Infectious Diseases Practice Questions

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

High grade fever with rigors. **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 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 ( 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.

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

Pegylated interferon. 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.

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

101 F. ### 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].

Q: 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?

Serial monitoring. ### 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).

Q: Tropical splenomegaly is caused by which of the following?

All of the above. **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].

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

Absence of definitive evidence of infection. **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 90 beats/min. 3. Respiratory rate >20 breaths/min or PaCO2 12,000/mm³, 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.

Q: 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?

HBV precore mutant. 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 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].

Question 1

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

Accepted Answer

High grade fever with rigors

Answer

Severe anemia

Answer

Acidosis

Answer

Pulmonary edema

Question 2

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

Accepted Answer

Pegylated interferon

Answer

Lamivudine

Answer

Adefovir

Answer

Telbivudine

Question 3

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

Accepted Answer

101
F

Answer

98.4
F

Answer

99.4
F

Answer

100
F

Question 4

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?

Accepted Answer

Serial monitoring

Answer

Antiviral treatment with Lamivudine monotherapy

Answer

Antiviral treatment with Lamivudine and pulsed Interferon

Answer

Antiviral treatment with Interferon Alfa alone

Question 5

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

Accepted Answer

Nevirapine

Answer

Didanosine

Answer

Indinavir

Answer

Nelfinavir

Question 6

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?

Accepted Answer

Segmental sclerosis of some of the glomeruli

Answer

Diffuse thickening of the glomerular basement membrane

Answer

Hypercellular glomeruli with thickening of the GBM

Answer

Proliferation of the parietal cells filling Bowman's space

Question 7

Tropical splenomegaly is caused by which of the following?

Accepted Answer

All of the above

Answer

Malaria

Answer

Kala azar

Answer

Schistosomiasis

Question 8

Which of the following is true regarding influenza?

Accepted Answer

Primary infectious pneumonia is less common than secondary bacterial pneumonia.

Answer

It is caused by an enveloped RNA virus.

Answer

Laboratory studies may show neutropenia early in the course of disease.

Answer

Antiviral agents given early prevent complications.

Question 9

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

Accepted Answer

Absence of definitive evidence of infection

Answer

Heart rate > 90 beats per minute

Answer

Temperature > 38 degrees Celsius

Answer

White blood cell count > 12,000 cells/mm³

Question 10

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?

Accepted Answer

HBV precore mutant

Answer

HBV surface mutant

Answer

Wild HBsAg

Answer

Inactive HBV carrier

Infectious Diseases — MCQs

Infectious Diseases — MCQs

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