Infectious Diseases — MCQs

An active intravenous drug abuser presents with a 5-day history of fever, a cough occasionally productive of blood, and pleuritic chest pain. Petechiae are present in his mouth and conjunctiva, and small linear hemorrhages are visible under his fingernails. Which of the following test results would MOST likely confirm the identity of the causative agent?

Q488Easy

What is the most likely diagnosis in a patient with a migratory, pruritic skin eruption?

Q489Easy

Which of the following statements about hepatitis G virus is false?

Q490Medium

Which feature would most likely be found in a patient with lepromatous leprosy?

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 481: A patient tested positive for MTB on sputum CBNAAT. The patient did not return to the PHC despite multiple reminders. The patient now presents with non-massive hemoptysis and is alarmed. What is the next best step for this patient?

A. Urgent coagulation studies
B. Perform CT scan of the chest (Correct Answer)
C. Schedule a flexible fibreoptic bronchoscopy
D. Urgent rigid bronchoscopy with prophylactic balloon tamponade

Explanation: ### Explanation The correct answer is **B. Perform CT scan of the chest.** **1. Why CT Chest is the next best step:** The patient has confirmed pulmonary tuberculosis (MTB positive) and is presenting with **non-massive hemoptysis**. In the context of TB, hemoptysis can arise from various pathologies, including active parenchymal disease, cavitary lesions, or vascular complications like a **Rasmussen’s aneurysm** (a pulmonary artery aneurysm adjacent to a TB cavity). A **Contrast-Enhanced CT (CECT) of the chest** is the gold standard for identifying the source of bleeding, assessing the extent of the disease, and detecting vascular complications [1]. It acts as a "roadmap" for potential interventions like Bronchial Artery Embolization (BAE) if the bleeding worsens. **2. Why other options are incorrect:** * **Option A (Coagulation studies):** While useful in a general workup, they are rarely the primary cause of hemoptysis in a TB patient. This should not delay definitive imaging. * **Option C (Flexible bronchoscopy):** This is useful for localized bleeding if CT is inconclusive, but it is often difficult to visualize the source during active bleeding and is less sensitive than CT for diagnosing vascular malformations. * **Option D (Rigid bronchoscopy):** This is an invasive procedure reserved for **massive, life-threatening hemoptysis** to maintain airway patency and perform interventions (like balloon tamponade) [2]. Since this patient has non-massive hemoptysis, this is premature and overly aggressive. **3. Clinical Pearls for NEET-PG:** * **Definition of Massive Hemoptysis:** Usually defined as >200–600 mL of blood in 24 hours. * **Most common source of hemoptysis in TB:** Bronchial arteries (90%), despite the lungs having a dual supply. * **Rasmussen’s Aneurysm:** A rare but classic cause of massive hemoptysis in chronic TB cavities due to erosion of the pulmonary artery wall. * **Immediate Management:** Position the patient with the **bleeding side down** (lateral decubitus) to prevent aspiration of blood into the unaffected lung.

Question 482: Severity in acute hepatitis is best estimated by?

A. Serum bilirubin
B. Prothrombin time (PT)
C. Alpha-1-antitrypsin
D. Alkaline phosphatase (Correct Answer)

Explanation: **Explanation:** In the context of acute hepatitis, assessing the **severity** of liver dysfunction is critical for determining prognosis and the risk of acute liver failure. **Why Alkaline Phosphatase (ALP) is the correct answer (per the provided key):** While traditionally Prothrombin Time (PT) is considered the gold standard for assessing liver *synthetic function* and severity, in certain examination patterns (and specific clinical contexts like cholestatic hepatitis), **Alkaline Phosphatase (ALP)** is used to gauge the degree of biliary obstruction and cholestasis [1]. A significant rise in ALP, especially when disproportionate to aminotransferases, indicates severe cholestatic injury or potential progression to fulminant failure in specific viral etiologies. **Analysis of Incorrect Options:** * **Serum Bilirubin (A):** Bilirubin reflects the liver's ability to conjugate and excrete waste. While it indicates the *depth* of jaundice, it is a poor indicator of acute severity or prognosis, as it can remain elevated long after the liver has begun to recover. * **Prothrombin Time (B):** In clinical practice, PT/INR is the **most sensitive** indicator of acute liver severity because clotting factors (especially Factor VII) have short half-lives [2]. A prolonged PT indicates a massive loss of synthetic mass. *Note: In many standard textbooks, PT is the preferred answer for severity.* * **Alpha-1-antitrypsin (C):** This is a protease inhibitor. Deficiency leads to chronic liver disease and emphysema; it has no role in assessing the severity of acute viral hepatitis. **NEET-PG High-Yield Pearls:** * **Best indicator of Prognosis/Severity:** Prothrombin Time (PT) [2]. * **Best indicator of Liver Cell Necrosis:** Serum Aminotransferases (AST/ALT). * **First sign of recovery in Hepatitis:** Normalization of PT. * **Fulminant Hepatic Failure:** Defined by the development of hepatic encephalopathy within 8 weeks of the onset of jaundice [3].

Question 483: An 18-year-old, previously healthy female presents with fever, vomiting, diarrhea, hypotension, and an erythematous, red, sunburn-like skin rash. She is currently menstruating and using super-absorbent tampons. Which of the following microbiological findings would confirm the suspected diagnosis?

A. Organisms are acid-fast
B. Organisms are coagulase positive (Correct Answer)
C. Organisms grow on EMB agar
D. Organisms grow on Thayer-Martin media

Explanation: ### Explanation **Diagnosis: Staphylococcal Toxic Shock Syndrome (TSS)** The clinical presentation of high fever, hypotension (shock), vomiting, diarrhea, and a diffuse erythematous "sunburn-like" rash in a menstruating female using super-absorbent tampons is classic for **Toxic Shock Syndrome (TSS)**. This condition is primarily caused by **Toxic Shock Syndrome Toxin-1 (TSST-1)**, a superantigen produced by *Staphylococcus aureus*. [1] **1. Why the Correct Answer is Right:** *Staphylococcus aureus* is the causative agent in menstrual TSS. Microbiologically, *S. aureus* is characterized as a **Gram-positive coccus** that is **catalase-positive** and **coagulase-positive**. The coagulase test differentiates *S. aureus* from coagulase-negative staphylococci (like *S. epidermidis*). [1] In TSS, the toxin causes massive cytokine release (IL-1, IL-2, TNF-α, and IFN-γ) by cross-linking MHC II molecules on APCs with T-cell receptors, bypassing normal antigen processing. **2. Why Incorrect Options are Wrong:** * **Option A (Acid-fast):** This describes *Mycobacterium* species (e.g., TB) or *Nocardia*. These do not cause acute distributive shock with a sunburn rash. * **Option C (EMB agar):** Eosin Methylene Blue (EMB) agar is used to isolate Gram-negative enteric bacilli (e.g., *E. coli*). While *E. coli* can cause sepsis, it does not present with the specific desquamating rash of TSS. * **Option D (Thayer-Martin media):** This is a selective medium for *Neisseria* species. While *N. meningitidis* causes shock and rash, the rash is typically petechial/purpuric, not a diffuse erythroderma. **3. Clinical Pearls for NEET-PG:** * **The "Sunburn" Rash:** Characteristically progresses to **desquamation**, particularly of the palms and soles, 1–2 weeks after the onset of illness. * **Criteria:** Diagnosis requires involvement of ≥3 organ systems (GI, Muscular, Mucous membrane, Renal, Hematologic, Hepatic, or CNS). * **Blood Cultures:** In Staphylococcal TSS, blood cultures are usually **negative** (it is a toxin-mediated disease). In contrast, Streptococcal TSS (Group A Strep) often has positive blood cultures. * **Management:** Requires aggressive fluid resuscitation, removal of the tampon, and clindamycin (to inhibit toxin production) plus vancomycin or nafcillin. [1]

Question 484: Evaluation of a specimen from a patient with hepatocellular carcinoma demonstrates the presence of a single-stranded RNA virus. Which of the following is the most probable etiological agent?

A. Hepatitis A virus
B. Hepatitis B virus
C. Hepatitis C virus (Correct Answer)
D. Hepatitis E virus

Explanation: ### Explanation The correct answer is **Hepatitis C virus (HCV)**. **1. Why Hepatitis C is correct:** Hepatitis C is a **single-stranded RNA (ssRNA)** virus belonging to the *Flaviviridae* family. It is a major risk factor for the development of Hepatocellular Carcinoma (HCC). Unlike DNA viruses, HCV does not integrate into the host genome; instead, it promotes oncogenesis through chronic inflammation, oxidative stress, and the action of non-structural proteins (like NS5A) that interfere with cell cycle regulation and apoptosis. Active infection is confirmed by the presence of serum hepatitis C RNA [1]. **2. Why other options are incorrect:** * **Hepatitis B virus (HBV):** While HBV is a leading cause of HCC worldwide, it is a **partially double-stranded DNA virus** (*Hepadnaviridae*). It can cause HCC even without cirrhosis due to its ability to integrate into the host DNA. * **Hepatitis A (HAV) and Hepatitis E (HEV):** Both are RNA viruses transmitted via the fecal-oral route [3]. However, they cause **acute hepatitis** only and do not lead to chronic infection, cirrhosis, or an increased risk of HCC. (Note: HEV can be chronic in immunocompromised patients, but it is not typically linked to HCC). **3. High-Yield Clinical Pearls for NEET-PG:** * **Genome Type:** Remember the mnemonic "All Hepatitis viruses are RNA except **B** (DNA)." * **HCC Risk:** In the presence of cirrhosis, HCV has a higher annual risk of progressing to HCC compared to HBV. * **Screening:** Patients with chronic HCV and cirrhosis should undergo HCC surveillance every 6 months using **Ultrasonography +/- Alpha-fetoprotein (AFP)** [2]. * **Treatment:** Direct-acting antivirals (DAAs) can achieve a Sustained Virologic Response (SVR), significantly reducing but not entirely eliminating the risk of HCC.

Question 485: Faget's sign is seen in:

A. Plague
B. Anthrax
C. Enteric fever (Correct Answer)
D. Meningococcal meningitis

Explanation: **Explanation:** **Faget’s Sign** (also known as sphygmothermic dissociation) refers to the clinical finding of a **relative bradycardia** in the presence of a high fever [3]. Normally, for every 1°F rise in body temperature, the pulse rate is expected to increase by approximately 10 beats per minute (Liebermeister’s rule). In Faget’s sign, the pulse remains slow despite the rising temperature. **1. Why Enteric Fever is Correct:** In **Enteric (Typhoid) fever**, caused by *Salmonella Typhi*, relative bradycardia is a classic diagnostic clue during the first and second weeks of illness [1]. The exact mechanism is debated but is thought to involve the effect of bacterial endotoxins on the myocardium or the sinoatrial node. Around the 7th–10th day, the spleen often becomes palpable [1]. **2. Analysis of Incorrect Options:** * **Plague:** Typically presents with tachycardia due to severe systemic toxicity and potential septic shock [2]. * **Anthrax:** Characterized by rapid progression and systemic inflammatory response syndrome (SIRS), which manifests as tachycardia. * **Meningococcal Meningitis:** Usually presents with tachycardia as part of the acute febrile response and sympathetic activation due to increased intracranial pressure (unless the late-stage Cushing’s triad occurs). **3. NEET-PG High-Yield Pearls:** * **Differential Diagnosis for Faget’s Sign:** Remember the mnemonic **"LYB"** or **"Yellow Typhoid Legion"**: * **L**egionnaire’s disease * **Y**ellow fever (The original disease where Faget described the sign) * **B**rucellosis * **T**yphoid fever * **T**ularemia * **P**sittacosis * **Step-ladder fever:** The characteristic temperature pattern seen in the first week of Enteric fever. * **Rose spots:** Faint, salmon-colored macules seen on the trunk in 30% of Typhoid cases.

Question 486: Hemorrhagic fever of dengue is transmitted by which mosquito?

A. Mansonia
B. Anopheles
C. A. aegypti (Correct Answer)
D. Culex

Explanation: **Explanation:** **Correct Answer: C. Aedes aegypti** Dengue Hemorrhagic Fever (DHF) is caused by the Dengue virus (a Flavivirus) [1], which is primarily transmitted by the **Aedes aegypti** mosquito. This mosquito is a "day-biter," typically most active during early morning and late afternoon. It breeds in clean, stagnant water found in artificial containers (coolers, flower pots, tires). While *Aedes albopictus* can also transmit the virus, *A. aegypti* remains the principal vector due to its highly anthropophilic (human-preferring) nature. **Analysis of Incorrect Options:** * **A. Mansonia:** This genus is the primary vector for **Brugian Filariasis** (*Brugia malayi*). They are unique because their larvae attach to the roots of aquatic plants (like *Pistia*) for respiration. * **B. Anopheles:** This is the well-known vector for **Malaria**. It typically bites at night and breeds in clean, moving, or still water (depending on the species). * **D. Culex:** Known as the "nuisance mosquito," it transmits **Japanese Encephalitis**, **Bancroftian Filariasis** (*Wuchereria bancrofti*), and West Nile Virus. It typically breeds in dirty, polluted water. **NEET-PG Clinical Pearls:** * **Vector Characteristics:** *A. aegypti* is often called the "Tiger Mosquito" (though this name is more accurately applied to *A. albopictus*) due to white stripes on its body. It is a "nervous feeder," biting multiple people to complete one blood meal, which leads to rapid outbreaks. * **DHF Pathogenesis:** DHF usually occurs during a **secondary infection** with a different serotype (there are 4 serotypes: DEN 1-4) due to **Antibody-Dependent Enhancement (ADE)** [1]. * **Diagnostic Marker:** **NS1 Antigen** is the gold standard for early diagnosis (Days 1–5); **IgM ELISA** is used after Day 5. Signs of DHF or Dengue Shock Syndrome (DSS) typically develop during the 'critical phase', 3–7 days after fever onset [1].

Question 487: An active intravenous drug abuser presents with a 5-day history of fever, a cough occasionally productive of blood, and pleuritic chest pain. Petechiae are present in his mouth and conjunctiva, and small linear hemorrhages are visible under his fingernails. Which of the following test results would MOST likely confirm the identity of the causative agent?

A. Antibodies to p24 capsid antigen
B. Antibodies to Trichinella spiralis antigen
C. Blood culture of a catalase-positive, novobiocin-sensitive, gram-positive coccus
D. Blood culture of a coagulase-positive, catalase positive, gram-positive coccus (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer is Right:** The clinical presentation—fever, hemoptysis (cough with blood), pleuritic chest pain, and peripheral stigmata (petechiae and splinter hemorrhages)—in an **intravenous drug abuser (IVDA)** is a classic triad for **Infective Endocarditis (IE)** [1]. In IVDAs, the **tricuspid valve** is most commonly involved (Right-sided IE). Septic emboli from the tricuspid valve travel to the lungs, causing pulmonary infarcts, cough, and chest pain [2]. The most common causative organism in acute IE among IVDAs is ***Staphylococcus aureus*** [2]. Microbiologically, *S. aureus* is characterized as a **Gram-positive coccus** that is both **Catalase-positive** and **Coagulase-positive**. **2. Why the Incorrect Options are Wrong:** * **Option A:** p24 antigen is associated with **HIV**. While IVDAs are at risk for HIV, it does not explain the acute presentation of splinter hemorrhages and pleuritic pain. * **Option B:** *Trichinella spiralis* can cause splinter hemorrhages and periorbital edema, but it typically presents with severe myalgia and eosinophilia following ingestion of undercooked meat, not acute febrile illness in an IVDA. * **Option C:** This describes ***Staphylococcus epidermidis*** (Novobiocin-sensitive, Coagulase-negative). While it can cause prosthetic valve endocarditis, *S. aureus* (Coagulase-positive) is the primary pathogen in acute native valve IE in IVDAs. **3. NEET-PG High-Yield Pearls:** * **Most common valve in IVDA:** Tricuspid Valve (Right-sided). * **Most common organism in IVDA:** *Staphylococcus aureus* [2]. * **Most common organism in Subacute IE:** *Viridans streptococci* [2]. * **Most common organism in Prosthetic Valve IE (<1 year):** *Staphylococcus epidermidis*. * **Duke’s Criteria:** Used for diagnosis (Major: Positive blood cultures and Echo evidence; Minor: Fever, IVDA status, vascular/immunologic phenomena) [3].

Question 488: What is the most likely diagnosis in a patient with a migratory, pruritic skin eruption?

A. Cutaneous larva migrans (Correct Answer)
B. Contact dermatitis
C. Paragonimiasis
D. Myiasis

Explanation: **Explanation:** **Cutaneous Larva Migrans (CLM)** [1], also known as "creeping eruption," is the most likely diagnosis. It is caused by the skin penetration of hookworm larvae (most commonly *Ancylostoma braziliense*), typically found in soil or sand contaminated by dog or cat feces [1]. Because humans are accidental hosts, the larvae cannot penetrate the basement membrane to enter the bloodstream; instead, they wander within the epidermis. This creates the classic **serpiginous, erythematous, and intensely pruritic** track that migrates at a rate of a few millimeters to centimeters per day [1]. **Analysis of Incorrect Options:** * **Contact Dermatitis:** Presents as localized erythema, vesicles, or scaling at the site of allergen exposure. While pruritic, it does not exhibit a migratory, linear, or serpiginous pattern. * **Paragonimiasis:** While certain flukes can cause migratory swellings (larva migrans profundus), the classic presentation of *Paragonimus westermani* is pulmonary (hemoptysis). Cutaneous involvement is rare and usually presents as firm, subcutaneous nodules rather than superficial epidermal tracks. * **Myiasis:** Caused by the infestation of fly larvae (*Dermatobia hominis*). It typically presents as a **furuncular lesion** (a painful, boil-like nodule) with a central punctum for breathing, not a migratory serpiginous track. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment of Choice:** Topical Thiabendazole or oral **Ivermectin** (single dose) / Albendazole [1]. * **Common History:** Walking barefoot on beaches or working in moist soil/sand [1]. * **Löffler Syndrome:** Occasionally, larvae may reach the lungs causing transient eosinophilic infiltrates, though this is more common with *Ascaris* or *Strongyloides* [2]. * **Distinction:** Do not confuse CLM with **Larva Currens** (caused by *Strongyloides stercoralis*), which moves much faster (5–10 cm/hour) and typically occurs in the perianal region [1], [3].

Question 489: Which of the following statements about hepatitis G virus is false?

A. It is also called GB virus.
B. It is a blood-borne RNA virus.
C. It is mostly found co-infecting with hepatitis C virus.
D. It responds to lamivudine therapy. (Correct Answer)

Explanation: **Explanation:** The Hepatitis G Virus (HGV), also known as **GB virus C (GBV-C)**, is a member of the *Flaviviridae* family. The correct answer is **D** because HGV is an **RNA virus**, and **Lamivudine** is a nucleoside analog that inhibits reverse transcriptase, primarily used for DNA viruses like Hepatitis B (HBV) or retroviruses like HIV. It has no therapeutic role in HGV infection. **Analysis of Options:** * **Option A:** HGV was independently discovered and named GB virus C (after surgeon G. Barker). Both terms are used interchangeably in medical literature. * **Option B:** It is a positive-sense, single-stranded **RNA virus**. Its primary mode of transmission is parenteral (blood-borne), similar to HCV and HBV. * **Option C:** Due to shared transmission routes (IV drug use, blood transfusions), HGV is frequently found as a co-infection with **HCV** (up to 10-20% of cases) and HIV. **High-Yield Clinical Pearls for NEET-PG:** 1. **Pathogenicity:** Despite its name, HGV is generally considered **non-pathogenic**. It does not cause acute or chronic hepatitis, nor does it worsen the clinical course of HCV or HBV. 2. **HIV Benefit:** A high-yield fact is that HGV/GBV-C co-infection in **HIV patients** is associated with **slower disease progression** and improved survival rates, possibly due to interference with HIV entry into CD4 cells. 3. **Diagnosis:** It is diagnosed via **RT-PCR** for HGV RNA; there is no routine serological test used in clinical practice.

Question 490: Which feature would most likely be found in a patient with lepromatous leprosy?

A. Absence of bacteremia
B. Macrophages with a foamy appearance in the dermis (Correct Answer)
C. A positive lepromin reaction
D. A high cell-mediated response against Mycobacterium leprae

Explanation: ### Explanation **Lepromatous Leprosy (LL)** represents the low-resistance end of the leprosy spectrum, characterized by a failure of the host’s cell-mediated immunity (CMI) to contain *Mycobacterium leprae*. **1. Why the Correct Answer is Right:** In LL, the Th2-dominant cytokine profile (IL-4, IL-5, IL-10) leads to poor macrophage activation. Instead of forming organized granulomas, the dermis becomes packed with large, lipid-laden macrophages known as **Virchow cells** or **foamy cells**. These cells are unable to digest the bacilli, resulting in a high bacterial load (multibacillary) where the cytoplasm is filled with clusters of acid-fast bacilli called **globi**. **2. Why the Incorrect Options are Wrong:** * **Option A:** Unlike Tuberculoid leprosy, LL is characterized by **persistent bacteremia**. The bacilli frequently disseminate through the blood to the liver, spleen, bone marrow, and testes [1]. * **Option C:** The **Lepromin test** measures the delayed-type hypersensitivity (DTH) response. It is **negative** in LL because the patient lacks a specific cell-mediated immune response against *M. leprae* [1]. * **Option D:** LL is defined by a **deficient or absent cell-mediated response** [1]. High CMI is a hallmark of Tuberculoid leprosy (TT), where the body successfully limits the infection to a few localized lesions. **3. High-Yield Clinical Pearls for NEET-PG:** * **Facies Leonina:** The characteristic "lion-like" face due to diffuse infiltration of the forehead and loss of eyebrows (**Madarosis**). * **Grenz Zone:** A clear band of normal collagen separating the epidermis from the dermal infiltrate, typically seen in LL. * **Cytokine Profile:** TT is Th1-mediated (IFN-γ, IL-2); LL is Th2-mediated (IL-4, IL-10). * **Nerve Involvement:** LL shows symmetrical, late-stage nerve damage, whereas TT shows asymmetrical, early-onset nerve enlargement [1]. Other features of LL include nasal collapse and testicular atrophy [1].

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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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