Tropical Dermatology — MCQs

Tropical Dermatology Indian Medical PG Practice Questions and MCQs

Question 41: Type 2 lepra reaction is an example of which type of hypersensitivity reaction?

A. Type 1 hypersensitivity reaction
B. Type 2 hypersensitivity reaction
C. Type 3 hypersensitivity reaction (Correct Answer)
D. Type 4 hypersensitivity reaction

Explanation: **Explanation:** **Type 2 Lepra Reaction (Erythema Nodosum Leprosum - ENL)** is a classic example of a **Type 3 Hypersensitivity Reaction**, which is mediated by the deposition of **immune complexes**. In patients with multibacillary leprosy (BL and LL), there is a high bacterial load and high levels of circulating antigens. When chemotherapy (MDT) is initiated, rapid killing of bacilli releases massive amounts of antigens that react with circulating antibodies to form antigen-antibody complexes. These complexes deposit in small blood vessels, activate the complement system, and lead to **vasculitis**. This manifests clinically as painful, evanescent erythematous nodules, fever, arthralgia, and neuritis. **Analysis of Incorrect Options:** * **Option A (Type 1):** This is IgE-mediated (anaphylactic) hypersensitivity. It is not involved in leprosy reactions. * **Option B (Type 2):** This involves antibody-mediated cytotoxic reactions (e.g., autoimmune hemolytic anemia). While the name "Type 2 Lepra Reaction" is similar, the mechanism is different. * **Option D (Type 4):** This is delayed-type hypersensitivity (cell-mediated). This is the mechanism for **Type 1 Lepra Reaction (Reversal Reaction)**, where a sudden increase in cell-mediated immunity occurs. **High-Yield Clinical Pearls for NEET-PG:** * **Trigger:** Usually occurs after starting MDT (due to antigen release), but can occur spontaneously. * **Key Cytokine:** **TNF-alpha** plays a central role in the pathogenesis of ENL. * **Drug of Choice:** **Thalidomide** is the most effective treatment for Type 2 reactions. Oral corticosteroids are also used. * **Systemic Involvement:** Unlike Type 1 reactions (which are localized to skin/nerves), Type 2 reactions are systemic and can cause iridocyclitis, orchitis, and glomerulonephritis.

Question 42: What is true about ROM therapy?

A. For a single lesion
B. Minocycline is used
C. A single dose is given
D. All the above (Correct Answer)

Explanation: **ROM Therapy** (Rifampicin, Ofloxacin, and Minocycline) is a specialized WHO-recommended treatment regimen designed specifically for **Single Lesion Paucibacillary (SLPB) Leprosy**. ### **Explanation of Options:** * **A. For a single lesion:** ROM therapy is indicated only for patients presenting with a single skin lesion that lacks nerve trunk involvement. This is classified as SLPB leprosy. * **B. Minocycline is used:** The regimen consists of a fixed-dose combination of three potent bactericidal drugs: 1. **R**ifampicin (600 mg) 2. **O**floxacin (400 mg) 3. **M**inocycline (100 mg) * **C. A single dose is given:** Unlike standard Multi-Drug Therapy (MDT) which lasts for months, ROM therapy is administered as a **stat (single) dose** under supervision. Since all three statements accurately describe the protocol, **Option D (All the above)** is correct. ### **Clinical Pearls for NEET-PG:** * **Inclusion Criteria:** The patient must have a single skin lesion with definite sensory loss but **no** enlarged nerves. * **Contraindications:** ROM therapy is generally avoided in children under 5 years and pregnant women (due to the side effects of Ofloxacin and Minocycline on bone/teeth development). * **U-MDT (Uniform MDT):** Do not confuse ROM with U-MDT. U-MDT is a 6-month regimen (Rifampicin + Dapsone + Clofazimine) proposed to treat both PB and MB leprosy patients to simplify logistics. * **Drug of Choice:** While ROM is an option for SLPB, the standard WHO MDT (6 months of Rifampicin + Dapsone) remains the gold standard for Paucibacillary leprosy.

Question 43: Immune-mediated destruction of tissue bearing a high concentration of Mycobacterium leprae bacilli occurs, usually several months after the initiation of effective therapy. This results in cutaneous ulcers in patients with lepromatous leprosy. What is this phenomenon called?

A. Raynaud's phenomenon
B. Placebo phenomenon
C. Lucio's phenomenon (Correct Answer)
D. Cutaneous anthrax

Explanation: ### Explanation **Correct Option: C. Lucio’s Phenomenon** Lucio’s phenomenon is a rare, life-threatening variant of a **Type 2 Leprosy Reaction** (though some classify it distinctly). It occurs almost exclusively in patients with **Diffuse Lepromatous Leprosy** (Lucio-Latapi leprosy). * **Pathogenesis:** It involves a severe necrotizing panvasculitis. High bacterial loads lead to direct invasion of endothelial cells by *M. leprae*, triggering immune-mediated vascular occlusion, thrombosis, and subsequent ischemic infarction of the skin. * **Clinical Presentation:** It manifests as painful, erythematous, jagged purpuric patches that evolve into **large, necrotic cutaneous ulcers**, typically appearing after starting multidrug therapy (MDT). **Why Incorrect Options are Wrong:** * **A. Raynaud’s Phenomenon:** A vasospastic disorder causing discoloration of fingers/toes in response to cold or stress; it is not associated with mycobacterial infection or necrotic ulceration. * **B. Placebo Phenomenon:** A psychological or physiological effect following a "sham" treatment; irrelevant to leprosy pathology. * **D. Cutaneous Anthrax:** Caused by *Bacillus anthracis*, it presents as a painless "malignant pustule" with a characteristic central black eschar, not related to chronic leprosy reactions. **High-Yield NEET-PG Pearls:** * **Lucio-Latapi Leprosy:** Characterized by "pure primitive diffuse infiltration," loss of eyebrows/eyelashes (madarosis), and a shiny "moon-face" appearance. * **Geographic Distribution:** Most common in Mexico and Central America. * **Treatment:** While MDT is continued, systemic corticosteroids and intensive wound care are vital. Unlike Erythema Nodosum Leprosum (ENL), Thalidomide is generally **not** effective for Lucio’s phenomenon. * **Histology:** Look for acid-fast bacilli (AFB) within the walls of blood vessels and endothelial cells.

Question 44: What are the characteristics of Type II lepra reaction?

A. Erythema and edema
B. Erythema nodosum leprosum (ENL)
C. Lymphadenopathy
D. All of the above (Correct Answer)

Explanation: **Explanation:** Type II Lepra Reaction, also known as **Erythema Nodosum Leprosum (ENL)**, is a **Type III hypersensitivity reaction** (immune-complex mediated) that typically occurs in patients with multibacillary leprosy (BL and LL types). It is characterized by a systemic inflammatory response due to the deposition of antigen-antibody complexes in various tissues. * **Why Option D is correct:** ENL is a multisystem disorder. The hallmark is the sudden appearance of tender, evanescent, **erythematous** nodules and plaques (**Option A and B**). Because it is a systemic immune response, it frequently involves the reticuloendothelial system, leading to **lymphadenopathy** (**Option C**), fever, malaise, and organ involvement such as neuritis, arthritis, iridocyclitis, and orchitis. * **Analysis of Options:** * **Erythema and edema:** These are local inflammatory signs seen in the skin lesions of ENL. * **ENL:** This is the clinical synonym for Type II reactions. * **Lymphadenopathy:** A common systemic feature reflecting the widespread immune activation. **High-Yield Clinical Pearls for NEET-PG:** * **Trigger:** Often precipitated by chemotherapy (MDT), pregnancy, or stress. * **Timing:** Usually occurs later in the course of treatment compared to Type I reactions. * **Drug of Choice:** **Thalidomide** is the most effective treatment for severe ENL. For mild cases or when thalidomide is contraindicated (e.g., pregnancy), **Prednisolone** or **Clofazimine** (at higher doses) are used. * **Key Difference:** Unlike Type I reactions (Type IV hypersensitivity), Type II reactions do not occur in paucibacillary (TT/BT) leprosy.

Question 45: Which of the following oral structures are not affected in Leprosy?

A. Gingiva (Correct Answer)
B. Tongue
C. Hard Palate
D. Soft Palate

Explanation: **Explanation:** Leprosy, specifically the **Multibacillary (Lepromatous)** spectrum, frequently involves the oral cavity due to the systemic dissemination of *Mycobacterium leprae*. The primary factor determining the site of involvement is **temperature**; the bacilli prefer cooler areas of the body. **Why Gingiva is the correct answer:** The **gingiva** is rarely affected in leprosy. While the oral mucosa can harbor lepromas, the gingival tissue is relatively resistant compared to other oral structures. In clinical practice, even in advanced Lepromatous Leprosy (LL), the gingiva remains largely spared, making it the most appropriate "except" choice for this question. **Analysis of Incorrect Options:** * **Hard Palate:** This is the **most common** site of oral involvement in leprosy. It often presents with chronic congestion, followed by the formation of "lepromas" (nodules) which may ulcerate or lead to perforation. * **Soft Palate and Uvula:** These are frequently involved after the hard palate. Infiltration can lead to scarring, fibrosis, and a "shrunken" appearance of the uvula. * **Tongue:** The tongue is a common site for lepromatous lesions, typically presenting as **"Glossitis centralis"** or nodules on the dorsum. It may also show "cobblestone" appearance or macroglossia. **High-Yield Clinical Pearls for NEET-PG:** * **Most common oral site:** Hard Palate. * **Sequence of involvement:** Hard palate > Soft palate > Tongue > Uvula. * **Temperature Sensitivity:** Oral lesions occur because the air passing through the mouth cools the mucosa, creating an environment below $37^\circ C$ favorable for *M. leprae*. * **Facies Leprosa (Bergen Syndrome):** Includes atrophy of the anterior nasal spine, atrophy of the maxillary alveolar process, and endonasal inflammatory changes.

Question 46: Skin lesions following visceral leishmaniasis typically present as which of the following?

A. Hyperpigmented macules
B. Hypopigmented macules (Correct Answer)
C. Ecchymosis
D. All of the above

Explanation: **Explanation:** The question describes **Post-Kala-Azar Dermal Leishmaniasis (PKDL)**, a non-ulcerative cutaneous manifestation that occurs in patients following the clinical recovery from Visceral Leishmaniasis (Kala-azar), caused by *Leishmania donovani*. **Why Hypopigmented Macules are Correct:** PKDL typically presents in two stages. The earliest and most common presentation is **hypopigmented macules**, which usually start on the face and later spread to the trunk and extremities. These macules are characteristically non-anesthetic (unlike Leprosy). Over time, these may progress into malar erythema, followed by the development of yellowish-pink non-ulcerating nodules or plaques. **Why Other Options are Incorrect:** * **Hyperpigmented Macules:** While Kala-azar itself is known as "Black Fever" due to generalized hyperpigmentation (especially on the hands, feet, and abdomen), the specific dermal sequel (PKDL) is characterized by a loss of pigment (hypopigmentation), not an increase. * **Ecchymosis:** This refers to subcutaneous bleeding/bruising. While Visceral Leishmaniasis can cause thrombocytopenia leading to bleeding tendencies, it is not a characteristic feature of the post-treatment skin lesions (PKDL). **High-Yield Clinical Pearls for NEET-PG:** * **Incidence:** In the Indian subcontinent, PKDL occurs in about 5-10% of cases, usually **2–3 years** after the visceral phase. In Sudan, it occurs in up to 50% of cases, much sooner (weeks to months). * **Diagnosis:** Slit-skin smear or biopsy shows **LD bodies** (Amastigotes), though they are harder to find in macules compared to nodules. * **Treatment:** The drug of choice in India is **Miltefosine** (for 12 weeks) or Amphotericin B. * **Public Health Significance:** Patients with PKDL act as an important **environmental reservoir** for the parasite, as the lesions are highly infectious to sandflies (*Phlebotomus argentipes*).

Question 47: What is the treatment for Lucio phenomenon?

A. Steroids
B. Lenalidomide
C. Clofazimine
D. Exchange transfusion (Correct Answer)

Explanation: ### Explanation **Lucio phenomenon** is a rare, life-threatening variant of Type 2 Lepra reaction (ENL) seen exclusively in patients with **Diffuse Lepromatous Leprosy (Lucio Leprosy)**. **Why Exchange Transfusion is the Correct Answer:** The pathogenesis involves a severe, necrotizing occlusive vasculitis. Large numbers of *M. leprae* invade the endothelial cells of dermal blood vessels, leading to endothelial proliferation, thrombus formation, and subsequent ischemic infarction of the skin. This results in the characteristic "star-shaped" or polygonal necrotic ulcers. Because the condition is driven by a massive bacterial load and circulating immune complexes causing hypercoagulability and systemic toxicity, **Exchange Transfusion** (or Plasmapheresis) is considered the definitive treatment to rapidly clear these mediators and improve survival in severe cases. **Analysis of Incorrect Options:** * **A. Steroids:** While used in standard Type 1 and Type 2 reactions, steroids have limited efficacy in Lucio phenomenon because the primary pathology is thrombotic vasculitis rather than purely inflammatory. * **B. Lenalidomide:** This is a derivative of Thalidomide. While Thalidomide is the drug of choice for standard ENL, it is generally **ineffective** in Lucio phenomenon. * **C. Clofazimine:** This is part of the MDT regimen and has anti-inflammatory properties, but it acts too slowly to manage the acute, life-threatening crisis of Lucio phenomenon. **High-Yield Clinical Pearls for NEET-PG:** * **Geographic distribution:** Most common in Mexico and Central America. * **Clinical hallmark:** Painful, jagged, violaceous purpuric macules that evolve into **polygonal necrotic ulcers**, typically on the extremities. * **Histopathology:** Shows acid-fast bacilli (AFB) within the endothelial cells and "thrombotic vasculitis." * **Mnemonic:** Remember **"Lucio = Lethal"** – it requires aggressive intervention like exchange transfusion, unlike standard ENL which responds to Thalidomide.

Question 48: A boy from Bihar presents with a non-anesthetic, hypopigmented, atrophic patch over his face. What is the diagnosis?

A. Pityriasis alba
B. Pityriasis versicolor
C. Indeterminate leprosy (Correct Answer)
D. Borderline leprosy

Explanation: ### **Explanation** The correct diagnosis is **Indeterminate Leprosy**. This is the earliest clinical stage of leprosy, often seen in children. **1. Why Indeterminate Leprosy is Correct:** * **Clinical Presentation:** It typically presents as a single, poorly defined, **hypopigmented patch**, most commonly on the face, outer arms, or thighs. * **Sensory Findings:** Unlike other forms of leprosy, the patch in the indeterminate stage is often **non-anesthetic** (or has only vague sensory loss) because nerve damage is minimal at this early phase. * **Epidemiology:** The patient is from Bihar, an endemic belt for leprosy in India, which increases clinical suspicion. **2. Why Other Options are Incorrect:** * **Pityriasis alba:** Presents as multiple, scaly, hypopigmented patches with indistinct borders, usually associated with atopy. It does not show atrophy. * **Pityriasis versicolor:** A fungal infection (Malassezia) presenting as multiple small, "dusty" scaly macules. It is diagnosed by a "spaghetti and meatballs" appearance on KOH mount, not by atrophy or endemicity. * **Borderline leprosy:** These lesions are usually multiple, well-defined, and show **definite sensory loss** and nerve enlargement, which are absent in this case. **3. NEET-PG High-Yield Pearls:** * **Fate of Indeterminate Leprosy:** About 75% of cases heal spontaneously; the rest evolve into a specific type (Tuberculoid, Borderline, or Lepromatous) based on the patient's CMI (Cell-Mediated Immunity). * **Histopathology:** Shows a non-specific perivascular and periappendageal lymphocytic infiltrate. Acid-fast bacilli (AFB) are rarely found. * **Key Differentiator:** If a hypopigmented patch on a child's face in an endemic area is non-anesthetic, always suspect Indeterminate Leprosy first.

Question 49: Which among the following organisms causes Buruli ulcer?

A. M. Marinum
B. M. Ulcerans (Correct Answer)
C. M. kansasii
D. M. Smegmatis

Explanation: **Explanation:** **Buruli ulcer** is a chronic, debilitating necrotizing disease of the skin and soft tissue caused by **Mycobacterium ulcerans**. It is the third most common mycobacterial disease in immunocompetent hosts, following tuberculosis and leprosy. 1. **Why M. ulcerans is correct:** * **Pathogenesis:** The hallmark of *M. ulcerans* is the production of a potent polyketide lipid toxin called **Mycolactone**. This toxin has cytotoxic and immunosuppressive properties, leading to extensive tissue necrosis and the characteristic "painless" ulcer with **undermined edges**. * **Transmission:** It is typically associated with slow-moving water bodies (swamps, wetlands), though the exact mode of transmission remains under study (aquatic insects or minor trauma). 2. **Analysis of Incorrect Options:** * **M. marinum:** Causes **Fish Tank Granuloma** or Swimming Pool Granuloma. It typically presents as a localized granulomatous lesion or sporotrichoid spread following exposure to contaminated water or fish. * **M. kansasii:** A photochromogen that primarily causes **pulmonary disease** resembling tuberculosis, though it can occasionally cause skin lesions in immunocompromised patients. * **M. smegmatis:** A rapid-grower (Runyon Group IV) usually considered a commensal or saprophyte, rarely causing skin or soft tissue infections post-surgery or trauma. **High-Yield Clinical Pearls for NEET-PG:** * **Characteristic Feature:** Large, **painless** ulcer with deeply **undermined edges**. * **Toxin:** Mycolactone (essential for virulence). * **Diagnosis:** PCR is the gold standard (IS2404 target). * **Treatment:** WHO recommends a combination of **Rifampicin and Clarithromycin** (or Streptomycin) for 8 weeks. * **Geographic Distribution:** Most common in West and Central Africa (e.g., Benin, Côte d'Ivoire).

Question 50: The 'groove sign' is characteristic of which condition?

A. Syphilis
B. Dermatomyositis
C. Lymphogranuloma venereum (LGV) (Correct Answer)
D. Systemic lupus erythematosus (SLE)

Explanation: ### Explanation **1. Why the Correct Answer is Right:** The **'Groove Sign' (Greenblatt’s Sign)** is a pathognomonic clinical finding in **Lymphogranuloma venereum (LGV)**, caused by *Chlamydia trachomatis* (serovars L1, L2, L3). It occurs during the secondary stage of the disease when the inguinal and femoral lymph nodes enlarge simultaneously. These two groups of nodes are separated by the **Poupart’s (inguinal) ligament**, which creates a visible depression or "groove" between the matted clusters of lymph nodes. **2. Why the Other Options are Wrong:** * **Syphilis:** Characterized by a painless, indurated ulcer (chancre) in the primary stage and a generalized maculopapular rash in the secondary stage. Lymphadenopathy is typically bilateral and non-suppurative, without a groove sign. * **Dermatomyositis:** A rheumatological condition characterized by Gottron papules, Heliotrope rash, and proximal muscle weakness. It does not involve suppurative inguinal lymphadenopathy. * **Systemic Lupus Erythematosus (SLE):** Presents with a malar rash, photosensitivity, and multi-organ involvement. While lymphadenopathy can occur, it is non-specific and does not form the characteristic groove sign. **3. Clinical Pearls for NEET-PG:** * **Causative Agent:** *Chlamydia trachomatis* L1-L3 (obligate intracellular). * **Stages of LGV:** 1. *Primary:* Small, painless, transient papule/ulcer. 2. *Secondary (Inguinal Syndrome):* Painful "buboes" and the **Groove Sign**. 3. *Tertiary (Genito-anorectal Syndrome):* Proctocolitis, strictures, and elephantiasis (Esthiomene). * **Treatment of Choice:** Doxycycline (100 mg BID for 21 days). Erythromycin is the alternative for pregnant patients. * **Differential Diagnosis:** Don't confuse the "Groove Sign" with the "School of Fish" appearance (Chancroid) or "Donovan bodies" (Granuloma Inguinale).

Practice by Chapter

Cutaneous Leishmaniasis

Practice Questions

Leprosy

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Tropical Ulcers

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Onchocerciasis

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Filariasis

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Tropical Mycoses

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Cutaneous Larva Migrans

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Tungiasis

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Myiasis

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Cutaneous Manifestations of Malaria

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Dengue and Other Viral Hemorrhagic Fevers

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Global Health Perspectives in Dermatology

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