required for infected gangrenous digits

7. Gynaecomastia and Testicular Atrophy

In LL leprosy due to direct bacillary infiltration of testes
Loss of testosterone → gynaecomastia, loss of libido, infertility

Prevention of Disabilities - POD Programme

The Prevention of Disabilities (POD) programme under NLEP:

Monthly examination of eyes, hands, feet at PHC level
Self-care training for all leprosy patients
Provision of MCR footwear and protective aids
Referral to PMRC (Physiotherapy, Medical, Rehabilitation Centres)
Reconstructive surgery at district/referral centres

Reconstructive Surgery Indications (Timing)

Only after completion of MDT
Patient must be bacteriologically inactive
No active reactions
Aim: improve function, prevent further damage, cosmetic correction

Q7. (A) Congenital Syphilis (B) Non-Treponemal Serological Tests in Syphilis

A. Congenital Syphilis

Definition

Congenital syphilis results from transplacental transmission of Treponema pallidum from an infected mother to the fetus, typically after the 16th week of gestation (when Langerhans cells disappear, allowing fetal infection).

Transmission Risk

Primary syphilis: ~75-90% transmission
Secondary: ~90%
Early latent: ~40%
Late latent: ~10%

Classification

Early Congenital Syphilis (< 2 years of age)

Skin and Mucous Membranes:

Syphilitic pemphigus: Bullae on palms and soles (pathognomonic at birth)
Snuffles: Serosanguineous nasal discharge (earliest sign); highly infectious
Condylomata lata: broad, flat moist lesions around anus/genitals
Mucous patches in mouth

Systemic:

Hepatosplenomegaly (most common internal finding)
Jaundice, anaemia (haemolytic)
Osteochondritis: metaphyseal irregularity on X-ray; Wimberger's sign (bilateral symmetric tibial destruction)
Periostitis
Chorioretinitis, uveitis
Meningitis (neurosyphilis in neonates)
"Pseudoparalysis of Parrot" - refusal to move limb due to bone pain

Late Congenital Syphilis (> 2 years of age)

These are stigmata from earlier inflammation and scarring:

Hutchinson's Triad (pathognomonic):

Hutchinson's teeth - upper permanent central incisors: notched, barrel-shaped, smaller, widely spaced (appear at 6-8 years with permanent teeth)
Interstitial keratitis - corneal vascularization and scarring; appears at 5-15 years; may cause blindness
Eighth nerve deafness - sensorineural; progressive; appears in adolescence

Other Stigmata:

Rhagades (perioral fissures): Linear scars radiating from angles of mouth, nose, anus due to healing of early mucocutaneous lesions
Saddle nose: Due to nasal septal destruction
Frontal bossing (Olympian brow)
Short maxilla with relative mandibular prominence
High palatal arch
Sabre tibia (Saber shin): Anterior bowing due to periostitis with new bone formation
Clutton's joints: Bilateral painless synovitis of knee joints (immune-mediated)
Moon's molars (mulberry molars): First lower molars - irregular, rounded, multiple cusps
Higoumenakis sign: Unilateral thickening of sternoclavicular portion of clavicle

Diagnosis

VDRL/RPR on infant serum (note: maternal IgG crosses placenta - may be passively transferred)
Infant VDRL titre >4x maternal titre: diagnostic
IgM-FTA-ABS (detects fetal-specific antibody - cannot cross placenta)
Dark-field microscopy of nasal discharge (snuffles), skin lesions
Long bone X-rays: metaphyseal irregularity, periostitis, Wimberger's sign
CSF analysis for neurosyphilis

Management

Early (< 1 year):

Aqueous Crystalline Penicillin G 50,000 units/kg IV every 12 hours x 10-14 days
OR Procaine Penicillin G 50,000 units/kg IM once daily x 10-14 days

Late (> 1 year):

Aqueous Crystalline Penicillin G 50,000 units/kg IV every 6 hours x 10-14 days

Prevention: Screening all pregnant women with VDRL at first ANC visit (and third trimester in high-prevalence areas); treat seropositive mothers.

B. Non-Treponemal Serological Tests (NTT) in Syphilis

Principle

Non-treponemal tests detect IgG and IgM antibodies directed against cardiolipin-lecithin-cholesterol antigen (a phospholipid released from host cell membranes damaged by T. pallidum). These are NOT specific to T. pallidum.

Tests

1. VDRL (Venereal Disease Research Laboratory Test)

Type: Flocculation test
Antigen: Cardiolipin-lecithin-cholesterol suspension
Reading: Macroscopic in test tube (flocculation = positive)
Quantitative: Reported as titres (e.g., 1:4, 1:32); reflect disease activity
Use: Screening + monitoring treatment response + CSF (ONLY NTT validated for CSF)
Sensitivity: Primary 70-80%, Secondary 99-100%, Late 70-80%

2. RPR (Rapid Plasma Reagin)

Type: Flocculation test
Antigen: Cardiolipin + charcoal particles (allows macroscopic reading)
Reading: Macroscopic on card test (agglutination = positive)
Advantage over VDRL: Can use unheated serum (plasma); field-friendly; no microscope needed
Same sensitivity as VDRL but more convenient
Cannot be used on CSF

3. TRUST (Toluidine Red Unheated Serum Test)

Modification of RPR with toluidine red indicator; similar performance to RPR

Titres and Clinical Correlation

Stage	Typical VDRL Titre
Primary	1:4 to 1:16
Secondary	1:16 to 1:512 (highest)
Latent (early)	Moderate
Latent (late/Tertiary)	Low or negative

Treatment response: 4-fold (2 dilution) fall in titre at 6-12 months = adequate treatment

Biological False Positive (BFP) VDRL

Acute BFP (<6 months):

Viral infections (EBV, CMV, HIV, Hepatitis, Varicella)
Bacterial: SBE, TB
Malaria
Post-vaccination

Chronic BFP (>6 months):

SLE (most important - antiphospholipid antibodies)
Rheumatoid arthritis
Lepromatous leprosy
Thyroid diseases
Old age
Pregnancy
IV drug use

Rule: BFP titre is usually LOW (<1:8); true syphilis with high titre + treponemal test negative = BFP

Treponemal Confirmatory Tests (for comparison)

FTA-ABS (Fluorescent Treponemal Antibody Absorption) - most sensitive
TPHA (Treponema pallidum Haemagglutination Assay)
MHA-TP
TPPA (T. pallidum Particle Agglutination)
These remain positive for life (cannot monitor treatment)

Q8. Herpes Genitalis

Introduction

Herpes genitalis is a chronic, recurrent viral STI caused primarily by Herpes Simplex Virus type 2 (HSV-2) and increasingly by HSV-1 (due to orogenital contact). It is one of the most prevalent STIs globally and is characterized by recurrent painful ulcers.

Etiology

HSV-2: Responsible for ~80% of genital herpes; strongly associated with genital tract; tends to recur more frequently
HSV-1: Increasing cause of primary genital herpes, particularly in young adults; recurs less frequently genitally
Both are enveloped double-stranded DNA viruses

Pathogenesis

Virus enters via mucosa/abraded skin
Replicates locally → produces primary lesion
Ascends peripheral sensory nerves → establishes latency in dorsal root ganglia (sacral ganglia S2-S4 for genital herpes)
Periodic reactivation → anterograde transport → recurrent lesions or asymptomatic shedding

Triggers for reactivation: Fever, trauma, UV light, stress, immunosuppression, menstruation

Clinical Features

Primary Genital Herpes (First Episode)

Incubation: 2-12 days (mean 4 days)
Prodrome: Tingling, burning, neuralgia 24-48 hours before lesions
Vesicles: Grouped vesicles on erythematous base → rupture → shallow, painful ulcers with scalloped margins
Sites: Glans, prepuce, shaft (males); labia majora/minora, cervix, vagina (females)
Constitutional symptoms: Fever, malaise, myalgia, headache (more severe in primary)
Tender bilateral inguinal lymphadenopathy
Dysuria, urinary retention (sacral radiculopathy)
Cervicitis (most common manifestation in women - may be asymptomatic)
Duration: 2-3 weeks without treatment

Recurrent Genital Herpes

Less severe, shorter duration (7-10 days)
Prodrome in ~50%
Unilateral involvement common
Constitutional symptoms minimal/absent
Typically 4-5 episodes per year (HSV-2); 1-2/year (HSV-1)

Asymptomatic Shedding

Occurs in ~70% of HSV-2 seropositive individuals
Responsible for most transmission events (majority of partners infected during asymptomatic periods)

Complications

Sacral radiculopathy: Urinary retention, constipation, neurogenic bladder
Herpes encephalitis (rare in immunocompetent; HSV-1 more common for CNS)
Disseminated herpes in immunocompromised (hepatitis, pneumonitis, encephalitis)
Neonatal herpes (peripartum transmission during vaginal delivery): highest risk when primary infection occurs near delivery; case fatality rate ~50% untreated
Herpetic whitlow: HSV infection of finger (inoculation)
Erythema multiforme: Recurrent HSV is most common trigger
Increased HIV susceptibility: Genital ulcers disrupt mucosal barrier; HSV ulcers increase HIV acquisition 3-fold and transmission

Diagnosis

Clinical Diagnosis

Classic grouped vesicles/ulcers with prodrome and recurrence pattern is often sufficient

Laboratory Tests

Test	Sensitivity	Notes
Tzanck smear	60-70%	Multinucleated giant cells + intranuclear inclusions (Cowdry type A); does not distinguish HSV-1 from HSV-2
Viral culture	Gold standard	Cells from base of fresh vesicle; CPE in 24-48 hours; sensitivity highest from vesicles
PCR (nucleic acid amplification)	Most sensitive	Method of choice for CSF in encephalitis; preferred over culture
Antigen detection (DFA)	Rapid
Serology (HSV-2 IgG)	Type-specific	Confirm HSV-2 seroprevalence; not useful for acute diagnosis; useful for counselling

Histology: Intranuclear inclusions (Cowdry type A), multinucleated giant cells with "ground glass" nuclei, "moulding" of nuclei

Management

Antiviral Drugs

Mechanism: Thymidine kinase-dependent phosphorylation → nucleoside analogue → inhibits viral DNA polymerase

Primary Episode:

Acyclovir 400 mg TDS x 7-10 days OR 200 mg 5 times/day x 7-10 days
Valacyclovir 1 g BD x 7-10 days (better bioavailability, simpler dosing)
Famciclovir 250 mg TDS x 7-10 days
Start ASAP, ideally within 72 hours; may extend if new lesions forming

Recurrent Episode:

Acyclovir 400 mg TDS x 5 days OR 800 mg BD x 5 days
Valacyclovir 500 mg BD x 3 days
Famciclovir 1000 mg BD x 1 day (single-day regimen)

Suppressive Therapy (≥6 recurrences/year, or for partner protection):

Acyclovir 400 mg BD (daily suppression)
Valacyclovir 500 mg once daily OR 1 g once daily
Famciclovir 250 mg BD
Reduces recurrences by ~75%; reduces asymptomatic shedding; reduces transmission to partners by ~50%

Severe/Disseminated/Immunocompromised:

IV Acyclovir 5-10 mg/kg every 8 hours x 5-7 days

Neonatal Herpes:

IV Acyclovir 20 mg/kg every 8 hours x 14-21 days
Caesarean section when active genital lesions at term

Counselling Points

Explain lifelong, recurrent nature
Asymptomatic shedding and transmission risk
Condom use reduces but does not eliminate transmission
Suppressive therapy for partners / frequent recurrences
Neonatal risk - inform obstetrician if pregnant
No cure but manageable

Q9. (A) Nerve Biopsy in Leprosy (B) Clofazimine

A. Nerve Biopsy in Leprosy

Introduction

Nerve biopsy is an important diagnostic and research tool in leprosy, providing histopathological evidence of nerve involvement and granulomatous inflammation.

Indications

Diagnostic challenge: Pure neuritic leprosy (no skin lesions) where slit-skin smear and skin biopsy are non-contributory
Atypical presentations: When clinical diagnosis uncertain
Mononeuropathy multiplex: To distinguish leprosy from other causes (vasculitis, sarcoidosis, hereditary neuropathy)
Research purposes: To study immunopathology of leprosy neuropathy
Occasionally: In reactions to confirm nerve involvement

Nerve Most Commonly Biopsied

Sural nerve (posterior to lateral malleolus) - most commonly used

Purely sensory nerve; biopsy causes only sensory loss over lateral foot
Accessible, superficial
Also used: Superficial peroneal nerve, radial cutaneous nerve

Technique

Local anaesthesia (lignocaine without adrenaline)
Longitudinal incision over nerve
Excise 2-3 cm segment
Divide: one portion for histology (formalin-fixed), one for Wade-Fite stain, one for electron microscopy (glutaraldehyde)
Gentle handling to avoid crush artefact

Histopathological Findings

Tuberculoid End (TT/BT):

Well-formed epithelioid cell granulomas within nerve fascicles
Langhans giant cells
Dense lymphocytic cuffing
Nerve fibres obliterated (destruction)
AFB: absent or rare

Borderline (BT-BL):

Granulomas less well formed
Perineural infiltration
"Onion peel" perineural fibrosis (characteristic of BL - concentric layers of fibroblasts)
Partial nerve destruction

Lepromatous End (BL/LL):

Foamy macrophages (lepra cells) within nerve
No granuloma formation
Dense bacillary load in nerves
Schwann cells infected with bacilli
"Onion peel" perineural fibrosis: most pronounced
Loss of myelinated and unmyelinated fibres

Pure Neuritic Leprosy (PNL):

Granulomas in nerve, sometimes with AFB
Classified along R-J spectrum based on nerve histology
No skin lesions clinically

Special Stains

Wade-Fite stain (modified AFB stain): Used for M. leprae in tissue (gentler - preserves lipid coat of M. leprae unlike Ziehl-Neelsen)
S-100: Schwann cell marker - shows Schwann cell involvement
EMA (Epithelial Membrane Antigen): Perineurium marker

Limitations

Permanent sensory deficit at biopsy site
Sampling error (skip lesions)
Replaced by less invasive methods (skin biopsy, nerve ultrasound) in many centres
Requires expertise in interpretation

B. Clofazimine

Classification

Rimino-phenazine dye; lipophilic compound

Mechanism of Action

Bactericidal against M. leprae (slower action than Rifampicin; acts primarily on MB leprosy)
Binds to mycobacterial DNA (guanine-specific) → inhibits template function → inhibits DNA replication
Anti-inflammatory property: Inhibits neutrophil migration, lysosomal enzyme release, and suppresses TNF-α → used for ENL
Promotes reactive oxygen species generation within mycobacteria

Pharmacokinetics

Highly lipophilic → stored in fat, skin, reticuloendothelial system
Half-life: ~70 days (range 35-100 days) - extremely long
This long t½ accounts for prolonged skin pigmentation even after stopping drug
Excreted in faeces, bile, sputum, sebaceous secretions
NOT removed by dialysis
Accumulates in macrophages

Dose in MDT

MB MDT supervised: 300 mg once monthly
MB MDT self-administered: 50 mg daily
ENL treatment: 100-300 mg/day (in 3 divided doses)

Side Effects (Important for Exams)

Skin Pigmentation (most characteristic):

Red-brown to slate-grey/black discolouration of skin, especially in leprosy lesions and sun-exposed areas
Due to drug deposition in macrophages + lipofuscin-like pigment
Reversible but takes 1-2 years after stopping drug
Also causes red discolouration of tears, sweat, urine, faeces, breast milk, sputum

GI Side Effects:

Nausea, vomiting, diarrhoea, abdominal pain
Crystal-storing histiocytosis: Clofazimine crystals deposited in intestinal wall and mesenteric lymph nodes → eosinophilic enteritis, small bowel obstruction (rare but serious)
Anorexia, weight loss

Ichthyosis: Dry, scaly skin (especially limbs) - due to drug deposition in skin

Other: Splenic infarction (rare), elevated blood glucose (rare)

Uses Beyond Leprosy

Multidrug-resistant TB (MDR-TB): WHO-recommended Group B drug in MDR-TB regimens
MAC (Mycobacterium avium complex) infection in AIDS patients
Crohn's disease (experimental)
Chronic discoid lupus erythematosus (DLE) - as immunomodulator

Contraindications / Cautions

Pregnancy: Category C - limited data; generally used if benefits outweigh risks
GI disease: use cautiously
Inform patients about inevitable skin discolouration (important for compliance)

Q10. (A) ENL (Erythema Nodosum Leprosum) (B) OHL (Oral Hairy Leukoplakia)

A. ENL (Erythema Nodosum Leprosum) - Type 2 Lepra Reaction

Definition

ENL is an acute inflammatory reaction occurring in multibacillary leprosy (BL and LL types), characterized by the eruption of NEW tender erythematous nodules with systemic features, superimposed on the existing clinical picture of leprosy.

Epidemiology

Occurs in ~50% of LL and ~25% of BL patients
More common during first year of MDT; also occurs after completion of treatment
Can recur and become chronic/recurrent in some patients

Immunopathogenesis

Type III hypersensitivity (Immune Complex Mediated)
Antigen (M. leprae fragments, especially PGL-1) + high levels of circulating antibodies → immune complex formation → complement activation → neutrophil recruitment → acute inflammation
TNF-α plays a central role (explains efficacy of Thalidomide/Pentoxifylline)
Associated with massive antigen release (during bacillary death from MDT, concurrent infection, pregnancy)

Clinical Features

Skin:

NEW crops of tender, erythematous papules and nodules (2-4 cm)
Mainly on face (especially malar region), extensor surface of forearms, thighs, trunk
Lesions may vesiculate, pustulate, become necrotic (ENL necroticans), ulcerate
Subside in 1-2 weeks, leaving pigmentation
Recurrent crops common

Systemic Features (distinguish from Type 1):

Fever (may be high and hectic) - most common
Malaise, anorexia, weight loss
Iridocyclitis (uveitis) → pain, photophobia → risk of blindness if untreated
Neuritis: Acute nerve pain and tenderness (without upgrading)
Orchitis/Epididymo-orchitis: Painful swollen testes; may → testicular atrophy, infertility
Arthritis/Arthralgia
Lymphadenopathy, hepatosplenomegaly
Dactylitis: Sausage-shaped swollen digits
Proteinuria, glomerulonephritis (immune complex deposition in kidney)

Histology of ENL

Dense neutrophilic infiltration in dermis (vasculitis with neutrophils)
Immune complexes in vessel walls
Fragmented bacilli (as opposed to solid bacilli in quiescent LL)
Foamy macrophages with globi (background LL histology)
Fibrinoid necrosis of vessel walls in severe cases

Laboratory Findings

Raised ESR, CRP
Leucocytosis (neutrophilia)
Elevated circulating immune complexes
C3/C4 complement consumed (low levels)
Proteinuria in renal involvement

Differential Diagnosis

Erythema nodosum (sarcoidosis, infections - lesions on shins, no systemic features of leprosy)
Sweet's syndrome
Lucio's phenomenon (specific to Lucio leprosy - LL variant; ischaemic ulceration, not nodules)
Type 1 reaction: OLD existing lesions inflamed, no systemic features, no new nodules, no neutrophilic infiltrate

Management

Mild ENL (skin only, no systemic features):

Aspirin/NSAIDs
Continue MDT

Moderate to Severe ENL:

First Line:

Thalidomide: 100-300 mg/day (MOST EFFECTIVE for ENL)
- Mechanism: Inhibits TNF-α mRNA stabilization → reduces TNF-α
- ONLY in males or post-menopausal females (severe teratogen)
- Side effects: Sedation, peripheral neuropathy, DVT
Prednisolone: 40-60 mg/day, tapered over 3-6 months
- Preferred in females of childbearing age
- Also first choice when neuritis or iridocyclitis present

For Recurrent/Chronic ENL:

Clofazimine 300 mg/day (100 mg TDS) for 3-6 months - has anti-inflammatory property
- Slower onset (4-6 weeks) but steroid-sparing effect
- Preferred for chronic ENL to reduce steroid dependence

Supportive:

Rest, adequate nutrition
Treat precipitating factors (infections, pregnancy stress)
Ophthalmology review for iridocyclitis (mydriatics + topical steroids)
Urological review for orchitis
Continue MDT (do NOT stop MDT during reactions)

B. OHL (Oral Hairy Leukoplakia)

Definition

OHL is a white, non-removable, corrugated ("hairy") plaque occurring on the lateral borders of the tongue, caused by Epstein-Barr Virus (EBV) replication in oral epithelial cells, almost exclusively in immunocompromised individuals, particularly HIV-infected patients.

Etiology and Pathogenesis

EBV (Human Herpesvirus 4) - lytic infection of oral epithelium
Unlike EBV-associated B-cell lymphoma (latent infection), OHL is due to productive/lytic EBV replication
Immunosuppression (HIV, organ transplant, haematological malignancies) allows EBV to replicate unchecked in epithelium
CD4 count usually <200 cells/mm³ when OHL appears in HIV patients

Clinical Features

Site: Lateral border of tongue (most characteristic); bilateral in 50%
- Rarely: dorsal tongue, buccal mucosa, floor of mouth, soft palate
Appearance: White, corrugated ("hairy") plaques with vertical folds/ridges; shaggy or "hairy" surface texture; cannot be wiped off (unlike candidiasis)
Symptoms: Usually asymptomatic; occasionally mild discomfort or altered taste
No malignant potential (does not transform to carcinoma)

Significance in HIV

OHL as an AIDS indicator: Marks significant immunosuppression
Associated with rapid HIV progression to AIDS
CD4 count typically <200/mm³
Presence of OHL in an otherwise healthy person → screen for HIV

Histology (Definitive Diagnosis)

Epithelial hyperparakeratosis with "balloon cells" in spinous layer (koilocytosis)
Herpetic-type nuclear changes (Cowdry type A inclusions in some cells)
No dysplasia (unlike oral leukoplakia)
Minimal or absent inflammatory infiltrate
EBER in-situ hybridization (ISH): Demonstrates EBV-encoded RNA (EBER) in epithelial cells - gold standard histological confirmation

Diagnosis

Method	Findings
Clinical	Non-removable white corrugated plaque on lateral tongue
Cytology/scrape	Balloon cells, koilocytes
Histology (biopsy)	Hyperparakeratosis, balloon cells, minimal inflammation
EBER-ISH	EBV in epithelial cells (confirmatory)
EBV PCR	High viral load in epithelial scraping

Differential Diagnosis

Condition	Distinguishing Feature
Oral Candidiasis	White plaques REMOVABLE with spatula; KOH shows hyphae; responds to antifungals
Oral leukoplakia (idiopathic)	Unilateral; non-HIV; biopsy shows dysplasia; NOT removable
Lichen planus	Lace-like Wickham's striae; bilateral buccal mucosa; histology: band-like lymphocytic infiltrate
Geographic tongue	Migratory red patches with white borders; dorsal tongue
White sponge naevus	Hereditary; extensive white plaques; autosomal dominant

Management

No specific treatment required in most cases; reassurance if HIV well-controlled.

Indications for Treatment:

Symptomatic (pain, discomfort)
Patient concern (cosmesis)

Options:

HAART: Most effective - as immune recovery occurs (CD4 rises), OHL resolves spontaneously in >90% cases
Topical Podophyllin resin (25%): Weekly application; causes regression
Acyclovir/Valacyclovir: High-dose oral antiviral (4-8 g/day Acyclovir) - EBV-directed; OHL resolves but recurs when drug stopped
Topical Tretinoin: Some evidence
Foscarnet IV: For refractory cases in severely immunosuppressed

Prognosis: Recurrence is common if immunosuppression persists; resolves with effective HAART.

All 10 answers are now complete. Here is a quick reference summary:

Index of Answers

Q	Topic	Key Exam Points
1	Inguinal Bubo	DD: LGV (groove sign), Chancroid, Syphilis, Plague; Aspirate - never incise
2	Leprosy	Full R-J spectrum; BI scale; Th1 vs Th2 immunity; Type 1 vs Type 2 reactions; MDT regimens
3A	Esthiomene	Tertiary LGV; vulvar elephantiasis; anorectal stricture; Doxycycline x 21 days
3B	HAART	5 drug classes; TDF+3TC+DTG first-line; IRIS; U=U principle
4	STI Counselling	Pre/post-test; partner notification timelines; ICTC framework; 5 C's; leprosy-specific counselling
5A	Newer drugs in leprosy	ROM regimen; Moxifloxacin; Minocycline; Thalidomide for ENL; MDR-leprosy protocol
5B	Vaccines in leprosy	BCG (20-80%); MIP/ICRC (65%, licensed India); SDR prophylaxis (57% at 2 years)
6	Leprosy deformities	WHO Grade 0-2; claw hand surgeries (Brand's/Fowler's); foot drop (tibialis posterior transfer); POD programme
7A	Congenital Syphilis	Hutchinson's triad; Wimberger's sign; snuffles; Penicillin G treatment
7B	NTT in Syphilis	VDRL (flocculation, CSF-valid); RPR (card test); BFP causes; 4-fold titre fall = cure
8	Herpes Genitalis	HSV-2 > HSV-1; sacral ganglia latency; Tzanck smear; Acyclovir/Valacyclovir; suppressive therapy
9A	Nerve biopsy	Sural nerve; PNL diagnosis; onion-peel perineural fibrosis (BL); Wade-Fite stain
9B	Clofazimine	DNA binding + anti-TNF; t½ 70 days; red-brown pigmentation; crystal-storing histiocytosis
10A	ENL	Immune complex (Type III); NEW nodules + systemic features; Thalidomide (males), Prednisolone; Clofazimine for chronic
10B	OHL	EBV lytic; lateral tongue; non-removable; EBER-ISH; resolves with HAART; no malignant potential

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3rd Year Dermatology PG Theory Examination

Model Answers (10 Marks Each)

Q1. Differential Diagnosis & Management of Inguinal Bubo

Definition

Differential Diagnosis

A. STI-Related (Infective) Causes

Disease	Causative Agent	Character of Bubo
Lymphogranuloma Venereum (LGV)	Chlamydia trachomatis L1, L2, L3	Matted, multi-locular; groove sign (pathognomonic); fluctuant; may rupture
Chancroid	Haemophilus ducreyi	Unilocular, tender, fluctuant, overlying erythema; ruptures forming "kissing ulcers"
Primary Syphilis	Treponema pallidum	Non-tender, rubbery, discrete, bilateral - "Bubo of steel"
Herpes Genitalis	HSV-2 (mainly)	Tender, bilateral, does not suppurate
Donovanosis	Klebsiella granulomatis	Pseudo-bubo (subcutaneous granuloma, not true lymphadenopathy)

B. Non-STI Infective Causes

Bubonic Plague - Yersinia pestis; extremely tender, rapidly suppurating; systemic toxaemia; flea bite history
Tuberculosis - cold abscess; matted, non-tender; central caseation; sinuses
Filariasis - Wuchereria bancrofti; recurrent lymphangitis, lymphoedema
Cat-scratch disease - Bartonella henselae; scratch history; self-limiting
Pyogenic lymphadenitis - secondary to infected wounds of lower limb

C. Non-Infective Causes

Lymphoma (Hodgkin's/Non-Hodgkin's) - rubbery, non-tender, progressive
Metastatic carcinoma - hard, fixed, irregular (from vulva, penis, rectum, lower limb)
Reactive lymphadenopathy

Distinguishing Feature: Groove Sign of LGV

The inguinal ligament (Poupart's ligament) divides enlarged nodes above and below, creating a pathognomonic groove - present in ~20% of LGV cases.

Management

General Principles

Syndromic management when laboratory confirmation unavailable
Treat both partners simultaneously
Aspiration preferred over incision and drainage (I&D causes sinus formation)
Screen for other STIs (HIV, Syphilis, HBV)

Specific Treatment

LGV:

First line: Doxycycline 100 mg BD x 21 days
Alternative: Azithromycin 1 g weekly x 3 weeks OR Erythromycin 500 mg QID x 21 days
Pregnancy: Erythromycin 500 mg QID x 21 days

Chancroid:

Azithromycin 1 g single dose OR
Ceftriaxone 250 mg IM single dose OR
Ciprofloxacin 500 mg BD x 3 days OR
Erythromycin 500 mg TDS x 7 days

Syphilis (with bubo):

Benzathine Penicillin G 2.4 MU IM single dose

Plague:

Streptomycin 1 g IM BD OR Doxycycline 100 mg BD x 10 days
Strict isolation; notifiable disease

Bubo Aspiration Technique

Insert needle from healthy adjacent skin at an angle
Aspirate pus (avoids fistula formation)
Never perform cruciate incision (leads to chronic discharging sinus)

Partner Management

LGV: trace contacts within 30 days of symptom onset
Chancroid: trace within 10 days
Syphilis: trace within 3 months (primary), 6 months (secondary)

Q2. Leprosy - Clinical, Bacteriological, Histological, Immunological Features

Introduction

Leprosy (Hansen's Disease) is a chronic granulomatous infection caused by Mycobacterium leprae, an obligate intracellular bacillus affecting skin, peripheral nerves, mucous membranes, and eyes. Classified by Ridley-Jopling (R-J) spectrum and WHO classification.

Causative Organism - Bacteriological Features

Gram-positive, acid-fast bacillus (Ziehl-Neelsen stain)
Obligate intracellular; cannot be cultured on artificial media
Doubling time: 12-13 days (slowest of all bacteria)
Optimum growth temperature: 27-30°C (explains predilection for cooler body parts)
Viable bacilli stain solid; dead bacilli appear fragmented (Morphological Index - MI)
Bacteriological Index (BI): Logarithmic Ridley scale 1+ to 6+

BI Score	Bacilli per field
1+	1-10 in 100 fields
2+	1-10 in 10 fields
3+	1-10 per average field
4+	10-100 per average field
5+	100-1000 per average field
6+	>1000 per average field

Ridley-Jopling Classification

1. Tuberculoid Leprosy (TT)

Clinical: 1-3 well-defined hypopigmented/erythematous macules or plaques; sharply defined edges; completely anaesthetic, anhidrotic, alopecic; single thickened nerve asymmetrically

Bacteriological: BI = 0; AFB absent on slit-skin smear (paucibacillary)

Histological:

Well-formed epithelioid cell granulomas
Langhans giant cells present
Dense lymphocytic infiltration
Granulomas erode sub-epidermal zone (NO Grenz zone)
Nerve: perineural granuloma, obliterated architecture

Immunological:

Strong CMI (Th1 response)
Lepromin test (Mitsuda): strongly positive (>10 mm at 28 days)
High IL-2, IFN-γ, IL-12
Low/absent anti-PGL-1 antibodies
CD4:CD8 ratio HIGH in lesions

2. Borderline Tuberculoid (BT)

Clinical: 3-10 plaques; satellite lesions (characteristic); impaired sensation; multiple nerve trunks involved

Bacteriological: BI = 0-1+ (paucibacillary)

Histological: Epithelioid granulomas with fewer Langhans cells; narrow Grenz zone beginning; nerve twigs infiltrated

Immunological: Lepromin: mildly positive; moderate CMI

3. Borderline Borderline (BB) - Unstable

Clinical: Many lesions; "Swiss cheese" appearance; dimorphic annular lesions; moderate sensory loss; symmetric distribution

Bacteriological: BI = 3+ (multibacillary)

Histological: Epithelioid cells without Langhans cells; prominent Grenz zone; "naked" lymphocytes

Immunological: Lepromin: negative; unstable - shifts toward TT (upgrading) or LL (downgrading)

4. Borderline Lepromatous (BL)

Clinical: Numerous lesions; some with defined edges, some vague; sloping inner/sharp outer edge; papules, nodules, plaques; moderate sensory loss

Bacteriological: BI = 4-5+ (multibacillary)

Histological:

Macrophages replacing epithelioid cells
Prominent Grenz zone
"Onion-peel" perineural fibrosis (pathognomonic of BL)
Foamy macrophages beginning to appear

Immunological: Lepromin: negative; predominantly humoral (Th2) response

5. Lepromatous Leprosy (LL)

Clinical:

Early: vague hypopigmented macules; madarosis (loss of lateral eyebrows - first sign)
Late: leonine facies; pendulous earlobes; gynaecomastia; saddle nose
Bilateral symmetric nerve thickening; stocking-glove anaesthesia
Corneal anaesthesia, lagophthalmos, iritis

Bacteriological: BI = 5-6+; globi (packets of bacilli within macrophages)

Histological:

Foamy (lipid-laden) macrophages = Virchow cells/lepra cells
Dense subepidermal Grenz zone (Unna's clear zone)
No lymphocytes, no giant cells
Wade-Fite stain: lepra cells with globi

Immunological:

Absent CMI (complete anergy)
Lepromin: negative
HIGH anti-PGL-1 antibodies
High IL-4, IL-5, IL-10 (Th2 dominance)
CD4:CD8 ratio LOW in lesions
Polyclonal hypergammaglobulinaemia
False-positive VDRL, RF, ANA

WHO Classification

Type	Skin Lesions	Smear	Regimen
Paucibacillary (PB)	1-5	Negative	6 months MDT
Multibacillary (MB)	>5	Positive/Negative	12 months MDT

Leprosy Reactions

Type 1 (Reversal Reaction) - Delayed Hypersensitivity (Type IV)

Occurs in borderline types (BT, BB, BL)
EXISTING lesions become inflamed, erythematous, oedematous, tender
Acute neuritis - most damaging feature
No systemic features
Treat: Prednisolone 40-60 mg/day, taper over 6 months

Type 2 (ENL) - Immune Complex (Type III)

Occurs in BL and LL
NEW erythematous tender nodules on face/extensor limbs
Systemic: fever, iridocyclitis, orchitis, arthritis, neuritis
Treat: Thalidomide (males) or Prednisolone; Clofazimine for recurrent ENL

MDT Regimens (WHO)

PB (6 months): Rifampicin 600 mg monthly (supervised) + Dapsone 100 mg daily

MB (12 months): Rifampicin 600 mg monthly + Clofazimine 300 mg monthly + 50 mg daily + Dapsone 100 mg daily

Q3. (A) Esthiomene (B) HAART

A. Esthiomene

Definition

Esthiomene (Greek: "eating away") is chronic, progressive, destructive ulceration and lymphoedema of the female external genitalia, classically associated with tertiary LGV.

Causes

LGV (C. trachomatis L1-L3) - most common
Donovanosis (Klebsiella granulomatis)
Filariasis (Wuchereria bancrofti)
TB of the vulva (rare)
Crohn's disease (metastatic)

Pathogenesis (in LGV)

Tertiary stage of LGV (years after primary infection)
Chronic lymphatic obstruction → elephantiasis of vulva
Progressive fibrosis, ulceration, scarring
Rectovaginal fistulae, anorectal strictures (more common in women due to lymphatic drainage pattern)

Clinical Features

Gross brawny oedema of vulva and labia (elephantiasis vulvae)
Polypoid hypertrophic lymphoedematous tissue ("lymphorrhoids")
Chronic indolent ulcers with undermined edges
Anorectal stricture: crampy pain, ribbon-like stools, constipation
Rectovaginal/vesicovaginal fistulae
Risk of squamous cell carcinoma in long-standing esthiomene

Management

Medical: Doxycycline 100 mg BD x 21 days minimum; Azithromycin 1 g weekly x 3+ weeks

Surgical: Excision of lymphoedematous tissue; dilatation of anorectal strictures; fistula repair; skin grafting

B. HAART (Highly Active Antiretroviral Therapy)

Definition

Combination antiretroviral therapy using at least 3 antiretroviral agents from 2+ drug classes, designed to suppress HIV replication to undetectable levels (<50 copies/mL).

Drug Classes and Mechanisms

Class	Mechanism	Examples
NRTIs	Competitive inhibition + chain termination of reverse transcriptase	TDF/TAF, AZT, Lamivudine, FTC, Abacavir
NNRTIs	Non-competitive binding to RT (different site)	Efavirenz, Nevirapine, Rilpivirine, Doravirine
PIs	Block HIV protease, prevent viral maturation	Lopinavir/r, Darunavir/r, Atazanavir
INSTIs	Block integration of viral DNA into host genome	Dolutegravir (DTG), Raltegravir, Bictegravir
Entry/Fusion Inhibitors	Block CCR5 (Maraviroc) or gp41 fusion (Enfuvirtide)	Maraviroc, Enfuvirtide

Preferred First-Line Regimen (WHO/NACO India)

TDF + 3TC (or FTC) + DTG - high barrier to resistance; single daily pill; well tolerated

Goals of HAART

Viral suppression: HIV RNA <50 copies/mL
CD4 count recovery (>500 cells/mm³)
Prevention of AIDS-defining illnesses
Prevention of transmission (U=U: Undetectable = Untransmittable)

HAART in STI/Dermatology Context

IRIS: Paradoxical worsening of OIs after HAART initiation (restored immune response)
OHL resolves with immune recovery
Molluscum contagiosum, Kaposi's sarcoma resolve with CD4 recovery

Key Side Effects

Tenofovir: nephrotoxicity, Fanconi syndrome, bone density loss
Efavirenz: CNS effects (vivid dreams), teratogenic
Dolutegravir: weight gain, neural tube defects (peri-conception)
Zidovudine: bone marrow suppression, myopathy

Q4. Role of Counselling in Management of STI

Introduction

Counselling in STI management addresses behaviour, partner notification, and prevention - integral alongside medication.

Goals of STI Counselling

Reduce stigma and facilitate disclosure
Promote testing and treatment compliance
Ensure partner treatment (prevent re-infection)
Encourage behaviour change (condom use, partner reduction)
Prevent complications (PID, infertility, congenital infection)
Address psychosocial issues (anxiety, depression, relationship strain)

Types of Counselling

1. Pre-Test Counselling

Explain nature and purpose of test; discuss window period (3-4 weeks for 4th generation HIV Ag/Ab assay)
Discuss implications of positive and negative results
Obtain informed consent
Risk assessment (sexual history, risk behaviours)
Dispel myths; address confidentiality

2. Post-Test Counselling

If Positive:

Break news sensitively, in private, non-judgmentally
Explain diagnosis, treatment, prognosis
Discuss partner notification (voluntary or assisted)
Address denial, anger, fear
Reinforce treatment adherence; safer sex counselling with condom demonstration
Plan follow-up

If Negative:

Explain window period - may need repeat testing
Reinforce continued safe sex practices
Not a "clearance certificate"

3. Partner Notification and Contact Tracing

STI	Look-back Period
Primary Syphilis	3 months
Secondary Syphilis	6 months
Early Latent Syphilis	1 year
Gonorrhoea	2 months
Chlamydia	6 months
LGV	30 days before symptoms

Methods:

Patient referral: patient informs partners
Provider referral: healthcare provider notifies
Contract referral: patient agrees within set time, provider follows up

4. Behaviour Change Communication (BCC)

Condom promotion and correct usage
Reduction of concurrent partners
Avoidance of commercial sex/needle sharing
Prompt STI treatment reduces HIV risk

5. Specific Counselling Situations

HIV/AIDS (ICTC):

SA-ICTC (Standalone): district hospitals
F-ICTC (Facility-based): integrated in ANC/TB clinics
Mobile ICTC: outreach
PPTCT: ANC counselling for HIV+ mothers

Herpes: Lifelong nature; asymptomatic shedding; antiviral suppression for frequent recurrences/partners

Leprosy Counselling (special):

Reassure leprosy is curable with MDT
Dispel myths about heredity and curse
Complete 6/12 months MDT; self-care of anaesthetic limbs
Recognize reaction symptoms early; social rehabilitation
Stigma reduction in community

6. The 5 C's of Effective STI Counselling

Consent - informed, voluntary
Confidentiality - protected health information
Counselling - adequate pre/post test
Correct results - quality-assured testing
Connections - to care, treatment, and support services

Documentation and Follow-up

Record in confidential register
Test of cure: Gonorrhoea 1 week; Syphilis 3/6/12 months VDRL (4-fold titre fall = cure)

Q5. (A) Newer Drugs in Leprosy (B) Vaccines in Leprosy

A. Newer Drugs in Leprosy

1. Fluoroquinolones

Ofloxacin

Mechanism: Inhibits DNA gyrase (topoisomerase II) and topoisomerase IV
Bactericidal against M. leprae
Dose: 400 mg/day
Used in Rifampicin-resistant leprosy or Dapsone intolerance

Moxifloxacin

Most potent fluoroquinolone against M. leprae
Dose: 400 mg/day
Faster bacterial killing than Ofloxacin; used in MDR leprosy regimens

Sparfloxacin

400 mg/day; phototoxicity more common

2. Minocycline

Semi-synthetic tetracycline; inhibits 30S ribosomal subunit
Dose: 100 mg/day
Unique: bactericidal against M. leprae among tetracyclines
Avoids Clofazimine's skin pigmentation

3. Clarithromycin

Macrolide; inhibits 50S ribosomal subunit
Dose: 500 mg/day; used in alternative regimens

4. Rifapentine

Long-acting rifamycin; longer half-life for less frequent dosing

ROM Regimen (Single-Dose for Single Lesion PB Leprosy)

Rifampicin 600 mg + Ofloxacin 400 mg + Minocycline 100 mg - single dose

WHO-recommended for single skin lesion PB leprosy
Cure rate comparable to 6-month PB MDT
Advantage: single supervised dose, no compliance issues

MDR Leprosy Regimen (WHO 2018)

6 months: Clarithromycin 500 mg + Moxifloxacin 400 mg + Minocycline 100 mg (all daily)
18 months: Moxifloxacin 400 mg + Minocycline 100 mg (or Clofazimine 50 mg) daily

Drugs for Reactions

Thalidomide:

Mechanism: TNF-alpha inhibition + immunomodulation
Highly effective for ENL; Dose: 100-300 mg/day
STRICT CONTRAINDICATION: Teratogenic (phocomelia) - cannot use in women of childbearing age
Side effects: sedation, peripheral neuropathy, DVT

Pentoxifylline: TNF-alpha inhibitor; alternative to Thalidomide for ENL; 400 mg TDS

B. Vaccines in Leprosy

1. BCG - Most Evidence

Live attenuated Mycobacterium bovis
Protection rate: 20-80% (variable by geography; ~34% in India)
Cross-reactive immunity between BCG and M. leprae (shared antigens, especially PGL-1)
Part of India's National Immunization Programme (given at birth)

2. MIP (Mycobacterium indicus pranii) - Licensed in India

Formerly: ICRC bacillus (Indian Cancer Research Centre)
Heat-killed, non-pathogenic mycobacterium with cross-reactive antigens
Developed by JALMA, Agra (ICMR)
Protection: ~65% in contacts of leprosy patients
Also accelerates bacterial clearance in MB patients when used adjuvant to MDT
Dose: 2 intradermal injections (0.1 mL each) at 0 and 6 months
Licensed by DCGI in India; available under NLEP for contacts in endemic areas

3. BCG + Killed M. leprae

Combination with armadillo-sourced killed M. leprae; superior to BCG alone in some studies
Limited by armadillo supply

4. Chemoprophylaxis: Single-Dose Rifampicin (SDR-PEP)

Household and social contacts of newly diagnosed leprosy patients
Dose: Adults 600 mg; Children (2-15 yrs) 300 mg; <2 yrs 150 mg
COLEP Trial (Bangladesh): 57% reduction in leprosy incidence at 2 years
WHO-recommended (2016 guidelines) for contacts in hyperendemic areas

Summary Table:

Vaccine	Type	Efficacy	Status
BCG	Live attenuated	20-80%	National programme
MIP (ICRC)	Killed	~65%	Licensed in India
BCG + killed M. leprae	Combined	Higher than BCG alone	Research/limited
SDR Rifampicin (PEP)	Chemoprophylaxis	~57% at 2 years	WHO-recommended

Q6. Deformities in Leprosy and Their Management

Introduction

Deformities result from nerve damage (neuritis), trauma to anaesthetic limbs, muscle weakness/paralysis, and bone resorption. Prevention is more important than late surgical correction.

WHO Disability Grading (2016)

Grade	Eyes	Hands	Feet
0	No problem	No problem	No problem
1	Anaesthesia present, no visible problem	Anaesthesia present, no visible problem	Anaesthesia present, no visible problem
2	Visible problem: lagophthalmos, corneal opacity	Claw hand, absorption, contracture, wound	Claw foot, absorption, contracture, wound

Nerves and Resultant Deformities

Nerve	Site	Deformity
Ulnar nerve	Elbow	Claw hand (ring and little fingers)
Median nerve	Wrist/forearm	Thenar wasting; claw index/middle fingers; ape thumb
Combined ulnar + median	-	Complete claw hand (main-en-griffe)
Radial nerve	Spiral groove	Wrist drop
Common peroneal	Fibula neck	Foot drop
Posterior tibial	Ankle	Clawing of toes; plantar anaesthesia; plantar ulcers
Facial nerve (zygomatic)	-	Lagophthalmos

Specific Deformities

1. Claw Hand (Main-en-griffe)

Cause: Intrinsic muscle paralysis (lumbrical and interossei) due to ulnar/median nerve damage
Hyperextension at MCPs, flexion at IPJs
Prevention: passive stretching, cocking-up splint

Surgery:

Fowler's operation: EDC re-routing to lumbrical position
Brand's operation: FDS transfer to replace intrinsic muscles
Bunnel's lasso procedure: Dynamic tenodesis
Capsulodesis for MCP hyperextension correction

2. Foot Drop

Cause: Common peroneal nerve palsy
High-stepping gait; equinovarus deformity
Prevention: Plastic AFO (ankle-foot orthosis), physical therapy

Surgery: Tibialis posterior transfer through interosseous membrane to dorsum of foot

3. Plantar Ulcers (Trophic Ulcers)

Cause: Posterior tibial nerve anaesthesia + repeated trauma/pressure
Usually under metatarsal heads; painless; punched-out; secondary infection → osteomyelitis

Management:

Rest, offloading with Total Contact Cast (TCC) or Scotchcast boot
Wound debridement; antibiotics for secondary infection
MCR (Microcellular rubber) footwear with moulded insoles
Patient education: daily foot inspection, soaking and oiling, no barefoot walking

4. Lagophthalmos

Cause: Facial nerve (zygomatic branch) palsy
Consequence: Corneal exposure → ulceration → blindness

Management:

Protective spectacles/goggles
Artificial tears (methyl cellulose) QID
Eye pad at night
Tarsorrhaphy (lateral suturing of eyelids)
Gold weight implant in upper eyelid (gravity-assisted closure)
Lateral fascial sling procedure

5. Saddle Nose

Cause: Granulomatous destruction of nasal cartilage and bone (LL)
Surgery: Rhinoplasty with cartilage graft (rib/ear) or silastic implant

6. Absorption of Digits

Cause: Repeated trauma, trophic ulcers, osteomyelitis in anaesthetic fingers/toes
Progressive resorption → "pencil-tip" tapering
Prevention: self-care regimen (soaking 20 min, oil, protective gloves)

POD Programme

Prevention of Disabilities (POD) under NLEP:

Monthly examination of eyes, hands, feet at PHC level
Self-care training; MCR footwear provision
Referral to PMRC (Physiotherapy, Medical, Rehabilitation Centres)
Reconstructive surgery at district/referral centres (only after completing MDT, bacteriologically inactive, no active reactions)

Q7. (A) Congenital Syphilis (B) Non-Treponemal Serological Tests

A. Congenital Syphilis

Definition

Congenital syphilis results from transplacental transmission of Treponema pallidum from infected mother to fetus, typically after the 16th week of gestation.

Transmission Risk

Primary syphilis: ~75-90%; Secondary: ~90%; Early latent: ~40%; Late latent: ~10%

Early Congenital Syphilis (< 2 years)

Skin and Mucous Membranes:

Syphilitic pemphigus: Bullae on palms and soles (pathognomonic at birth)
Snuffles: Serosanguineous nasal discharge (earliest sign; highly infectious)
Condylomata lata around anus/genitals
Mucous patches in mouth

Systemic:

Hepatosplenomegaly (most common internal finding)
Jaundice, haemolytic anaemia
Osteochondritis: metaphyseal irregularity; Wimberger's sign (bilateral symmetric tibial destruction)
Periostitis
Chorioretinitis, uveitis
Meningitis
Pseudoparalysis of Parrot - refusal to move limb due to bone pain

Late Congenital Syphilis (> 2 years) - Stigmata

Hutchinson's Triad (pathognomonic):

Hutchinson's teeth - upper permanent central incisors: notched, barrel-shaped, widely spaced (appear at 6-8 years)
Interstitial keratitis - corneal vascularization and scarring; appears at 5-15 years
Eighth nerve deafness - sensorineural; progressive; appears in adolescence

Other Stigmata:

Rhagades: Linear perioral scars radiating from angles of mouth, nose, anus
Saddle nose: Nasal septal destruction
Frontal bossing (Olympian brow)
Sabre tibia (Saber shin): Anterior bowing due to periostitis
Clutton's joints: Bilateral painless synovitis of knees (immune-mediated)
Moon's molars (mulberry molars): First lower molars - irregular, multiple cusps
Higoumenakis sign: Unilateral thickening of sternoclavicular clavicle

Diagnosis

VDRL/RPR on infant serum
Infant VDRL titre >4x maternal titre: diagnostic
IgM-FTA-ABS (detects fetal-specific antibody - cannot cross placenta)
Dark-field microscopy of snuffles, skin lesions
Long bone X-rays: metaphyseal irregularity, periostitis, Wimberger's sign

Management

Early (<1 year): Aqueous Crystalline Penicillin G 50,000 units/kg IV every 12 hours x 10-14 days OR Procaine Penicillin G 50,000 units/kg IM once daily x 10-14 days

Late (>1 year): Aqueous Crystalline Penicillin G 50,000 units/kg IV every 6 hours x 10-14 days

Prevention: Screen all pregnant women with VDRL at first ANC visit; treat seropositive mothers

B. Non-Treponemal Serological Tests (NTT) in Syphilis

Principle

Detect IgG and IgM antibodies against cardiolipin-lecithin-cholesterol antigen (phospholipid released from host cell membranes damaged by T. pallidum). NOT specific to T. pallidum.

Tests

1. VDRL (Venereal Disease Research Laboratory Test)

Type: Flocculation test
Antigen: Cardiolipin-lecithin-cholesterol suspension
Reading: Macroscopic in test tube (flocculation = positive)
Quantitative: Titres reflect disease activity
Only NTT validated for CSF (neurosyphilis diagnosis)
Sensitivity: Primary 70-80%; Secondary 99-100%; Late 70-80%

2. RPR (Rapid Plasma Reagin)

Type: Flocculation test with charcoal particles
Reading: Macroscopic on card (agglutination = positive)
Advantage over VDRL: Uses unheated serum; field-friendly; no microscope needed
Same sensitivity as VDRL; cannot be used on CSF

3. TRUST (Toluidine Red Unheated Serum Test)

Modification of RPR with toluidine red indicator; similar performance to RPR

Titres and Clinical Correlation

Stage	Typical VDRL Titre
Primary	1:4 to 1:16
Secondary	1:16 to 1:512 (highest)
Late/Tertiary	Low or negative

Treatment response: 4-fold (2 dilution) fall in titre at 6-12 months = adequate treatment

Biological False Positive (BFP) VDRL

Acute BFP (<6 months): Viral infections (EBV, CMV, HIV, Hepatitis); Malaria; post-vaccination

Chronic BFP (>6 months):

SLE (most important - antiphospholipid antibodies)
Rheumatoid arthritis
Lepromatous leprosy
Thyroid diseases; old age; pregnancy; IV drug use

Rule: BFP titre usually LOW (<1:8); true syphilis at high titre with treponemal test negative = BFP

Treponemal Confirmatory Tests (for comparison)

FTA-ABS, TPHA, TPPA, MHA-TP - remain positive for life; cannot monitor treatment response

Q8. Herpes Genitalis

Introduction

Chronic, recurrent viral STI caused primarily by HSV-2 (and increasingly HSV-1 due to orogenital contact). Characterized by recurrent painful ulcers; one of the most prevalent STIs globally.

Etiology

HSV-2: ~80% of genital herpes; recurs more frequently genitally
HSV-1: Increasing cause in young adults; recurs less frequently genitally
Both are enveloped double-stranded DNA viruses

Pathogenesis

Virus enters via mucosa/abraded skin → replicates locally → primary lesion
Ascends peripheral sensory nerves → establishes latency in sacral dorsal root ganglia (S2-S4)
Periodic reactivation → anterograde transport → recurrent lesions or asymptomatic shedding

Triggers: Fever, trauma, UV light, stress, immunosuppression, menstruation

Clinical Features

Primary Genital Herpes

Incubation: 2-12 days (mean 4 days)
Prodrome: Tingling, burning, neuralgia 24-48 hours before lesions
Grouped vesicles on erythematous base → rupture → shallow painful ulcers with scalloped margins
Sites: glans, prepuce, shaft (males); labia majora/minora, cervix, vagina (females)
Constitutional symptoms: fever, malaise, myalgia, headache (more severe in primary)
Tender bilateral inguinal lymphadenopathy
Dysuria, urinary retention (sacral radiculopathy)
Cervicitis (most common manifestation in women - may be asymptomatic)
Duration: 2-3 weeks without treatment

Recurrent Genital Herpes

Less severe, shorter (7-10 days); prodrome in ~50%
Unilateral involvement common; minimal constitutional symptoms
Typically 4-5 episodes/year (HSV-2); 1-2/year (HSV-1)

Asymptomatic Shedding

~70% of HSV-2 seropositive individuals; responsible for most transmission events

Complications

Sacral radiculopathy: Urinary retention, neurogenic bladder
Herpes encephalitis (rare in immunocompetent)
Disseminated herpes in immunocompromised (hepatitis, pneumonitis, encephalitis)
Neonatal herpes: Peripartum transmission; case fatality ~50% untreated
Herpetic whitlow: HSV inoculation of finger
Erythema multiforme: Recurrent HSV is most common trigger
Increased HIV susceptibility: Genital ulcers increase HIV acquisition 3-fold

Diagnosis

Test	Sensitivity	Notes
Tzanck smear	60-70%	Multinucleated giant cells + Cowdry type A intranuclear inclusions; does not distinguish HSV-1 from HSV-2
Viral culture	Gold standard	From base of fresh vesicle; CPE in 24-48 hours
PCR	Most sensitive	Method of choice for CSF in encephalitis
Type-specific IgG serology	-	Confirms HSV-2 seroprevalence; not for acute diagnosis

Histology: Cowdry type A intranuclear inclusions, multinucleated giant cells with "ground glass" nuclei and moulding

Management

Antiviral Drugs

Mechanism: Thymidine kinase phosphorylation → nucleoside analogue → inhibits viral DNA polymerase

Primary Episode:

Acyclovir 400 mg TDS x 7-10 days
Valacyclovir 1 g BD x 7-10 days
Famciclovir 250 mg TDS x 7-10 days
Start within 72 hours

Recurrent Episode:

Acyclovir 800 mg BD x 5 days
Valacyclovir 500 mg BD x 3 days
Famciclovir 1000 mg BD x 1 day

Suppressive Therapy (≥6 recurrences/year):

Acyclovir 400 mg BD (daily)
Valacyclovir 500 mg once daily
Famciclovir 250 mg BD
Reduces recurrences by ~75%; reduces transmission to partners by ~50%

Severe/Immunocompromised: IV Acyclovir 5-10 mg/kg every 8 hours x 5-7 days

Neonatal Herpes: IV Acyclovir 20 mg/kg every 8 hours x 14-21 days; Caesarean section when active lesions at term

Counselling Points

Lifelong recurrent nature; asymptomatic shedding risk
Condom use reduces but does not eliminate transmission
Suppressive therapy for partners/frequent recurrences
Neonatal risk - inform obstetrician if pregnant

Q9. (A) Nerve Biopsy in Leprosy (B) Clofazimine

A. Nerve Biopsy in Leprosy

Indications

Pure neuritic leprosy (PNL): No skin lesions; slit-skin smear and skin biopsy non-contributory
Atypical presentations; uncertain clinical diagnosis
Mononeuropathy multiplex: distinguish from vasculitis, sarcoidosis, hereditary neuropathy
Research purposes: study immunopathology of leprosy neuropathy
Confirm nerve involvement in reactions

Nerve Most Commonly Biopsied

Sural nerve (posterior to lateral malleolus)

Purely sensory; biopsy causes only lateral foot sensory loss
Accessible, superficial
Also used: Superficial peroneal nerve, radial cutaneous nerve

Technique

Local anaesthesia (lignocaine without adrenaline)
Longitudinal incision over nerve
Excise 2-3 cm segment
Divide: formalin-fixed (histology), Wade-Fite stain portion, glutaraldehyde (electron microscopy)
Gentle handling to avoid crush artefact

Histopathological Findings

Tuberculoid End (TT/BT):

Well-formed epithelioid cell granulomas within nerve fascicles
Langhans giant cells; dense lymphocytic cuffing
Nerve fibres obliterated; AFB absent or rare

Borderline (BL):

Granulomas less well formed
"Onion peel" perineural fibrosis (concentric layers of fibroblasts - characteristic)
Partial nerve destruction

Lepromatous End (BL/LL):

Foamy macrophages (lepra cells) within nerve
Dense bacillary load; Schwann cells infected
"Onion peel" perineural fibrosis: most pronounced
Loss of myelinated and unmyelinated fibres

Pure Neuritic Leprosy (PNL):

Granulomas in nerve, sometimes with AFB
Classified along R-J spectrum based on nerve histology

Special Stains

Wade-Fite stain: Modified AFB stain for M. leprae in tissue (gentler - preserves lipid coat)
S-100: Schwann cell marker
EMA: Perineurium marker

Limitations

Permanent sensory deficit at biopsy site
Sampling error (skip lesions)
Replaced by nerve ultrasound in many centres
Requires expertise in interpretation

B. Clofazimine

Classification

Rimino-phenazine dye; highly lipophilic compound

Mechanism of Action

Bactericidal against M. leprae: binds mycobacterial DNA (guanine-specific) → inhibits template function → inhibits DNA replication
Anti-inflammatory: Inhibits neutrophil migration, lysosomal enzyme release, suppresses TNF-α → useful for ENL
Promotes reactive oxygen species generation within mycobacteria

Pharmacokinetics

Highly lipophilic → stored in fat, skin, reticuloendothelial system
Half-life: ~70 days (range 35-100 days) - extremely long
Long t½ accounts for prolonged skin pigmentation after stopping drug
Excreted in faeces, bile, sputum, sebaceous secretions; accumulates in macrophages

Dose in MDT

MB MDT supervised: 300 mg once monthly
MB MDT self-administered: 50 mg daily
ENL treatment: 100-300 mg/day (in 3 divided doses)

Side Effects

Skin Pigmentation (most characteristic):

Red-brown to slate-grey/black discolouration of skin, especially in leprosy lesions and sun-exposed areas
Due to drug deposition in macrophages + lipofuscin-like pigment
Reversible but takes 1-2 years after stopping drug
Red discolouration of tears, sweat, urine, faeces, breast milk, sputum

GI Side Effects:

Nausea, vomiting, diarrhoea, abdominal pain
Crystal-storing histiocytosis: Clofazimine crystals in intestinal wall and mesenteric lymph nodes → eosinophilic enteritis; small bowel obstruction (rare but serious)

Ichthyosis: Dry scaly skin (especially limbs)

Other: Splenic infarction (rare), elevated blood glucose (rare)

Uses Beyond Leprosy

MDR-TB: WHO-recommended Group B drug in MDR-TB regimens
MAC infection in AIDS patients
Crohn's disease (experimental)
Chronic discoid lupus erythematosus (DLE) - as immunomodulator

Q10. (A) ENL (Erythema Nodosum Leprosum) (B) OHL (Oral Hairy Leukoplakia)

A. ENL (Erythema Nodosum Leprosum) - Type 2 Lepra Reaction

Definition

An acute inflammatory reaction in multibacillary leprosy (BL and LL), characterized by NEW tender erythematous nodules with systemic features, superimposed on existing leprosy.

Epidemiology

~50% of LL; ~25% of BL patients
Most common during first year of MDT; also occurs after treatment completion
Can become chronic/recurrent

Immunopathogenesis

Type III hypersensitivity (Immune Complex Mediated)
M. leprae antigens (especially PGL-1) + high circulating antibodies → immune complex formation → complement activation → neutrophil recruitment → acute inflammation
TNF-α plays central role (explains efficacy of Thalidomide/Pentoxifylline)
Triggered by: antigen release during bacillary death from MDT, concurrent infection, pregnancy

Clinical Features

Skin:

NEW crops of tender erythematous papules and nodules (2-4 cm)
Mainly face (malar region), extensor forearms, thighs, trunk
Lesions may vesiculate, pustulate, necrose (ENL necroticans), ulcerate
Subside in 1-2 weeks leaving pigmentation; recurrent crops

Systemic Features (distinguish from Type 1):

Fever (most common; may be high and hectic)
Malaise, anorexia, weight loss
Iridocyclitis (uveitis): Pain, photophobia; risk of blindness
Neuritis: Acute nerve pain and tenderness
Orchitis/Epididymo-orchitis: Painful swollen testes → testicular atrophy, infertility
Arthritis/Arthralgia; lymphadenopathy; hepatosplenomegaly
Dactylitis: Sausage-shaped swollen digits
Proteinuria, glomerulonephritis (immune complex deposition)

Histology of ENL

Dense neutrophilic infiltration in dermis; vasculitis with neutrophils
Immune complexes in vessel walls; fibrinoid necrosis in severe cases
Fragmented bacilli (vs solid bacilli in quiescent LL)
Background foamy macrophages with globi (LL histology)

Laboratory Findings

Raised ESR, CRP; leucocytosis (neutrophilia)
Elevated circulating immune complexes; low C3/C4
Proteinuria in renal involvement

ENL vs Type 1 Reaction

Feature	ENL (Type 2)	Type 1 (Reversal)
Type	BL and LL	Borderline (BT, BB, BL)
Lesions	NEW nodules	EXISTING lesions inflamed
Systemic features	Present (fever, iritis, orchitis)	Absent
Mechanism	Type III (immune complex)	Type IV (delayed hypersensitivity)
Histology	Neutrophilic vasculitis	Epithelioid granulomas upgrading
Lucio's phenomenon	Different entity (ischaemic ulceration in Lucio LL)	-

Management

Mild (skin only): Aspirin/NSAIDs; continue MDT

Moderate to Severe:

First Line:

Thalidomide: 100-300 mg/day - MOST EFFECTIVE
- Mechanism: Inhibits TNF-α mRNA stabilization
- Only in males or post-menopausal females (severe teratogen - phocomelia)
- Side effects: sedation, peripheral neuropathy, DVT
Prednisolone: 40-60 mg/day tapered over 3-6 months
- Preferred in females of childbearing age
- First choice when neuritis or iridocyclitis present

Recurrent/Chronic ENL:

Clofazimine 300 mg/day (100 mg TDS) x 3-6 months
- Anti-inflammatory property; steroid-sparing
- Slower onset (4-6 weeks); preferred to reduce steroid dependence

Supportive:

Ophthalmology review (mydriatics + topical steroids for iridocyclitis)
Urological review for orchitis
Continue MDT - do NOT stop during reactions

B. OHL (Oral Hairy Leukoplakia)

Definition

OHL is a white, non-removable, corrugated ("hairy") plaque on the lateral borders of the tongue caused by EBV (Epstein-Barr Virus) replication in oral epithelial cells, almost exclusively in immunocompromised individuals.

Etiology and Pathogenesis

EBV (Human Herpesvirus 4) - lytic/productive infection of oral epithelium
Unlike EBV-associated lymphoma (latent), OHL = lytic EBV replication
Immunosuppression (HIV, organ transplant, haematological malignancies) allows unchecked EBV replication
CD4 count usually <200 cells/mm³ in HIV patients

Clinical Features

Site: Lateral border of tongue (most characteristic); bilateral in 50%
- Rarely: dorsal tongue, buccal mucosa, floor of mouth, soft palate
Appearance: White, corrugated ("hairy") plaques with vertical folds/ridges; cannot be wiped off (unlike candidiasis)
Symptoms: Usually asymptomatic; occasional mild discomfort
No malignant potential

Significance in HIV

Marks significant immunosuppression; associated with rapid HIV progression to AIDS
CD4 typically <200/mm³
Presence in otherwise healthy person → screen for HIV

Histology (Definitive Diagnosis)

Epithelial hyperparakeratosis
"Balloon cells" in spinous layer (koilocytosis)
Herpetic-type nuclear changes (Cowdry type A inclusions in some cells)
No dysplasia
Minimal or absent inflammatory infiltrate
EBER in-situ hybridization (ISH): Demonstrates EBV-encoded RNA in epithelial cells - gold standard

Differential Diagnosis

Condition	Key Differentiator
Oral Candidiasis	Plaques REMOVABLE with spatula; KOH shows hyphae; responds to antifungals
Oral leukoplakia (idiopathic)	Unilateral; non-HIV; biopsy shows dysplasia; malignant potential
Lichen planus	Lace-like Wickham's striae; bilateral buccal mucosa; band-like lymphocytic infiltrate
Geographic tongue	Migratory red patches with white borders; dorsal tongue
White sponge naevus	Hereditary; extensive; autosomal dominant

Management

Usually no treatment required - reassure if HIV well-controlled.

Indications for treatment: Symptomatic; patient concern (cosmesis)

Options:

HAART: Most effective - OHL resolves spontaneously in >90% with immune recovery (CD4 rises)
Topical Podophyllin resin (25%): Weekly application; causes regression
Acyclovir/Valacyclovir: High-dose oral antiviral - OHL resolves but recurs when drug stopped
Topical Tretinoin: Some evidence
Foscarnet IV: Refractory cases in severely immunosuppressed

Prognosis: Recurrence common if immunosuppression persists; resolves with effective HAART.

Quick Reference Index

Q	Topic	Key Exam Points
1	Inguinal Bubo	DD: LGV (groove sign), Chancroid, Syphilis, Plague; Aspirate - never incise
2	Leprosy	Full R-J spectrum; BI scale; Th1 vs Th2; Type 1 vs Type 2 reactions; MDT
3A	Esthiomene	Tertiary LGV; vulvar elephantiasis; anorectal stricture; Doxycycline x 21 days
3B	HAART	5 drug classes; TDF+3TC+DTG first-line; IRIS; U=U
4	STI Counselling	Pre/post-test; partner notification timelines; ICTC; 5 C's; leprosy counselling
5A	Newer drugs in leprosy	ROM regimen; Moxifloxacin; Minocycline; Thalidomide; MDR-leprosy protocol
5B	Vaccines in leprosy	BCG (20-80%); MIP/ICRC (65%, licensed India); SDR-PEP (57% at 2 years)
6	Leprosy deformities	WHO Grade 0-2; claw hand surgery (Brand's/Fowler's); foot drop; POD programme
7A	Congenital Syphilis	Hutchinson's triad; Wimberger's sign; snuffles; Penicillin G
7B	NTT in Syphilis	VDRL (flocculation, CSF-valid); RPR (card test); BFP causes; 4-fold titre fall = cure
8	Herpes Genitalis	HSV-2 > HSV-1; sacral ganglia latency; Tzanck smear; Acyclovir; suppressive therapy
9A	Nerve biopsy	Sural nerve; PNL; onion-peel perineural fibrosis (BL); Wade-Fite stain
9B	Clofazimine	DNA binding + anti-TNF; t½ 70 days; red-brown pigmentation; crystal-storing histiocytosis
10A	ENL	Type III hypersensitivity; NEW nodules + systemic features; Thalidomide/Prednisolone/Clofazimine
10B	OHL	EBV lytic; lateral tongue; non-removable; EBER-ISH; resolves with HAART; no malignant transformation

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