Infectious Diseases — MCQs
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What is the mechanism of acute rheumatic fever?
A 40-year-old man presents with a year-long history of oral candidiasis, fever, and diarrhea. Physical examination reveals muscle wasting, with his weight at 70% of normal for his height and age. He has generalized nontender lymphadenopathy but no hepatosplenomegaly. Over the past 3 months, he has developed three irregular, 1- to 2-cm, reddish-purple, nodular skin lesions on his forearm. Laboratory findings show hemoglobin, 12.2 g/dL; hematocrit, 36.5%; MCV, 85 mm3; platelet count, 188,000/mm3; and WBC count, 2460/mm3 with 82% segmented neutrophils, 4% bands, 6% lymphocytes, 6% monocytes, and 2% eosinophils. Infection with which of the following organisms is most likely to produce these findings?
Kaposi sarcoma is caused by:
A 30-year-old man presents with persistent cough, night sweats, low-grade fever, and general malaise. A chest X-ray shows findings consistent with a Ghon complex, and sputum cultures are positive for acid-fast bacilli. Examination of the hilar lymph nodes in this patient would most likely demonstrate which of the following pathologic changes?
Which of the following are granulomatous diseases?
Infectious Diseases Indian Medical PG Practice Questions and MCQs
Question 1: What is the mechanism of acute rheumatic fever?
- A. Cross-reactivity with endogenous antigen (Correct Answer)
- B. Innocent bystander effect
- C. Due to toxin secretion by streptococci
- D. Release of pyrogenic cytokines
Explanation: ### Explanation **Correct Answer: A. Cross-reactivity with endogenous antigen** The pathogenesis of Acute Rheumatic Fever (ARF) is based on the concept of **Molecular Mimicry** (Type II Hypersensitivity). Following an infection with **Group A Beta-Hemolytic Streptococci (GABHS)**, the body produces antibodies against the streptococcal **M-protein** [1]. Because the M-protein shares structural homology with human molecules, these antibodies "cross-react" with endogenous antigens [2]. Specifically, they target **cardiac myosin**, sarcolemmal membrane proteins, and valvular glycoproteins, leading to the characteristic inflammatory lesions (Aschoff bodies) in the heart [1]. **Analysis of Incorrect Options:** * **B. Innocent bystander effect:** This refers to tissue damage where healthy cells are destroyed during an immune response against a nearby pathogen (often seen in Type III hypersensitivity or viral infections). ARF is a direct autoimmune attack due to structural similarity, not collateral damage. * **C. Due to toxin secretion:** While streptococci produce toxins (like Streptolysin O or Erythrogenic toxin), these cause direct tissue damage (e.g., Scarlet Fever or Toxic Shock Syndrome) rather than the delayed, immune-mediated multi-system inflammation seen in ARF. * **D. Release of pyrogenic cytokines:** While cytokines mediate the resulting fever and inflammation, they are the *mediators* of the response, not the primary *mechanism* of disease initiation. **High-Yield Clinical Pearls for NEET-PG:** * **Latent Period:** ARF typically occurs 2–3 weeks after streptococcal pharyngitis (never after skin infections like impetigo). * **Jones Criteria:** Diagnosis is clinical, requiring 2 Major or 1 Major + 2 Minor criteria plus evidence of preceding GABHS infection. * **Pathognomonic Feature:** **Aschoff bodies** (granulomatous foci) containing **Anitschkow cells** ("caterpillar cells" with condensed chromatin) [1]. * **Most Common Valve Involved:** Mitral valve (Mitral Regurgitation in acute phase; Mitral Stenosis in chronic phase). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 65-66.
Question 2: A 40-year-old man presents with a year-long history of oral candidiasis, fever, and diarrhea. Physical examination reveals muscle wasting, with his weight at 70% of normal for his height and age. He has generalized nontender lymphadenopathy but no hepatosplenomegaly. Over the past 3 months, he has developed three irregular, 1- to 2-cm, reddish-purple, nodular skin lesions on his forearm. Laboratory findings show hemoglobin, 12.2 g/dL; hematocrit, 36.5%; MCV, 85 mm3; platelet count, 188,000/mm3; and WBC count, 2460/mm3 with 82% segmented neutrophils, 4% bands, 6% lymphocytes, 6% monocytes, and 2% eosinophils. Infection with which of the following organisms is most likely to produce these findings?
- A. Hepatitis C virus
- B. Herpes simplex virus
- C. HIV (Correct Answer)
- D. Mycobacterium leprae
Explanation: **Explanation:** The clinical presentation is a classic case of **Acquired Immunodeficiency Syndrome (AIDS)** caused by **HIV**. The diagnosis is established through a constellation of findings: 1. **Opportunistic Infection:** Recurrent oral candidiasis in an adult is a major red flag for immunosuppression [1]. 2. **Wasting Syndrome:** Weight loss to 70% of normal (Cachexia) is a WHO clinical stage 4 defining criterion for AIDS [1]. 3. **Kaposi Sarcoma (KS):** The "reddish-purple, nodular skin lesions" are pathognomonic for KS, caused by **HHV-8** in the setting of HIV infection [2]. 4. **Lymphopenia:** The WBC count is 2460/mm³ with only 6% lymphocytes, resulting in an absolute lymphocyte count (ALC) of **147/mm³**. An ALC <1500/mm³ (specifically a CD4+ count <200/mm³) is diagnostic of the profound immunosuppression seen in HIV [3]. **Analysis of Incorrect Options:** * **Hepatitis C Virus:** Primarily causes chronic hepatitis, cirrhosis, or hepatocellular carcinoma. While it can cause cryoglobulinemia, it does not present with opportunistic infections or Kaposi-like lesions. * **Herpes Simplex Virus:** Typically causes vesicular/ulcerative lesions (cold sores or genital herpes). While common in HIV patients, it does not explain the systemic wasting or the nodular vascular tumors. * **Mycobacterium leprae:** Causes Leprosy, characterized by hypopigmented patches, nerve thickening, and skin nodules (in lepromatous leprosy), but not generalized lymphadenopathy, profound lymphopenia, or oral candidiasis. **NEET-PG High-Yield Pearls:** * **Kaposi Sarcoma:** Look for "spindle cells," "slit-like vascular spaces," and "extravasated RBCs" on histology. * **HIV Indicators:** Generalized nontender lymphadenopathy (Persistent Generalized Lymphadenopathy - PGL) is often the earliest clinical sign of HIV [3]. * **CD4+ Thresholds:** Oral Candidiasis (<250-500 cells/mm³); Kaposi Sarcoma (<200 cells/mm³); CMV Retinitis/MAC (<50 cells/mm³). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 260-261. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 259-260.
Question 3: Kaposi sarcoma is caused by:
- A. HHV 6
- B. HHV 7
- C. HHV 8 (Correct Answer)
- D. All of the above
Explanation: **Explanation:** **Kaposi Sarcoma (KS)** is a low-grade vascular neoplasm caused by **Human Herpesvirus 8 (HHV-8)**, also known as Kaposi Sarcoma-associated Herpesvirus (KSHV) [1]. **Why HHV-8 is the correct answer:** HHV-8 is a gamma-herpesvirus that infects vascular and lymphatic endothelial cells [1]. It carries oncogenes (like the viral G protein-coupled receptor and viral cyclin D) that drive cellular proliferation, inhibit apoptosis, and promote angiogenesis. In the setting of immune deficiency (especially HIV/AIDS), the virus replicates uncontrollably, leading to the characteristic spindle cell proliferation and slit-like vascular spaces filled with red blood cells seen histologically [1]. **Why other options are incorrect:** * **HHV-6:** This virus is the primary cause of **Roseola Infantum** (Exanthem Subitum), characterized by high fever followed by a rash in infants. * **HHV-7:** Similar to HHV-6, it is also associated with Roseola Infantum and pityriasis rosea, but it does not possess the oncogenic potential to cause KS. **High-Yield Clinical Pearls for NEET-PG:** * **Four Clinical Variants:** Classic (older Mediterranean men), Endemic (African), Iatrogenic (transplant-related), and AIDS-associated (most common and aggressive) [1]. * **Histology:** Look for "spindle-shaped cells," "slit-like spaces" containing extravasated RBCs, and "hyaline droplets." * **Markers:** HHV-8 LNA-1 (Latent Nuclear Antigen) is the most specific immunohistochemical marker. * **Associated Malignancy:** HHV-8 is also linked to **Primary Effusion Lymphoma (PEL)** and **Multicentric Castleman Disease** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262.
Question 4: A 30-year-old man presents with persistent cough, night sweats, low-grade fever, and general malaise. A chest X-ray shows findings consistent with a Ghon complex, and sputum cultures are positive for acid-fast bacilli. Examination of the hilar lymph nodes in this patient would most likely demonstrate which of the following pathologic changes?
- A. Caseous necrosis (Correct Answer)
- B. Coagulative necrosis
- C. Fat necrosis
- D. Fibrinoid necrosis
Explanation: **Explanation:** The clinical presentation of persistent cough, night sweats, low-grade fever, and acid-fast bacilli (AFB) in sputum, combined with a **Ghon complex** on X-ray, is diagnostic of **Primary Pulmonary Tuberculosis (TB)**. **Why Caseous Necrosis is Correct:** Tuberculosis is the classic example of **caseous necrosis** [2]. This is a form of cell death that combines features of both coagulative and liquefactive necrosis. Microscopically, it appears as a "cheese-like" (caseous), structureless, eosinophilic area of debris surrounded by a granulomatous inflammatory border (epithelioid histiocytes, Langhans giant cells, and lymphocytes) [2]. This process is mediated by a Type IV hypersensitivity reaction where macrophages attempt to wall off the *Mycobacterium tuberculosis* [1]. **Why Other Options are Incorrect:** * **Coagulative Necrosis:** Characterized by the preservation of cell outlines ("ghost cells"). It is typically seen in **ischemic infarction** of solid organs (heart, kidney, spleen), but not the brain. * **Fat Necrosis:** Occurs due to the release of activated lipases (as in **acute pancreatitis**) or trauma to breast tissue, resulting in saponification (chalky white deposits). * **Fibrinoid Necrosis:** Seen in **immune-mediated vascular damage** (e.g., Polyarteritis Nodosa, SLE) or malignant hypertension. It involves the leakage of fibrin into vessel walls, appearing bright pink on H&E stain. **NEET-PG High-Yield Pearls:** * **Ghon Focus:** The initial subpleural lesion (usually mid/lower lobes). * **Ghon Complex:** Ghon focus + involved hilar lymph nodes. * **Ranke Complex:** A calcified Ghon complex (visible on X-ray). * **Stain of Choice:** Ziehl-Neelsen (ZN) stain for Acid-Fast Bacilli. * **Cytokine Key:** **IFN-γ** (Interferon-gamma) is the most critical cytokine for activating macrophages to kill *M. tuberculosis* [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 380-381. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384.
Question 5: Which of the following are granulomatous diseases?
- A. Lichen planus
- B. Histoplasmosis
- C. Sarcoidosis (Correct Answer)
- D. Asbestosis
Explanation: **Explanation:** A **granuloma** is a focal collection of inflammatory cells, primarily activated macrophages (epithelioid cells), surrounded by a rim of lymphocytes and occasionally plasma cells [1]. It is a form of Type IV hypersensitivity reaction occurring in response to a persistent irritant. **Correct Option: C. Sarcoidosis** Sarcoidosis is a classic example of a **non-caseating granulomatous disease** [1], [2]. It is characterized by the presence of "naked" granulomas (lacking a dense lymphocytic rim) containing epithelioid cells and multinucleated giant cells (Langhans or foreign-body type) [1]. High-yield microscopic findings in sarcoid granulomas include **Schaumann bodies** (laminated calcium-protein concretions) and **Asteroid bodies** (stellate inclusions). **Analysis of Incorrect Options:** * **A. Lichen planus:** This is an inflammatory dermatological condition characterized by **interface dermatitis** [4]. Histology shows a "saw-tooth" appearance of rete ridges and Civatte bodies, but no granulomas. * **B. Histoplasmosis:** While fungal infections like Histoplasmosis *can* cause granulomas (often caseating) [3], in the context of this specific question and standard NEET-PG patterns, Sarcoidosis is the most definitive "textbook" answer for a primary granulomatous disease. (Note: If multiple options were allowed, B would also be correct). * **D. Asbestosis:** This is a form of pneumoconiosis characterized by **diffuse interstitial fibrosis**. The hallmark is the presence of **Ferruginous bodies** (asbestos fibers coated with iron-containing protein), not granulomas. **High-Yield Clinical Pearls for NEET-PG:** * **Caseating Granuloma:** Tuberculosis (central cheesy necrosis). * **Non-caseating Granuloma:** Sarcoidosis, Crohn’s disease, Lepromatous leprosy (early), and Berylliosis [1]. * **Suppurative Granuloma:** Cat-scratch disease, Lymphogranuloma venereum. * **Stellate Granuloma:** Cat-scratch disease. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 198-200. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 717. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 654-655.
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