Infectious Diseases — MCQs
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A previously healthy 43-year-old man presents with symptoms of cough, fever, weight loss, and lymphadenopathy for the past 2 months. His physical examination reveals multiple axillary and cervical lymph nodes and oropharyngeal ulcerations. His CXR reveals fibronodular pulmonary infiltrates in the apex, his sputum is negative for TB, and the HIV test is negative. A bronchoalveolar lavage (BAL) confirms the diagnosis. For the above patient, select the most likely diagnosis?
A 30-year-old patient has persistent antibodies to HCV for 6 months with normal AST/ALT levels and no symptoms or stigmata of liver disease. What is the most appropriate next step in management?
Primary tuberculosis most commonly involves which organ?
A patient on a urinary catheter has a catheter tip culture that shows extended-spectrum beta-lactamase (ESBL)-positive Klebsiella. Which of the following drugs can be given?
Which of the following is NOT true about Pneumocystis jirovecii pneumonia?
Basal exudates, infarcts, and hydrocephalus are findings observed in brain imaging studies. The most likely diagnosis is:
Which of the following is the best method to evaluate alpha interferon therapy for Hepatitis C Virus (HCV) infection?
Apex of the lung is commonly involved by which pathogen?
Regarding Hepatitis E, which of the following statements is true?
Which of the following statements regarding HIV-associated TB is FALSE?
Infectious Diseases Indian Medical PG Practice Questions and MCQs
Question 401: A previously healthy 43-year-old man presents with symptoms of cough, fever, weight loss, and lymphadenopathy for the past 2 months. His physical examination reveals multiple axillary and cervical lymph nodes and oropharyngeal ulcerations. His CXR reveals fibronodular pulmonary infiltrates in the apex, his sputum is negative for TB, and the HIV test is negative. A bronchoalveolar lavage (BAL) confirms the diagnosis. For the above patient, select the most likely diagnosis?
- A. brucellosis
- B. coccidioidomycosis
- C. histoplasmosis (Correct Answer)
- D. leprosy
Explanation: **Explanation:** The clinical presentation of chronic cough, fever, weight loss, and apical fibronodular infiltrates closely mimics pulmonary tuberculosis [1]. However, the presence of **oropharyngeal ulcerations** and generalized **lymphadenopathy** in a TB-negative patient is a classic hallmark of **Histoplasmosis** (*Histoplasma capsulatum*). 1. **Why Histoplasmosis is correct:** While often associated with immunocompromised states (HIV), Histoplasmosis can occur in immunocompetent individuals. It is a dimorphic fungus that primarily affects the lungs but can disseminate to the reticuloendothelial system (lymph nodes, liver, spleen) and mucous membranes. Oropharyngeal ulcers are a high-yield diagnostic clue for disseminated or chronic histoplasmosis. 2. **Why other options are incorrect:** * **Brucellosis:** Typically presents with undulant fever, arthralgia, and hepatosplenomegaly, but does not usually cause apical pulmonary infiltrates or oropharyngeal ulcers. * **Coccidioidomycosis:** Known as "Valley Fever," it causes pulmonary symptoms and erythema nodosum, but oropharyngeal ulceration is not a characteristic feature. * **Leprosy:** While it involves skin and nerves, it does not present with apical pulmonary fibronodular infiltrates or acute systemic symptoms like weight loss and fever mimicking TB [2]. **NEET-PG High-Yield Pearls:** * **The "Great Mimicker":** Histoplasmosis is the fungal equivalent of Tuberculosis. * **Morphology:** On biopsy/BAL, look for **small intracellular yeast cells** within macrophages (Gomori Methenamine Silver stain). * **Habitat:** Associated with **bird or bat droppings** (caving, cleaning chicken coops). * **Treatment:** Mild cases may resolve spontaneously; moderate-to-severe cases require **Itraconazole**, while disseminated disease requires **Amphotericin B**.
Question 402: A 30-year-old patient has persistent antibodies to HCV for 6 months with normal AST/ALT levels and no symptoms or stigmata of liver disease. What is the most appropriate next step in management?
- A. Reassure the patient
- B. Repeat antibody titre every three years
- C. Repeat liver enzymes every year
- D. Determine HCV RNA levels (Correct Answer)
Explanation: ### Explanation The presence of **HCV antibodies (Anti-HCV)** indicates that the patient has been exposed to the Hepatitis C virus at some point. However, it does not distinguish between an active (chronic) infection and a resolved past infection [1]. **1. Why Option D is Correct:** In Hepatitis C, approximately 15–25% of patients clear the virus spontaneously but remain antibody-positive for life [1]. Furthermore, chronic HCV infection is often "clinically silent," where patients may have **persistently normal ALT/AST levels** despite ongoing viral replication and progressive liver fibrosis [1]. Therefore, the presence of antibodies must always be followed by a **qualitative or quantitative HCV RNA test (PCR)** to confirm active viremia [1]. If HCV RNA is detected, the patient has chronic hepatitis C and requires treatment, regardless of enzyme levels. **2. Why Other Options are Incorrect:** * **Option A & B:** Reassurance or simply repeating antibody titers is inappropriate because the patient may have active, transmissible chronic infection that can lead to cirrhosis or HCC if left untreated. Antibody titers do not correlate with disease activity. * **Option C:** Normal liver enzymes are not a reliable indicator of viral clearance. Up to 30% of patients with chronic HCV have normal ALT levels. Relying on enzymes alone would miss a significant number of chronic cases. **Clinical Pearls for NEET-PG:** * **Screening Test:** Anti-HCV (ELISA). * **Confirmatory/Gold Standard for Active Infection:** HCV RNA by PCR [1]. * **Treatment Goal:** Sustained Virologic Response (SVR), defined as undetectable HCV RNA 12–24 weeks after completing antiviral therapy. * **High-Yield Fact:** Unlike Hepatitis B, Hepatitis C does not integrate into the host genome; therefore, it is potentially curable with Direct-Acting Antivirals (DAAs).
Question 403: Primary tuberculosis most commonly involves which organ?
- A. Brain
- B. Lymph node
- C. Lung (Correct Answer)
- D. Intestine
Explanation: **Explanation:** **Primary Tuberculosis (TB)** occurs in a person who has not been previously exposed to *Mycobacterium tuberculosis*. The most common route of transmission is the inhalation of infectious airborne droplets (droplet nuclei) [1]. 1. **Why Lung is Correct:** Since the primary mode of infection is inhalation, the **Lung** is the most common site of primary tuberculosis [1]. When the bacilli reach the subpleural area of the mid or lower lung zones, they form a **Ghon focus** [1]. When this is associated with involved hilar lymph nodes, it is termed the **Ghon complex** (or Primary Complex) [1]. In most cases, this lesion heals, leaving a calcified nodule known as a **Ranke complex** [1]. 2. **Why Other Options are Incorrect:** * **Brain:** CNS involvement (like TB meningitis) is a severe form of disseminated or miliary TB [2], but it is never the primary site of entry [4]. * **Lymph node:** While lymphadenopathy (especially hilar) is a component of the primary complex [1], the lung parenchyma is the initial site of deposition. Extrapulmonary lymph node TB (Scrofula) is common in secondary TB or reactivation [3]. * **Intestine:** This was historically common due to the ingestion of *M. bovis* via unpasteurized milk (Primary Intestinal TB), but with modern pasteurization, it is now rare compared to the pulmonary route. **High-Yield Clinical Pearls for NEET-PG:** * **Ghon Focus:** Subpleural lesion, usually in the lower part of the upper lobe or upper part of the lower lobe [1]. * **Ranke Complex:** Ghon complex + Calcification [1]. * **Simon’s Focus:** Secondary TB focus at the lung apex (due to high oxygen tension). * **Most common site of Extrapulmonary TB:** Lymph nodes (Tuberculous lymphadenitis) [3]. * **Most common site of Hematogenous spread:** Bone marrow.
Question 404: A patient on a urinary catheter has a catheter tip culture that shows extended-spectrum beta-lactamase (ESBL)-positive Klebsiella. Which of the following drugs can be given?
- A. Ceftriaxone
- B. A beta-lactamase inhibitor (Correct Answer)
- C. Aminoglycoside
- D. Tetracycline
Explanation: ### **Explanation** **Correct Answer: B. A beta-lactamase inhibitor** **Mechanism and Rationale:** Extended-spectrum beta-lactamases (ESBLs) are enzymes produced by certain Gram-negative bacteria (most commonly *Klebsiella pneumoniae* and *E. coli*) that confer resistance to most beta-lactam antibiotics, including third-generation cephalosporins and monobactams [2]. However, these enzymes are typically **inhibited by beta-lactamase inhibitors** such as Clavulanic acid, Sulbactam, and Tazobactam [1]. Combining a beta-lactam with an inhibitor (e.g., Piperacillin-Tazobactam) can restore the activity of the antibiotic against ESBL-producing strains, particularly in non-bacteremic urinary tract infections [1]. **Analysis of Incorrect Options:** * **A. Ceftriaxone:** This is a third-generation cephalosporin. By definition, ESBL-producing organisms are resistant to all first, second, and third-generation cephalosporins [2]. * **C. Aminoglycoside:** While some ESBL strains may remain sensitive to aminoglycosides (like Amikacin), they are not the primary class defined by the ESBL resistance mechanism. Furthermore, ESBL genes are often carried on plasmids that also harbor resistance to aminoglycosides (co-resistance) [3]. * **D. Tetracycline:** These are generally bacteriostatic and are not the preferred treatment for complicated urinary infections caused by multi-drug resistant *Klebsiella*. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** For **severe or systemic infections** (bacteremia) caused by ESBL-producing organisms, **Carbapenems** (e.g., Meropenem, Imipenem) are the gold standard. * **Marker for ESBL:** Resistance to **Ceftazidime** or **Cefotaxime** in a laboratory report is a strong indicator of ESBL production. * **The "Inhibitor Squeeze":** ESBLs are characterized by their susceptibility to inhibition by clavulanic acid in *in vitro* synergy tests. * **Carbapenemase (KPC):** If a *Klebsiella* strain becomes resistant to Carbapenems, the drug of choice shifts to **Colistin, Polymyxin B, or Tigecycline.**
Question 405: Which of the following is NOT true about Pneumocystis jirovecii pneumonia?
- A. Characterized by respiratory alkalosis
- B. Associated with decreased diffusion capacity
- C. Leads to cyanosis
- D. Associated with an increased alveolar-arterial oxygen gradient (PAO2 - PaO2) (Correct Answer)
Explanation: The question asks for the statement that is **NOT** true regarding *Pneumocystis jirovecii* pneumonia (PCP). **Understanding the Correct Answer (Option D):** The correct answer is D because the statement is actually **true**, making it a "distractor" in a "NOT true" question format. In PCP, the accumulation of intra-alveolar exudate and interstitial thickening severely impairs gas exchange. This leads to a significant **increase in the Alveolar-arterial (A-a) oxygen gradient**. An elevated A-a gradient is a hallmark of PCP and is used clinically to stratify the severity of the disease and determine the need for adjunctive corticosteroids (indicated if A-a gradient ≥ 35 mmHg or PaO2 < 70 mmHg) [1]. **Analysis of Incorrect Options:** * **Option A (Respiratory Alkalosis):** This is **true**. Patients with PCP typically present with tachypnea and hyperventilation due to hypoxia, which leads to a decrease in PaCO2 and subsequent respiratory alkalosis. * **Option B (Decreased Diffusion Capacity):** This is **true**. The characteristic "foamy" eosinophilic exudate in the alveoli increases the distance for gas diffusion, leading to a significantly reduced DLCO (Diffusion Capacity of the Lung for Carbon Monoxide). A normal DLCO virtually rules out PCP. * **Option C (Cyanosis):** This is **true**. Severe PCP causes profound hypoxemia due to V/Q mismatch and diffusion defects, which clinically manifests as central cyanosis, especially during exertion. **NEET-PG High-Yield Pearls for PCP:** * **Organism:** Reclassified as a **fungus** (formerly a protozoan). * **Stain of Choice:** **Gomori Methenamine Silver (GMS)** stain (shows crushed ping-pong ball appearance) [1]. * **Radiology:** Classic **bilateral perihilar ground-glass opacities** [1]. * **Treatment:** **Trimethoprim-Sulfamethoxazole (TMP-SMX)** is the first-line drug for both prophylaxis and treatment [1]. * **Prophylaxis Criteria:** CD4 count **< 200 cells/µL** in HIV-positive patients [1].
Question 406: Basal exudates, infarcts, and hydrocephalus are findings observed in brain imaging studies. The most likely diagnosis is:
- A. Tubercular Meningitis (Correct Answer)
- B. Viral Meningitis
- C. Herpes encephalitis
- D. Cerebral Malaria
Explanation: ### Explanation The correct answer is **Tubercular Meningitis (TBM)**. This diagnosis is characterized by a classic triad of neuroimaging findings: 1. **Basal Exudates:** *Mycobacterium tuberculosis* has a predilection for the base of the brain. The inflammatory response leads to thick, gelatinous exudates in the basal cisterns, which can entrap cranial nerves [1]. 2. **Infarcts:** The intense inflammation causes **Vasculitis** (specifically affecting the Circle of Willis), leading to ischemic strokes, most commonly in the basal ganglia and internal capsule (Medial Striate artery territory). 3. **Hydrocephalus:** Exudates obstruct the flow of CSF at the level of the aqueduct or the basal cisterns, leading to **communicating or non-communicating hydrocephalus**. #### Why the other options are incorrect: * **Viral Meningitis:** Typically presents with normal imaging or mild meningeal enhancement. It does not cause thick exudates or infarcts. * **Herpes Encephalitis (HSV-1):** Characteristically involves the **temporal lobes** and limbic system. Imaging shows edema and hemorrhage in the temporal/frontal lobes, not basal exudates. * **Cerebral Malaria:** Imaging is often normal or shows diffuse cerebral edema. While micro-hemorrhages (Durck’s granulomas) can occur, the classic triad of TBM is absent. #### NEET-PG High-Yield Pearls: * **Gold Standard Diagnosis:** CSF Culture (MGIT) or GeneXpert (NAAT). * **CSF Findings in TBM:** High protein, low sugar, and **lymphocytic pleocytosis** [1]. * **Hydrocephalus Management:** Often requires a VP shunt; steroids (Dexamethasone) are added to ATT to reduce mortality and complications from exudates. * **Stage of TBM:** The presence of infarcts or altered sensorium usually indicates Stage II or III disease.
Question 407: Which of the following is the best method to evaluate alpha interferon therapy for Hepatitis C Virus (HCV) infection?
- A. Quantification of HCV RNA (Correct Answer)
- B. ALT and AST levels
- C. Serum bilirubin level
- D. Serum IgM and IgG levels
Explanation: ### Explanation The primary goal of treating Hepatitis C Virus (HCV) infection is the achievement of a **Sustained Virologic Response (SVR)**, defined as the absence of detectable HCV RNA in the blood 12 to 24 weeks after completing therapy. **Why Option A is Correct:** **Quantification of HCV RNA** using nucleic acid testing (like RT-PCR) is the "gold standard" for monitoring treatment efficacy [1]. It directly measures the viral load. A rapid decline in HCV RNA levels during therapy (Early Virologic Response) and its total disappearance post-therapy (SVR) are the only definitive indicators that the interferon-based treatment has successfully cleared the virus. **Why the Other Options are Incorrect:** * **B. ALT and AST levels:** While these enzymes indicate liver inflammation (hepatocellular injury), they are non-specific. Aminotransferase levels can normalize even if the virus persists, or they may remain elevated due to other factors (like fatty liver or drug-induced injury), making them unreliable for evaluating viral clearance. * **C. Serum bilirubin level:** Bilirubin is a marker of liver synthetic and excretory function. It is used to assess the severity of cirrhosis or acute liver failure but does not correlate with the presence or quantity of HCV. * **D. Serum IgM and IgG levels:** HCV antibodies (Anti-HCV) often persist for life even after successful treatment [1]. Therefore, serology cannot distinguish between an active infection and a resolved one. **NEET-PG High-Yield Pearls:** * **SVR (Sustained Virologic Response):** Defined as undetectable HCV RNA 12 weeks (SVR12) or 24 weeks (SVR24) after stopping treatment. It is considered a "virologic cure." * **Current Standard:** While this question focuses on Interferon, modern treatment has shifted to **Direct-Acting Antivirals (DAAs)** (e.g., Sofosbuvir), which have higher SVR rates (>95%) and fewer side effects. * **Screening vs. Diagnosis:** Anti-HCV is the screening test; HCV RNA is the confirmatory and monitoring test [1].
Question 408: Apex of the lung is commonly involved by which pathogen?
- A. Chlamydia
- B. Coxiella burnetti
- C. Klebsiella (Correct Answer)
- D. Actinomyces israelii
Explanation: **Explanation:** **Why Klebsiella is Correct:** *Klebsiella pneumoniae* is a Gram-negative encapsulated bacillus that typically causes severe, necrotizing lobar pneumonia. It has a strong predilection for the **upper lobes**, particularly the **apex of the lung**. This is attributed to the organism's tendency to cause infection in patients with impaired host defenses (e.g., chronic alcoholics, diabetics), where aspiration of oropharyngeal flora occurs [1]. The resulting inflammatory response is so intense that it leads to "bulging fissures" on X-ray due to heavy alveolar exudate. **Analysis of Incorrect Options:** * **Chlamydia:** *Chlamydia pneumoniae* typically causes "atypical pneumonia" characterized by diffuse, patchy interstitial infiltrates rather than localized apical consolidation [1]. * **Coxiella burnetii:** The causative agent of Q fever usually presents with non-specific radiological findings, most commonly multiple rounded opacities or segmental consolidation in the **lower lobes**. * **Actinomyces israelii:** While *Actinomyces* can cross anatomical boundaries and involve the pleura or chest wall, it most commonly involves the **lower lobes** via aspiration [1]. It is known for causing "sulfur granules" in abscesses rather than isolated apical pneumonia. **High-Yield Clinical Pearls for NEET-PG:** * **"Currant Jelly" Sputum:** A classic board-style descriptor for *Klebsiella* pneumonia due to blood and mucus. * **Friedländer’s Pneumonia:** An older eponym for *Klebsiella* pneumonia. * **Differential Diagnosis for Apical Lesions:** Remember the mnemonic **"SET"** for upper lobe involvement: **S**ilicosis, **E**xtrinsic allergic alveolitis, and **T**uberculosis (the most common cause of apical cavitary lesions). *Klebsiella* is the classic bacterial (non-TB) cause. * **Alcoholism Link:** Always suspect *Klebsiella* in an alcoholic patient presenting with sudden onset of productive cough and upper lobe consolidation [1].
Question 409: Regarding Hepatitis E, which of the following statements is true?
- A. It occurs with Hepatitis B.
- B. It is a single-stranded DNA virus.
- C. It occurs along with HIV.
- D. Mortality is increased in pregnancy. (Correct Answer)
Explanation: **Explanation:** **Hepatitis E Virus (HEV)** is a non-enveloped, **single-stranded RNA virus** primarily transmitted via the fecal-oral route. It is a major cause of acute viral hepatitis worldwide, particularly in developing countries with poor sanitation. **Why Option D is correct:** The most characteristic clinical feature of HEV is its high virulence in pregnant women, especially during the **third trimester**. While the overall mortality rate for HEV is low (0.5–4%), it escalates dramatically to **15–25% in pregnancy**. This is attributed to a combination of altered immune responses (Th2 shift), high viral loads, and a predisposition to **Fulminant Hepatic Failure (FHF)** and Disseminated Intravascular Coagulation (DIC). **Why other options are incorrect:** * **Option A:** Hepatitis **D** (Delta virus) is the one that requires Hepatitis B (HBsAg) for its replication and infection. HEV is independent. * **Option B:** HEV is an **RNA virus** (Hepeviridae family). Hepatitis B is the only major hepatitis virus that is a DNA virus. * **Option C:** While HEV can occur in HIV patients (potentially leading to chronic hepatitis in immunocompromised states), there is no specific mandatory co-infection or epidemiological link like that seen between HBV/HCV and HIV. **High-Yield Pearls for NEET-PG:** * **Transmission:** Fecal-oral (similar to Hep A). * **Genotypes:** Genotypes 1 and 2 are human-restricted (epidemic); Genotypes 3 and 4 are zoonotic (pigs/boars) and can cause **chronic hepatitis** in transplant recipients. * **Diagnosis:** IgM anti-HEV is the gold standard for acute infection. * **Extra-hepatic manifestations:** Guillain-Barré syndrome and Neuralgic amyotrophy.
Question 410: Which of the following statements regarding HIV-associated TB is FALSE?
- A. Extrapulmonary TB is common among HIV-infected patients.
- B. The diagnosis of TB in HIV-infected patients may be difficult.
- C. Immune reconstitution inflammatory syndrome (IRIS) is more common among patients with advanced immunosuppression and extrapulmonary TB.
- D. Patients with both HIV infection and TB are more infectious than persons without HIV co-infection. (Correct Answer)
Explanation: ### Explanation **Why Option D is the Correct (False) Statement:** The infectivity of a TB patient depends primarily on the presence of cavitary lesions and the concentration of bacilli in the sputum. In HIV-infected patients, the immune response is often too weak to form cavitary lesions (which require a robust T-cell mediated response) [1]. Consequently, HIV-positive patients are **less likely to have cavitary disease** and often have lower sputum bacterial loads. Therefore, they are generally **less infectious** to others compared to HIV-negative individuals with classic cavitary pulmonary TB. **Analysis of Other Options:** * **Option A (True):** As CD4 counts decline, the risk of dissemination increases. Extrapulmonary TB (EPTB) and disseminated TB are significantly more common in HIV patients than in the general population [2]. * **Option B (True):** Diagnosis is challenging because HIV patients often present with atypical chest X-ray findings (lower lobe infiltrates, lack of cavities) and are more likely to have **sputum smear-negative** disease due to lower bacterial loads in the airways [1]. * **Option C (True):** IRIS occurs when the immune system recovers after starting ART and "over-reacts" to TB antigens. It is most frequent in patients with **CD4 counts <50 cells/µL** and those with disseminated or extrapulmonary involvement. **High-Yield Clinical Pearls for NEET-PG:** * **Most common opportunistic infection** in HIV patients in India: **Tuberculosis** [1]. * **Screening:** All HIV-positive patients should be screened for TB using the **WHO 4-symptom screen** (Cough, Fever, Night sweats, Weight loss). * **Diagnosis:** **NAAT (CBNAAT/GeneXpert)** is the preferred initial diagnostic test for TB in people living with HIV (PLHIV). * **Treatment Timing:** Start TB treatment first, followed by ART within **2 weeks** (regardless of CD4 count) to reduce mortality, except in TB meningitis where ART is delayed.
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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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