Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 121: All of the following special histology stains are used to demonstrate H. pylori in gastric biopsies, except:

A. Giemsa stain
B. Fite's stain (Correct Answer)
C. Warthin-Starry stain
D. Modified Steiner's stain

Explanation: ***Fite's stain*** - **Fite's stain** (or Fite-Faraco stain) is a modified acid-fast stain primarily used to detect **mycobacteria**, particularly **Mycobacterium leprae**, in tissue sections [2]. - It is not used for the identification of **Helicobacter pylori**. *Giemsa stain* - **Giemsa stain** is a common special stain used to visualize **Helicobacter pylori** directly in gastric biopsies due to its ability to stain the bacterial cytoplasm a characteristic **blue color**. - It works by staining the cytoplasmic and nuclear components of cells, making bacteria and inflammatory cells easily identifiable. *Modified Steiner's stain* - **Modified Steiner's stain** is a silver impregnation stain used to demonstrate spirochetes and other bacteria, including **Helicobacter pylori**, by staining them **black**. - It involves a silver solution that precipitates onto the bacterial surface, followed by a reducing agent to visualize the organisms. *Warthin-Starry stain* - The **Warthin-Starry stain** is another silver impregnation method widely employed for detecting spirochetes and bacteria like **Helicobacter pylori** in tissue [1]. - It renders the bacteria visible as **black** or dark brown structures against a pale yellow background, providing excellent contrast [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 771. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 385-386.

Question 122: Earliest feature of TB:

A. Caseation
B. Lymphocytosis (Correct Answer)
C. Granuloma
D. Langerhans' Giant cells

Explanation: ***Lymphocytosis*** - While the very earliest response to *Mycobacterium tuberculosis* involves neutrophils (acute inflammation), among the given options, **lymphocytosis is the earliest feature** [1]. - Within 2-3 weeks of initial infection, the immune system mounts a cellular response with increased **lymphocytes** (particularly CD4+ T cells) and macrophages attempting to contain the bacteria [2]. - This lymphocytic infiltration precedes the organized granuloma formation and represents the early cell-mediated immune response to TB [3]. *Granuloma* - **Granuloma formation** is a hallmark of tuberculosis, where epithelioid macrophages organize into structured aggregates to wall off the infection. - This organized structure typically develops around 3-4 weeks after infection, following the initial lymphocytic response [4]. *Caseation* - **Caseous necrosis** is the characteristic cheese-like necrosis seen in the center of TB granulomas. - This represents tissue death and is a later feature (4+ weeks), developing as granulomas mature and central hypoxia leads to cell death [4]. *Langerhans' Giant cells* - **Langhans giant cells** (not Langerhans cells of skin) are multinucleated giant cells formed by fusion of epithelioid macrophages within established granulomas [5]. - These appear in mature granulomas and represent a late organized response, not an early feature. **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. 195-196. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 379-380. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 380. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 380-381. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Question 123: Ghon’s focus is found in

A. Asbestosis
B. Leprosy
C. Pulmonary tuberculosis (Correct Answer)
D. Sarcoidosis

Explanation: ***Pulmonary tuberculosis*** - A **Ghon's focus** is a primary lesion in the lung, typically a granuloma, that develops after initial infection with ***Mycobacterium tuberculosis*** [1]. - It results from the body's immune response to wall off the infection, often calcifying over time and visible on imaging [1]. *Asbestosis* - This is a chronic lung disease caused by inhaling **asbestos fibers**, leading to diffuse **pulmonary fibrosis** and pleural plaques. - It does not involve the formation of a Ghon's focus, which is specific to tuberculosis. *Leprosy* - **Leprosy** is a chronic infectious disease caused by ***Mycobacterium leprae***, primarily affecting the skin, nerves, and upper respiratory tract. - It does not cause pulmonary Ghon's foci; its manifestations are mostly peripheral and mucocutaneous. *Sarcoidosis* - **Sarcoidosis** is a multi-system inflammatory disease characterized by the formation of **non-caseating granulomas** in various organs, most commonly the lungs and lymph nodes [2]. - While it involves granulomas in the lung, these are distinct from the specific primary lesion of tuberculosis known as a Ghon's focus [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321. [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. 198-200.

Question 124: In spinal tuberculosis, the commoner route of spread is:

A. Lymphatics
B. Blood (Correct Answer)
C. All of the options
D. Direct spread

Explanation: ***Blood*** - Spinal tuberculosis, also known as **Pott's disease**, primarily spreads via the **hematogenous route** [1] from a primary infection elsewhere, most commonly the lungs [1]. - Bacilli reach the vertebral bodies through the **arterial circulation** or via the **paravertebral (Batson's) venous plexus**, which allows retrograde spread without passing through the lungs. - The rich vascular supply of the vertebral bodies, particularly the **metaphyseal regions adjacent to intervertebral discs**, facilitates the deposition and growth of **Mycobacterium tuberculosis**. - This accounts for the typical involvement of two adjacent vertebrae with disc destruction in spinal TB [2]. *Lymphatics* - While lymphatic spread is important in other forms of tuberculosis, it is **not the primary route** for the initial seeding of the spine. - Lymphatic involvement tends to be secondary to established bony lesions or occurs in cases of extensive soft tissue involvement with paravertebral abscess formation. *Direct spread* - Direct spread is **rare** in spinal tuberculosis and typically occurs from an adjacent infected structure, such as a psoas abscess that erodes into the spine or from mediastinal lymph nodes. - It is not the most common initial mode of dissemination to the vertebrae. *All of the options* - While other routes like lymphatics and direct spread can contribute in specific circumstances, **hematogenous spread (via blood)** is overwhelmingly the most common and primary route for spinal tuberculosis. - The question asks for the "commoner route," which is definitively the bloodstream. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 379-380. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1197-1198.

Question 125: The following features are hallmarks of postprimary pulmonary tuberculosis except-

A. If cavity formation occurs, satellite lesions result from the discharge of liquefied contents into the airways
B. It results from endogenous reactivation of latent infection
C. Up to one-third of untreated patients die due to severe pulmonary TB within a few weeks or months after onset
D. The disease is usually localized to the anterior segment of the upper lobe (Correct Answer)

Explanation: ***The disease is usually localized to the anterior segment of the upper lobe*** - **Postprimary pulmonary tuberculosis** typically localizes to the **apical and posterior segments of the upper lobes** and the superior segment of the lower lobes, due to better oxygen tension in these areas [1]. - The anterior segment of the upper lobe is **less commonly affected** as the primary site of reactivation. *If cavity formation occurs, satellite lesions result from the discharge of liquefied contents into the airways* - This statement is **correct** for postprimary TB, as the liquefaction of caseous necrosis and subsequent expulsion of contents can spread the infection within the airways, leading to **satellite lesions** and further spread. - **Cavitation** is a hallmark of postprimary pulmonary tuberculosis and is responsible for significant tissue destruction and transmissibility. *It results from endogenous reactivation of latent infection* - This is a **defining characteristic** of postprimary (or secondary) tuberculosis, where the disease develops years after an initial **primary infection** due to the reactivation of dormant *Mycobacterium tuberculosis* [1]. - Reactivation is often triggered by **compromised immune status**, such as in HIV infection, immunosuppressive therapy, or old age [1]. *Up to one-third of untreated patients die due to severe pulmonary TB within a few weeks or months after onset* - This statement accurately reflects the **severe morbidity and mortality** associated with untreated postprimary pulmonary tuberculosis. - Without treatment, the disease can lead to **progressive lung destruction**, severe symptoms, and systemic complications. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 319-320.

Question 126: Levinthal-Coles-Lillie bodies are seen in:

A. Chicken pox
B. LGV
C. Kala-Azar
D. Psittacosis (Correct Answer)

Explanation: ***Psittacosis*** - **Levinthal-Coles-Lillie (LCL) bodies** are characteristic cytoplasmic inclusions found in cells infected with *Chlamydophila psittaci*, the causative agent of **psittacosis**. - These bodies represent aggregations of elementary and reticulate bodies within the host cell cytoplasm, visible on microscopy. *Chicken pox* - Chickenpox, caused by the **varicella-zoster virus**, is characterized by **Cowdry type A intranuclear inclusions**, not LCL bodies [1]. - These inclusions are typically seen in skin lesions and are indicative of herpesvirus infections [1]. *LGV* - **Lymphogranuloma venereum (LGV)** is caused by specific serovars of *Chlamydia trachomatis* and is characterized by **chlamydial inclusions**. - While *Chlamydia* species form inclusions, they are not specifically termed LCL bodies, which are unique to *Chlamydophila psittaci*. *Kala-Azar* - **Kala-Azar (visceral leishmaniasis)** is caused by **Leishmania donovani** parasites. - Diagnostic features include the presence of **amastigotes** within macrophages in various tissues, not LCL bodies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 366-367.

Question 127: The following pathological features are associated with Plasmodium falciparum except-

A. Cytoadherence
B. Sequestration
C. Rosetting
D. Tissue phase (Correct Answer)

Explanation: ***Tissue phase*** (Correct Answer - NOT associated with P. falciparum) - While *Plasmodium falciparum* does have a **hepatic (liver) phase** in its life cycle, the term "**tissue phase**" specifically refers to the **persistent dormant liver stage (hypnozoites)** seen in **relapsing malarias** [1]. - **Hypnozoites** are found in *Plasmodium vivax* and *Plasmodium ovale* but **NOT in *P. falciparum***. - These dormant forms can reactivate months or years later, causing relapse—a feature absent in *P. falciparum* infection. *Cytoadherence* (Incorrect - IS associated with P. falciparum) - This is a **key virulence factor** of *P. falciparum*, where **infected red blood cells (iRBCs)** bind to the **vascular endothelium** via adhesion molecules (PfEMP1) [1]. - This binding leads to **sequestration** in deep capillaries and avoidance of splenic clearance, contributing to severe malaria pathology [1]. *Sequestration* (Incorrect - IS associated with P. falciparum) - Refers to the confinement of **iRBCs** in the **deep microvasculature** of vital organs such as the brain, lungs, and kidneys. - Results from **cytoadherence** and is the primary mechanism behind severe complications like **cerebral malaria** in *P. falciparum*. *Rosetting* (Incorrect - IS associated with P. falciparum) - Involves **iRBCs** binding to uninfected red blood cells, forming **rosette structures**. - This phenomenon impedes blood flow in capillaries and contributes to **microvascular obstruction** and tissue hypoxia in severe *P. falciparum* infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 398-400.

Question 128: Xanthogranulomatous infection is caused by:

A. Nephrolithiasis
B. Proteus Mirabilis
C. All of the options (Correct Answer)
D. Urinary obstruction

Explanation: ***All of the options*** - **Xanthogranulomatous pyelonephritis (XGP)** is a severe, chronic infectious process of the kidney, often associated with a combination of factors including **urinary tract obstruction**, specific bacterial infections, and the presence of kidney stones (nephrolithiasis) [1]. - **Proteus mirabilis** is a common cause of XGP due to its ability to produce urease, which hydrolyzes urea into ammonia, increasing urinary pH and promoting the formation of struvite stones, thus acting in concert with obstruction and stones [1]. *Nephrolithiasis* - While **kidney stones** are a major predisposing factor for XGP, they do not solely cause the infection; they primarily create an environment conducive to bacterial colonization and obstruction. - The presence of stones, particularly **struvite stones**, can lead to persistent infection and the characteristic inflammatory response seen in XGP. *Proteus Mirabilis* - **Proteus mirabilis** is frequently isolated in cases of XGP, but it typically acts in conjunction with urinary obstruction and/or nephrolithiasis [1]. - This bacterium contributes significantly to the pathophysiology by promoting stone formation and maintaining a chronic infectious state, but it is not the sole cause. *Urinary obstruction* - **Urinary tract obstruction** is a key predisposing factor that prevents proper drainage, leading to stasis and increasing susceptibility to infection [1]. - While essential for the development of XGP, obstruction alone does not directly cause the characteristic xanthogranulomatous inflammation without the presence of bacteria and often stones. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940.

Question 129: Which of the following is NOT a fungal infection?

A. Black Piedra
B. White Piedra
C. Tinea nigra Palmaris
D. Mycoses fungoides (Correct Answer)

Explanation: ***Mycoses fungoides*** - This is a type of **cutaneous T-cell lymphoma**, which is a **malignancy of lymphocytes**, not a fungal infection [1]. - It presents with skin lesions that can mimic various dermatological conditions but is characterized by abnormal T-cells infiltrating the skin [1], [2]. *Black Piedra* - This is a superficial fungal infection of the **hair shaft** caused by **Piedraia hortae**, forming hard, black nodules. - It is an example of a **dermatomycosis**. *White Piedra* - This is a fungal infection of the **hair shaft** caused by **Trichosporon species**, leading to soft, white to light brown nodules. - Like black piedra, it is also a **dermatomycosis**. *Tinea nigra Palmaris* - This is a superficial fungal infection of the **stratum corneum** of the skin, primarily on the palms and soles, caused by **Hortaea werneckii**. - It presents as irregular, darkly pigmented (brown to black) macules and is a true **mycosis**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 613-614. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 564-565.

Question 130: Which of the following is a special stain used to diagnose fungal hyphae in tissues-

A. Masson trichrome
B. Silver methenamine (Correct Answer)
C. Congo Red
D. Alizarin Red

Explanation: ***Silver methenamine*** - **Grocott's methenamine silver (GMS) stain** is widely used to visualize **fungal elements** in tissue sections. - It works by staining the **polysaccharides** in the fungal cell walls, making them appear **black** against a green or grayish-green background. *Masson trichome* - This stain is primarily used to differentiate **collagen fibers** from smooth muscle and other tissues. - It stains **collagen blue or green**, cytoplasm red, and nuclei black, and is not suitable for identifying fungi. *Congo Red* - **Congo Red stain** is used to identify **amyloid deposits** in tissues, which appear red-pink and show apple-green birefringence under polarized light [1]. - It does not specifically stain fungal hyphae. *Alizarin Red* - **Alizarin Red S stain** is used to demonstrate the presence of **calcium deposits** in tissues. - It stains calcium salts **orange-red** or scarlet, and is not utilized for fungal identification. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269.

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Host-Pathogen Interactions

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Bacterial Infections

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Viral Infections

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Parasitic Diseases

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Emerging Infections

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Healthcare-Associated Infections

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Infectious Disease Pathology in Immunocompromised Hosts

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Laboratory Diagnosis of Infections

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Antimicrobial Resistance

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