Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 671: Ketoconazole is useful in all of the following except?

A. Tinea cruris
B. Tinea versicolor
C. Tinea capitis (Correct Answer)
D. Tinea corporis

Explanation: **Explanation:** The correct answer is **Tinea capitis** because Ketoconazole (a first-generation imidazole) has poor penetration into hair follicles and does not achieve therapeutic concentrations in the hair shaft. **1. Why Tinea capitis is the correct answer:** Tinea capitis involves infection of the hair shaft and follicles [3]. Management requires systemic antifungal agents that accumulate in keratinized tissues. **Griseofulvin** remains the gold standard (DOC), while Terbinafine and Itraconazole are effective alternatives. Ketoconazole is generally avoided for Tinea capitis due to its limited efficacy in hair and its significant side-effect profile, which include severe hepatitis and inhibition of enzymes involved in steroid hormone biosynthesis [1]. **2. Why the other options are incorrect:** * **Tinea cruris (A), Tinea versicolor (B), and Tinea corporis (D):** These are superficial fungal infections of the glabrous (smooth) skin or the stratum corneum [2]. Ketoconazole, especially in topical formulations (creams/shampoos), is highly effective against these dermatophytes and *Malassezia furfur* [1]. Since these infections do not involve deep hair follicle penetration, topical imidazoles are first-line treatments. **Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Ketoconazole inhibits the enzyme **14-α demethylase**, preventing the conversion of lanosterol to ergosterol, a vital component of the fungal cell membrane. * **Endocrine Side Effects:** It inhibits Cytochrome P450 enzymes, leading to decreased testosterone and cortisol [1]. This can cause **gynecomastia**, loss of libido, and menstrual irregularities. * **Drug of Choice (DOC):** While Ketoconazole is used for Tinea versicolor, **Griseofulvin** is the DOC for Tinea capitis, and **Terbinafine** is the DOC for Onychomycosis.

Question 672: What is the most common neoplasm among HIV-positive homosexual males?

A. Non-Hodgkin's lymphoma
B. Glomus tumor
C. Kaposi's sarcoma (Correct Answer)
D. None of the above

Explanation: **Explanation:** **Kaposi’s Sarcoma (KS)** is the most common neoplasm associated with HIV infection, particularly among men who have sex with men (MSM). It is an angioproliferative disorder caused by **Human Herpesvirus 8 (HHV-8)**, also known as Kaposi’s sarcoma-associated herpesvirus (KSHV). In the context of HIV, it is classified as an AIDS-defining illness [1]. **Analysis of Options:** * **Option A: Non-Hodgkin's Lymphoma (NHL):** While NHL is the second most common malignancy in HIV patients and is also an AIDS-defining illness (specifically Burkitt’s and Diffuse Large B-Cell Lymphoma), its overall incidence remains lower than Kaposi’s sarcoma in the MSM population. * **Option B: Glomus Tumor:** This is a rare, benign vascular neoplasm typically found in the subungual region (under the fingernails). It has no established association with HIV or HHV-8. * **Option D: None of the above:** Incorrect, as Kaposi’s sarcoma is the well-documented leading neoplasm in this group. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Characterized by painless, non-pruritic, violaceous (purple/red) macules, plaques, or nodules [1]. It can involve the skin, oral mucosa (especially the hard palate), and visceral organs (GI tract and lungs) [1]. * **Histology:** Features spindle-shaped cells, slit-like vascular spaces, and extravasated red blood cells. * **Treatment:** The primary treatment is the initiation of **Highly Active Antiretroviral Therapy (HAART)**, which often leads to lesion regression. For advanced cases, systemic chemotherapy (e.g., liposomal doxorubicin) may be used. * **Other HIV-Associated Cancers:** Invasive cervical cancer and Primary CNS Lymphoma are also AIDS-defining. Non-AIDS-defining cancers (like Anal Cancer) are also increasing in incidence due to prolonged survival on HAART.

Question 673: All are true regarding typhoid ulcer EXCEPT?

A. Ileum is the common site
B. Bleeding is common
C. Stricture is usual and causes obstruction (Correct Answer)
D. Perforation is common

Explanation: Enriched Explanation: Typhoid fever, caused by Salmonella typhi, primarily affects the gastrointestinal tract by targeting the Peyer’s patches (lymphoid tissue) in the small intestine [1]. Why Option C is the Correct Answer (The "Except"): Unlike Tuberculosis or Crohn’s disease, typhoid ulcers are longitudinal (oriented along the long axis of the bowel). Because they do not encircle the bowel lumen, they heal without significant fibrosis. Therefore, stricture formation and intestinal obstruction are extremely rare in typhoid fever. Analysis of Other Options: * A. Ileum is the common site: Peyer’s patches are most numerous and prominent in the terminal ileum; hence, this is the most common site for typhoid-related pathology. * B. Bleeding is common: During the 3rd week of infection, the sloughing of the necrotic Peyer’s patches (forming the ulcer) can erode into small vessels, leading to occult or frank gastrointestinal hemorrhage [1]. * D. Perforation is common: This is a dreaded complication occurring in the 3rd week [1]. As the ulcer deepens through the muscularis and serosa, it can lead to ileal perforation, typically presenting as sudden abdominal pain and peritonitis. High-Yield Clinical Pearls for NEET-PG: * Ulcer Orientation: Typhoid ulcers are Longitudinal (parallel to the long axis); Tubercular ulcers are Transverse (leading to strictures). * Timeline: Complications like bleeding and perforation typically occur in the 3rd week of illness [1]. * Pathology: The characteristic histological finding is the presence of Typhoid nodules (aggregates of macrophages/Kupffer cells containing ingested bacilli and RBCs—erythrophagocytosis). * Widal Test: Usually becomes positive after the 1st week (best in the 2nd week).

Question 674: What is the commonest cause of spleen rupture?

A. Chronic malaria
B. Infectious mononucleosis
C. Leukemia (Correct Answer)
D. Chronic kala azar

Explanation: **Explanation:** The spleen is a highly vascular organ, and its rupture can be categorized into traumatic (most common overall) [1] and **spontaneous (pathological) rupture**. **1. Why Leukemia is the correct answer:** In the context of pathological rupture, **Leukemia** (specifically Chronic Myeloid Leukemia or Acute Leukemias) is considered the most common cause [3]. The underlying mechanism involves rapid infiltration of the splenic parenchyma by malignant cells. This leads to massive splenomegaly, which stretches the splenic capsule. Furthermore, the hypercellularity causes "splenic infarction" and increased intra-capsular pressure, making the organ extremely friable and prone to rupture even with negligible or no trauma. **2. Analysis of Incorrect Options:** * **Infectious Mononucleosis (EBV):** This is the most common **infectious** cause of spontaneous splenic rupture [3]. While high-yield, it occurs less frequently than rupture due to hematological malignancies in a clinical aggregate. * **Chronic Malaria & Chronic Kala-azar:** These conditions cause massive splenomegaly (especially "Tropical Splenomegaly Syndrome" in malaria). While they increase the risk of rupture due to minor trauma, spontaneous rupture is statistically less common compared to the acute infiltrative process of leukemia. **NEET-PG High-Yield Pearls:** * **Most common cause of splenic rupture overall:** Blunt trauma to the abdomen (e.g., RTA) [1], [2]. * **Most common infectious cause of rupture:** Infectious Mononucleosis [3] (Avoid contact sports for 3–4 weeks). * **Kehr’s Sign:** Referred pain to the left shoulder due to diaphragmatic irritation by splenic blood (classic sign of rupture). * **Massive Splenomegaly:** Defined as a spleen crossing the midline or reaching the iliac fossa (Common causes: CML, Malaria, Kala-azar, Myelofibrosis).

Question 675: Which is the drug of choice for prophylaxis of meningococcal meningitis in pregnancy?

A. Penicillin
B. Ceftriaxone (Correct Answer)
C. Rifampicin
D. Ampicillin

Explanation: **Explanation:** The primary goal of chemoprophylaxis in meningococcal meningitis is to eradicate the nasopharyngeal carriage of *Neisseria meningitidis* to prevent the spread of the disease to close contacts [1]. **1. Why Ceftriaxone is the Correct Answer:** Ceftriaxone is the **drug of choice for pregnant women** because it is highly effective at eradicating the carrier state and has an established safety profile in pregnancy (FDA Category B). It is administered as a single intramuscular (IM) dose of 250 mg. It is also the preferred choice for children. **2. Why Other Options are Incorrect:** * **Rifampicin:** While it is the standard drug of choice for the general population (600 mg twice daily for 2 days), it is **contraindicated in pregnancy** due to potential teratogenicity (demonstrated in animal studies) [1]. * **Penicillin & Ampicillin:** Although these are used for the *treatment* of active meningococcal disease, they are ineffective for *prophylaxis* because they do not achieve sufficient concentrations in nasopharyngeal secretions to reliably eradicate the carrier state. **3. High-Yield Clinical Pearls for NEET-PG:** * **Standard Prophylaxis (Non-pregnant adults):** Rifampicin is the first-line agent [1]. Ciprofloxacin (500 mg single dose) is an alternative but is generally avoided in pregnancy and children due to concerns regarding cartilage damage. * **Close Contacts:** Prophylaxis is indicated for "close contacts" (household members, daycare contacts, or healthcare workers exposed to respiratory secretions) and should ideally be started within 24 hours of identification of the index case [1]. * **Azithromycin:** Can be used as a single-dose oral alternative if other options are unavailable.

Question 676: What is the most common malignancy in AIDS patients?

A. Kaposi sarcoma (Correct Answer)
B. Hodgkin lymphoma
C. Leukemia
D. Multiple myeloma

Explanation: **Explanation:** **Kaposi Sarcoma (KS)** is the most common malignancy associated with HIV/AIDS [1]. It is caused by **Human Herpesvirus 8 (HHV-8)**, also known as Kaposi Sarcoma-associated Herpesvirus (KSHV). In the context of AIDS, it typically presents as painless, violaceous (purple) macules, plaques, or nodules on the skin, mucous membranes, or visceral organs [1]. It is considered an **AIDS-defining illness** [1]. While the incidence has significantly decreased with the advent of Highly Active Antiretroviral Therapy (HAART), it remains the most frequent neoplasm in this population. **Analysis of Incorrect Options:** * **B. Hodgkin Lymphoma:** While HIV patients have a significantly higher risk of Hodgkin Lymphoma compared to the general population, it is less common than Kaposi Sarcoma. Note that **Non-Hodgkin Lymphoma (NHL)**, specifically Burkitt and Diffuse Large B-cell Lymphoma, is the *second* most common malignancy in AIDS. * **C. Leukemia:** There is no strong epidemiological link between HIV and an increased incidence of primary leukemias compared to the general population. * **D. Multiple Myeloma:** Although plasma cell dyscrasias can occur in HIV patients due to chronic B-cell stimulation, it is not a defining or common malignancy in this group. **High-Yield Clinical Pearls for NEET-PG:** 1. **Top 3 AIDS-Defining Malignancies:** 1. Kaposi Sarcoma, 2. Non-Hodgkin Lymphoma, 3. Invasive Cervical Carcinoma. 2. **Histology of KS:** Characterized by **spindle-shaped cells**, slit-like vascular spaces, and extravasated RBCs. 3. **Most common site:** The skin is most common, but the **gastrointestinal tract** and lungs are common visceral sites [1]. 4. **Primary Effusion Lymphoma:** Another HHV-8 associated malignancy seen specifically in AIDS patients.

Question 677: What is the minimum duration required for post-exposure chemoprophylaxis for HIV?

A. 4 weeks (Correct Answer)
B. 6 weeks
C. 8 weeks
D. 12 weeks

Explanation: The correct answer is **4 weeks (A)**. Post-exposure prophylaxis (PEP) for HIV is a medical emergency aimed at preventing viral replication and systemic dissemination following a potential exposure (e.g., needle-stick injury or sexual assault). According to current WHO and NACO guidelines, the standard duration for PEP is **28 days (4 weeks)**. **Why 4 weeks?** The rationale is based on the window of opportunity for intervention. Animal studies have demonstrated that while HIV begins to replicate at the site of entry within hours, it takes approximately 48–72 hours to reach regional lymph nodes and several days to become systemic. A 28-day course of Highly Active Antiretroviral Therapy (HAART) is sufficient to inhibit viral replication during this critical period, allowing the host immune system to clear the initial inoculum before a permanent infection is established. **Analysis of Incorrect Options:** * **6, 8, and 12 weeks (B, C, D):** These durations are unnecessarily long. Extending PEP beyond 28 days does not provide additional protection but significantly increases the risk of drug toxicity, side effects (like nausea and hepatotoxicity), and poor patient compliance. **High-Yield Clinical Pearls for NEET-PG:** * **Timing:** PEP should be started as soon as possible, ideally within **2 hours**, and no later than **72 hours** post-exposure. * **Preferred Regimen (NACO):** A 3-drug regimen is now standard, typically consisting of **Tenofovir (300mg) + Lamivudine (300mg) + Dolutegravir (50mg)** as a single daily tablet for 28 days. * **Follow-up:** HIV testing should be performed at baseline, 6 weeks, and 3 months post-exposure to confirm serostatus [1]. * **Efficacy:** PEP is highly effective but not 100%; it reduces the risk of HIV transmission by approximately 81%.

Question 678: Acute infectious purpura fulminans is caused by which of the following agents?

A. Neisseria meningitidis and varicella (Correct Answer)
B. Gonococci
C. E. coli
D. Proteus

Explanation: **Explanation:** **Purpura Fulminans (PF)** is a life-threatening hematological emergency characterized by skin necrosis, disseminated intravascular coagulation (DIC), and microvascular thrombosis. It is classified into three types: neonatal (Protein C/S deficiency), idiopathic (post-infectious), and **acute infectious**. **Why Option A is correct:** Acute infectious purpura fulminans is most commonly associated with **Neisseria meningitidis** (Meningococcemia). In this setting, bacterial endotoxins trigger a massive inflammatory response, leading to the consumption of Protein C, Protein S, and Antithrombin III. This results in a prothrombotic state and hemorrhagic skin infarction. **Varicella** (Chickenpox) is the classic viral trigger for the post-infectious (idiopathic) form, often mediated by transient autoantibodies against Protein S. Other notable causes include *Streptococcus pneumoniae* and *Capnocytophaga canimorsus* (following dog bites). **Why other options are incorrect:** * **Option B (Gonococci):** While *N. gonorrhoeae* causes Disseminated Gonococcal Infection (DGI), it typically presents with a triad of tenosynovitis, dermatitis (pustules), and polyarthralgia, rather than the fulminant DIC seen in PF. * **Options C & D (E. coli and Proteus):** These are common causes of Gram-negative sepsis, but they rarely present with the specific clinical picture of purpura fulminans unless there is underlying asplenia or extreme immunosuppression. **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark:** Symmetric peripheral gangrene and "retiform" (branching) purpura. * **Pathophysiology:** Severe deficiency of **Protein C** is the central metabolic derangement. * **Treatment:** Aggressive fluid resuscitation, antibiotics, and replacement of coagulation factors (Fresh Frozen Plasma) or **Protein C concentrate**. * **Waterhouse-Friderichsen Syndrome:** Adrenal hemorrhage associated with meningococcemia, often seen alongside PF.

Question 679: A 6-year-old child presented with perianal pruritus, skin excoriation, and nocturnal enuresis, and was found to be infected with a parasite that causes autoinfection. How is the causative agent diagnosed?

A. NIH swab method (Correct Answer)
B. String test
C. Hetrazan test
D. Encysted larvae on muscle biopsy

Explanation: The clinical presentation of **perianal pruritus** (worse at night), skin excoriation, and **nocturnal enuresis** in a child is classic for **Enterobius vermicularis** (Pinworm or Seatworm). The female worm migrates to the perianal skin at night to lay eggs, causing intense itching. Scratching leads to the transfer of eggs to the mouth, facilitating **autoinfection** and retro-infection. **Why Option A is Correct:** Standard stool microscopy is often negative because eggs are deposited on the perianal folds, not in the feces. The **NIH swab** (National Institutes of Health) or the **Scotch Tape/Cellophane Tape test** is the gold standard. It involves applying the adhesive side of the tape to the perianal area early in the morning to collect the characteristic **planoconvex (D-shaped)** eggs for microscopic examination. **Why Other Options are Incorrect:** * **B. String test (Entero-test):** Used for diagnosing parasites in the upper small intestine, primarily *Giardia lamblia* and *Strongyloides stercoralis* [1]. * **C. Hetrazan test (Mazzotti test):** Used to diagnose *Onchocerca volvulus*. It involves giving a dose of Diethylcarbamazine (DEC), which causes an intense pruritic reaction if microfilariae are present. * **D. Encysted larvae on muscle biopsy:** This is the diagnostic method for **Trichinella spiralis**, which causes trichinosis. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Albendazole or Mebendazole (single dose, repeated after 2 weeks to kill newly hatched larvae). * **Public Health:** Always treat the **entire family** simultaneously to prevent reinfection. * **Morphology:** Eggs are non-bile stained and have a double-layered shell.

Question 680: All of the following are features of CD4 count dropping below 50 cells/mm³ EXCEPT?

A. HIV associated dementia. (Correct Answer)
B. CMV retinitis.
C. Disseminated Mycobacterium avium intracellulare.
D. None of the above.

Explanation: In HIV/AIDS, the CD4 T-lymphocyte count is the most important predictor of disease progression and the risk for specific opportunistic infections (OIs) [1]. **Explanation of the Correct Answer:** **Option A (HIV-associated dementia)** is the correct answer because it typically occurs when the CD4 count falls below **200 cells/mm³**, though it becomes more severe as the count drops further. Unlike the other options, it is not specifically defined by the ultra-low threshold of <50 cells/mm³. It is a result of direct HIV infection of the CNS microglia and macrophages rather than a secondary opportunistic pathogen. **Analysis of Incorrect Options:** * **Option B (CMV Retinitis):** This is a classic "late-stage" opportunistic infection. Cytomegalovirus (CMV) manifestations, particularly retinitis and colitis, characteristically occur only when the CD4 count is **<50 cells/mm³**. * **Option C (Disseminated MAC):** *Mycobacterium avium* complex (MAC) is a hallmark of profound immunosuppression. Disseminated disease is rarely seen unless the CD4 count is **<50 cells/mm³**. Prophylaxis (historically with Azithromycin) was specifically indicated at this threshold. **NEET-PG High-Yield Pearls:** * **CD4 <200:** Pneumocystis jirovecii pneumonia (PCP), HIV Dementia, Progressive Multifocal Leukoencephalopathy (PML). * **CD4 <100:** Toxoplasmosis, Cryptococcosis, Cryptosporidiosis. * **CD4 <50:** CMV Retinitis, Disseminated MAC, CNS Lymphoma. * **Mnemonic:** As the CD4 count drops, the "C" infections appear: **C**ryptococcus (<100) → **C**MV/MAC (<50). * **Note:** Kaposi Sarcoma and Tuberculosis can occur at any CD4 level, though risk increases as the count declines.

Practice by Chapter

Principles of Antimicrobial Therapy

Practice Questions

Fever of Unknown Origin

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HIV/AIDS and Related Infections

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Tuberculosis and Mycobacterial Diseases

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Tropical and Parasitic Infections

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Viral Infections (Hepatitis, Herpes, etc.)

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Healthcare-Associated Infections

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Fungal Infections

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Sepsis and Septic Shock

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Infection in Immunocompromised Hosts

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Emerging and Re-emerging Infections

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Antimicrobial Resistance

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Vaccination Principles

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