Infectious Diseases — MCQs
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What is the most common presentation of hepatitis A?
CMV retinitis in HIV occurs when the CD4 count falls below which value?
A 23-year-old female patient presents with a 2-month history of low-grade fever and moderate right-sided pleural effusion. Pleural fluid shows lymphocyte predominance with ADA levels of 120 IU/L. The patient is started on anti-tubercular therapy (WHO category 1). Two months later, the patient presents with progressive breathlessness, generalized body swelling, and raised JVP. Pleural fluid is now predominantly transudate. What is this patient likely to have developed?
A patient presented with fever, jaundice, and neurological symptoms during the rainy season. What is the most probable diagnosis?
A patient presents with fever of unknown origin (FUO). Empirical anti-tuberculosis treatment (ATT) was initiated, but the symptoms persisted after several weeks. How long should ATT be continued in the absence of a clinical response before discontinuation?
Which of the following tumors is not commonly associated with Acquired Immunodeficiency Syndrome (AIDS)?
Which of the following conditions is commonly referred to as "Breakbone fever"?
An untreated AIDS patient (CD4+ count of 180 cells/mm3) has developed progressively severe headache and mental confusion, along with ataxia and retinochoroiditis. Focal lesions are present on a computed tomography scan of his brain. No mucocutaneous lesions are found. His level of immunoglobulin G (IgG) to the infectious agent is high. What is the most likely explanation for how this current infection started?
A 38-year-old homeless man presents with 2 days of shortness of breath, chills, fever, drooling, painful swallowing, and a 'croupy' cough. Physical examination reveals bluish discoloration of the skin and a tough, gray membrane adhered to the pharynx. What is the underlying mechanism through which this disease affects normal cells?
Which of the following etiologic agents is the most common cause of infection in liver transplant patients?
Infectious Diseases Indian Medical PG Practice Questions and MCQs
Question 581: What is the most common presentation of hepatitis A?
- A. Asymptomatic
- B. Fulminant hepatitis
- C. Chronic carrier state
- D. Transient illness with jaundice (Correct Answer)
Explanation: Hepatitis A virus (HAV) is an RNA virus transmitted primarily via the fecal-oral route. The most common clinical presentation of Hepatitis A is a **self-limiting, transient illness with jaundice** [1]. While the severity is age-dependent (often asymptomatic in children <6 years), in the adolescent and adult populations typically seen in clinical practice, the classic presentation involves a prodromal phase (fever, malaise, nausea) followed by an icteric phase (jaundice, dark urine, and hepatomegaly) [1]. **Analysis of Options:** * **A. Asymptomatic:** While common in young children (up to 70%), it is not the "classic" or most common presentation in the general symptomatic population. * **B. Fulminant hepatitis:** This is a rare complication of HAV, occurring in less than 1% of cases. It is more common in patients with pre-existing chronic liver disease. * **C. Chronic carrier state:** **Hepatitis A never causes chronic infection.** Unlike Hepatitis B or C, HAV does not progress to a carrier state, chronic hepatitis, or cirrhosis. **High-Yield Clinical Pearls for NEET-PG:** * **Incubation Period:** 2–6 weeks (Average 28 days). * **Diagnosis:** Acute infection is confirmed by **Anti-HAV IgM** [1]. Anti-HAV IgG indicates past infection or vaccination and confers lifelong immunity [1]. * **Extrahepatic Manifestations:** Though rare, the most common is **evanescent rash and arthralgia**. * **Relapsing Hepatitis:** A unique feature of HAV where symptoms recur weeks after initial recovery; however, it still remains self-limiting. * **Vaccine:** Inactivated vaccines are part of the recommended schedule for high-risk groups [1].
Question 582: CMV retinitis in HIV occurs when the CD4 count falls below which value?
- A. 50 cells/microL (Correct Answer)
- B. 100 cells/microL
- C. 200 cells/microL
- D. 150 cells/microL
Explanation: **Explanation:** Cytomegalovirus (CMV) is a late-stage opportunistic infection in HIV patients. The correct answer is **50 cells/microL** because CMV retinitis typically manifests only when there is profound immunosuppression. **1. Why 50 cells/microL is correct:** CMV is a ubiquitous herpesvirus that remains latent in most individuals. In HIV-infected patients, clinical disease (reactivation) occurs almost exclusively when the CD4 T-cell count drops below **50 cells/microL**. CMV retinitis is the most common clinical manifestation, characterized by "pizza-pie" or "cottage cheese and ketchup" funduscopic appearance (hemorrhage and exudates). **2. Analysis of Incorrect Options:** * **200 cells/microL:** This is the threshold for defining AIDS and the level at which prophylaxis for *Pneumocystis jirovecii* pneumonia (PCP) is initiated. * **150 cells/microL:** This level is associated with an increased risk of fungal infections like *Histoplasmosis* (especially in endemic areas). * **100 cells/microL:** This is the critical threshold for *Toxoplasma gondii* encephalitis and *Cryptococcus neoformans* meningitis. **Clinical Pearls for NEET-PG:** * **Symptoms:** Patients often complain of floaters, blurred vision, or scotomas. It is usually unilateral but can become bilateral [1]. * **Diagnosis:** Primarily clinical via funduscopy. * **Treatment:** Intravenous **Ganciclovir** is the drug of choice. Valganciclovir, Foscarnet, and Cidofovir are alternatives. * **IRIS:** Starting ART in a patient with CMV retinitis can lead to Immune Reconstitution Inflammatory Syndrome (Immune Recovery Uveitis).
Question 583: A 23-year-old female patient presents with a 2-month history of low-grade fever and moderate right-sided pleural effusion. Pleural fluid shows lymphocyte predominance with ADA levels of 120 IU/L. The patient is started on anti-tubercular therapy (WHO category 1). Two months later, the patient presents with progressive breathlessness, generalized body swelling, and raised JVP. Pleural fluid is now predominantly transudate. What is this patient likely to have developed?
- A. Hypoproteinemia
- B. Drug-resistant TB
- C. Collagen vascular disease
- D. Constrictive pericarditis (Correct Answer)
Explanation: ### Explanation **1. Why Constrictive Pericarditis is the Correct Answer:** The patient initially presented with **Tuberculous Pleuritis** (low-grade fever, lymphocytic effusion, and high ADA >40 IU/L). Despite starting Anti-Tubercular Therapy (ATT), she developed progressive breathlessness, generalized edema, and raised JVP. These are classic signs of **Right Heart Failure**. In the context of tuberculosis, the most common cause of this progression is **Constrictive Pericarditis** [1]. Tuberculosis is the leading cause of constrictive pericarditis in developing countries. The inflammatory process can involve the pericardium, leading to fibrosis and calcification [1]. This restricts diastolic filling, causing elevated venous pressures (raised JVP, edema) and the development of **transudative** effusions (due to increased hydrostatic pressure), replacing the initial exudative tubercular effusion. **2. Why the Other Options are Incorrect:** * **A. Hypoproteinemia:** While TB can cause malnutrition, it would not typically present with a raised JVP. Raised JVP indicates a cardiac/obstructive etiology rather than simple osmotic loss. * **B. Drug-resistant TB:** If the patient had DR-TB, the pleural effusion would likely remain an exudate with high ADA and persistent constitutional symptoms (fever, weight loss), rather than shifting to a transudative profile with signs of heart failure. * **C. Collagen Vascular Disease:** While SLE or RA can cause pleuritis, the clinical sequence (initial high ADA followed by right heart failure) strongly points toward a complication of the primary infection (TB) rather than a new-onset autoimmune disease. **3. Clinical Pearls for NEET-PG:** * **ADA (Adenosine Deaminase):** Levels >40 IU/L in pleural fluid are highly suggestive of TB (Sensitivity >90%). * **Kussmaul’s Sign:** A paradoxical rise in JVP during inspiration, often seen in Constrictive Pericarditis. * **Pericardial Knock:** A high-pitched sound heard in early diastole, characteristic of constriction. * **Treatment:** Definitive management for Constrictive Pericarditis is **Pericardiectomy** [1]. Steroids are often used in TB pericarditis to reduce the risk of constriction, though their efficacy remains debated [1].
Question 584: A patient presented with fever, jaundice, and neurological symptoms during the rainy season. What is the most probable diagnosis?
- A. Leptospirosis (Correct Answer)
- B. Dengue fever
- C. Brucellosis
- D. Lyme disease
Explanation: The clinical triad of **fever, jaundice, and neurological symptoms** (often presenting as aseptic meningitis) occurring during the **rainy season** is a classic presentation of **Leptospirosis** [1]. This zoonotic disease, caused by the spirochete *Leptospira interrogans*, is typically transmitted through water contaminated with the urine of infected rodents [1]. The severe form, known as **Weil’s Disease**, is characterized by the triad of jaundice, renal failure, and hemorrhage. **Why the other options are incorrect:** * **Dengue Fever:** While common in the rainy season, it typically presents with severe retro-orbital pain, arthralgia ("breakbone fever"), and a characteristic rash. While jaundice can occur in severe cases (Dengue Hemorrhagic Fever), neurological symptoms are less common than in Leptospirosis [1]. * **Brucellosis:** This is usually a chronic or subacute illness associated with unpasteurized dairy or livestock exposure. It presents with "undulant fever" and hepatosplenomegaly, but the acute seasonal/rainy association is absent. * **Lyme Disease:** Caused by *Borrelia burgdorferi*, it is transmitted by Ixodes ticks. While it can cause neurological symptoms (Bell’s palsy, meningitis), it does not typically present with jaundice or a rainy-season surge in the same epidemiological pattern as Leptospirosis. **High-Yield NEET-PG Pearls:** * **Gold Standard Diagnosis:** Microscopic Agglutination Test (MAT) [1]. * **Drug of Choice:** Doxycycline (mild cases) or IV Penicillin G (severe cases). * **Prophylaxis:** Doxycycline 200 mg once weekly for high-risk exposure. * **Pathognomonic Sign:** Conjunctival suffusion (redness without inflammatory exudate) is a highly specific clinical clue.
Question 585: A patient presents with fever of unknown origin (FUO). Empirical anti-tuberculosis treatment (ATT) was initiated, but the symptoms persisted after several weeks. How long should ATT be continued in the absence of a clinical response before discontinuation?
- A. 4 weeks
- B. 6 weeks (Correct Answer)
- C. 8 weeks
- D. 10 weeks
Explanation: **Explanation:** In the diagnostic workup of Fever of Unknown Origin (FUO), empirical anti-tuberculosis treatment (ATT) is often initiated in TB-endemic regions like India when clinical suspicion is high but microbiological confirmation is lacking. Pyrexia of unknown origin (PUO) is defined as a temperature persistently above 38.0°C for more than 3 weeks, without diagnosis, despite initial investigation [1]. **Why 6 weeks is the correct answer:** According to standard clinical guidelines (including Harrison’s Principles of Internal Medicine), if a patient with FUO is started on empirical ATT, a clinical response (defervescence and improvement in constitutional symptoms) is typically expected within **2 to 4 weeks**. If there is no clinical improvement after **6 weeks**, it is highly unlikely that the fever is due to tuberculosis. At this point, ATT should be discontinued, and the clinician must re-evaluate the patient for other etiologies, such as lymphoma, collagen vascular diseases, or deep-seated fungal infections. **Analysis of Incorrect Options:** * **4 weeks:** While many patients respond by this time, 4 weeks is considered slightly premature to definitively rule out a response in slow-growing mycobacterial infections. * **8 weeks and 10 weeks:** Continuing ineffective treatment for 2 months or longer unnecessarily increases the risk of drug-induced liver injury (DILI) and delays the diagnosis of the actual underlying condition. **Clinical Pearls for NEET-PG:** * **Most common cause of FUO in India:** Infections (specifically Tuberculosis). * **Most common cause of FUO globally:** Infections, followed by Malignancy and Connective Tissue Disorders. * **Naproxen Challenge:** Historically used to differentiate infectious fever from neoplastic fever (malignancy-related fever often responds rapidly to Naproxen), though its specificity is debated. * **Key Rule:** Never start empirical ATT in FUO unless a thorough search for other causes has been exhausted, as it can mask other diagnoses or lead to unnecessary toxicity.
Question 586: Which of the following tumors is not commonly associated with Acquired Immunodeficiency Syndrome (AIDS)?
- A. Kaposi sarcoma
- B. Gastrointestinal adenocarcinoma
- C. Non-Hodgkin's lymphoma
- D. Astrocytoma (Correct Answer)
Explanation: The association between HIV/AIDS and specific malignancies is primarily driven by profound immunosuppression and the reactivation of oncogenic viruses. **1. Why Astrocytoma is the Correct Answer:** Astrocytomas are primary glial tumors of the central nervous system. Unlike Primary CNS Lymphoma [2], astrocytomas do **not** have an increased incidence in HIV-infected individuals compared to the general population. They are not considered AIDS-defining illnesses and do not share a pathophysiological link with viral reactivation or CD4+ T-cell depletion. **2. Analysis of Incorrect Options:** * **Kaposi Sarcoma (KS):** The most common AIDS-associated neoplasm [1]. It is caused by **Human Herpesvirus 8 (HHV-8)**. It typically presents as violaceous skin lesions but can involve viscera [1]. * **Non-Hodgkin’s Lymphoma (NHL):** AIDS patients have a significantly higher risk of aggressive B-cell lymphomas (e.g., Diffuse Large B-cell Lymphoma or Burkitt Lymphoma). These are often associated with **Epstein-Barr Virus (EBV)** [2]. * **Gastrointestinal Adenocarcinoma:** While not "AIDS-defining," patients with HIV have a higher age-adjusted risk for various non-AIDS-defining cancers (NADCs), including colorectal and gastric adenocarcinomas, due to chronic inflammation and lifestyle factors. However, compared to Astrocytoma, GI malignancies show a more documented epidemiological link in the HAART era [3]. **High-Yield Clinical Pearls for NEET-PG:** * **AIDS-Defining Malignancies:** Kaposi Sarcoma (HHV-8), Non-Hodgkin Lymphoma (EBV), and Invasive Cervical Carcinoma (HPV) [3]. * **Primary CNS Lymphoma:** Always suspect this in an AIDS patient with a ring-enhancing lesion on MRI that is **EBV DNA positive** in the CSF (Distinguish from Toxoplasmosis) [2]. * **CD4 Count Correlation:** KS can occur at higher CD4 counts, but NHL and CNS Lymphoma typically occur when **CD4 <100-50 cells/mm³**.
Question 587: Which of the following conditions is commonly referred to as "Breakbone fever"?
- A. Rheumatic fever
- B. Dengue fever (Correct Answer)
- C. Rat-bite fever
- D. Relapsing fever
Explanation: **Explanation:** **Dengue fever** is classically known as **"Breakbone fever"** because of the intense, debilitating muscle and joint pain (myalgia and arthralgia) that patients experience, which feels as though their bones are breaking. It is caused by the Dengue virus (DENV 1-4), a flavivirus transmitted primarily by the *Aedes aegypti* mosquito. [1] **Analysis of Options:** * **A. Rheumatic fever:** This is an autoimmune sequela of Group A Streptococcal pharyngitis. While it involves "migratory polyarthritis," it is characterized by the Jones criteria (e.g., carditis, chorea) rather than the "breakbone" sensation. * **C. Rat-bite fever:** Caused by *Streptobacillus moniliformis* or *Spirillum minus*, it presents with fever, rash, and joint pain following a rodent bite, but lacks the specific "breakbone" nomenclature. * **D. Relapsing fever:** Caused by *Borrelia* species (transmitted by lice or ticks), it is characterized by recurring febrile episodes due to antigenic variation, not primary bone/joint pain. **High-Yield Clinical Pearls for NEET-PG:** * **Vector:** *Aedes aegypti* (Daytime biter; breeds in stagnant clean water). * **Laboratory Findings:** Leukopenia and **Thrombocytopenia** are hallmark features. [1] * **Tourniquet Test:** A positive test (≥10 petechiae per square inch) indicates capillary fragility. [1] * **Saddleback Fever:** Dengue often presents with a biphasic fever pattern. * **Warning Signs:** Abdominal pain, persistent vomiting, mucosal bleed, and rapid drop in platelet count signify progression to severe dengue. [1]
Question 588: An untreated AIDS patient (CD4+ count of 180 cells/mm3) has developed progressively severe headache and mental confusion, along with ataxia and retinochoroiditis. Focal lesions are present on a computed tomography scan of his brain. No mucocutaneous lesions are found. His level of immunoglobulin G (IgG) to the infectious agent is high. What is the most likely explanation for how this current infection started?
- A. Earlier exposure to pigeons
- B. Earlier exposure to desert sand
- C. Reactivation of bradyzoites in cysts from an earlier infection (Correct Answer)
- D. Recent exposure to cat feces
Explanation: ### Explanation The clinical presentation of headache, confusion, ataxia, and focal brain lesions in an AIDS patient with a CD4+ count <200 cells/mm³ is highly suggestive of **CNS Toxoplasmosis**, caused by *Toxoplasma gondii*. The presence of **retinochoroiditis** and positive **IgG antibodies** further confirms this diagnosis [1]. **1. Why the Correct Answer is Right:** In immunocompromised patients, CNS Toxoplasmosis is almost always due to the **reactivation of a latent infection** rather than a primary (recent) acquisition. When the CD4+ count drops, dormant **bradyzoites** contained within tissue cysts (formed during a previous subclinical infection) transform back into rapidly dividing **tachyzoites**, causing tissue destruction and focal abscesses [1]. **2. Why the Other Options are Wrong:** * **Option A (Pigeons):** Exposure to pigeon droppings is associated with *Cryptococcus neoformans*. While it causes meningitis in AIDS, it typically presents with diffuse symptoms rather than focal CT lesions and retinochoroiditis. * **Option B (Desert Sand):** This refers to *Coccidioides immitis* (Valley Fever), which causes pulmonary disease or meningitis, primarily in the Southwestern US. * **Option D (Recent exposure to cat feces):** While *T. gondii* oocysts are shed in cat feces, primary infection in an AIDS patient is rare. The high IgG titer indicates a past infection, making reactivation the most likely mechanism. **3. NEET-PG High-Yield Pearls:** * **Imaging:** CT/MRI typically shows **multiple ring-enhancing lesions** with a predilection for the basal ganglia [1]. * **Treatment:** The drug of choice is **Pyrimethamine + Sulfadiazine** (plus Leucovorin to prevent bone marrow suppression) [1]. * **Prophylaxis:** Start **TMP-SMX** in HIV patients when CD4+ count is **<100 cells/mm³** and IgG is positive. * **Differential:** If a single lesion is present and does not respond to anti-toxoplasma therapy, suspect **Primary CNS Lymphoma** (associated with EBV) [1].
Question 589: A 38-year-old homeless man presents with 2 days of shortness of breath, chills, fever, drooling, painful swallowing, and a 'croupy' cough. Physical examination reveals bluish discoloration of the skin and a tough, gray membrane adhered to the pharynx. What is the underlying mechanism through which this disease affects normal cells?
- A. DNA synthesis is inhibited in the target cells.
- B. RNA synthesis is inhibited in the target cells.
- C. The process of protein synthesis is inhibited in the target cells. (Correct Answer)
- D. The plasma membrane becomes leaky in the target cells.
Explanation: ### Explanation The clinical presentation of a **tough, gray membrane** (pseudomembrane) adhered to the pharynx [2], coupled with drooling, "croupy" cough (stridor), and bluish discoloration (cyanosis), is a classic description of **Diphtheria**, caused by *Corynebacterium diphtheriae*. **1. Why the Correct Answer is Right:** The primary virulence factor of *C. diphtheriae* is the **Diphtheria toxin**, an A-B exotoxin. The 'B' subunit binds to the cell surface, while the 'A' (Active) subunit enters the cytosol. The A subunit catalyzes the **ADP-ribosylation of Elongation Factor-2 (EF-2)** [1]. EF-2 is essential for the translocation step of polypeptide chain elongation during translation. By inactivating EF-2, the toxin completely **inhibits protein synthesis**, leading to cell death and the formation of the characteristic necrotic pseudomembrane [1]. **2. Why Incorrect Options are Wrong:** * **Option A & B:** While some toxins or drugs interfere with nucleic acid synthesis (e.g., Quinolones or Rifampin), the Diphtheria toxin specifically targets the translation machinery (ribosomes/EF-2), not transcription or DNA replication. * **Option D:** Toxins that make the plasma membrane "leaky" are typically pore-forming toxins (e.g., *Staphylococcus aureus* alpha-toxin or *Clostridium perfringens* lecithinase). This is not the mechanism of *C. diphtheriae*. **3. NEET-PG High-Yield Pearls:** * **Diagnosis:** Culture on **Löffler’s serum slope** or **Potassium Tellurite agar** (black colonies). * **Virulence Testing:** **Elek’s gel precipitation test** detects the production of the exotoxin. * **Complications:** The toxin has an affinity for the heart and nerves, leading to **Myocarditis** (most common cause of death) and **Polyneuritis** (e.g., palatal paralysis). * **Morphology:** Gram-positive bacilli with club-shaped ends, often arranged in "Chinese letter" patterns (cuneiform). They contain **metachromatic granules** (Volutin/Babes-Ernst granules) which stain with Albert’s stain.
Question 590: Which of the following etiologic agents is the most common cause of infection in liver transplant patients?
- A. Candida
- B. Cytomegalovirus (Correct Answer)
- C. Herpes simplex virus
- D. Pneumocystis jirovecii pneumonia
Explanation: **Explanation:** **Cytomegalovirus (CMV)** is the most common clinically significant viral pathogen in solid organ transplant (SOT) recipients, particularly liver transplant patients [2]. The risk is highest between **1 to 6 months post-transplant**, coinciding with peak immunosuppression [2]. CMV infection in liver transplant patients often manifests as "CMV syndrome" (fever, malaise, leukopenia) or tissue-invasive disease, most commonly causing **hepatitis** in the allograft. **Analysis of Options:** * **A. Candida:** While fungal infections are common in the early post-operative period (first 30 days) due to surgical complications or indwelling catheters, they are less frequent overall than CMV [2]. * **C. Herpes simplex virus (HSV):** HSV is common but usually presents as mucocutaneous lesions [1]. Due to the routine use of viral prophylaxis (like Acyclovir or Valganciclovir), its incidence is significantly lower than CMV [1], [2]. * **D. Pneumocystis jirovecii (PJP):** PJP is a potential opportunistic fungal infection; however, its incidence has drastically reduced due to the standard use of **Trimethoprim-Sulfamethoxazole (TMP-SMX)** prophylaxis [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Timeline of Infection:** * *<1 month:* Bacterial and Candidal infections (nosocomial/surgical) [2]. * *1–6 months:* Opportunistic infections (CMV, HBV, HCV, PJP, Toxoplasmosis) [2]. * *>6 months:* Community-acquired infections [2]. * **Risk Factor:** The highest risk for CMV is a **Seronegative Recipient (R-) receiving an organ from a Seropositive Donor (D+)** [1]. * **Diagnosis:** Quantitative PCR for CMV DNA is the gold standard [2]. * **Treatment:** Intravenous **Ganciclovir** or oral Valganciclovir [1], [2].
Practice by Chapter
Principles of Antimicrobial Therapy
Practice Questions
Fever of Unknown Origin
Practice Questions
HIV/AIDS and Related Infections
Practice Questions
Tuberculosis and Mycobacterial Diseases
Practice Questions
Tropical and Parasitic Infections
Practice Questions
Viral Infections (Hepatitis, Herpes, etc.)
Practice Questions
Healthcare-Associated Infections
Practice Questions
Fungal Infections
Practice Questions
Sepsis and Septic Shock
Practice Questions
Infection in Immunocompromised Hosts
Practice Questions
Emerging and Re-emerging Infections
Practice Questions
Antimicrobial Resistance
Practice Questions
Vaccination Principles
Practice Questions
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