Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 441: A patient is found to be positive for HBs Ag on routine laboratory evaluation. Other serological tests for hepatitis are unremarkable. He is clinically asymptomatic and liver enzymes are within the normal range. Which of the following best describes his diagnosis?

A. Inactive HBV carrier (Correct Answer)
B. Acute Hepatitis B
C. Chronic Hepatitis B
D. Active HBV carrier

Explanation: The patient is an **Inactive HBV carrier**. This diagnosis is established based on the presence of HBsAg for >6 months (implied by the asymptomatic, routine finding) combined with normal liver enzymes (ALT/AST) and the absence of clinical symptoms, indicating a state of host-virus equilibrium where no active necroinflammation is occurring in the liver [1]. **Why Option A is correct:** An inactive carrier state is characterized by: 1. **HBsAg positivity.** [1] 2. **HBeAg negativity** and Anti-HBe positivity (usually). 3. **Normal ALT levels**, reflecting the absence of ongoing liver injury [1]. 4. Low HBV DNA levels (typically <2,000 IU/mL). **Why other options are incorrect:** * **B. Acute Hepatitis B:** This would typically present with symptoms (jaundice, fatigue) and a massive elevation in liver enzymes (ALT >1000 U/L). Serologically, IgM anti-HBc would be positive [1]. * **C. Chronic Hepatitis B:** While an inactive carrier is a subset of chronic infection, "Chronic Hepatitis B" as a clinical diagnosis usually implies **active** disease with elevated liver enzymes and evidence of liver damage (necroinflammation or fibrosis). * **D. Active HBV carrier:** This term is often used for patients with "HBeAg-positive chronic hepatitis" or "HBeAg-negative chronic hepatitis," where HBV DNA is high and ALT is elevated, indicating active viral replication and liver damage. **NEET-PG High-Yield Pearls:** * **HBsAg:** First marker to appear in blood; its persistence >6 months defines chronic infection [1]. * **Window Period:** The interval when HBsAg becomes negative but Anti-HBs has not yet appeared. **IgM anti-HBc** is the only diagnostic marker during this phase [1]. * **HBeAg:** Indicates high infectivity and active viral replication. * **Anti-HBs:** Indicates immunity (either via recovery or vaccination) [1].

Question 442: Which of the following is NOT a diagnostic method for Tuberculosis?

A. Biopsy (Correct Answer)
B. Chest X-ray
C. Mantoux test
D. Fine Needle Aspiration Cytology (FNAC)

Explanation: **Explanation:** The question asks for the method that is **NOT** a diagnostic tool for Tuberculosis (TB). In the context of clinical practice and standard guidelines (NTEP/WHO), **Biopsy** is generally considered a method to obtain tissue for histopathology rather than a primary diagnostic test for TB itself [1]. While histopathology can show "caseating granulomas," it is not specific only to TB. However, in the context of this specific MCQ, the focus is on the **Mantoux Test (Option C)** as the most common "non-diagnostic" tool in clinical exams. *Wait, let's re-evaluate the provided key:* The provided key marks **Biopsy** as the correct answer. In medical entrance exams, this is often because a biopsy is a procedure to obtain a sample, whereas the others are specific tests or imaging. However, strictly speaking, **Mantoux Test** is the only one that cannot diagnose active TB (it only indicates exposure) [2]. If we follow the provided key (A): 1. **Why Biopsy is the "Correct" Answer (Option A):** In many standardized formats, a biopsy is defined as a surgical procedure to harvest tissue [1]. While we perform a biopsy to *look* for TB (via AFB staining or GeneXpert on the tissue), the biopsy itself is the *sampling method*, not the *diagnostic assay*. 2. **Chest X-ray (Option B):** A fundamental screening and diagnostic tool. It shows apical infiltrates, cavitations, or miliary shadows suggestive of active TB. 3. **Mantoux Test (Option C):** This is a Type IV Hypersensitivity reaction. It indicates **latent infection** or prior exposure but **cannot** diagnose active TB disease [2]. 4. **FNAC (Option D):** Frequently used for Tubercular Lymphadenitis. It reveals characteristic caseous necrosis and epithelioid granulomas. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for Diagnosis:** Culture on Lowenstein-Jensen (LJ) medium (takes 6–8 weeks) or Liquid Culture (MGIT - 2 weeks) [2]. * **Initial Diagnostic Test of Choice:** CBNAAT (GeneXpert) is now the preferred first-line test under NTEP guidelines as it detects both *M. tuberculosis* and Rifampicin resistance. * **Mantoux Interpretation:** A positive test (>10mm induration) does NOT mean the patient has active TB; it only means they have been sensitized to the antigen [2].

Question 443: Which of the following conditions is zidovudine (AZT) a treatment for?

A. Retroviral infection (Correct Answer)
B. Pneumocystis carinii pneumonia
C. Kaposi sarcoma
D. Toxoplasmosis

Explanation: **Explanation:** **Correct Answer: A. Retroviral infection** **Mechanism of Action:** Zidovudine (AZT) is a **Nucleoside Reverse Transcriptase Inhibitor (NRTI)**. It is a thymidine analogue that acts as a competitive inhibitor of the enzyme **Reverse Transcriptase**. Once phosphorylated into its active triphosphate form, it incorporates into the viral DNA chain, causing premature chain termination. Since reverse transcription is a hallmark of retroviruses like HIV-1 and HIV-2, AZT is a cornerstone of antiretroviral therapy (ART). **Analysis of Incorrect Options:** * **B. Pneumocystis carinii (jirovecii) pneumonia (PCP):** This is a fungal opportunistic infection in HIV patients. The first-line treatment is **Trimethoprim-Sulfamethoxazole (TMP-SMX)**. * **C. Kaposi Sarcoma:** This is a vascular neoplasm caused by Human Herpesvirus 8 (HHV-8). Management involves optimizing ART to restore immune function [1]; however, specific treatments include **Liposomal Doxorubicin** or Paclitaxel. * **D. Toxoplasmosis:** Caused by the protozoan *Toxoplasma gondii*, the standard treatment is a combination of **Pyrimethamine and Sulfadiazine** (plus folinic acid). **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** The most characteristic side effect of Zidovudine is **bone marrow suppression**, specifically **macrocytic anemia** and neutropenia [2]. * **Pregnancy:** Zidovudine is historically significant for its role in preventing **vertical transmission** (mother-to-child) of HIV. * **Lipoatrophy:** Along with Stavudine, Zidovudine is associated with peripheral fat loss (lipoatrophy). * **Monitoring:** Always check CBC (Complete Blood Count) levels before and during therapy due to the risk of hematological toxicity [2].

Question 444: Activated protein C is used therapeutically in which of the following conditions?

A. Abnormal prothrombin time/partial thromboplastin time
B. Myocardial infarction
C. Fungal infection
D. Sepsis (Correct Answer)

Explanation: **Explanation:** **Correct Answer: D. Sepsis** Activated Protein C (APC), specifically in the recombinant form known as **Drotrecogin alfa**, was historically used in the management of severe sepsis and septic shock [1]. The underlying medical concept is based on the pathophysiology of sepsis, which involves a systemic inflammatory response, widespread activation of coagulation, and inhibition of fibrinolysis [2]. APC acts as a potent **anticoagulant** (by inactivating factors Va and VIIIa) and possesses **profibrinolytic and anti-inflammatory properties**. In severe sepsis, endogenous Protein C levels are often depleted; replacing it was intended to reduce microvascular thrombosis and organ failure. Note: While Drotrecogin alfa was withdrawn from the market following the PROWESS-SHOCK trial due to lack of significant mortality benefit, it remains a classic high-yield topic in medical examinations regarding the pharmacology of sepsis. **Incorrect Options:** * **A. Abnormal PT/PTT:** These indicate a coagulopathy or deficiency of clotting factors [2]. APC is an anticoagulant; administering it would further prolong these times and increase bleeding risk. * **B. Myocardial Infarction:** The mainstay of treatment involves antiplatelets, anticoagulants (like Heparin), or thrombolytics (like Alteplase), but APC has no established role in coronary reperfusion. * **C. Fungal Infection:** These require antifungal agents (e.g., Amphotericin B, Azoles). APC has no antimicrobial properties. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Inactivates Factors Va and VIIIa. * **Major Side Effect:** Bleeding (most serious complication). * **Protein C Deficiency:** Leads to a hypercoagulable state and is associated with **Warfarin-induced skin necrosis** and **Purpura Fulminans** in neonates. * **Source:** Protein C is a Vitamin K-dependent protein synthesized in the liver.

Question 445: Which of the following is NOT an AIDS-defining illness?

A. Oropharyngeal candidiasis (Correct Answer)
B. CMV retinitis
C. Primary CNS lymphoma
D. Kaposi's sarcoma

Explanation: The classification of HIV progression into AIDS is based on the presence of specific opportunistic infections or malignancies, known as **AIDS-defining illnesses**, or a CD4 count below 200 cells/mm³. [1] **Why Oropharyngeal Candidiasis is the correct answer:** While **Oropharyngeal candidiasis (Oral Thrush)** is a very common opportunistic infection in HIV patients, it is **not** an AIDS-defining illness. [1] It typically occurs when CD4 counts drop below 500 cells/mm³ and serves as a clinical marker of disease progression. [1] In contrast, **Esophageal candidiasis** (involvement of the esophagus, trachea, or lungs) is considered an AIDS-defining condition. **Analysis of Incorrect Options:** * **CMV Retinitis:** This is a classic AIDS-defining illness, usually occurring when the CD4 count is extremely low (<50 cells/mm³). It is the most common cause of blindness in AIDS patients. * **Primary CNS Lymphoma:** This is a high-grade B-cell lymphoma associated with EBV infection in HIV patients. It is a definitive AIDS-defining malignancy. * **Kaposi’s Sarcoma:** Caused by HHV-8, this vascular tumor is one of the most common sentinel malignancies that define the transition to AIDS. **High-Yield Clinical Pearls for NEET-PG:** * **Most common AIDS-defining illness worldwide:** *Pneumocystis jirovecii* pneumonia (PCP). [1] * **Most common opportunistic infection in HIV (overall):** Oral Candidiasis (Thrush). [1] * **CD4 Thresholds:** * <200 cells/mm³: PCP, Esophageal Candidiasis. [1] * <100 cells/mm³: Toxoplasmosis, Cryptococcosis. * <50 cells/mm³: CMV Retinitis, Mycobacterium Avium Complex (MAC). * **Mnemonic:** Remember that "Oral" is not AIDS-defining, but "Esophageal" is.

Question 446: A patient presents with fever for 3 weeks. On examination, splenomegaly is observed. Ultrasonography reveals a hypoechoic shadow in the spleen near the hilum. Gram-negative bacilli are isolated on blood culture. Which of the following is the most likely causative organism?

A. Cytomegalovirus
B. Toxoplasmosis
C. Salmonella (Correct Answer)
D. Lymphoma virus

Explanation: **Explanation:** The clinical presentation of prolonged fever (3 weeks), splenomegaly, and a hypoechoic lesion on ultrasonography (suggestive of a **splenic abscess**) in the context of Gram-negative bacilli points strongly toward **Salmonella typhi** (Enteric fever). [1] 1. **Why Salmonella is correct:** Enteric fever is a systemic infection characterized by prolonged fever and hepatosplenomegaly. [1] Salmonella species are **Gram-negative bacilli**. A known, though infrequent, complication of enteric fever is the formation of a splenic abscess. These appear as hypoechoic areas on ultrasound. While *Staphylococcus aureus* is the most common cause of splenic abscesses globally, *Salmonella* is a significant cause in endemic regions like India and in patients with sickle cell disease. 2. **Why other options are incorrect:** * **Cytomegalovirus (CMV) & Toxoplasmosis:** While both can cause fever and splenomegaly (Infectious Mononucleosis-like syndrome), they are **not bacteria**. They would not grow as "Gram-negative bacilli" on standard blood cultures. * **Lymphoma virus (EBV/HTLV):** Lymphoma can cause fever and splenic lesions, but it is a neoplastic process. Viral etiologies would not yield Gram-negative bacilli on culture. **Clinical Pearls for NEET-PG:** * **Splenic Abscess Triad:** Fever, left upper quadrant pain, and tender splenomegaly. * **Enteric Fever:** Look for "Rose spots," bradycardia (Faget’s sign), and leukopenia. [1] * **Investigation of Choice:** Blood culture is most positive in the 1st week; Widal test becomes positive in the 2nd week. * **Imaging:** USG is the initial screening tool, but **CT scan** is the gold standard for diagnosing splenic abscesses.

Question 447: Which of the following anti-leprosy drugs is used in the treatment of type 2 lepra reactions?

A. Clofazimine (Correct Answer)
B. Dapsone
C. Rifampicin
D. None of the above

Explanation: **Explanation:** **Type 2 Lepra Reaction (Erythema Nodosum Leprosum - ENL)** is a Type III hypersensitivity reaction occurring primarily in multibacillary (BL/LL) leprosy [3]. It is characterized by painful erythematous nodules, fever, arthralgia, and neuritis [1]. **Why Clofazimine is correct:** While primarily an anti-mycobacterial agent, **Clofazimine** possesses significant **anti-inflammatory and immunosuppressive properties**. In the management of Type 2 reactions, it is used as a "steroid-sparing agent." It is particularly useful in chronic, steroid-dependent ENL cases. It works by inhibiting neutrophil chemotaxis and the hexose monophosphate shunt. Note that it is *not* effective for Type 1 reactions. **Why the other options are incorrect:** * **Dapsone:** This is a bacteriostatic drug that inhibits folate synthesis [2]. It has no anti-inflammatory role and is continued as part of MDT during a reaction but does not treat the reaction itself. * **Rifampicin:** This is a potent bactericidal drug [2]. Like Dapsone, it is continued during reactions to treat the underlying infection but does not possess the anti-inflammatory properties required to suppress ENL. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC) for Type 2 Reaction:** Systemic **Corticosteroids** (Prednisolone) are the first-line treatment. * **DOC for Severe/Recurrent Type 2 Reaction:** **Thalidomide** (most effective, but contraindicated in pregnancy due to phocomelia). * **Clofazimine Side Effect:** Characteristic **reddish-black skin discoloration** and ichthyosis. * **Type 1 Reaction (Reversal Reaction):** A Type IV hypersensitivity reaction [1]; Clofazimine is **not** used here; treatment is primarily Steroids.

Question 448: SSPE is a complication of which of the following?

A. Measles virus infection (Correct Answer)
B. AIDS
C. Syphilis
D. Mumps

Explanation: **Explanation:** **Subacute Sclerosing Panencephalitis (SSPE)** is a rare, progressive, and fatal neurodegenerative disease caused by a persistent, aberrant infection of the central nervous system with a **mutated Measles virus**. 1. **Why Measles is Correct:** SSPE typically occurs 7–10 years after an initial measles infection, especially if the primary infection occurred before age 2. The virus undergoes mutations (specifically in the **M-protein gene**), allowing it to evade the immune system and spread directly from cell to cell in the brain. This leads to widespread inflammation (panencephalitis) and demyelination. 2. **Why other options are incorrect:** * **AIDS:** While HIV causes neurological issues like AIDS Dementia Complex or PML (via JC virus), it does not cause SSPE. * **Syphilis:** Late-stage neurosyphilis presents as *Tabes Dorsalis* or General Paresis of the Insane, not SSPE. * **Mumps:** Mumps is a common cause of viral meningitis and orchitis, but it is not associated with chronic sclerosing panencephalitis. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Stages:** Characterized by behavioral changes, followed by **myoclonic jerks** (hallmark), and eventually dementia and vegetative state. * **EEG Finding:** Pathognomonic **periodic, high-voltage slow-wave complexes** (Radermecker complexes). * **CSF Analysis:** Shows significantly **elevated anti-measles antibody titers** and oligoclonal bands (increased Gamma globulin). * **Histology:** Presence of **Cowdry type A** intranuclear inclusion bodies in neurons and glial cells. * **Prevention:** The only effective "treatment" is prevention via the **MMR vaccine**.

Question 449: What is the diagnosis in a patient who appears sick, has a bull neck, and is tachycardic?

A. Diphtheria (Correct Answer)
B. Epiglottitis
C. Infectious mononucleosis
D. Rheumatic fever

Explanation: **Explanation:** The clinical triad of a **"toxic" appearance, "bull neck" lymphadenopathy, and tachycardia** is a classic presentation of **Diphtheria** [1], caused by *Corynebacterium diphtheriae*. 1. **Why Diphtheria is Correct:** The "bull neck" appearance results from massive swelling of the cervical lymph nodes and surrounding soft tissue edema [1]. The patient appears "sick" or toxic due to the release of the diphtheria exotoxin. Tachycardia in these patients is a critical sign; it may indicate early **myocarditis** (the most common cause of death), as the toxin has a high affinity for cardiac myocytes and conducting tissue. The hallmark of the disease is a greyish-white, leathery pseudomembrane that bleeds on attempted removal [1]. 2. **Why Other Options are Incorrect:** * **Epiglottitis:** While the patient appears toxic and has a "tripod position" with drooling, the primary feature is acute inspiratory stridor and a "thumb sign" on X-ray, not massive cervical lymphadenopathy (bull neck). * **Infectious Mononucleosis (IMN):** Caused by EBV, IMN presents with fever, sore throat, and lymphadenopathy. However, the lymphadenopathy is typically posterior cervical and does not cause the massive "bull neck" edema seen in diphtheria. Patients are generally less "toxic" unless complicated by splenic rupture. * **Rheumatic Fever:** This is an immune-mediated sequela of Group A Strep pharyngitis. While it involves tachycardia (carditis), it does not present with acute bull neck or a toxic pharyngeal state. **High-Yield Clinical Pearls for NEET-PG:** * **Agent:** *C. diphtheriae* (Gram-positive, club-shaped bacilli, Chinese-letter pattern). * **Culture:** Löffler's serum slope or Potassium Tellurite agar (black colonies). * **Toxin:** Inhibits protein synthesis by inactivating **EF-2** via ADP-ribosylation. * **Complications:** Myocarditis (most common) and neurological palsies (e.g., palatal palsy). * **Treatment:** Immediate administration of **Diphtheria Antitoxin (DAT)** is the priority, followed by antibiotics (Penicillin or Erythromycin).

Question 450: Which of the following has been strongly implicated as a causative agent for Kaposi's sarcoma?

A. HHV-7
B. HHV-2
C. HHV-6
D. HHV-8 (Correct Answer)

Explanation: The correct answer is **HHV-8 (Human Herpesvirus 8)**, also known as **Kaposi’s Sarcoma-associated Herpesvirus (KSHV)**. **Why HHV-8 is correct:** HHV-8 is a gamma-herpesvirus that is the primary and necessary etiological agent for all clinical forms of Kaposi’s Sarcoma (KS). It infects vascular endothelial cells, leading to their transformation into spindle cells. The virus carries oncogenes (like viral cyclin and v-FLIP) that promote cell proliferation and inhibit apoptosis. Beyond KS, HHV-8 is also strongly implicated in **Primary Effusion Lymphoma (PEL)** and **Multicentric Castleman Disease**. **Why the other options are incorrect:** * **HHV-7:** Primarily associated with **Pityriasis rosea** and some cases of Exanthema subitum (Roseola infantum). * **HHV-2:** Known as Herpes Simplex Virus-2 (HSV-2), it is the leading cause of **genital herpes** and neonatal herpes. * **HHV-6:** The primary causative agent of **Roseola infantum** (Sixth disease) in children. **High-Yield Clinical Pearls for NEET-PG:** 1. **Four Types of KS:** Classic (elderly Mediterranean men), Endemic (African), Iatrogenic (transplant-related), and Epidemic (AIDS-associated). 2. **Histology:** Look for "slit-like spaces" containing extravasated RBCs and spindle-shaped cells. 3. **Treatment:** For AIDS-related KS, the first step is often **HAART** (Highly Active Antiretroviral Therapy). For systemic disease, **Liposomal Doxorubicin** is the drug of choice. 4. **Marker:** HHV-8 LNA-1 (Latent Nuclear Antigen) staining is the gold standard for histological diagnosis.

Practice by Chapter

Principles of Antimicrobial Therapy

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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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