Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 381: Acute viral hepatitis is diagnosed by?

A. Hepatic injury related with transaminase level
B. Variable increase in transaminase level (Correct Answer)
C. IgG anti-HAV used for diagnosis
D. No rise of transaminase at all

Explanation: **Explanation:** In acute viral hepatitis, the hallmark of diagnosis is the biochemical evidence of hepatocellular necrosis [1]. **Why Option B is correct:** The characteristic feature of acute viral hepatitis is a **variable but significant increase in serum transaminases** (ALT and AST) [1]. These enzymes are released into the bloodstream following hepatocyte injury. In acute cases, these levels typically rise above 500 U/L and often exceed 1000 U/L [3]. The increase is "variable" because the peak level depends on the timing of the blood draw relative to the onset of symptoms and the severity of the viral insult. **Analysis of Incorrect Options:** * **Option A:** While hepatic injury is related to transaminase levels, the term "variable increase" more accurately describes the clinical presentation where levels fluctuate during the prodromal and icteric phases. * **Option C:** **IgG** anti-HAV indicates past infection or immunity (vaccination). For the diagnosis of *acute* Hepatitis A, **IgM** anti-HAV is the specific marker required. * **Option D:** This is factually incorrect. Transaminases are the most sensitive indicators of acute liver cell injury; a "no rise" scenario would rule out acute hepatitis. **High-Yield Clinical Pearls for NEET-PG:** * **ALT vs. AST:** In viral hepatitis, **ALT is typically higher than AST** (ALT > AST). This is the opposite of Alcoholic Hepatitis, where AST:ALT is > 2:1. * **Decline of Enzymes:** A rapid fall in transaminases accompanied by a rising Prothrombin Time (PT/INR) and increasing bilirubin is a grave sign indicating **fulminant hepatic failure** (massive hepatocyte loss) [2]. * **Gold Standard for Acute Diagnosis:** Serology (e.g., HBsAg, IgM anti-HBc for Hep B; IgM anti-HAV for Hep A) is used to identify the specific viral etiology [4].

Question 382: A 48-year-old HIV-positive male presents with 3 weeks of cough, fever, night sweats, weight loss, and diarrhea. He is not taking any treatment for HIV and has a CD4 count of <50. What is the most likely diagnosis?

A. Cytomegalovirus
B. Mycobacterium avium complex (Correct Answer)
C. Candidiasis
D. Pneumocystis jiroveci

Explanation: ### Explanation The clinical presentation of chronic constitutional symptoms (fever, weight loss, night sweats) combined with gastrointestinal symptoms (diarrhea) in a patient with advanced immunosuppression (**CD4 count <50 cells/mm³**) is classic for **Disseminated Mycobacterium avium complex (MAC)**. **Why MAC is the correct answer:** MAC is an opportunistic infection caused by *M. avium* or *M. intracellulare*. It typically occurs when CD4 counts fall below 50. Key diagnostic features include: * **Systemic symptoms:** High-grade fever, night sweats, and profound weight loss. * **GI involvement:** Diarrhea and abdominal pain (due to mesenteric lymphadenopathy) [1]. * **Laboratory findings:** Anemia and elevated alkaline phosphatase (ALP) are common due to bone marrow and liver involvement. **Why other options are incorrect:** * **A. Cytomegalovirus (CMV):** While CMV also occurs at CD4 <50, it most commonly presents as **retinitis** (painless vision loss) or **colitis** (bloody diarrhea). It is less likely to cause this specific triad of chronic cough and systemic wasting. * **C. Candidiasis:** Oropharyngeal candidiasis occurs at CD4 <250, and esophageal candidiasis at CD4 <100 [2]. It presents with dysphagia or odynophagia (Fig. 14.7), not chronic systemic/pulmonary symptoms [1]. * **D. Pneumocystis jiroveci (PJP):** PJP typically presents at **CD4 <200** [3]. While it causes cough and fever, it is primarily a pulmonary infection characterized by exertional dyspnea and hypoxia; it does not cause chronic diarrhea or significant systemic wasting. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Gold standard is **Blood Culture** (using BACTEC bottles) or bone marrow biopsy showing Acid-Fast Bacilli (AFB). * **Prophylaxis:** Historically, Azithromycin was given if CD4 <50; however, current guidelines suggest deferring prophylaxis if ART is started immediately. * **Treatment:** Preferred regimen is **Clarithromycin + Ethambutol**. * **Differential:** Always differentiate MAC from *M. tuberculosis* (MTB). MTB can occur at any CD4 count, whereas MAC is almost exclusive to severe immunosuppression (CD4 <50) [3].

Question 383: A patient presents with high fever, signs of raised intracranial pressure, and a history of chronic otitis media. What is the most likely diagnosis?

A. Brain abscess (Correct Answer)
B. Pyogenic meningitis
C. Acute subarachnoid hemorrhage
D. Acute osteomyelitis of skull bone

Explanation: ### Explanation **1. Why Brain Abscess is the Correct Answer:** The clinical triad of **fever, signs of raised intracranial pressure (ICP)** (such as headache, vomiting, or papilledema), and a **predisposing focus of infection** is classic for a brain abscess [1]. In this case, the history of **chronic otitis media (COM)** is the definitive clue. Infections from the middle ear or mastoid air cells typically spread via direct extension or retrograde thrombophlebitis to the **temporal lobe** or **cerebellum**, making COM the most common cause of brain abscess in adults [1]. **2. Why the Other Options are Incorrect:** * **Pyogenic Meningitis:** While it presents with fever and raised ICP, it typically features **meningeal signs** (nuchal rigidity, Kernig’s/Brudzinski’s signs) which are often absent in brain abscess. Furthermore, meningitis is less specifically linked to a chronic focal ear infection compared to an abscess. * **Acute Subarachnoid Hemorrhage:** This presents with a "thunderclap headache" and signs of meningeal irritation. It is usually non-febrile unless complicated by secondary infections or chemical meningitis. * **Acute Osteomyelitis of Skull Bone:** This would present with localized scalp swelling (e.g., Pott’s Puffy Tumor in frontal sinusitis), tenderness, and fever, but it does not typically cause signs of raised ICP unless it progresses to an intracranial collection. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Temporal lobe (from COM) or Frontal lobe (from Sinusitis). * **Most common organism:** *Streptococcus* species (viridans group); however, in post-traumatic cases, think *Staphylococcus aureus*. * **Imaging of choice:** Contrast-enhanced MRI is superior, but CT shows a characteristic **"Ring-enhancing lesion"** with surrounding edema. * **Management:** Small abscesses (<2.5 cm) may be managed medically; larger ones require surgical aspiration or excision plus long-term antibiotics.

Question 384: In an HIV-positive patient with tuberculosis, all are true except?

A. Decreased cavitation in the lungs
B. Increased sputum positivity for AFB (Correct Answer)
C. Highly variable tuberculin tests
D. Decreased fibrosis

Explanation: In HIV-positive patients, the presentation of Tuberculosis (TB) is significantly altered due to the depletion of CD4+ T-lymphocytes, which are essential for granuloma formation and containment of the bacilli [1]. **Explanation of the Correct Answer:** * **Option B (Increased sputum positivity for AFB):** This is **false**. In advanced HIV, the lack of an effective immune response leads to poor granuloma formation and less cavitation. Since cavities are the primary sites where high concentrations of bacilli reside and communicate with the airways, their absence results in **decreased sputum positivity** (paucibacillary disease) [1][2]. This makes diagnosis via traditional smear microscopy more challenging in HIV patients. **Explanation of Incorrect Options:** * **Option A (Decreased cavitation):** True. Cavitation is a result of a robust delayed-type hypersensitivity (DTH) response. As CD4 counts fall, the immune system cannot mount this response, leading to "non-cavitary" disease [1]. * **Option C (Highly variable tuberculin tests):** True. Due to **anergy** (the inability to mount a delayed-type hypersensitivity response), the TST/Mantoux test is often negative or unreliable in patients with low CD4 counts [2]. * **Option D (Decreased fibrosis):** True. Fibrosis is a feature of chronic, contained inflammation. In HIV, the disease is often more disseminated and acute, with less organized healing and scarring. **NEET-PG High-Yield Pearls:** * **Radiology:** In early HIV (high CD4), TB looks like classic post-primary TB (upper lobe infiltrates/cavities). In late HIV (low CD4 <200), it resembles **Primary TB** (intrathoracic lymphadenopathy, lower lobe involvement, and miliary patterns) [1]. * **Diagnosis:** Because of low sputum positivity, **NAAT (CBNAAT/Xpert MTB/RIF)** is the preferred initial diagnostic test in HIV-TB co-infection. * **Treatment:** Start Anti-Retroviral Therapy (ART) in all TB patients regardless of CD4 count, usually within 2 weeks of starting ATT.

Question 385: What is the most common causative organism causing lobar pneumonia?

A. Staphylococcus aureus
B. Streptococcus pyogenes
C. Streptococcus pneumonia (Correct Answer)
D. Hemophilus influenza

Explanation: **Explanation:** **Streptococcus pneumoniae** (Pneumococcus) remains the most common cause of community-acquired pneumonia (CAP) [1] and the classic cause of **lobar pneumonia**. The underlying medical concept involves its virulence factor, the polysaccharide capsule, which allows it to evade phagocytosis and spread rapidly through the Pores of Kohn, leading to uniform consolidation of an entire lobe. **Analysis of Options:** * **Streptococcus pneumoniae (Correct):** It is responsible for nearly 60-80% of bacterial lobar pneumonia cases. It typically presents with sudden onset chills, fever, and "rusty" sputum [1]. * **Staphylococcus aureus:** More commonly associated with **bronchopneumonia** (patchy distribution) rather than lobar. It often occurs post-influenza and is notorious for causing complications like lung abscesses and pneumatoceles [1]. * **Streptococcus pyogenes:** A rare cause of pneumonia; it more frequently causes pharyngitis, skin infections, or necrotizing fasciitis. When it does cause pneumonia, it is often severe with rapid pleural effusion. * **Hemophilus influenzae:** A common cause of CAP, especially in patients with underlying **COPD** [1] or cystic fibrosis, but it typically presents as bronchopneumonia rather than classic lobar consolidation. **High-Yield Clinical Pearls for NEET-PG:** 1. **Stages of Lobar Pneumonia:** Congestion → Red Hepatization (RBCs/fibrin) → Gray Hepatization (WBCs/fibrin) → Resolution. 2. **Sputum Color:** *S. pneumoniae* (Rusty) [1], *Klebsiella* (Currant jelly), *S. aureus* (Purulent/Golden). 3. **Radiology:** A "silhouette sign" on X-ray helps localize the affected lobe (e.g., loss of right heart border in right middle lobe pneumonia). 4. **Vaccination:** The PCV13 and PPSV23 vaccines are crucial for preventing invasive pneumococcal disease in elderly and immunocompromised patients.

Question 386: Stage III of Lyme's disease is characterized by what?

A. Meningoencephalitis
B. Myocarditis
C. Arthritis (Correct Answer)
D. Nephritis

Explanation: **Explanation:** Lyme disease, caused by the spirochete *Borrelia burgdorferi* (transmitted by the *Ixodes* tick), progresses through three distinct clinical stages [1]. Understanding the chronicity of symptoms is key to distinguishing these stages. **1. Why Arthritis is Correct:** **Stage III (Late Disseminated Infection)** occurs months to years after the initial tick bite. Its hallmark manifestation is **chronic large-joint arthritis**, most commonly affecting the **knee** [1]. Other Stage III features include acrodermatitis chronica atrophicans (skin atrophy) and subtle encephalopathy. The arthritis is typically episodic or persistent and results from an immune-mediated response to the persistent spirochetes [1]. **2. Why Other Options are Incorrect:** * **Meningoencephalitis & Myocarditis:** These are classic features of **Stage II (Early Disseminated Infection)**, which occurs weeks to months after the bite. Stage II is characterized by the "triad" of cranial nerve palsies (especially bilateral Bell’s palsy), meningitis/radiculoneuropathy, and AV nodal blocks (myocarditis). * **Nephritis:** This is not a standard clinical feature of Lyme disease in humans (though "Lyme nephritis" is a recognized entity in veterinary medicine, specifically dogs). **3. NEET-PG High-Yield Pearls:** * **Stage I (Early Localized):** Characterized by **Erythema Chronicum Migrans** (target/bull’s eye rash) and flu-like symptoms [1]. * **Drug of Choice:** **Doxycycline** is the first-line treatment for early stages [1]. * **Neurological/Cardiac involvement:** Treated with IV **Ceftriaxone** [1]. * **Vector:** *Ixodes scapularis* (Deer tick); the same tick transmits Babesiosis and Anaplasmosis (co-infections) [1]. * **Prophylaxis:** A single dose of Doxycycline (200mg) if the tick was attached for >36 hours.

Question 387: Which of the following is the optimum treatment in a patient with chronic hepatitis B and elevated serum AST levels?

A. Lamivudine (Correct Answer)
B. Lamivudine and interferons
C. Immunoglobulins
D. Interferons

Explanation: **Explanation:** The goal of treating chronic Hepatitis B (CHB) is to achieve sustained suppression of HBV replication and prevent disease progression to cirrhosis or hepatocellular carcinoma. **Why Lamivudine is the correct answer:** Lamivudine is a nucleoside analogue that inhibits HBV DNA polymerase. In patients with chronic Hepatitis B and elevated transaminases (AST/ALT), it effectively reduces viral load, normalizes liver enzymes, and improves histology. While newer agents like Tenofovir or Entecavir are now preferred in modern guidelines due to lower resistance rates, **Lamivudine** remains a classic, high-yield answer in the context of standard medical examinations for initiating oral antiviral therapy in CHB. **Analysis of Incorrect Options:** * **B. Lamivudine and Interferons:** Combination therapy has not consistently shown superior long-term outcomes compared to monotherapy and significantly increases the risk of adverse effects. * **C. Immunoglobulins (HBIG):** These provide passive immunity. They are used for post-exposure prophylaxis (e.g., needle-stick injuries) or to prevent reinfection post-liver transplant [1], but they have no role in treating established chronic infection. * **D. Interferons:** While Interferon-alpha is a treatment option, it is contraindicated in patients with decompensated cirrhosis as it may precipitate liver failure [1] and has a poor side-effect profile, including fatigue, depression, and bone marrow suppression [1]. In many clinical scenarios, oral nucleoside analogues are preferred for their safety and ease of administration. **Clinical Pearls for NEET-PG:** * **Indications for treatment:** HBsAg positive >6 months [2] AND HBV DNA >20,000 IU/mL (HBeAg positive) or >2,000 IU/mL (HBeAg negative) AND elevated ALT/AST. * **Drug of Choice (Current):** Tenofovir or Entecavir (due to high genetic barrier to resistance). * **Lamivudine Resistance:** Long-term use often leads to the **YMDD mutation** in the HBV polymerase gene. * **Interferon Contraindication:** Never give Interferons to patients with decompensated liver disease (risk of hepatic flare) [1].

Question 388: Which one of the following is not a feature of leptospirosis?

A. Aminotransferase elevation to less than five times
B. Elevated creatinine phosphokinase
C. Hepatorenal syndrome (Correct Answer)
D. Thrombocytopenia

Explanation: **Explanation:** Leptospirosis, caused by the spirochete *Leptospira interrogans*, is a zoonotic infection characterized by a wide spectrum of clinical manifestations. The severe form, known as **Weil’s Disease**, is defined by the triad of jaundice, acute kidney injury (AKI), and hemorrhage. **Why Hepatorenal Syndrome (C) is the Correct Answer:** In leptospirosis, renal failure is primarily caused by **acute tubular necrosis (ATN)** or **interstitial nephritis** due to direct bacterial invasion and toxin-mediated damage. **Hepatorenal Syndrome (HRS)**, however, is a specific functional renal failure occurring in the setting of advanced cirrhosis or portal hypertension due to splanchnic vasodilation [1]. While leptospirosis involves both the liver and kidneys, the pathophysiology is direct organ damage, not the hemodynamic shifts characteristic of HRS. **Analysis of Incorrect Options:** * **A. Aminotransferase elevation (<5 times):** Characteristically, leptospirosis causes significant jaundice (high bilirubin) but only mild-to-moderate elevations in ALT/AST (usually <500 U/L). This "bilirubin-enzyme dissociation" helps distinguish it from viral hepatitis. * **B. Elevated Creatinine Phosphokinase (CPK):** Muscle tenderness and elevated CPK are hallmark features of the septicemic phase, reflecting myositis. This is a high-yield diagnostic clue. * **D. Thrombocytopenia:** Common in severe cases, it contributes to the hemorrhagic manifestations (petechiae, epistaxis, or pulmonary hemorrhage) seen in Weil’s disease. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Microscopic Agglutination Test (MAT). * **Renal Feature:** Unlike most causes of AKI, leptospirosis often presents with **hypokalemia** (due to proximal tubular dysfunction). * **Drug of Choice:** Doxycycline (mild); Penicillin G (severe). * **Classic Sign:** Conjunctival suffusion (redness without inflammatory exudate).

Question 389: What is the recommended post-exposure prophylaxis for HIV?

A. Tenofovir + Lamivudine for 4 weeks (Correct Answer)
B. Lamivudine + Ritonavir for 4 weeks
C. Zidovudine + Lamivudine + Indinavir for 4 weeks
D. Single dose Zidovudine + Lamivudine + Indinavir

Explanation: **Explanation:** The current standard of care for HIV Post-Exposure Prophylaxis (PEP) has shifted towards simplified, highly effective regimens with better safety profiles. According to the latest **NACO (National AIDS Control Organization) and WHO guidelines**, the preferred regimen for PEP is a combination of two or three antiretroviral drugs for a duration of **28 days (4 weeks)**. **1. Why Option A is correct:** The combination of **Tenofovir (TDF) 300 mg + Lamivudine (3TC) 300 mg** (or Emtricitabine) is the backbone of PEP. In many updated protocols, a third drug—an Integrase Inhibitor like **Dolutegravir (DTG)**—is added (TDF + 3TC + DTG). However, in the context of standard MCQ options based on basic NACO dual-therapy recommendations, Tenofovir + Lamivudine for 4 weeks is the most appropriate choice. **2. Why the other options are incorrect:** * **Option B:** Ritonavir is a protease inhibitor used as a "booster" for other drugs (like Lopinavir); it is not used as a primary dual-therapy backbone with Lamivudine. * **Option C:** This was an older "expanded regimen" (Zidovudine + Lamivudine + Indinavir). Indinavir is rarely used now due to significant side effects like nephrolithiasis. * **Option D:** A single dose is insufficient to prevent viral replication and integration into the host genome. PEP must be continued for the full 28-day course. **High-Yield Clinical Pearls for NEET-PG:** * **Timing:** PEP should be initiated as soon as possible, ideally within **2 hours**, and no later than **72 hours** after exposure. * **Duration:** Always **28 days**. * **Baseline Testing:** Perform HIV testing at baseline, 6 weeks, 12 weeks, and 6 months post-exposure. * **Preferred Triple Regimen (Latest):** TDF (300mg) + 3TC (300mg) + DTG (50mg) once daily.

Question 390: Which of the following is NOT a predisposing factor for Pneumococcal Pneumonia?

A. Chronic renal failure (CRF)
B. Lymphoma
C. Old age
D. Thalassemia (Correct Answer)

Explanation: ### Explanation **Pneumococcal Pneumonia**, caused by *Streptococcus pneumoniae*, primarily affects individuals with compromised host defenses. The organism is an encapsulated bacterium, meaning its clearance depends heavily on **splenic function** and **humoral immunity** (B-cell response). **Why Thalassemia is the Correct Answer:** While patients with Thalassemia Major often undergo **splenectomy** (which *is* a major risk factor for Pneumococcal sepsis), Thalassemia itself is not a direct predisposing factor for pneumonia. In the context of this question, Thalassemia is categorized as a hemoglobinopathy rather than a primary state of immunosuppression or chronic organ failure that leads to pulmonary vulnerability. **Analysis of Incorrect Options:** * **Chronic Renal Failure (CRF):** Uremia impairs leukocyte function and suppresses cell-mediated immunity, making these patients highly susceptible to pyogenic infections like *S. pneumoniae*. [2] * **Lymphoma:** Malignancies of the lymphoid system (especially CLL and Hodgkin’s) lead to **hypogammaglobulinemia** and impaired antibody production. Since opsonization is required to clear encapsulated bacteria, these patients are at high risk. * **Old Age:** Immunosenescence (the natural decline of the immune system with age) and a decrease in the cough reflex/mucociliary clearance make the elderly a classic high-risk demographic. [1] --- ### High-Yield Clinical Pearls for NEET-PG * **Most Common Cause:** *S. pneumoniae* remains the #1 cause of Community-Acquired Pneumonia (CAP) worldwide. [1] * **Classic Presentation:** Sudden onset of rigors, fever, and **"rusty sputum"** (due to alveolar hemorrhage). [2] * **The Spleen Connection:** The most significant risk factor for overwhelming post-splenectomy infection (OPSI) is *S. pneumoniae*. * **Vaccination:** Two types are available—**PPSV23** (T-cell independent, for adults) and **PCV13** (Conjugate vaccine, more immunogenic, used in children). * **Radiology:** Typically presents as **lobar consolidation** with air bronchograms.

Practice by Chapter

Principles of Antimicrobial Therapy

Practice Questions

Fever of Unknown Origin

Practice Questions

HIV/AIDS and Related Infections

Practice Questions

Tuberculosis and Mycobacterial Diseases

Practice Questions

Tropical and Parasitic Infections

Practice Questions

Viral Infections (Hepatitis, Herpes, etc.)

Practice Questions

Healthcare-Associated Infections

Practice Questions

Fungal Infections

Practice Questions

Sepsis and Septic Shock

Practice Questions

Infection in Immunocompromised Hosts

Practice Questions

Emerging and Re-emerging Infections

Practice Questions

Antimicrobial Resistance

Practice Questions

Vaccination Principles

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free