Infectious Diseases — MCQs

A 32-year-old African-American male presents with recurrent edema of the feet and periorbital swelling. He has a history of high-risk sexual behavior. The blood pressure was 110/85 mm Hg. Results of laboratory investigations are as follows: HBs Ag: Negative, Blood glucose: Normal, HIV ELISA: Positive, 24-hour urine protein: 3.9 g, Urine microscopy: Fatty casts, oval fat bodies. An H and E stain of the renal biopsy is most likely to show what?

Q207Easy

Tropical splenomegaly is caused by which of the following?

Q208Medium

Which of the following is true regarding influenza?

Q209Easy

Which of the following differentiates Systemic Inflammatory Response Syndrome (SIRS) from sepsis?

Q210Medium

A male patient is HBsAg positive, HBeAg negative, and anti-HBe antibody positive. HBV DNA copies are 100,000/mL, and SGOT and SGPT are elevated to 6 times the upper limit of normal. What is the likely diagnosis?

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 201: Which of the following clinical presentations does NOT qualify for the term "Severe Falciparum Malaria"?

A. Severe anemia
B. Acidosis
C. Pulmonary edema
D. High grade fever with rigors (Correct Answer)

Explanation: **Explanation:** The definition of **Severe Falciparum Malaria** is based on the presence of clinical or laboratory evidence of vital organ dysfunction. According to the WHO criteria, severe malaria is a medical emergency characterized by complications that significantly increase the risk of mortality [1]. **Why Option D is Correct:** **High-grade fever with rigors** is a classic symptom of uncomplicated malaria [1]. While distressing to the patient, it does not indicate organ failure or a life-threatening complication. Therefore, it does not meet the criteria for "Severe Malaria." **Why the other options are Incorrect (Criteria for Severe Malaria):** * **Severe Anemia (Option A):** Defined as a hemoglobin concentration <5 g/dL (or hematocrit <15%) in the presence of parasitemia [1]. It results from the massive destruction of infected and uninfected RBCs. * **Acidosis (Option B):** Specifically metabolic acidosis (plasma bicarbonate <15 mmol/L or venous lactate >5 mmol/L). This is often a result of microvascular sequestration leading to tissue hypoxia. * **Pulmonary Edema (Option C):** This is a grave complication (often presenting as ARDS) caused by increased capillary permeability or fluid overload, carrying a high mortality rate [1]. **NEET-PG High-Yield Pearls:** 1. **Drug of Choice:** For severe malaria, **Intravenous Artesunate** is the gold standard (superior to Quinine) [1]. 2. **Other Severe Criteria:** Hypoglycemia (<40 mg/dL), Cerebral malaria (GCS <11), Acute Kidney Injury (Creatinine >3 mg/dL), and Jaundice (Bilirubin >3 mg/dL with parasite count >100,000/µL) [1]. 3. **Blackwater Fever:** Characterized by massive intravascular hemolysis and hemoglobinuria, leading to dark-colored urine.

Question 202: Which of the following drugs used for chronic hepatitis B therapy is not administered orally?

A. Lamivudine
B. Adefovir
C. Telbivudine
D. Pegylated interferon (Correct Answer)

Explanation: The management of Chronic Hepatitis B (CHB) involves two main classes of drugs: **Nucleos(t)ide Analogues (NAs)** and **Immunomodulators**. **1. Why Pegylated Interferon (Peg-IFN) is correct:** Pegylated interferon-alpha (2a or 2b) is a protein-based immunomodulator. Because it is a protein, it would be degraded by gastric enzymes if taken orally. Therefore, it must be administered via **subcutaneous injection** (usually once weekly) [1]. It works by enhancing the host immune response and exerting direct antiviral effects. **2. Why the other options are incorrect:** * **Lamivudine (A):** A nucleoside analogue that inhibits HBV DNA polymerase. It was the first oral agent approved for HBV. * **Adefovir (B):** A nucleotide analogue administered orally. It is now less commonly used due to its lower potency and risk of nephrotoxicity compared to newer agents. * **Telbivudine (C):** An oral L-nucleoside analogue. Like Lamivudine, it has a high rate of resistance, leading to its decreased use in modern clinical practice. **Clinical Pearls for NEET-PG:** * **First-line Oral Agents:** Currently, **Tenofovir (TDF/TAF)** and **Entecavir** are the preferred oral agents due to their high potency and high genetic barrier to resistance. * **Interferon Contraindications:** Peg-IFN should be avoided in patients with decompensated cirrhosis, psychiatric disorders, or autoimmune diseases [1]. * **HBeAg Seroconversion:** Peg-IFN has a higher rate of HBeAg and HBsAg clearance compared to oral NAs but is associated with more side effects (flu-like symptoms, bone marrow suppression) [1]. * **Pregnancy:** Tenofovir is the preferred agent for preventing vertical transmission in highly viremic mothers.

Question 203: According to current criteria for Fever of Unknown Origin (FUO), what body temperature is considered significant?

A. 98.4 F
B. 99.4 F
C. 100 F
D. 101 F (Correct Answer)

Explanation: ### Explanation The definition of **Fever of Unknown Origin (FUO)** was first standardized by Petersdorf and Beeson in 1961 and remains a cornerstone of clinical medicine. To qualify as FUO, a patient must meet specific criteria regarding temperature, duration, and diagnostic effort [1]. **Why Option D is Correct:** The classic and current criteria for FUO require a documented body temperature of **$\geq$ 101°F (38.3°C)** on several occasions. This threshold is set higher than the physiological "normal" (98.6°F) to exclude individuals with normal circadian temperature variations or low-grade habitual hyperthermia, ensuring that the diagnostic workup focuses on clinically significant pathology [1], [3]. **Analysis of Incorrect Options:** * **Option A (98.4°F):** This is considered a normal baseline body temperature. * **Option B (99.4°F):** While this may represent a "low-grade fever" in some clinical contexts, it does not meet the stringent threshold required for an FUO diagnosis. * **Option C (100°F):** This is often the threshold for defining a simple fever (pyrexia), but FUO criteria specifically require $\geq$ 101°F to increase diagnostic specificity [3]. **High-Yield NEET-PG Pearls:** * **The Three Criteria for FUO:** 1. **Temperature:** $\geq$ 101°F (38.3°C) on several occasions [1]. 2. **Duration:** Fever lasting for **> 3 weeks** [1]. 3. **Diagnostic Effort:** Failure to reach a diagnosis after **1 week** of inpatient investigation (or 3 outpatient visits in modern modified criteria) [1]. * **Etiology:** In adults, the most common causes of FUO are **Infections** (e.g., TB, Abscesses), followed by **Malignancies** (e.g., Lymphoma, RCC), and **Non-infectious Inflammatory Diseases** (e.g., Still’s disease, SLE) [1]. * **Factitious Fever:** Always consider this in patients with high temperatures but no tachycardia or sweating (dissociation of pulse and temperature) [2].

Question 204: A 26-year-old man is positive for HBsAg but negative for HBeAg. His AST and ALT levels are within normal limits. What is the next step in the management of this patient?

A. Serial monitoring (Correct Answer)
B. Antiviral treatment with Lamivudine monotherapy
C. Antiviral treatment with Lamivudine and pulsed Interferon
D. Antiviral treatment with Interferon Alfa alone

Explanation: ### Explanation The patient is in the **Inactive HBsAg Carrier State** (also known as the Immune Control phase). This is characterized by the presence of HBsAg for >6 months, HBeAg negativity, anti-HBe positivity, and persistently normal ALT/AST levels. **1. Why Serial Monitoring is Correct:** In the inactive carrier state, the viral load is typically very low (HBV DNA <2,000 IU/mL) and there is minimal to no hepatic inflammation or fibrosis. According to AASLD and EASL guidelines, these patients do **not** require immediate antiviral therapy. Instead, they require **serial monitoring** (ALT every 3–6 months and HBV DNA periodically) to detect potential reactivation or progression to HBeAg-negative chronic hepatitis. **2. Why the Other Options are Incorrect:** * **Options B, C, & D:** Antiviral therapy (Interferon or Nucleoside analogs) is indicated only when there is evidence of active liver disease, characterized by **elevated ALT** (≥2x upper limit of normal) or **high viral load** (HBV DNA >2,000 IU/mL for HBeAg-negative patients) with significant fibrosis. * **Lamivudine Monotherapy (B):** Even if treatment were indicated, Lamivudine is no longer a first-line agent due to its high rate of resistance. Tenofovir or Entecavir are preferred. **Clinical Pearls for NEET-PG:** * **HBsAg (+):** Indicates infection (Acute or Chronic). * **HBeAg (+):** Indicates high infectivity and active viral replication. * **Normal ALT + HBsAg (+):** Usually implies either the "Immune Tolerant" phase (HBeAg positive, very high DNA) or the "Inactive Carrier" phase (HBeAg negative, low DNA). Neither typically requires immediate treatment. * **Goal of Monitoring:** To catch the transition to **HBeAg-negative Chronic Hepatitis**, where ALT rises and DNA levels increase despite being HBeAg negative (often due to precore/core promoter mutations).

Question 205: Which drug is recommended for the prevention of mother-to-child transmission of HIV infection?

A. Didanosine
B. Nevirapine (Correct Answer)
C. Indinavir
D. Nelfinavir

Explanation: **Explanation:** The prevention of mother-to-child transmission (PMTCT) is a critical component of HIV management. **Nevirapine**, a Non-Nucleoside Reverse Transcriptase Inhibitor (NNRTI), is the drug of choice in many resource-limited settings due to its long half-life and excellent placental transfer [1]. **Why Nevirapine is Correct:** Nevirapine rapidly crosses the placenta and achieves therapeutic levels in the neonate. Historically, the **WHO and NACO guidelines** (specifically the Single-Dose Nevirapine regimen) recommended giving a single dose to the mother at the onset of labor and a single dose to the newborn within 72 hours of birth. While modern protocols have shifted toward multi-drug ART (Antiretroviral Therapy) for all pregnant women, Nevirapine remains the classic high-yield answer for PMTCT in examination contexts. **Why Other Options are Incorrect:** * **A. Didanosine (ddI):** A Nucleoside Reverse Transcriptase Inhibitor (NRTI) that is rarely used today due to significant toxicities like pancreatitis and peripheral neuropathy. It is not a first-line agent for PMTCT. * **C. Indinavir & D. Nelfinavir:** These are Protease Inhibitors (PIs). While PIs can be used in pregnancy as part of a combination regimen, they are not the specific "single-drug" recommendation for PMTCT prevention in the same way Nevirapine is recognized. Nelfinavir is also less preferred due to lower efficacy compared to newer PIs like Lopinavir/Ritonavir. **High-Yield Clinical Pearls for NEET-PG:** * **Current NACO Guidelines:** All HIV-positive pregnant women should be started on **Lifelong ART** (usually TLE regimen: Tenofovir + Lamivudine + Efavirenz) regardless of CD4 count. * **Infant Prophylaxis:** The newborn typically receives Nevirapine syrup for 6 weeks [1]. * **Risk of Transmission:** Without intervention, the risk is 20–45%; with proper ART and PMTCT protocols, it can be reduced to <2%. * **Breastfeeding:** In India, exclusive breastfeeding for the first 6 months is recommended even if the mother is HIV-positive, provided she is on ART [1].

Question 206: A 32-year-old African-American male presents with recurrent edema of the feet and periorbital swelling. He has a history of high-risk sexual behavior. The blood pressure was 110/85 mm Hg. Results of laboratory investigations are as follows: HBs Ag: Negative, Blood glucose: Normal, HIV ELISA: Positive, 24-hour urine protein: 3.9 g, Urine microscopy: Fatty casts, oval fat bodies. An H and E stain of the renal biopsy is most likely to show what?

A. Segmental sclerosis of some of the glomeruli (Correct Answer)
B. Diffuse thickening of the glomerular basement membrane
C. Hypercellular glomeruli with thickening of the GBM
D. Proliferation of the parietal cells filling Bowman's space

Explanation: ### Explanation The clinical presentation of nephrotic-range proteinuria (3.9 g/24h), edema, fatty casts, and a positive HIV status in an African-American male strongly points toward **HIV-Associated Nephropathy (HIVAN)**. **1. Why Option A is Correct:** HIVAN is a specific form of **Collapsing Focal Segmental Glomerulosclerosis (FSGS)** [1]. Histologically, FSGS is characterized by the involvement of some, but not all, glomeruli (focal) and only a portion of the glomerular tuft (segmental). In HIVAN, there is typically a "collapsing" variant where the glomerular capillaries collapse, accompanied by podocyte hypertrophy and hyperplasia. This is the most common cause of nephrotic syndrome in HIV-positive patients, especially those of African descent (linked to APOL1 gene variants). **2. Why the Other Options are Incorrect:** * **Option B (Diffuse thickening of GBM):** This describes **Membranous Nephropathy** [1]. While it can be associated with Hepatitis B or C, it is not the classic presentation for HIV-related renal disease. * **Option C (Hypercellularity with GBM thickening):** This describes **Membranoproliferative Glomerulonephritis (MPGN)** [1], often seen in Hepatitis C infection (Type I) or complement dysregulation (Type II). * **Option D (Proliferation of parietal cells):** This describes **Crescentic Glomerulonephritis** [1], seen in Rapidly Progressive Glomerulonephritis (RPGN), which presents with an acute nephritic syndrome rather than chronic nephrotic syndrome. **3. NEET-PG High-Yield Pearls:** * **HIVAN Hallmark:** Collapsing FSGS + Microcystic tubular dilatation + Tubuloreticular inclusions (seen on Electron Microscopy). * **Epidemiology:** Strongly associated with the **APOL1 gene** in African Americans. * **Clinical Clue:** Patients with HIVAN often have normal or small-to-normal sized kidneys on ultrasound, despite advanced renal failure, though classic teaching sometimes mentions enlarged echogenic kidneys. * **Treatment:** Initiation of HAART (Highly Active Antiretroviral Therapy) is the most effective way to slow progression.

Question 207: Tropical splenomegaly is caused by which of the following?

A. Malaria
B. Kala azar
C. Schistosomiasis
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Tropical Splenomegaly Syndrome (TSS)**, also known as **Hyperreactive Malarial Splenomegaly (HMS)**, is a clinical syndrome characterized by massive enlargement of the spleen resulting from an abnormal immunological response to chronic or repeated exposure to infectious agents, most commonly in tropical regions. **Why "All of the Above" is correct:** While **Malaria** (*Plasmodium falciparum* and *P. vivax*) is the most frequent cause of TSS due to chronic B-cell stimulation and IgM overproduction, other tropical infections also lead to significant splenomegaly through similar or overlapping mechanisms: * **Kala-azar (Visceral Leishmaniasis):** Causes massive splenomegaly due to the proliferation of the Reticuloendothelial (RE) system as macrophages become packed with Amastigotes (LD bodies) [1]. * **Schistosomiasis:** Specifically *S. mansoni* and *S. japonicum*, causes portal hypertension via periportal (Symmer’s pipestem) fibrosis, leading to congestive splenomegaly [2]. **Clinical Pearls for NEET-PG:** 1. **Diagnostic Criteria for HMS:** * Massive splenomegaly (>10 cm below the costal margin). * Elevated serum **IgM** levels (>2 standard deviations above the local mean). * High titers of antimalarial antibodies. * Clinical and immunological response to long-term **antimalarial prophylaxis** (e.g., Proguanil or Chloroquine). 2. **Histology:** Shows hepatic sinusoidal lymphocytosis. 3. **Differential Diagnosis:** Always rule out Chronic Myeloid Leukemia (CML) and Myelofibrosis in cases of massive splenomegaly. In the context of tropical infections, **Kala-azar** is the closest mimic to Malarial TSS regarding spleen size [1].

Question 208: Which of the following is true regarding influenza?

A. It is caused by an enveloped RNA virus.
B. Laboratory studies may show neutropenia early in the course of disease.
C. Primary infectious pneumonia is less common than secondary bacterial pneumonia. (Correct Answer)
D. Antiviral agents given early prevent complications.

Explanation: **Explanation:** Influenza is a major cause of respiratory morbidity. Understanding its complications and clinical presentation is crucial for NEET-PG [1]. **1. Why Option C is Correct:** While influenza primarily affects the upper respiratory tract, it can lead to pneumonia. **Secondary bacterial pneumonia** (most commonly caused by *S. pneumoniae*, *S. aureus*, or *H. influenzae*) is significantly **more common** than primary viral influenza pneumonia [1],[2]. Primary viral pneumonia is a severe, often fatal complication characterized by rapid progression and diffuse interstitial infiltrates, but it occurs less frequently than bacterial superinfection [1]. **2. Why the other options are incorrect:** * **Option A:** Influenza is caused by an **enveloped RNA virus** (Orthomyxoviridae) [1]. While this statement is technically true, in the context of standard medical examinations, Option C is the "most true" clinical fact regarding disease progression and complications. *Note: In some versions of this question, Option A is considered a "distractor" if the focus is on clinical complications.* * **Option B:** Laboratory findings in influenza typically show **leukopenia** (low WBC count), but specifically, **lymphopenia** is more characteristic than neutropenia early in the course. * **Option C:** While Neuraminidase inhibitors (Oseltamivir) reduce the duration of symptoms by 1–1.5 days if given within 48 hours, there is **no definitive evidence** that they prevent major complications like pneumonia or hospitalization in healthy individuals. **Clinical Pearls for NEET-PG:** * **Most common secondary bacterial cause:** *Streptococcus pneumoniae* [1],[2]. * **Most serious/aggressive secondary cause:** *Staphylococcus aureus* (including MRSA), often presenting with cavitary lesions [1],[2]. * **Reye’s Syndrome:** Associated with Influenza B and Aspirin use in children (presents with fatty liver and encephalopathy). * **Gold Standard Diagnosis:** RT-PCR (Nasopharyngeal swab).

Question 209: Which of the following differentiates Systemic Inflammatory Response Syndrome (SIRS) from sepsis?

A. Heart rate > 90 beats per minute
B. Temperature > 38 degrees Celsius
C. Absence of definitive evidence of infection (Correct Answer)
D. White blood cell count > 12,000 cells/mm³

Explanation: **Explanation:** The fundamental difference between **Systemic Inflammatory Response Syndrome (SIRS)** and **Sepsis** lies in the etiology. SIRS is a clinical syndrome representing a generalized state of inflammation that can be triggered by both infectious (e.g., pneumonia) and non-infectious insults [1]. **Sepsis** is defined specifically as **SIRS caused by a documented or suspected infection.** Therefore, the absence of definitive evidence of infection is what characterizes SIRS in isolation. **Analysis of Options:** * **Option C (Correct):** As per the classic criteria, SIRS becomes Sepsis only when an infectious source is identified [1]. * **Options A, B, and D (Incorrect):** These are all constituent **criteria for SIRS**. To diagnose SIRS, at least two of the following must be present: 1. Temperature >38°C (100.4°F) or <36°C (96.8°F) [2]. 2. Heart rate >90 beats/min. 3. Respiratory rate >20 breaths/min or PaCO2 <32 mmHg. 4. WBC count >12,000/mm³, <4,000/mm³, or >10% bands. Since these parameters are present in *both* SIRS and Sepsis, they cannot be used to differentiate between the two. **High-Yield Clinical Pearls for NEET-PG:** * **Sepsis-3 Definitions:** Modern guidelines (Sepsis-3) have shifted away from SIRS, defining Sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection, measured by a **SOFA score ≥ 2**. * **qSOFA (Quick SOFA):** A bedside tool to identify patients at risk (Altered mental status, Systolic BP ≤100 mmHg, Respiratory rate ≥22/min). * **Septic Shock:** Sepsis plus persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg AND serum lactate >2 mmol/L despite adequate fluid resuscitation.

Question 210: A male patient is HBsAg positive, HBeAg negative, and anti-HBe antibody positive. HBV DNA copies are 100,000/mL, and SGOT and SGPT are elevated to 6 times the upper limit of normal. What is the likely diagnosis?

A. HBV surface mutant
B. HBV precore mutant (Correct Answer)
C. Wild HBsAg
D. Inactive HBV carrier

Explanation: The clinical presentation describes a patient with active chronic hepatitis B who lacks the HBeAg marker. This is the classic profile of an **HBV Precore Mutant** infection [1]. 1. **Why the correct answer is right:** In "wild-type" HBV infection, the presence of HBeAg signifies high viral replication. However, a mutation in the **precore region** (most commonly a G-to-A substitution at nucleotide 1896) creates a stop codon that prevents the synthesis of HBeAg. Despite the absence of HBeAg and the presence of anti-HBe antibodies, the virus continues to replicate efficiently [1]. This is evidenced here by the high **HBV DNA (100,000 copies/mL)** and significant liver injury (**ALT/AST 6x normal**). 2. **Why the incorrect options are wrong:** * **HBV Surface Mutant:** This involves mutations in the 'a' determinant of HBsAg (e.g., G145R). It allows the virus to escape detection by standard HBsAg assays or vaccine-induced antibodies, but it does not specifically explain the HBeAg-negative/DNA-high discordance. * **Wild HBsAg:** In a typical wild-type active infection, high viral DNA and elevated enzymes would almost always be accompanied by a **positive HBeAg**. * **Inactive HBV Carrier:** While these patients are HBeAg negative and anti-HBe positive, they must have **low HBV DNA** (<2,000 IU/mL) and **normal SGOT/SGPT** levels [1]. **Clinical Pearls for NEET-PG:** * **Precore Mutant:** Suspect when HBeAg is negative, Anti-HBe is positive, but HBV DNA is >2,000 IU/mL and transaminases are elevated. * **Core Promoter Mutant:** Another variant (A1762T, G1764A) that decreases HBeAg production but increases viral replication. * **Treatment:** Precore mutants often have a more severe clinical course and higher rates of progression to cirrhosis compared to HBeAg-positive patients [1].

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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