Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 171: In primary tuberculosis, what is seen?

A. Ghon's focus (Correct Answer)
B. Pleural effusion
C. Miliary mottling
D. Fibrosis

Explanation: ***Ghon's focus*** - A **Ghon's focus** is the primary parenchymal lesion that develops at the site of initial infection in **primary tuberculosis**. - It consists of a small area of caseous necrosis in the lung parenchyma, typically in the **mid or lower zones**. - Combined with hilar lymph node involvement, it forms the **Ghon complex (primary complex)**, which is the pathological hallmark of primary TB. - This represents the **characteristic pathological finding** that defines primary tuberculosis [2]. *Pleural effusion* - **Pleural effusion** is actually a **common manifestation of primary tuberculosis**, particularly in adolescents and adults [3]. - It develops due to a hypersensitivity reaction to tubercular antigens in the pleural space. - While frequently seen in primary TB, it is a **clinical manifestation** rather than the defining pathological lesion (Ghon's focus). - Can occur in both primary and post-primary TB [3]. *Miliary mottling* - **Miliary mottling** on chest X-ray is characteristic of **miliary tuberculosis**, a severe form where the infection disseminates hematogenously [1]. - This represents a **complication of primary TB** due to lymphohematogenous spread, not the typical presentation [1]. - Shows multiple small nodules (1-3mm) scattered throughout both lung fields. *Fibrosis* - **Fibrosis** refers to scarring of lung tissue that occurs during the **healing phase** of tuberculosis. - It is a **sequela of TB infection**, not an acute finding in primary tuberculosis. - Develops after the active infection has been controlled or treated [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321. [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. The Lung, pp. 728-729.

Question 172: Which of the following is a histological feature of Whipple's disease?

A. Granuloma formation in the lamina
B. Macrophages with PAS (+) material in the lamina propria (Correct Answer)
C. Eosinophils in the lamina
D. Infiltration of histiocytes without PAS (+) material in the lamina

Explanation: ***Macrophages with PAS (+) material inside the lamina propria*** - A hallmark of Whipple's disease is the presence of **macrophages laden with PAS-positive material** in the lamina propria, indicating the storage of *Tropheryma whipplei* [1]. - This histological finding is crucial for diagnosis, highlighting its **unique lipid composition** and impaired lipid digestion. *Granuloma in the lamina* - Granulomas are typically associated with **sarcoidosis** or **Crohn's disease**, not Whipple's disease. - Whipple's disease features **foamy macrophages** instead of granulomatous inflammation [1]. *Eosinophils in the lamina propria* - Eosinophils are often seen in conditions like **allergic reactions** or **parasitic infections**, which are not characteristic of Whipple's disease. - The predominant inflammatory cells in Whipple's disease are **macrophages**, not eosinophils [1]. *Infiltration of histiocytes in the lamina propria* - While histiocytes may be present, they are not a specific histological hallmark of Whipple's disease compared to the **PAS-positive macrophages**. - This finding is more non-specific and can occur in various other chronic inflammatory conditions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 798-799.

Question 173: Which of the following is diagnostic of rabies?

A. Guarneri bodies
B. Negri bodies (Correct Answer)
C. Cowdry A body
D. Bollinger bodies

Explanation: ***Negri bodies*** - **Negri bodies** are eosinophilic, sharply outlined, inclusion bodies found in the cytoplasm of certain nerve cells, particularly in the **hippocampus** and **Purkinje cells** of the cerebellum, in cases of rabies infection [1]. - Their presence in brain tissue is **pathognomonic** for rabies [1]. *Guarneri bodies* - **Guarneri bodies** are acidophilic cytoplasmic inclusion bodies found in cells infected with **variola (smallpox) virus** or **vaccinia virus**. - They are characteristic of poxvirus infections, not rabies. *Cowdry A body* - **Cowdry A bodies** are intranuclear inclusion bodies seen in cells infected with certain viruses like **herpes simplex virus (HSV)**, **varicella-zoster virus (VZV)**, and **cytomegalovirus (CMV)**. - They are not associated with rabies. *Bollinger bodies* - **Bollinger bodies** are eosinophilic cytoplasmic inclusion bodies primarily found in epithelial cells infected with **fowlpox virus**, a type of avian poxvirus. - They are not relevant to human rabies diagnosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1279-1280.

Question 174: What are the histological characteristics of Lepra cells in lepromatous leprosy?

A. Foamy macrophages (Histiocytes) (Correct Answer)
B. Neutrophils
C. Plasma cells
D. Epithelioid cells

Explanation: ***Foamy macrophages (Histiocytes)*** - **Lepra cells** in lepromatous leprosy are essentially **macrophages** that have engulfed a large number of **Mycobacterium leprae** [1]. - These macrophages appear **foamy** due to the accumulation of bacteria and their lipid-rich components within the cytoplasm [1]. *Epithelioid cells* - **Epithelioid cells** are typically found in **tuberculoid leprosy**, where the immune response is strong and forms well-organized **granulomas** [1]. - The immune response in lepromatous leprosy is largely ineffective, leading to a proliferation of infected macrophages rather than granuloma formation. *Plasma cells* - **Plasma cells** are responsible for producing antibodies and are usually seen in chronic inflammation as part of the humoral immune response [2]. - While they may be present to some extent in inflammatory infiltrates, they are not the characteristic and defining cell type of lepromatous leprosy lesions. *Neutrophils* - **Neutrophils** are primarily associated with **acute bacterial infections** and are responsible for phagocytosing and destroying pathogens [3]. - They are not the predominant or characteristic cell type in the chronic granulomatous inflammation of leprosy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 385-386. [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. 195-196. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.

Question 175: Macrophages containing large quantities of undigested and partially digested bacteria in the intestine, specifically PAS-positive macrophages, are seen in which of the following conditions?

A. Whipple's disease (Correct Answer)
B. Amyloidosis
C. Immunoproliferative small intestinal disease
D. Vibrio cholerae infection

Explanation: ***Whipple's disease*** - **Whipple's disease** is characterized by the accumulation of **PAS-positive macrophages** containing undigested **Tropheryma whipplei** bacteria in the lamina propria of the small intestine [1]. - These macrophages contain bacteria that appear as **foamy, distended cells** on histology [1]. - The PAS-positive staining is pathognomonic and distinguishes this condition from other causes of malabsorption. - Clinical features include **steatorrhea**, weight loss, arthralgia, and neurological symptoms [1]. *Amyloidosis* - **Amyloidosis** is characterized by the extracellular deposition of abnormal **fibrillar proteins (amyloid)** in various tissues, not by intracellular bacteria-laden macrophages. - Diagnosed by **Congo red staining** which shows apple-green birefringence under polarized light. - Can cause GI symptoms but histology shows acellular amyloid deposits, not macrophages. *Immunoproliferative small intestinal disease* - This condition involves the proliferation of **B lymphocytes** in the small intestine, producing **alpha heavy chains**. - Seen in regions with chronic parasitic infections and leads to malabsorption. - Histology shows lymphoplasmacytic infiltration, not PAS-positive macrophages with bacteria. *Vibrio cholerae infection* - **Vibrio cholerae** causes severe secretory diarrhea by producing **cholera toxin**, which activates adenylate cyclase in intestinal epithelial cells. - The bacteria colonize the intestinal lumen but do not invade tissues or lead to macrophage accumulation. - Histology shows preserved mucosal architecture without characteristic macrophage findings. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 798-799.

Question 176: Which of the following statements about the CSF findings in pyogenic meningitis is true?

A. CSF contains no organisms
B. CSF is sterile and clear
C. Glucose is decreased and protein is elevated (Correct Answer)
D. Chloride is decreased and glucose is normal

Explanation: ***Glucose is decreased and protein is elevated*** - In **pyogenic (bacterial) meningitis**, bacteria consume glucose, leading to a **decreased CSF glucose** level. [1] - The inflammatory response increases the permeability of the blood-brain barrier, allowing proteins to leak into the CSF, resulting in **elevated CSF protein**. [1] *CSF contains no organisms* - This statement is incorrect; **pyogenic meningitis** is caused by bacterial infection, and therefore, **bacteria (organisms)** are typically present in the CSF. [1] - Microscopic examination and culture of the CSF are crucial for identifying the causative organism. [1] *CSF is sterile and clear* - CSF in **pyogenic meningitis** is **not sterile** due to the presence of bacteria, and it is typically **turbid or cloudy** due to the high leukocyte count. [1] - A clear and sterile CSF would suggest the absence of bacterial infection or a very early stage of viral meningitis. [1] *Chloride is decreased and glucose is normal* - While **CSF chloride** might be slightly decreased in severe meningitis cases, it is not a primary diagnostic marker, and **glucose is typically decreased**, not normal, in pyogenic meningitis. - **Normal CSF glucose** with decreased chloride might be observed in other conditions, but not typically in established pyogenic meningitis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 708-709.

Question 177: What is the definitive method for diagnosing Pneumocystis jirovecii pneumonia?

A. Serological test
B. Chest X-ray
C. Finding cysts in tissue specimens (Correct Answer)
D. CT scan of thorax

Explanation: ***Finding cysts in tissue specimens*** - The definitive diagnosis of **Pneumocystis jirovecii pneumonia (PCP)** involves the microscopic identification of the **trophozoites** or **cysts** of the organism in respiratory secretions or tissue biopsies [1]. - This is typically achieved through techniques like **bronchoalveolar lavage (BAL)**, induced sputum, or transbronchial biopsy, followed by staining with methods such as **Gomori methenamine silver (GMS)** [1] or Giemsa. *Serological test* - Serological tests for PCP are **not definitive** for diagnosis, as antibodies to *P. jirovecii* can be found in a high percentage of healthy individuals due to widespread exposure. - These tests cannot distinguish between active infection, past exposure, or colonization, making them **unreliable** for acute diagnosis. *Chest X-ray* - A chest X-ray can show abnormalities like **diffuse bilateral interstitial infiltrates** or ground-glass opacities, which are highly suggestive of PCP in immunocompromised patients [1]. - However, these findings are **non-specific** and can be present in other pulmonary conditions, thus not providing a definitive diagnosis of PCP. *CT scan of thorax* - A CT scan of the thorax, particularly a **high-resolution CT (HRCT)**, is more sensitive than a chest X-ray and can reveal characteristic patterns such as **ground-glass opacities**, interstitial infiltrates, and sometimes cysts. - While highly suggestive, these imaging findings are **not specific enough** to definitively diagnose PCP and must be correlated with microbiological evidence. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-319.

Question 178: Which of the following is the most predominant constituent of sulfur granules in Actinomycosis?

A. Organisms (Correct Answer)
B. Monocytes and lymphocytes
C. Neutrophils and monocytes
D. Eosinophils

Explanation: ***Organisms*** - The characteristic "sulfur granules" in **Actinomycosis** are macroscopic colonies of the **Actinomyces bacteria** themselves. - These granules are formed by a dense tangled mass of bacterial filaments surrounded by host inflammatory cells. *Neutrophils and monocytes* - While **neutrophils** and other inflammatory cells are attracted to the site of infection and surround the bacterial colonies [1], [3], they are not the primary constituent of the granule itself. - They represent the host's immune response to the bacterial presence [1]. *Monocytes and lymphocytes* - **Monocytes** differentiate into macrophages that help in clearing infection, and **lymphocytes** are involved in specific immune responses [2]. - However, similar to neutrophils, these cells are part of the host's inflammatory response and not the main structural component of the sulfur granule [2], [3]. *Eosinophils* - **Eosinophils** are typically associated with parasitic infections and allergic reactions [3]. - They are not a predominant component of the sulfur granules found in bacterial infections like Actinomycosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 360-362. [3] 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.

Question 179: Which of the following tumors is not associated with an infective etiology?

A. Nasopharyngeal carcinoma
B. Hepatocellular carcinoma
C. Gastric carcinoma
D. Non-small cell lung carcinoma (Correct Answer)

Explanation: ***Non-small cell carcinoma lung*** - This cancer type is primarily linked with **smoking** and environmental factors rather than infectious agents. - Unlike other listed cancers, it lacks a recognized **infective etiology** in its pathogenesis. *Gastric ca* - Strongly associated with **Helicobacter pylori** infection, which contributes to gastric mucosal changes [2]. - This bacteria is a known risk factor for the development of **gastric malignancies**. *Nasopharyngeal ca* - Frequently linked with **Epstein-Barr Virus (EBV)**, highlighting its infective associations [1]. - Characterized by symptoms such as **nasal obstruction** and **otitis media**, often seen in endemic forms. *Hepatocellular ca* - Closely related to **chronic hepatitis B and C infections**, representing a significant infective cause [3]. - The presence of viral antigens in liver tissue correlates with the development of **hepatocellular carcinoma**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 744-745. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 348-350. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 336-337.

Question 180: Warthin-Finkeldey giant cells in lymphoid tissue are characteristic of which of the following infections?

A. Mumps infection
B. Measles infection (Correct Answer)
C. Congenital cytomegalovirus infection
D. HIV infection

Explanation: ***Measles infection*** - **Warthin-Finkeldey giant cells** are prominent multinucleated giant cells characteristic of lymphoid tissue changes in **measles (rubeola)** [1]. - These cells contain both eosinophilic nuclear and cytoplasmic inclusions and are crucial for the histological diagnosis of measles [1]. *Mumps infection* - Mumps primarily causes inflammation of the **parotid glands** but does not typically produce Warthin-Finkeldey giant cells in lymphoid tissue. - While mumps is also caused by a paramyxovirus, its histopathological features differ significantly from measles. *Congenital cytomegalovirus infection* - Characterized by the presence of large cells with prominent **intranuclear and intracytoplasmic inclusions** (owl's eye inclusions), especially in visceral organs. - It does not involve Warthin-Finkeldey giant cells in lymphoid tissues. *HIV infection* - HIV infection causes lymphoid depletion, germinal center hyperplasia followed by involution, and is associated with various opportunistic infections and lymphomas [1]. - It does not typically present with Warthin-Finkeldey giant cells in lymphoid tissue; these are specific to measles. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 362-363.

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Host-Pathogen Interactions

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Bacterial Infections

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Viral Infections

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Fungal 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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