Infectious Diseases — MCQs

Question 331: Which of the following infections does NOT typically cause acute hepatic and renal failure?

• A. Shigellosis (Correct Answer)
• B. Leptospirosis
• C. Malaria
• D. Hantavirus

Explanation: ### Explanation The combination of acute hepatic and renal failure is a classic presentation of several tropical and zoonotic infections. To identify the correct answer, one must recognize which pathogen primarily targets the gastrointestinal tract rather than systemic multi-organ systems. **1. Why Shigellosis is the correct answer:** Shigellosis is primarily an invasive **bacterial enteritis** caused by *Shigella* species. While it can cause severe complications like **Hemolytic Uremic Syndrome (HUS)**—leading to acute renal failure—it does **not** typically cause acute hepatic failure or significant jaundice. Its systemic manifestations are usually limited to neurotoxicity (seizures) or reactive arthritis. **2. Why the other options are incorrect:** * **Leptospirosis:** Specifically **Weil’s Disease**, is the classic cause of the "hepatorenal syndrome" triad: jaundice, hemorrhage, and acute kidney injury (AKI) [1]. After a brief bacteraemia, invading organisms are distributed throughout the body, mainly in kidneys, liver, meninges and brain [1]. * **Malaria:** Severe *Plasmodium falciparum* infection can lead to **"Bilious Remittent Fever,"** characterized by significant jaundice (hepatic involvement) and "Blackwater Fever" (hemoglobinuria leading to AKI). * **Hantavirus:** Specifically the **Hemorrhagic Fever with Renal Syndrome (HFRS)**, causes systemic vascular leak, acute interstitial nephritis, and can involve the liver, leading to elevated transaminases and multi-organ dysfunction. ### NEET-PG High-Yield Pearls * **Weil’s Disease Triad:** Jaundice + Renal Failure + Hemorrhage (often subconjunctival) [1]. * **Yellow Fever:** Another major differential for hepatorenal failure (Councilman bodies in the liver). * **Shigella & HUS:** *Shigella dysenteriae* type 1 produces Shiga toxin, which is a high-yield cause of HUS (Microangiopathic hemolytic anemia + Thrombocytopenia + Renal failure). * **Dengue:** While it causes hepatitis, renal failure is usually a late complication of shock (Dengue Shock Syndrome).

Question 332: A person presents with difficulty of breathing and a CD-4 count of 200. What is the most probable diagnosis?

• A. Tuberculosis
• B. Histoplasmosis
• C. Candidiasis
• D. Pneumocystis pneumonia (Correct Answer)

Explanation: **Explanation:** The clinical presentation of dyspnea in an immunocompromised patient with a **CD4 count of 200 cells/mm³** strongly points toward **Pneumocystis pneumonia (PCP)**, caused by *Pneumocystis jirovecii*. **Why Pneumocystis pneumonia is correct:** PCP is the most common opportunistic infection in patients with HIV when the CD4 count falls below **200 cells/mm³** [1]. It typically presents with a subacute onset of progressive dyspnea, non-productive cough, and low-grade fever. A hallmark feature is **exertional desaturation** (hypoxia out of proportion to radiologic findings). **Analysis of Incorrect Options:** * **Tuberculosis (A):** While common in HIV, TB can occur at **any CD4 count**. However, at CD4 >200, it usually presents with typical cavitary lesions. PCP is the more "classic" association specifically at the 200 threshold [1]. * **Histoplasmosis (B):** This fungal infection usually occurs when the CD4 count drops below **150 cells/mm³**. It often presents with systemic features like hepatosplenomegaly or lymphadenopathy. * **Candidiasis (C):** Mucocutaneous candidiasis (thrush) occurs at CD4 <250, but **Esophageal Candidiasis** (an AIDS-defining illness) typically occurs at CD4 <100. It presents with odynophagia rather than primary respiratory distress. **High-Yield Clinical Pearls for NEET-PG:** * **Investigation of Choice:** Induced sputum or Bronchoalveolar Lavage (BAL) with **Gomori Methenamine Silver (GMS)** stain showing "crushed ping-pong ball" cysts [1]. * **Radiology:** Characterized by bilateral perihilar **"ground-glass opacities."** * **Treatment:** High-dose **Trimethoprim-Sulfamethoxazole (TMP-SMX)** [1]. * **Steroid Indication:** Add corticosteroids if $PaO_2 < 70$ mmHg or A-a gradient $> 35$ mmHg to prevent inflammatory worsening [1]. * **Prophylaxis:** Started when CD4 count is **< 200 cells/mm³**.

Question 333: Following extraction of an upper central incisor, a patient develops ophthalmoplegia, meningitis, and lateral rectus paralysis. What is the most likely diagnosis?

• A. Cavernous sinus thrombosis (Correct Answer)
• B. Not related
• C. Cellulitis
• D. Ludwig's angina

Explanation: ### Explanation **Correct Answer: A. Cavernous Sinus Thrombosis (CST)** The clinical presentation of **ophthalmoplegia** (paralysis of ocular muscles), **meningitis**, and **lateral rectus paralysis** following a dental procedure in the upper jaw is classic for Cavernous Sinus Thrombosis. **Pathophysiology:** The cavernous sinus is a large venous plexus located on either side of the sella turcica. It receives venous drainage from the face and upper teeth via the **superior and inferior ophthalmic veins** and the **pterygoid plexus**. Because these veins are **valveless**, infections from the "danger area of the face" or maxillary teeth can spread retrogradely into the sinus. **Clinical Correlation:** * **Lateral Rectus Paralysis:** The **Abducens nerve (CN VI)** runs centrally through the cavernous sinus (unlike CN III and IV, which are in the lateral wall), making it the first nerve typically affected. * **Ophthalmoplegia:** Involvement of CN III and IV leads to total internal/external ophthalmoplegia. * **Meningitis:** Since the cavernous sinus is in close proximity to the meninges, septic thrombosis frequently leads to CNS spread. **Why Other Options are Incorrect:** * **B. Not related:** Incorrect, as there is a direct anatomical pathway between the maxillary dentition and the cavernous sinus. * **C. Cellulitis:** While facial cellulitis can precede CST, it does not explain intracranial complications like meningitis or specific cranial nerve palsies. * **D. Ludwig’s Angina:** This is a rapidly spreading cellulitis of the **submandibular, submental, and sublingual spaces**. It typically follows infections of the **lower molars** and presents with "woody" edema of the neck and airway obstruction, not ophthalmoplegia. **NEET-PG High-Yield Pearls:** * **Most common causative organism:** *Staphylococcus aureus* (~70%). * **Earliest Sign:** Usually a headache or deep facial pain (CN V1/V2 involvement). * **Most sensitive imaging:** MRI with MR venogram (MRV). * **Danger Area of Face:** Bound by the nasolabial folds, the upper lip, and the bridge of the nose.

Question 334: All are risk factors for antituberculosis treatment related hepatotoxicity, EXCEPT?

• A. CYP2E1 status
• B. HLA haplotype associations
• C. Female gender
• D. HBeAg negative hepatitis B (Correct Answer)

Explanation: Antituberculosis therapy (ATT)-induced hepatotoxicity is a common and potentially serious adverse effect, primarily associated with Isoniazid (INH), Rifampicin, and Pyrazinamide. [1] **Why HBeAg negative hepatitis B is the correct answer:** While chronic viral hepatitis (HBV and HCV) is a well-established risk factor for ATT-induced liver injury, the risk is specifically associated with **chronic carriers** or those with **active viral replication**. HBeAg (Hepatitis B e-antigen) is a marker of high viral replication and infectivity. Being "HBeAg negative" typically implies a lower viral load and lower replication state (unless it is a precore mutant), making it a less significant risk factor compared to active hepatitis or other systemic factors. [2] **Analysis of Incorrect Options:** * **CYP2E1 status:** Polymorphisms in the Cytochrome P450 2E1 gene (especially the c1/c1 genotype) are linked to increased production of hepatotoxic metabolites of INH, significantly increasing risk. * **HLA haplotype associations:** Genetic predisposition plays a major role. Specific HLA alleles (e.g., HLA-B*52, HLA-DQA1*0102, and HLA-DQB1*0502) have been strongly associated with an increased susceptibility to ATT-induced hepatotoxicity. * **Female gender:** Epidemiological studies consistently show that females are at a higher risk for developing drug-induced liver injury (DILI) from ATT compared to males. **High-Yield Clinical Pearls for NEET-PG:** * **Most hepatotoxic drug:** Pyrazinamide (PZA) > Isoniazid (INH) > Rifampicin (RIF). * **Other Risk Factors:** Age >35 years, malnutrition (low albumin), chronic alcohol consumption, and "Slow Acetylator" status (NAT2 polymorphism). * **Management Rule:** Discontinue ATT if Serum Bilirubin >1.5 mg/dL or if Transaminases are >3 times the upper limit of normal (with symptoms) or >5 times (if asymptomatic). [1]

Question 335: What is the most common hematologic finding associated with pulmonary tuberculosis?

• A. Mild anemia, leukocytosis, thrombocytosis with slightly elevated ESR (Correct Answer)
• B. Mild anemia, leukopenia, thrombocytopenia with marked elevation in ESR
• C. Mild anemia, Leukocytosis, Thrombocytopenia with marked elevation in ESR
• D. Mild anemia leukocytosis, thrombocytosis with normal ESR

Explanation: Pulmonary Tuberculosis (PTB) is a chronic granulomatous infection that triggers a systemic inflammatory response, leading to characteristic hematologic alterations. [1] **1. Why Option A is Correct:** * **Anemia:** The most common finding is **Anemia of Chronic Disease** (normocytic, normochromic), occurring in about 60-90% of patients due to iron sequestration by macrophages. [2] * **Leukocytosis:** A mild to moderate increase in the white cell count (neutrophilia or monocytosis) is typical as the body mounts an immune response against *M. tuberculosis*. [1][3] * **Thrombocytosis:** Platelet counts often rise as an **acute-phase reactant** stimulated by IL-6 and other inflammatory cytokines. [1] * **Elevated ESR:** The Erythrocyte Sedimentation Rate is almost always elevated due to increased plasma proteins (fibrinogen/globulins), though the degree can vary from slight to marked depending on disease activity. **2. Why Other Options are Incorrect:** * **Option B:** Leukopenia and thrombocytopenia are rare in isolated PTB. They are more suggestive of **Miliary TB** (bone marrow involvement) or adverse effects of anti-tubercular therapy (e.g., Rifampicin-induced thrombocytopenia). [2] * **Option C:** Thrombocytopenia is incorrect; reactive thrombocytosis is the standard physiological response to the chronic inflammation of TB. [1] * **Option D:** A "Normal ESR" is highly unlikely in active pulmonary TB, as it is a sensitive (though non-specific) marker of the underlying inflammatory process. **High-Yield Clinical Pearls for NEET-PG:** * **Monocytosis** is the most characteristic differential count finding in TB. [3] * **Pancytopenia** in a TB patient should raise suspicion for **Miliary Tuberculosis** or bone marrow granulomas. [2] * **Hyponatremia** (due to SIADH) is the most common electrolyte abnormality associated with pulmonary TB. * **Leukemoid reaction** (WBC >50,000) can occasionally occur in disseminated TB, mimicking leukemia.

Question 336: A 35-year-old man developed a lesion on his chest during treatment for a respiratory tract infection. What is the diagnosis?

• A. Acute urticaria
• B. Drug-induced pemphigus
• C. Erythema annulare
• D. Fixed drug eruption (Correct Answer)

Question 337: Which of the following is not used in post-exposure prophylaxis for HIV?

• A. Zidovudine + Lamivudine
• B. Nelfinavir
• C. Stavudine + Didanosine
• D. Acyclovir (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Acyclovir**. **1. Why Acyclovir is the correct answer:** Post-Exposure Prophylaxis (PEP) for HIV requires the use of **Antiretroviral Therapy (ART)** to prevent the integration of HIV into the host genome. Acyclovir is an **anti-herpetic antiviral** drug that inhibits DNA polymerase in Herpes Simplex Virus (HSV) and Varicella-Zoster Virus (VZV). It has no inhibitory activity against HIV (a retrovirus) and therefore plays no role in HIV prophylaxis. **2. Analysis of Incorrect Options:** * **A. Zidovudine + Lamivudine:** Historically, this dual Nucleoside Reverse Transcriptase Inhibitor (NRTI) backbone was the standard "basic regimen" for PEP. While current guidelines prefer Tenofovir, this combination remains a valid HIV treatment/prophylaxis option. * **B. Nelfinavir:** This is a Protease Inhibitor (PI). In older protocols, Nelfinavir was used as the third drug in "expanded regimens" for high-risk exposures. * **C. Stavudine + Didanosine:** Although rarely used now due to toxicity (lactic acidosis/peripheral neuropathy), these are NRTIs that were historically included in PEP protocols. **3. High-Yield Clinical Pearls for NEET-PG:** * **Ideal Timing:** PEP should be started as soon as possible, ideally within **2 hours**, and no later than **72 hours** after exposure. * **Duration:** The standard duration for PEP is **28 days**. * **Current WHO/NACO Preferred Regimen:** The current "all-in-one" preferred regimen is **Tenofovir (TDF) + Lamivudine (3TC) + Dolutegravir (DTG)**. * **Baseline Testing:** Always perform a baseline HIV test on the exposed individual to ensure they are not already HIV-positive before starting PEP.

Question 338: Which of the following drugs is NOT used in the treatment of candidiasis?

• A. Ketoconazole (Correct Answer)
• B. Itraconazole
• C. Voriconazole
• D. Fluconazole

Explanation: ### Explanation The correct answer is **Ketoconazole**. **1. Why Ketoconazole is the correct answer:** While Ketoconazole is an antifungal agent belonging to the imidazole class, it is **no longer used for the systemic treatment of Candidiasis**. This is due to its significant side-effect profile, specifically **severe hepatotoxicity** and its tendency to cause **adrenal insufficiency** by inhibiting steroidogenesis (CYP450 inhibition) [1]. In modern clinical practice, its use is largely restricted to topical formulations (e.g., shampoos for seborrheic dermatitis) or specifically for managing Cushing’s syndrome [1]. **2. Why the other options are incorrect:** * **Fluconazole:** This is the first-line agent for many forms of candidiasis (e.g., esophageal, vaginal, and urinary tract infections) due to its excellent bioavailability and safety profile [1]. * **Itraconazole:** Used as an alternative for mucosal candidiasis, especially in cases where there is resistance to fluconazole, though it has more erratic absorption. * **Voriconazole:** A second-generation triazole with a broad spectrum. It is highly effective against *Candida* species, including some fluconazole-resistant strains like *Candida krusei* [2]. **3. NEET-PG High-Yield Clinical Pearls:** * **Drug of Choice (DOC):** For **Invasive Candidiasis** in hemodynamically unstable patients, **Echinocandins** (e.g., Caspofungin, Micafungin) are now the preferred first-line agents over azoles [2]. * **Resistance Pattern:** *Candida krusei* is inherently resistant to Fluconazole. *Candida glabrata* often shows dose-dependent susceptibility or resistance. * **Side Effect Highlight:** Ketoconazole causes **Gynecomastia** and decreased libido in males because it inhibits the synthesis of testosterone [1]. * **Newer Agent:** **Ibrexafungerp** is a first-in-class triterpenoid antifungal recently approved for vulvovaginal candidiasis.

Question 339: Which one of the following is typically associated with the given clinical finding?

• A. Bulimia nervosa
• B. Recent endotracheal intubation
• C. Acquired immunodeficiency syndrome (AIDS)
• D. Treatment with a sulfonylurea (Correct Answer)

Explanation: ***Treatment with a sulfonylurea*** - **Diabetes mellitus** is the most typical association with **rhinocerebral mucormycosis**, accounting for approximately **70% of cases**. - **Sulfonylureas** are antidiabetic medications indicating underlying diabetes, which creates the **hyperglycemic** and **acidotic** environment that favors **Mucor** growth. *Bulimia nervosa* - Not a recognized risk factor for **mucormycosis** as it doesn't create the immunocompromised state necessary for fungal invasion. - Primarily associated with **dental erosion** and **electrolyte imbalances**, not opportunistic fungal infections. *Recent endotracheal intubation* - While trauma can predispose to infections, **endotracheal intubation** is not a classic risk factor for **mucormycosis**. - More commonly associated with **bacterial pneumonia** or **aspiration pneumonia** rather than invasive fungal infections. *Acquired immunodeficiency syndrome (AIDS)* - Although **AIDS** can predispose to mucormycosis, it is **less commonly** the typical association compared to diabetes. - **AIDS patients** are more prone to **Candida**, **Cryptococcus**, and **Pneumocystis** infections rather than mucormycosis.

Question 340: What is the common presenting symptom of Pneumocystis jirovecii pneumonia?

• A. Cavity on X-ray
• B. Hemoptysis
• C. Breathlessness (Correct Answer)
• D. Purulent sputum

Explanation: **Explanation:** *Pneumocystis jirovecii* pneumonia (PCP) is a classic opportunistic infection, most commonly seen in patients with HIV/AIDS (typically when CD4 counts fall below 200 cells/µL) or those on chronic immunosuppressants. **Why Breathlessness is Correct:** The hallmark presentation of PCP is a **triad of progressive exertional dyspnea (breathlessness), dry cough, and fever.** The underlying pathophysiology involves the organism causing alveolar damage and impaired gas exchange, leading to significant hypoxemia [1]. A characteristic clinical finding is "desaturation on exertion," where a patient’s oxygen levels drop significantly even with minimal physical activity. Diagnosis and management often involve silver stains, broncho-alveolar lavage, and high-dose co-trimoxazole [1]. **Analysis of Incorrect Options:** * **A. Cavity on X-ray:** PCP typically presents with **bilateral, diffuse interstitial infiltrates** (ground-glass opacities) [1]. Cavitation is rare in PCP and should raise suspicion for Tuberculosis, Fungal infections (Aspergillus), or *Staphylococcus aureus*. * **B. Hemoptysis:** This is not a feature of PCP. Hemoptysis is more commonly associated with Pulmonary TB, Bronchiectasis, or Pulmonary Infarction. * **D. Purulent Sputum:** The cough in PCP is characteristically **non-productive (dry)**. Purulent sputum suggests a bacterial pneumonia (e.g., *Streptococcus pneumoniae*). **High-Yield Clinical Pearls for NEET-PG:** * **Investigation of Choice:** Bronchoalveolar Lavage (BAL) is the most sensitive diagnostic tool [1]. * **Staining:** Silver stains (Gomori Methenamine Silver - GMS) or Toluidine blue are used to identify the cysts [1]. * **Drug of Choice:** Trimethoprim-Sulfamethoxazole (TMP-SMX) [1]. * **Steroid Indication:** Add corticosteroids if PaO2 < 70 mmHg or A-a gradient > 35 mmHg to prevent inflammatory worsening [1]. * **Radiology:** "Bat-wing" appearance or ground-glass opacities on HRCT.