Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 541: Which infectious disease among the following most closely resembles vasculitis?

A. Lyme disease (Correct Answer)
B. Rubella
C. Tuberculosis
D. Leprosy

Explanation: **Explanation:** **Lyme Disease (Option A)** is the correct answer because its clinical presentation often mimics systemic vasculitis. The causative agent, *Borrelia burgdorferi*, can trigger inflammatory responses in the blood vessels, leading to a "pseudovasculitis" picture. Pathologically, it can cause an obliterative vasculitis or perivascular lymphocytic infiltration. Clinically, the multi-system involvement—including migratory arthralgia, cranial nerve palsies (especially Bell’s palsy), and cardiac conduction blocks—closely mirrors the multisystemic nature of small-vessel vasculitis [1], [2]. **Why other options are incorrect:** * **Rubella (Option B):** Typically presents as a self-limiting viral exanthema with post-auricular lymphadenopathy. While it can cause arthritis, it does not mimic the chronic, multi-organ inflammatory damage seen in vasculitis. * **Tuberculosis (Option C):** While TB can cause "Poncet’s disease" (reactive arthritis), it is primarily a granulomatous infection. It is more likely to be a differential for malignancy or sarcoidosis rather than primary vasculitis. * **Leprosy (Option D):** Although Type 2 Lepra reaction (Erythema Nodosum Leprosum) involves vasculitis of the dermal vessels, the primary disease itself is characterized by peripheral nerve thickening and anesthetic skin patches, which are distinct from the systemic presentation of vasculitis. **High-Yield Clinical Pearls for NEET-PG:** * **Lyme Disease Triad:** Erythema chronicum migrans (Bull’s eye rash), bilateral facial nerve palsy, and AV nodal block [1]. * **The "Great Mimickers":** Syphilis, TB, and Lyme disease are often termed "great imitators" because they can present like various autoimmune and inflammatory conditions. * **Treatment of choice:** Doxycycline is the first-line treatment for early Lyme disease; IV Ceftriaxone is used for neurological or cardiac manifestations. * **Differential Diagnosis:** Systemic vasculitis should be considered in any patient involving fever and multi-system involvement in multiple organ systems [2].

Question 542: What is the most common opportunistic infection in patients with AIDS?

A. Cryptococcosis
B. Tuberculosis
C. Candidiasis (Correct Answer)
D. Aspergillosis

Explanation: **Explanation:** **Candidiasis (Option C)** is the correct answer because it is the most common opportunistic infection (OI) overall in patients with HIV/AIDS [1]. Specifically, **Oropharyngeal Candidiasis (Oral Thrush)** is the most frequent initial opportunistic fungal infection, often occurring when CD4 counts drop below 200-500 cells/mm³ [1]. While Esophageal Candidiasis is an AIDS-defining illness, the mucosal (oral) form remains the most prevalent clinical manifestation across the spectrum of the disease [2]. **Analysis of Incorrect Options:** * **Tuberculosis (Option B):** While TB is the most common **cause of death** in AIDS patients globally and the most common OI in the **Indian subcontinent**, it is not the most common infection overall worldwide. * **Cryptococcosis (Option A):** This is the most common **fungal meningitis** in AIDS patients (typically seen when CD4 <100 cells/mm³), but its incidence is lower than Candidiasis. * **Aspergillosis (Option D):** This is relatively uncommon in AIDS patients compared to other OIs; it usually occurs only in the setting of profound neutropenia or very advanced immunosuppression. **High-Yield Clinical Pearls for NEET-PG:** * **Most common OI overall:** Candidiasis [1]. * **Most common OI in India:** Tuberculosis. * **Most common life-threatening OI (USA/Global):** *Pneumocystis jirovecii* pneumonia (PCP) [1]. * **Most common CNS mass lesion:** Toxoplasmosis. * **Most common cause of blindness:** CMV Retinitis (CD4 <50 cells/mm³). * **Oral Thrush vs. Leukoplakia:** Unlike Oral Hairy Leukoplakia (caused by EBV), Candidial plaques **can** be scraped off, leaving an erythematous base.

Question 543: What is the treatment of choice for Pneumocystis jirovecii pneumonia?

A. Trimethoprim/sulfamethoxazole (Correct Answer)
B. Erythromycin
C. Ofloxacin
D. Tetracycline

Explanation: **Explanation:** **Pneumocystis jirovecii pneumonia (PCP)** is a life-threatening opportunistic fungal infection primarily seen in immunocompromised patients, particularly those with HIV/AIDS (typically when CD4 counts fall below 200 cells/mm³). **1. Why Trimethoprim/sulfamethoxazole (TMP-SMX) is the Correct Choice:** TMP-SMX (Co-trimoxazole) is the **first-line treatment and prophylaxis** for PCP [1]. It works by inhibiting two consecutive steps in the fungal folic acid synthesis pathway. For moderate-to-severe infections, it is administered intravenously; for mild cases, oral administration is sufficient. In patients with severe hypoxia (PaO₂ <70 mmHg or A-a gradient >35 mmHg), **adjunctive corticosteroids** must be added to reduce the inflammatory response triggered by dying organisms [1]. **2. Why Other Options are Incorrect:** * **B. Erythromycin:** A macrolide antibiotic used for atypical pneumonias (like *Legionella* or *Mycoplasma*). It has no activity against *P. jirovecii*. * **C. Ofloxacin:** A fluoroquinolone used for bacterial infections (UTIs, respiratory infections). It is ineffective against fungal pathogens. * **D. Tetracycline:** Primarily used for Rickettsial infections or *Chlamydia*. It does not cover *P. jirovecii*. **High-Yield Clinical Pearls for NEET-PG:** * **Radiology:** Classic "bat-wing" appearance or bilateral perihilar ground-glass opacities on CXR/HRCT [1]. * **Diagnosis:** Definitive diagnosis requires visualization of cysts via **Gomori Methenamine Silver (GMS)** stain or Giemsa stain from induced sputum or Bronchoalveolar Lavage (BAL) [1]. * **Alternative Treatment:** If the patient is allergic to sulfa drugs, the second-line treatment is **Primaquine plus Clindamycin** or **Pentamidine**. * **Marker:** Elevated **Serum Beta-D-Glucan** is a highly sensitive (though non-specific) marker for PCP.

Question 544: Opisthotonus is typically seen in which of the following conditions?

A. Tetanus (Correct Answer)
B. Anthrax
C. Tetany
D. Rabies

Explanation: **Explanation:** **Opisthotonus** is a state of severe hyperextension and spasticity in which an individual's head, neck, and spinal column enter into a complete "bridging" or arching position. **1. Why Tetanus is Correct:** Tetanus is caused by the toxin **tetanospasmin** produced by *Clostridium tetani* [2]. This toxin travels retrograde to the CNS and inhibits the release of inhibitory neurotransmitters (**GABA and Glycine**) from Renshaw cells. The loss of inhibition leads to unchecked muscular spasms. Opisthotonus occurs because the extensor muscles of the back are more powerful than the flexors, causing the characteristic backward arching during a generalized spasm. **2. Why Other Options are Incorrect:** * **Anthrax:** Caused by *Bacillus anthracis*, it typically presents as cutaneous eschars, hemorrhagic mediastinitis (inhalation), or GI distress, but does not cause generalized muscle arching. * **Tetany:** Caused by hypocalcemia, it presents with carpopedal spasm (Trousseau’s sign) and facial twitching (Chvostek’s sign), but not the full-body opisthotonic posturing seen in tetanus [3]. * **Rabies:** Characterized by hydrophobia, aerophobia, and localized spasms of the pharyngeal muscles (furious rabies) or ascending paralysis (dumb rabies), but not classic opisthotonus. **Clinical Pearls for NEET-PG:** * **Risus Sardonicus:** The "sardonic smile" caused by spasms of the facial muscles. * **Trismus (Lockjaw):** Usually the first clinical sign of tetanus. * **Management:** Neutralize unbound toxin with **Human Tetanus Immune Globulin (HTIG)** and use **Metronidazole** (preferred over Penicillin G as Penicillin is a GABA antagonist). * **Differential:** Opisthotonus can also be seen in **strychnine poisoning** [1], **phenothiazine toxicity** (extrapyramidal side effects), and **kernicterus**.

Question 545: Dengue fever is characterized by all except?

A. Rash
B. Fever
C. Thrombocytopenia
D. Increased clotting time (Correct Answer)

Explanation: Dengue fever, caused by the Flavivirus and transmitted by the Aedes aegypti mosquito, is characterized by a triad of high-grade fever, severe body aches, and hematological changes. In Dengue, the coagulation profile typically shows a prolonged Prothrombin Time (PT) and Activated Partial Thromboplastin Time (aPTT) due to hepatic dysfunction and consumption of clotting factors. However, Clotting Time (CT)—which measures the intrinsic pathway—is generally not a diagnostic hallmark or a consistent finding in Dengue. Bleeding manifestations in Dengue are primarily driven by thrombocytopenia and vascular leakage rather than a primary defect in the clotting time. * Fever: Characteristically "saddle-back" (biphasic) and high-grade [1]. It is the most common presenting symptom. * Rash: Typically appears as a "white islands in a sea of red" (maculopapular) rash during the recovery phase [1]. * Thrombocytopenia: A hallmark of Dengue (especially DHF). It results from bone marrow suppression and immune-mediated destruction of platelets. * Vector: Aedes aegypti (Day biter, breeds in clean stagnant water). * Tourniquet Test: Positive if >10-20 petechiae per square inch; used as a screening tool for capillary fragility [1]. * Gold Standard Diagnosis: PCR (Days 1-5) or NS1 Antigen (Days 1-7). IgM ELISA is used after day 5. * Critical Phase: Occurs during defervescence (when fever drops); this is when plasma leakage and shock (Dengue Shock Syndrome) are most likely to occur [1]. * Lab Findings: Leukopenia (common early finding), increased hematocrit (indicates plasma leakage), and elevated AST/ALT.

Question 546: Which of the following medications used to treat severe cerebral malaria can cause hypoglycemia?

A. Quinine (Correct Answer)
B. Chloroquine
C. Halofantrine
D. Mefloquine

Explanation: Explanation: 1. Why Quinine is Correct: Quinine is a potent stimulator of the pancreatic beta cells, leading to the hypersecretion of insulin (hyperinsulinemia). This often results in profound hypoglycemia, which is a common and serious side effect, especially in pregnant patients and those with severe malaria [1]. In the context of cerebral malaria, this is particularly dangerous as hypoglycemia can mimic or worsen the neurological symptoms of the disease (e.g., altered consciousness, seizures). 2. Why the Other Options are Incorrect: * Chloroquine: While it can occasionally cause gastrointestinal upset or pruritus, it does not stimulate insulin release [1]. Its primary toxicity concerns are cardiovascular (arrhythmias) and retinal (with chronic use). * Halofantrine: The major concern with Halofantrine is cardiotoxicity, specifically QT interval prolongation, which can lead to fatal arrhythmias. It does not affect blood glucose levels. * Mefloquine: This drug is primarily associated with neuropsychiatric side effects, such as vivid dreams, anxiety, psychosis, and dizziness. It is not linked to hypoglycemia. High-Yield Clinical Pearls for NEET-PG: * The "Double Whammy": In severe malaria, hypoglycemia can be caused by both the parasite (consuming host glucose) and the treatment (Quinine-induced insulin release) [1]. * Monitoring: Always monitor blood glucose levels frequently in patients receiving IV Quinine [1]. * Drug of Choice: While Quinine was the traditional choice, Artesunate is now the preferred first-line treatment for severe malaria due to its superior efficacy and better safety profile (less hypoglycemia). * Cinchonism: Remember the classic triad of Quinine toxicity: Tinnitus, headache, and nausea.

Question 547: Hepatitis B infection is most commonly associated with which of the following conditions?

A. Polyarteritis nodosa
B. Systemic lupus erythematosus
C. Serum sickness (Correct Answer)
D. Polymyositis

Explanation: The correct answer is **Serum sickness (Option C)**. This refers to the **prodromal, pre-icteric phase** of acute Hepatitis B virus (HBV) infection [1]. **Why Serum Sickness is Correct:** In the early stages of HBV infection, there is an excess of circulating Hepatitis B surface antigen (HBsAg) [1]. This leads to the formation of **Type III hypersensitivity immune complexes** (antigen-antibody complexes) that deposit in small vessels and joints. This manifests as a "serum sickness-like syndrome," characterized by the triad of **fever, skin rash (usually urticarial), and polyarthritis/arthralgia**. It typically resolves once jaundice appears [1]. **Analysis of Incorrect Options:** * **A. Polyarteritis nodosa (PAN):** While PAN is famously associated with HBV (10–30% of PAN cases are HBV-positive), it is a **late complication** or a chronic extrahepatic manifestation. In the context of "most common" early association or general prodromal presentation, serum sickness-like syndrome occurs more frequently during the acute phase. * **B. Systemic lupus erythematosus (SLE):** SLE is an autoimmune connective tissue disease with no direct causal link to HBV. In fact, chronic viral infections are sometimes studied as triggers for autoimmunity, but HBV is not a primary association for SLE. * **C. Polymyositis:** This is an inflammatory myopathy. While viral triggers are hypothesized, there is no established clinical association between HBV and polymyositis. **NEET-PG High-Yield Pearls:** * **Extrahepatic manifestations of HBV:** Serum sickness (most common prodrome), Polyarteritis Nodosa (PAN), and Membranous Glomerulonephritis (MGN). * **Hepatitis C associations:** Essential Mixed Cryoglobulinemia, Membranoproliferative Glomerulonephritis (MPGN), Porphyria Cutanea Tarda, and Lichen Planus. * **The "Gianotti-Crosti syndrome"** is a specific papular acrodermatitis of childhood associated with HBV.

Question 548: Primary atypical pneumonia is caused by all of the following organisms, EXCEPT:

A. Coxiella burnetii
B. Influenza
C. Measles
D. Mumps virus (Correct Answer)

Explanation: **Explanation:** Primary atypical pneumonia refers to a pulmonary infection where the clinical presentation differs from typical lobar pneumonia (e.g., *S. pneumoniae*). It is characterized by an insidious onset, non-productive cough, constitutional symptoms (headache, malaise), and a chest X-ray that shows diffuse interstitial infiltrates, often appearing "worse" than the patient's clinical state suggests. **Why Mumps virus is the correct answer:** While many viruses cause respiratory infections, the **Mumps virus** primarily targets the parotid glands and lymphoid tissue. It is **not** a recognized cause of primary atypical pneumonia. Its classic complications include orchitis, oophoritis, meningitis, and pancreatitis, but not interstitial lung disease. **Analysis of incorrect options:** * **Coxiella burnetii:** This is the causative agent of **Q fever**. It is a well-known cause of atypical pneumonia, often associated with exposure to livestock (cattle, sheep, goats). * **Influenza:** Influenza viruses (A and B) are common causes of viral atypical pneumonia, especially during seasonal outbreaks [1]. They can cause direct viral pneumonitis or predispose patients to secondary bacterial infections [1]. * **Measles:** The Measles virus can cause severe interstitial pneumonia (Hecht’s giant cell pneumonia), particularly in immunocompromised individuals or malnourished children. **NEET-PG High-Yield Pearls:** 1. **Most common cause:** *Mycoplasma pneumoniae* is the #1 cause of atypical pneumonia (associated with cold agglutinins and bullous myringitis). 2. **Legionella:** Often associated with hyponatremia, diarrhea, and exposure to contaminated water/AC systems [1]. 3. **Psittacosis (*C. psittaci*):** Look for a history of contact with birds/parrots and Horder’s spots. 4. **Radiology:** Atypical pneumonias typically show "reticulonodular" or "interstitial" patterns rather than consolidation.

Question 549: Which of the following is a FALSE statement regarding Pyrexia of Unknown Origin (PUO)?

A. Cause unknown despite more than 3 days of hospitalization
B. Cause unknown even after 3 outpatient department (OPD) visits
C. Fever persisting after 1 month of regular treatment (Correct Answer)
D. Usually, fever more than 38.3 degrees Celsius

Explanation: ### Explanation The concept of **Pyrexia of Unknown Origin (PUO)** was originally defined by Petersdorf and Beeson in 1961. The diagnosis is based on specific temporal and clinical criteria rather than the failure of "regular treatment." [1] **Why Option C is the Correct (False) Statement:** The definition of PUO does not include a criterion regarding "1 month of regular treatment." Instead, the classic definition requires the fever to persist for **more than 3 weeks**. [1] The term "regular treatment" is medically vague; PUO is defined by the inability to reach a diagnosis despite standardized investigations, not by the failure of empirical therapy. **Analysis of Other Options:** * **Option D (Fever >38.3°C):** This is a core requirement. The fever must be documented on several occasions as being higher than 38.3°C (101°F) to rule out normal physiological variations or low-grade thermoregulatory issues. [1] * **Options A & B (Investigation Threshold):** Modern definitions (Durack and Street) updated the "3 weeks" criteria to include a requirement for intensive investigation. This is defined as failure to reach a diagnosis after **3 days of in-hospital investigation** (Option A) or **3 outpatient visits** (Option B). [1] **High-Yield Clinical Pearls for NEET-PG:** 1. **Categories of PUO:** There are four distinct types: Classic, Nosocomial, Neutropenic, and HIV-associated. [1] 2. **Most Common Causes:** In developing countries like India, **Infections** (specifically Extrapulmonary Tuberculosis) remain the leading cause. In developed nations, **Malignancies** (Lymphoma) and **Non-infectious Inflammatory Diseases** (Still’s disease, Temporal Arteritis) are more frequent. 3. **Factitious Fever:** Always consider this in patients with a medical background who have a high temperature but no tachycardia or sweating. [2] 4. **NAPDH:** A useful mnemonic for causes—Neoplasm, Autoimmune, Parasitic/Infection, Drug fever, and Hematological.

Question 550: Which of the following hepatitis infections has the worst prognosis?

A. Hepatitis B Virus (HBV) Infection
B. Hepatitis D Virus (HDV) Infection
C. Hepatitis B Virus (HBV) and Hepatitis D Virus (HDV) Coinfection
D. Hepatitis D Virus (HDV) Superinfection on Hepatitis B Virus (HBV) Infection (Correct Answer)

Explanation: ### Explanation The correct answer is **Hepatitis D Virus (HDV) Superinfection on Hepatitis B Virus (HBV) Infection**. #### 1. Why Option D is Correct Hepatitis D is a defective RNA virus that requires the presence of Hepatitis B Surface Antigen (HBsAg) to replicate. **Superinfection** occurs when a chronic HBV carrier is subsequently infected with HDV. This carries the worst prognosis because: * It leads to **chronic HDV infection in >80% of cases**. * It causes rapid progression to **cirrhosis** (often within 5–10 years) and a significantly higher risk of **Hepatocellular Carcinoma (HCC)** compared to HBV monoinfection. * It often presents as an acute exacerbation of chronic hepatitis, frequently leading to liver failure. #### 2. Why Other Options are Incorrect * **Option A (HBV):** While HBV can cause chronic disease, its progression is generally slower than HDV-related disease. Full recovery occurs in 90-95% of adults following acute HBV infection, though chronic infection occurs in the remainder [1]. * **Option B (HDV alone):** HDV cannot exist or cause infection without the presence of HBV; it is an obligate satellite virus. * **Option C (Coinfection):** This occurs when a person acquires HBV and HDV simultaneously. While it can cause severe acute hepatitis (including fulminant failure), it leads to chronic infection in **<5% of cases**. Most patients recover completely, giving it a better long-term prognosis than superinfection. #### 3. High-Yield Clinical Pearls for NEET-PG * **Marker of HDV Replication:** HDV-RNA is the most sensitive marker; HDAg is transient. * **Serological Distinction:** * **Coinfection:** Anti-HBc **IgM** positive. * **Superinfection:** Anti-HBc **IgG** positive (indicating pre-existing chronic HBV) and HBsAg positive. * **Treatment:** Pegylated Interferon-alpha is the mainstay (though efficacy is limited) [1]. * **Prevention:** The HBV vaccine automatically protects against HDV (since HDV cannot infect without HBV).

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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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