Infectious Diseases Practice Questions

Q: Which one of the following is the drug of choice for treating systemic fungal infection?

Amphotericin B. **Explanation:** **Amphotericin B** remains the "Gold Standard" and drug of choice for most life-threatening systemic fungal infections (e.g., systemic Candidiasis, Cryptococcosis, Aspergillosis, and Mucormycosis) [2], [3]. Its mechanism of action involves binding to **ergosterol** in the fungal cell membrane, creating pores that lead to leakage of intracellular contents and cell death (fungicidal). While newer azoles and echinocandins are used for specific indications [2], Amphotericin B is preferred for its broad spectrum and rapid action in severe cases [3]. **Analysis of Incorrect Options:** * **Griseofulvin (A):** This is a fungistatic drug used exclusively for **superficial dermatophytoses** (skin, hair, nail infections). It is ineffective against systemic mycoses because it concentrates only in keratin precursor cells [4]. * **Ketoconazole (C):** An imidazole primarily used for topical fungal infections or specific endocrine conditions (Cushing’s syndrome). It is rarely used systemically today due to significant **hepatotoxicity** and inhibition of cytochrome P450 enzymes, which interferes with steroid synthesis [1]. * **Trimoxazole (D):** Also known as Co-trimoxazole, this is an antibacterial/antiprotozoal agent. While it is the drug of choice for *Pneumocystis jirovecii*, it is not a general antifungal agent for systemic mycoses. **High-Yield Clinical Pearls for NEET-PG:** * **Adverse Effects:** Amphotericin B is notorious for **nephrotoxicity** (causes distal Renal Tubular Acidosis) and infusion-related reactions ("shake and bake" – fever/chills). * **Liposomal Amphotericin B:** This formulation is preferred to reduce nephrotoxicity while maintaining efficacy [3]. * **Monitoring:** Always monitor serum **Potassium and Magnesium** levels, as hypokalemia and hypomagnesemia are common side effects.

Q: True about primary pulmonary tuberculosis is:

All of the above. Explanation: Primary Pulmonary Tuberculosis (TB) occurs in individuals not previously exposed to *Mycobacterium tuberculosis*. Understanding its manifestations is crucial for NEET-PG, as it differs significantly from secondary (reactivation) TB. * **Pleural Effusion (Option A):** This is a common manifestation of primary TB, often resulting from a hypersensitivity reaction to the tubercle bacilli or their antigens entering the pleural space from a subpleural focus [2]. It is typically exudative and lymphocytic. * **Fibrocaseous Lesion (Option B):** While more characteristic of secondary TB, the primary complex (Ghon complex) involves a parenchymal subpleural focus that undergoes caseous necrosis [1]. If the immune response is robust, these lesions undergo fibrosis and calcification (Ranke complex) [1]. * **Phlyctenular Keratitis (Option C):** This is a classic **hypersensitivity manifestation** of primary TB [2]. It is a non-infectious, inflammatory reaction of the cornea/conjunctiva to the tuberculo-protein. Other similar hypersensitivity markers include Erythema Nodosum. **Conclusion:** Since all three features can occur during the course of primary infection, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Ghon Focus:** The initial site of parenchymal inflammation (usually mid or lower lobes) [1]. * **Ghon Complex:** Ghon focus + Ipsilateral lymphadenopathy [1]. * **Ranke Complex:** Calcified Ghon complex (visible on X-ray) [1]. * **Epituberculosis:** A segmental collapse/consolidation occurring in children due to lymph node enlargement compressing a bronchus. * **Key Difference:** Cavitation is rare in primary TB but a hallmark of secondary TB.

Q: A 28-year-old sexually active man presents with a new, painless genital ulcer on his penis that he noticed 1 week ago. The ulcer is 1 cm in size, with an eroded base and an indurated margin. Dark-field examination of the ulcer fluid confirmed the diagnosis. What is the most likely infecting organism?

Syphilis. ### Explanation The clinical presentation describes a classic **Primary Syphilis** infection caused by the spirochete ***Treponema pallidum*** [1]. **Why Syphilis is correct:** The hallmark of primary syphilis is the **chancre**. It typically presents as a single, **painless**, well-circumscribed ulcer with a clean base and **indurated (firm) margins**. The incubation period is usually 3 weeks (range 10–90 days). **Dark-field microscopy** is the gold standard for immediate diagnosis of primary syphilis, as it allows for the direct visualization of motile spirochetes from the ulcer exudate before serological tests (like VDRL/RPR) become positive [1]. **Why the other options are incorrect:** * **Toxoplasmosis:** Caused by *Toxoplasma gondii*, it typically presents as a systemic febrile illness with lymphadenopathy or CNS involvement in immunocompromised patients, not genital ulcers. * **Tetanus:** Caused by *Clostridium tetani*, it presents with neuromuscular symptoms like lockjaw (trismus) and muscle spasms following a contaminated wound; it does not cause genital lesions. * **Smallpox:** Caused by the Variola virus, it presents with a systemic centrifugal rash (pustules) and has been eradicated globally. **NEET-PG High-Yield Pearls:** * **Painful vs. Painless:** Syphilis (Chancre) is **painless**, whereas Chancroid (*Haemophilus ducreyi*) is **painful** ("You *do cry* with *ducreyi*"). * **Diagnosis:** VDRL/RPR are screening tests (non-specific); FTA-ABS/TPPA are confirmatory (specific). * **Treatment:** The drug of choice for all stages of syphilis is **Benzathine Penicillin G**. * **Jarisch-Herxheimer Reaction:** An acute febrile reaction occurring within 24 hours of starting penicillin treatment for syphilis due to the release of endotoxins from dying spirochetes.

Q: A patient suffering from AIDS presents with a history of dyspnea and non-productive cough. X-ray shows bilateral perihilar opacities without pleural effusion and lymphadenopathy. What is the most probable etiological agent?

Pneumocystis jirovecii. ### Explanation The clinical presentation of a patient with AIDS, progressive dyspnea, and a non-productive cough, combined with the classic radiological finding of **bilateral perihilar (interstitial) opacities**, is the hallmark of **Pneumocystis jirovecii Pneumonia (PCP)**. **1. Why Pneumocystis jirovecii is correct:** PCP is the most common opportunistic infection in HIV patients with CD4 counts <200 cells/µL. The characteristic X-ray shows "ground-glass" or "bat-wing" perihilar infiltrates [1]. The absence of pleural effusion and lymphadenopathy is a key negative finding that strongly points toward PCP rather than bacterial or mycobacterial infections [1]. **2. Why other options are incorrect:** * **Tuberculosis (TB):** While common in AIDS, TB typically presents with upper lobe cavitary lesions (in early HIV) or mediastinal lymphadenopathy and pleural effusions (in advanced HIV) [1]. * **CMV Pneumonitis:** Though it causes interstitial patterns, it is rare as a primary cause of pneumonia in HIV unless the CD4 count is extremely low (<50 cells/µL) and is usually a diagnosis of exclusion. * **Kaposi’s Sarcoma:** Pulmonary involvement usually presents with nodular opacities, pleural effusions (often hemorrhagic), and characteristic skin lesions [2]. **3. NEET-PG High-Yield Pearls:** * **Diagnosis:** The gold standard is identifying the organism via **Gomori Methenamine Silver (GMS) stain** from induced sputum or Bronchoalveolar Lavage (BAL) [1]. * **Biomarker:** Elevated **Serum LDH** is a sensitive but non-specific marker for PCP. * **Treatment:** Drug of choice is **High-dose TMP-SMX** [1]. * **Steroid Indication:** Add Prednisone if $PaO_2 35$ mmHg to prevent respiratory failure triggered by inflammatory response to dying organisms [1].

Q: In a severe untreated case of tuberculous meningitis, what are the characteristic findings in CSF analysis?

Increased lymphocytes. ### Explanation **Tuberculous Meningitis (TBM)** is a chronic granulomatous inflammation of the meninges caused by *Mycobacterium tuberculosis* [1]. The CSF profile in TBM is classic and high-yield for NEET-PG. **1. Why "Increased Lymphocytes" is correct:** TBM typically presents with a **lymphocytic pleocytosis** (usually 10–500 cells/µL). Unlike pyogenic bacterial meningitis, which triggers an acute neutrophilic response [2], TB is a chronic infection that induces a Type IV hypersensitivity reaction [3]. This leads to the recruitment of mononuclear cells, specifically **lymphocytes**, to the subarachnoid space. **2. Why the other options are incorrect:** * **A. Increased sugar:** In TBM, CSF glucose is characteristically **decreased** (hypoglycorrhachia), usually <40 mg/dL or a CSF:Serum ratio <0.5. * **C. Increased polymorphs:** Polymorphonuclear leucocytes (neutrophils) are the hallmark of **acute pyogenic (bacterial) meningitis** [2]. While they may appear very early in TBM (the "neutrophilic phase"), the predominant and characteristic finding is lymphocytic. * **D. Increased RBCs:** CSF is typically clear or "cobweb" in appearance. Increased RBCs suggest a traumatic tap or subarachnoid hemorrhage, not a primary infectious process like TB. **3. High-Yield Clinical Pearls for NEET-PG:** * **The "Cobweb" Coagulum:** If CSF is left standing, a fine fibrin clot (pellicle/cobweb) often forms due to high protein content. * **Protein Levels:** Characteristically **very high** (100–500 mg/dL), often much higher than in viral meningitis. * **Basal Exudates:** TBM is notorious for thick exudates at the base of the brain [1], often leading to **cranial nerve palsies** [2] (CN VI is most common). * **Gold Standard:** CSF Culture (MGIT) is most sensitive, but **GeneXpert (CBNAAT)** is the preferred initial rapid test.

Q: Saddleback/biphasic fever is seen in:

Dengue. **Explanation:** **Dengue fever** is the classic cause of a **saddleback (biphasic) fever** pattern. This characteristic profile consists of an initial high-grade fever lasting 3–4 days, followed by a brief period of remission (defervescence) lasting 1–2 days, and a subsequent second rise in temperature for another 2–3 days. The second phase often coincides with the appearance of a generalized morbilliform rash [1]. **Analysis of Incorrect Options:** * **Typhoid (Enteric Fever):** Characterized by a **"Step-ladder"** pattern of fever, where the temperature rises gradually over the first week. * **Brucellosis:** Classically associated with an **"Undulant"** fever pattern, featuring waves of temperature that rise and fall over weeks to months. * **Trench Fever:** Caused by *Bartonella quintana*, it typically presents as a **"Quintan"** fever (recurring every 5 days). **High-Yield Clinical Pearls for NEET-PG:** 1. **Other causes of Saddleback fever:** Yellow fever, Colorado tick fever, Rift Valley fever, and occasionally Poliomyelitis or Leptospirosis [3]. 2. **Dengue Triad:** High fever, retro-orbital pain, and severe backache/myalgia (hence the name "Break-bone fever") [2]. 3. **Herman’s Sign:** Seen in Dengue; it is a late-onset maculopapular rash described as "islands of white in a sea of red." 4. **Tourniquet Test:** A positive test (≥10 petechiae per square inch) is a clinical indicator of capillary fragility in Dengue [1].

Q: Persistent marrow aplasia is caused by which hepatitis virus?

None of the above. **Explanation:** The correct answer is **None of the above** because persistent marrow aplasia (Aplastic Anemia) is most commonly associated with **Non-A, Non-B, Non-C, Non-E, and Non-G hepatitis viruses**. **1. Understanding the Concept:** Post-hepatitic aplastic anemia is a distinct clinical syndrome where bone marrow failure follows an episode of acute hepatitis. In approximately 90% of these cases, the known hepatotropic viruses (HAV, HBV, HCV, HEV) are **not** the causative agents. Instead, it is attributed to unidentified "Non-A-E" viruses or an aberrant T-cell mediated immune response triggered by an unknown viral infection that cross-reacts with hematopoietic stem cells. **2. Analysis of Options:** * **Hepatitis A (HAV):** While rare cases of transient marrow suppression have been reported, it does not typically cause persistent aplastic anemia. * **Hepatitis B (HBV) & Hepatitis C (HCV):** These are primarily associated with chronic liver disease, cirrhosis, and hepatocellular carcinoma. While they can cause extrahepatic manifestations (like polyarteritis nodosa for HBV or cryoglobulinemia for HCV), they are not the standard causes of post-hepatitic marrow aplasia. **3. NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Post-hepatitic aplastic anemia typically occurs 2–3 months after the acute hepatitis episode. * **Prognosis:** It is often severe and can be fatal if not treated with bone marrow transplantation or immunosuppressive therapy (Antithymocyte globulin + Cyclosporine). * **Most Common Cause:** Idiopathic (60-70%), followed by drugs/toxins and post-hepatitic (Non-A-E) syndromes. * **Hepatitis E (HEV):** In pregnant women, HEV is associated with high mortality due to Fulminant Hepatic Failure, not marrow aplasia.

Q: A patient with prosthetic valve replacement develops endocarditis 8 months later. Which organism is most likely responsible?

Staphylococcus epidermidis. **Explanation:** Prosthetic Valve Endocarditis (PVE) is classified based on the timing of symptom onset after surgery, which dictates the most likely causative organism: 1. **Early PVE (<12 months):** The correct answer is **Staphylococcus epidermidis** (Coagulase-negative Staphylococcus) [1]. During surgery, the prosthetic material is easily colonized by skin flora [1]. *S. epidermidis* produces a **biofilm** (extracellular polysaccharide matrix) that protects it from antibiotics and host immune responses, making it the most common cause of PVE within the first year. 2. **Late PVE (>12 months):** The microbiology resembles native valve endocarditis, where **Streptococcus viridans** becomes the most common cause due to transient bacteremia from dental or mucosal sources. **Analysis of Incorrect Options:** * **Staphylococcus aureus (A):** While a common cause of acute endocarditis and early PVE, it is generally less frequent than *S. epidermidis* in the subacute presentation of early prosthetic infections. * **Streptococcus viridans (B):** This is the leading cause of **Late PVE** (>1 year post-surgery) and community-acquired native valve endocarditis. * **HACEK group (D):** These are fastidious gram-negative organisms (e.g., *Haemophilus, Aggregatibacter*) that typically cause **culture-negative endocarditis** and are rarely the primary cause of early PVE. **High-Yield Pearls for NEET-PG:** * **Most common cause of NVE (Native Valve):** *Streptococcus viridans*. * **Most common cause in IV drug users:** *Staphylococcus aureus* (often affecting the **Tricuspid valve**). * **Duke’s Criteria:** The gold standard for diagnosis (requires 2 major, 1 major + 3 minor, or 5 minor criteria) [2]. * **Biofilm formation:** The key virulence factor for *S. epidermidis* in prosthetic device infections [1].

Question 1

Which one of the following is the drug of choice for treating systemic fungal infection?

Accepted Answer

Amphotericin B

Answer

Griseofulvin

Answer

Ketoconazole

Answer

Trimoxazole

Question 2

True about primary pulmonary tuberculosis is:

Accepted Answer

All of the above

Answer

Pleural effusion

Answer

Fibrocaseous lesion

Answer

Phlyctenular keratitis

Question 3

A 28-year-old sexually active man presents with a new, painless genital ulcer on his penis that he noticed 1 week ago. The ulcer is 1 cm in size, with an eroded base and an indurated margin. Dark-field examination of the ulcer fluid confirmed the diagnosis. What is the most likely infecting organism?

Accepted Answer

Syphilis

Answer

Toxoplasmosis

Answer

Tetanus

Answer

Smallpox

Question 4

A patient suffering from AIDS presents with a history of dyspnea and non-productive cough. X-ray shows bilateral perihilar opacities without pleural effusion and lymphadenopathy. What is the most probable etiological agent?

Accepted Answer

Pneumocystis jirovecii

Answer

Tuberculosis

Answer

CMV

Answer

Kaposi's sarcoma

Question 5

In a severe untreated case of tuberculous meningitis, what are the characteristic findings in CSF analysis?

Accepted Answer

Increased lymphocytes

Answer

Increased sugar

Answer

Increased polymorphs

Answer

Increased RBCs

Question 6

Saddleback/biphasic fever is seen in:

Accepted Answer

Dengue

Answer

Typhoid

Answer

Brucellosis

Answer

Trench fever

Question 7

Which parameter is best for monitoring HIV disease progression?

Accepted Answer

Peripheral blood CD4+ T-cell counts with plasma levels of HIV RNA

Answer

Peripheral blood CD4+ T-cell counts

Answer

Plasma levels of HIV RNA

Answer

Peripheral blood CD4+ T-cell counts or plasma levels of HIV RNA

Question 8

Persistent marrow aplasia is caused by which hepatitis virus?

Accepted Answer

None of the above

Answer

Hepatitis A virus (HAV)

Answer

Hepatitis B virus (HBV)

Answer

Hepatitis C virus (HCV)

Question 9

A patient with prosthetic valve replacement develops endocarditis 8 months later. Which organism is most likely responsible?

Accepted Answer

Staphylococcus epidermidis

Answer

Staphylococcus aureus

Answer

Streptococcus viridans

Answer

HACEK group

Question 10

Which of the following statements regarding brain abscess is FALSE?

Accepted Answer

Abscesses that develop as a result of direct spread of infection from the sinuses and dental infections are usually located in the frontal lobe.

Answer

The most common source of infection is direct spread from a contiguous cranial site of infection, such as paranasal sinusitis, otitis media, mastoiditis, or dental infection.

Answer

Hematogenous abscesses are often multiple, and multiple abscesses often (50%) have a hematogenous origin.

Answer

Hematogenous abscesses show a predilection for the territory of the middle cerebral artery.

Infectious Diseases — MCQs

Infectious Diseases — MCQs

On this page

Practice by Chapter

Want unlimited practice?