Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 21: Which of the following is NOT a causative agent of lymphatic filariasis?

A. Brugia malayi
B. Brugia timori
C. Loa loa (Correct Answer)
D. Wuchereria bancrofti

Explanation: Explanation: Lymphatic filariasis (Elephantiasis) is caused by thread-like filarial nematodes that occupy the lymphatic system, leading to lymphoedema and hydrocele. **Why Loa loa is the correct answer:** *Loa loa* is the causative agent of **Loiasis**, also known as "African Eye Worm." Unlike the agents of lymphatic filariasis, *Loa loa* resides in the **subcutaneous tissues** and is transmitted by the *Chrysops* (deer fly) [1]. It is clinically characterized by transient localized angioedema known as **Calabar swellings** and the visible migration of the adult worm across the subconjunctiva of the eye [1]. It does not cause lymphatic obstruction. **Why the other options are incorrect:** * **Wuchereria bancrofti:** The most common cause, responsible for approximately 90% of lymphatic filariasis cases worldwide. It is transmitted by *Culex*, *Anopheles*, and *Aedes* mosquitoes. * **Brugia malayi:** A major cause of lymphatic filariasis in South and Southeast Asia (including parts of India like Kerala). * **Brugia timori:** A localized cause of lymphatic filariasis restricted to the Timor islands of Indonesia. **High-Yield NEET-PG Pearls:** 1. **Vector Check:** *W. bancrofti* is primarily transmitted by the **Culex quinquefasciatus** mosquito in urban India. 2. **Diagnosis:** The gold standard is the identification of microfilariae in a **peripheral blood smear** collected at night (**Nocturnal Periodicity**, typically 10 PM – 2 AM). 3. **Drug of Choice:** **Diethylcarbamazine (DEC)** is the mainstay of treatment. However, it is contraindicated in patients with heavy *Loa loa* or *Onchocerca* co-infection due to the risk of encephalopathy or severe Mazzotti reaction [1]. 4. **Tropical Pulmonary Eosinophilia (TPE):** A hypersensitivity response to *W. bancrofti* or *B. malayi* antigens, characterized by nocturnal cough, wheezing, and high peripheral eosinophilia [1].

Question 22: A 29-year-old male is suspected of having viral encephalitis. Which of the following is the most likely result from CSF analysis?

A. Raised protein, raised lymphocytes, normal glucose (Correct Answer)
B. Raised protein, normal lymphocytes, normal glucose
C. Raised protein, raised lymphocytes, raised glucose
D. Normal protein, raised lymphocytes, raised glucose

Explanation: ### Explanation The hallmark of viral infections of the Central Nervous System (CNS), including meningitis and encephalitis, is **lymphocytic pleocytosis** with relatively preserved biochemical parameters compared to bacterial infections [1]. **Why Option A is correct:** In viral encephalitis, the inflammatory response leads to an influx of white blood cells, predominantly **lymphocytes**. The inflammation also causes a breakdown of the blood-brain barrier, resulting in **mildly to moderately raised protein** levels. Crucially, viruses do not consume glucose for metabolism; therefore, the **CSF glucose remains normal** (typically >60% of blood glucose) [1]. **Why the other options are incorrect:** * **Option B:** Encephalitis typically triggers an immune response [2]; a "normal lymphocyte" count is rare unless the patient is severely immunocompromised or in the very early hyperacute phase. * **Option C & D:** **Raised glucose** in CSF is not a diagnostic feature of any CNS infection. High CSF glucose usually reflects systemic hyperglycemia (as CSF glucose levels follow blood glucose levels). --- ### High-Yield Clinical Pearls for NEET-PG: 1. **The "Rule of Two":** In viral CNS infections, look for **Normal Glucose** and **Lymphocytic Predominance**. 2. **Bacterial vs. Viral:** Bacterial meningitis shows **low glucose** (hypoglycorrhachia) and **neutrophilic** predominance. 3. **HSV Encephalitis:** If the question mentions **hemorrhagic** CSF or involvement of the **temporal lobes** on MRI, think Herpes Simplex Virus (HSV-1) [2]. This is the most common cause of sporadic fatal encephalitis. 4. **Xanthochromia:** If the CSF is yellowish, it indicates old blood (Subarachnoid Hemorrhage), not typical viral encephalitis. 5. **TB Meningitis:** Characterized by very high protein, very low glucose, and lymphocytic pleocytosis (often confused with viral, but glucose is the differentiator).

Question 23: What are the investigations in a clinically suspected case of tuberculosis?

A. Mantoux test (in children) (Correct Answer)
B. Sputum AFB
C. QuantiFERON TB Gold
D. Bactec

Explanation: In the context of the NEET-PG exam, this question focuses on the **initial screening and diagnostic approach** for Tuberculosis (TB) across different age groups. ### **Explanation of the Correct Answer** **Option A (Mantoux test in children)** is the correct choice because, in pediatric clinical practice, the Mantoux test (Tuberculin Skin Test) remains a cornerstone for screening and diagnosis. Children often have **paucibacillary disease**, making sputum microscopy difficult. A positive Mantoux test (≥10mm induration), when combined with clinical symptoms and a suggestive chest X-ray, is a primary diagnostic criterion in the **Paediatric TB Diagnostic Algorithm** (under NTEP guidelines). ### **Analysis of Incorrect Options** * **Option B (Sputum AFB):** While essential for adult pulmonary TB, it has low sensitivity in children and extra-pulmonary cases. Furthermore, **CBNAAT (GeneXpert)** has now replaced Sputum AFB as the initial diagnostic test of choice under the National Tuberculosis Elimination Program (NTEP). Direct microscopy of sputum remains the most important first step in certain regions, but its detection threshold is typically 5000–10,000 organisms [1]. * **Option C (QuantiFERON TB Gold):** This Interferon-Gamma Release Assay (IGRA) cannot differentiate between Latent TB Infection (LTBI) and active disease. It is generally not recommended for routine diagnosis of active TB in high-burden countries like India. * **Option D (Bactec):** This is a rapid liquid culture system. While it is the "Gold Standard" for drug sensitivity testing, it is not the *initial* investigation due to the time required (1–3 weeks) compared to molecular or skin tests. ### **High-Yield Clinical Pearls for NEET-PG** * **Initial Test of Choice (NTEP):** CBNAAT (GeneXpert) is now the first-line investigation for all suspected TB cases. * **Gold Standard for Diagnosis:** Culture (Liquid culture/MGIT is faster than solid LJ medium). * **Mantoux Interpretation:** In HIV-positive patients or severely malnourished children, an induration of **≥5mm** is considered positive. * **False Negative Mantoux:** Seen in miliary TB, sarcoidosis, malnutrition, and recent viral infections (e.g., Measles).

Question 24: Which of the following is not a cause of rash?

A. Salmonella
B. Shigella (Correct Answer)
C. Meningococci
D. Staphylococcus

Explanation: The correct answer is **Shigella**. In clinical medicine, Shigella is primarily characterized by bacillary dysentery (fever, abdominal cramps, and mucoid/bloody stools). It is an invasive intestinal pathogen but does not typically cause a systemic cutaneous rash. **Why the other options are incorrect:** * **Salmonella (S. Typhi):** Causes **"Rose Spots."** These are 2–4 mm, blanching, erythematous maculopapules typically found on the upper abdomen and chest during the second week of Enteric Fever. * **Meningococci (N. meningitidis):** Classically causes a **petechial or purpuric rash**. In severe cases (Meningococcemia), it can lead to *Purpura Fulminans* due to disseminated intravascular coagulation (DIC). * **Staphylococcus (S. aureus):** Associated with various rashes, most notably the diffuse erythematous "sunburn-like" rash of **Toxic Shock Syndrome (TSS)**, which later undergoes desquamation. It also causes localized infections like impetigo and scalded skin syndrome. **NEET-PG High-Yield Pearls:** 1. **Rose Spots:** Pathognomonic for Enteric fever (Salmonella), seen in only ~25% of cases. 2. **Waterhouse-Friderichsen Syndrome:** Adrenal hemorrhage associated with fulminant Meningococcemia. 3. **Palmar/Sole Rash:** If a question mentions a rash involving palms and soles, think of **Syphilis (Secondary)**, **Rocky Mountain Spotted Fever**, or **Coxsackievirus (Hand-Foot-Mouth disease)**. 4. **Shigella Complication:** While it lacks a rash, remember its association with **HUS (Hemolytic Uremic Syndrome)** and **Reactive Arthritis** (HLA-B27).

Question 25: What is the outpatient treatment for community-acquired pneumonia?

A. Azithromycin (Correct Answer)
B. Cefotaxime
C. Ampicillin
D. Gentamicin

Explanation: The treatment of Community-Acquired Pneumonia (CAP) is guided by the likely causative organisms, most commonly *Streptococcus pneumoniae*, *Haemophilus influenzae*, and atypical pathogens like *Mycoplasma pneumoniae* [3]. **1. Why Azithromycin is correct:** In previously healthy outpatients with no risk factors for drug-resistant *S. pneumoniae*, **Macrolides** (Azithromycin or Clarithromycin) or **Doxycycline** are the first-line empirical treatments. Azithromycin is preferred due to its excellent coverage against atypical pathogens and its convenient once-daily dosing [3]. In regions with high macrolide resistance or for patients with comorbidities, a respiratory fluoroquinolone (e.g., Levofloxacin) or a combination of a Beta-lactam plus a Macrolide is indicated. **2. Why the other options are incorrect:** * **Cefotaxime:** This is a third-generation cephalosporin administered parenterally (IV/IM). It is used for inpatient management of CAP, not for routine outpatient treatment. * **Ampicillin:** While active against some gram-positive organisms, it is inactivated by beta-lactamase-producing strains of *H. influenzae* and has no activity against atypical pathogens, making it poor monotherapy for CAP [3]. * **Gentamicin:** This aminoglycoside is primarily active against aerobic gram-negative bacilli. It has poor lung penetration and no activity against *S. pneumoniae* or atypicals, making it inappropriate for CAP. **High-Yield Clinical Pearls for NEET-PG:** * **CURB-65 Score:** Used to decide the site of care (Outpatient vs. Inpatient) [2]. A score of 0-1 suggests outpatient treatment. * **Atypical Pneumonia:** Characterized by a subacute onset and "walking pneumonia" symptoms; Macrolides are the drug of choice [3]. * **Drug of Choice for MRSA Pneumonia:** Linezolid or Vancomycin [1]. * **Drug of Choice for *Legionella*:** Azithromycin or Levofloxacin.

Question 26: A nurse is evaluating a client who is HIV positive and prescribed IV Pentamidine for Pneumocystis jirovecii pneumonia. Which of the following assessments after administration is most important to relay to the physician?

A. Blood pressure of 100/62 mm Hg.
B. Redness and pain at the infusion site.
C. Sudden sweating and hunger. (Correct Answer)
D. Unusual taste or dryness in the mouth.

Explanation: **Explanation:** **Correct Option: C (Sudden Sweating and Hunger)** Pentamidine is a potent antiprotozoal agent used for *Pneumocystis jirovecii* pneumonia (PCP), but it is notorious for its metabolic side effects. It is directly toxic to the pancreatic islet cells. Initially, this causes an excessive release of insulin, leading to **severe hypoglycemia** [1]. Symptoms like sudden sweating, hunger, tremors, and confusion are classic signs of hypoglycemia and require immediate intervention to prevent seizures or coma [1]. Long-term use can eventually lead to islet cell destruction and secondary diabetes mellitus. **Analysis of Incorrect Options:** * **A (Blood pressure of 100/62 mm Hg):** While IV Pentamidine can cause hypotension if infused too rapidly, this specific reading is within a borderline normal range and is less acutely life-threatening than severe hypoglycemia. * **B (Redness and pain at the infusion site):** Pentamidine is an irritant and can cause local thrombophlebitis. While it requires nursing care (e.g., changing the site), it is not a systemic emergency. * **D (Unusual taste or dryness in the mouth):** A metallic taste (dysgeusia) is a common, benign side effect of Pentamidine and does not require urgent physician notification. **Clinical Pearls for NEET-PG:** 1. **Metabolic Profile:** Pentamidine causes a "double hit" on the pancreas—initial **hypoglycemia** (due to insulin leak) followed by potential **hyperglycemia/Diabetes** (due to B-cell cytolysis) [1]. 2. **Renal Impact:** Nephrotoxicity is common (up to 25% of patients); monitor serum creatinine closely. 3. **Cardiac Warning:** It can cause **QT prolongation** and Torsades de Pointes. 4. **PCP Prophylaxis:** While IV/IM is used for treatment, aerosolized Pentamidine is used for prophylaxis in patients who cannot tolerate Cotrimoxazole (TMP-SMX) [2].

Question 27: Which of the following is not a marker of the active replicative phase of chronic hepatitis B?

A. HBV DNA
B. HBV DNA polymerase
C. Anti-HBc (Correct Answer)
D. AST and ALT

Explanation: ### Explanation The correct answer is **C. Anti-HBc**. In Hepatitis B serology, markers are categorized based on whether they indicate active viral replication or the host's immune response [1]. **1. Why Anti-HBc is the correct answer:** **Anti-HBc (Antibody to Hepatitis B core antigen)** is a marker of **exposure**, not replication [1]. * **IgM anti-HBc** indicates acute infection (or a flare) [1]. * **IgG anti-HBc** indicates a past or chronic infection. Crucially, Anti-HBc persists for life regardless of whether the virus is actively replicating or has been cleared. Therefore, it cannot differentiate between the active replicative phase and the inactive carrier state. **2. Analysis of Incorrect Options (Markers of Replication):** * **HBV DNA (Option A):** This is the most sensitive and quantitative marker of viral load and active replication, often measured via PCR [1]. * **HBV DNA Polymerase (Option B):** This enzyme is required for viral synthesis; its presence directly correlates with active viral multiplication. * **AST and ALT (Option D):** While these are markers of hepatocellular injury, in the context of Chronic HBV, elevated transaminases typically signify the **Immune Clearance Phase**, where the host immune system attacks hepatocytes harboring replicating viruses. **3. High-Yield Clinical Pearls for NEET-PG:** * **HBeAg:** The classic serological marker for high infectivity and active replication. * **Window Period:** The interval where HBsAg and Anti-HBs are both negative; **IgM anti-HBc** is the only diagnostic marker during this time [1]. * **Inactive Carrier State:** Characterized by HBsAg (+), HBeAg (-), Anti-HBe (+), and low/undetectable HBV DNA with normal ALT [1]. * **Pre-core Mutant:** A scenario where the patient has high HBV DNA and active liver disease but is **HBeAg negative** (due to a mutation in the precore region) [1].

Question 28: Which of the following organisms can cause acalculous cholecystitis?

A. Leptospirosis (Correct Answer)
B. Malaria
C. Staphylococcus
D. Nocardiosis

Explanation: ### Explanation **Acalculous cholecystitis** refers to inflammation of the gallbladder in the absence of gallstones. It typically occurs in critically ill patients or as a complication of specific systemic infections [1]. #### 1. Why Leptospirosis is Correct **Leptospirosis** is a well-recognized cause of acalculous cholecystitis, particularly in the pediatric population and during the immune phase of the disease. The underlying mechanism involves **systemic vasculitis** and direct invasion of the gallbladder wall by *Leptospira* interrogans, leading to ischemia, stasis, and inflammation. It often presents with right upper quadrant pain and jaundice, which can be confused with Weil’s syndrome (icteric leptospirosis). #### 2. Why Other Options are Incorrect * **Malaria:** While malaria causes significant jaundice (due to hemolysis and hepatic dysfunction), it does not typically cause primary gallbladder inflammation or acalculous cholecystitis. * **Staphylococcus:** While *S. aureus* can cause sepsis and multi-organ failure, it is not a classic or high-yield causative agent for acalculous cholecystitis compared to Gram-negative bacilli or specific pathogens like *Salmonella typhi*. * **Nocardiosis:** This is primarily a pulmonary or CNS infection in immunocompromised hosts; it does not have a clinical association with gallbladder disease. #### 3. NEET-PG High-Yield Pearls * **Common Infectious Causes:** Apart from Leptospirosis, other high-yield organisms causing acalculous cholecystitis include **Salmonella typhi (Enteric fever)**, **Brucellosis**, **Cholera**, and **Cytomegalovirus (CMV)** (especially in HIV/AIDS patients). * **Non-infectious triggers:** Major trauma, severe burns, prolonged fasting (TPN), and post-cardiac surgery [1]. * **Diagnosis:** Ultrasound is the initial investigation (showing gallbladder wall thickening >4mm and pericholecystic fluid), but **HIDA scan** is the most sensitive confirmatory test. * **Management:** In critically ill patients, **percutaneous cholecystostomy** is often the preferred initial intervention over surgery.

Question 29: Post-transplant cytomegalovirus infection may cause which of the following?

A. Pyelonephritis
B. Gastrointestinal ulceration and hemorrhage (Correct Answer)
C. Cholecystitis
D. Intraabdominal abscess

Explanation: Cytomegalovirus (CMV) is the most common clinically significant viral infection in the post-transplant period (typically occurring 1–6 months post-transplant) [1]. In immunocompromised patients, CMV manifests as "tissue-invasive disease" rather than a self-limiting mononucleosis-like syndrome. **Why Option B is Correct:** CMV has a high tropism for vascular endothelial cells, leading to vasculitis and subsequent mucosal ischemia. In the gastrointestinal tract, this results in **mucosal ulcerations**, which can lead to life-threatening **hemorrhage** or perforation. It can affect any segment from the esophagus to the rectum, with CMV colitis being a frequent presentation in renal and hematopoietic stem cell transplant recipients [1]. **Why Other Options are Incorrect:** * **A. Pyelonephritis:** While CMV can cause graft dysfunction in renal transplants (CMV nephritis), it does not cause classic pyelonephritis, which is typically bacterial (e.g., *E. coli*). * **C. Cholecystitis:** CMV can occasionally cause acalculous cholecystitis in AIDS patients, but it is an extremely rare manifestation in the post-transplant setting compared to GI involvement. * **D. Intraabdominal abscess:** Abscesses are usually the result of bacterial or fungal infections related to surgical complications or bowel perforation; CMV itself causes diffuse or localized tissue inflammation/ulceration rather than primary abscess formation. **High-Yield NEET-PG Pearls:** * **Diagnosis:** The gold standard for tissue-invasive CMV is the presence of **"Owl’s Eye" intranuclear inclusion bodies** on histopathology. * **Treatment:** Intravenous **Ganciclovir** is the drug of choice [1]; Valganciclovir is used for prophylaxis and mild cases. * **Risk Factor:** The highest risk is in **D+/R-** (Seropositive Donor/Seronegative Recipient) cases. * **Other Manifestations:** CMV retinitis (more common in HIV), pneumonitis (high mortality in transplant patients), and hepatitis.

Question 30: A 21-year-old medical student suffered a needle stick injury. The patient has a history of illicit intravenous drugs abuse. One month later, the medical student develops jaundice. Which of the following findings would implicate hepatitis B as the etiology?

A. Positive hepatitis B surface antigen (Correct Answer)
B. Positive antihepatitis B surface antibody
C. Positive antihepatitis A antibody
D. Positive antihepatitis B-core antibody

Explanation: **Explanation:** The clinical presentation describes an acute onset of jaundice following a high-risk parenteral exposure (needle stick injury). To diagnose acute Hepatitis B Virus (HBV) infection, one must identify markers of active viral replication [1]. **Why Option A is Correct:** **Hepatitis B surface antigen (HBsAg)** is the first serological marker to appear in the blood after infection, often detectable 2 to 6 weeks before the onset of symptoms or jaundice [1]. Its presence indicates an active (acute or chronic) infection. In this scenario, one month post-exposure, HBsAg is the most reliable indicator that the student has contracted HBV [2]. **Why Other Options are Incorrect:** * **Option B (Anti-HBs):** This antibody indicates immunity, either from a successful vaccination or recovery from a past infection [2]. It does not signify an active, acute illness. * **Option C (Anti-HAV):** This indicates a past or present Hepatitis A infection [3]. HAV is transmitted via the fecal-oral route, not through needle stick injuries (parenteral). * **Option D (Anti-HBc):** While IgM anti-HBc is a marker of acute infection, "Anti-HBc" (Total) is non-specific as it remains positive for life after any natural infection [2]. Without specifying the IgM isotype, HBsAg is a more definitive marker for diagnosing the etiology of the current jaundice. **NEET-PG High-Yield Pearls:** 1. **Window Period:** The interval when HBsAg becomes negative but Anti-HBs has not yet appeared. During this time, **IgM Anti-HBc** is the only diagnostic marker of acute HBV [1]. 2. **HBeAg:** Indicates high viral replication and maximum infectivity. 3. **Post-Exposure Prophylaxis (PEP):** If a student is unvaccinated, PEP involves both the HBV vaccine and Hepatitis B Immune Globulin (HBIG), ideally within 24 hours.

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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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