Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 141: Multinucleated giant cells are seen in smear from the lesions of:

A. HIV
B. Poliovirus
C. Rabiesvirus
D. Herpes simplex virus (Correct Answer)

Explanation: ***Herpes simplex virus*** - **Multinucleated giant cells** with intranuclear inclusions are characteristic findings in Tzanck smears from **herpes simplex virus (HSV)** lesions [1]. - This cellular morphology results from the fusion of infected cells, a cytopathic effect of the virus [1]. *HIV* - HIV primarily infects **CD4+ T-cells** and macrophages, leading to immunosuppression, but does not typically cause multinucleated giant cells in skin lesion smears. - While HIV can be associated with various opportunistic skin lesions, the hallmark cytological finding from the primary infection itself is not multinucleated giant cells. *Poliovirus* - Poliovirus is an **enterovirus** that primarily affects the central nervous system, causing paralytic disease. - It does not cause skin lesions characterized by multinucleated giant cells. *Rabiesvirus* - Rabiesvirus is a **neurotropic virus** that causes acute encephalitis in mammals. - The characteristic pathological finding in rabies is the presence of **Negri bodies** (intracytoplasmic inclusions) in neurons, not multinucleated giant cells in skin smears. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 365-366.

Question 142: "Medlar bodies" are seen in

A. Coccidiomycosis
B. Sporotrichosis
C. Chromblastomycosis (Correct Answer)
D. Histoplasmosis

Explanation: ***Chromblastomycosis*** - "**Medlar bodies**" (also known as muriform cells or sclerotic bodies) are characteristic findings in the tissue biopsy of patients with **chromoblastomycosis**. - These are thick-walled, septate, dark brown fungal cells that reproduce by septation and are crucial for the diagnosis of this chronic fungal infection. *Coccidiomycosis* - This deep fungal infection is characterized by thick-walled **spherules containing endospores** in tissue, rather than Medlar bodies [1]. - It primarily affects the lungs but can disseminate to other organs. *Sporotrichosis* - The classic histological finding in sporotrichosis is the presence of **cigar-shaped budding yeasts** in tissue, especially in the suppurative granulomas. - **Asteroid bodies**, which are yeasts surrounded by eosinophilic material, may also be seen. *Histoplasmosis* - This fungal infection is identified by small, **intracellular budding yeasts** (2-4 µm) found within macrophages in tissue samples [1]. - It commonly affects the lungs and can disseminate, particularly in immunocompromised individuals [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 717.

Question 143: Warthin-Finkeldey giant cells are seen in?

A. Measles (Correct Answer)
B. Rubella
C. Rickettsial pox
D. Influenza

Explanation: ***Measles*** - **Warthin-Finkeldey giant cells** are characteristic large, multinucleated cells found in lymphoid tissues during the prodromal and eruptive phases of **measles** (rubeola) [1]. - These cells represent **syncytia** formed by the fusion of infected lymphocytes and macrophages, a hallmark of **measles virus infection** [1]. *Rubella* - Rubella (German measles) is a milder viral infection and does not typically involve the formation of **Warthin-Finkeldey giant cells**. - While it can cause lymphadenopathy, the characteristic histological findings differ significantly from measles. *Rickettsial pox* - Rickettsial pox is caused by *Rickettsia akari* and presents with a rash and flu-like symptoms. - The pathology primarily involves **vasculitis** and does not feature **Warthin-Finkeldey giant cells**. *Influenza* - Influenza is a respiratory viral infection primarily affecting the respiratory epithelium. - It does not lead to the formation of **Warthin-Finkeldey giant cells** in lymphoid tissues. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 362-363.

Question 144: Eosinophilic ovoid intranuclear inclusion bodies seen in herpes infection is called as:

A. Lipschutz bodies. (Correct Answer)
B. Rushton bodies.
C. Cowdry bodies
D. Howell-Jolly bodies

Explanation: ***Lipschutz bodies*** - **Lipschutz bodies** are characteristic **eosinophilic ovoid intranuclear inclusion bodies** found in cells infected with **herpes simplex virus (HSV)**. - They represent viral replication within the nucleus and are a key diagnostic feature in histopathology of herpes infections. - These inclusion bodies are typically seen in cervical, vulvar, and penile lesions caused by HSV. *Howell-Jolly bodies* - **Howell-Jolly bodies** are **round, dense, basophilic nuclear remnants** often seen in **red blood cells**. - Their presence indicates hyposplenism or asplenia, not viral infection. *Rushton bodies* - **Rushton bodies** are **hyaline bodies** found in the lining of **odontogenic cysts**, particularly radicular and dentigerous cysts. - They are not related to viral infections and represent keratin or mucous material. *Cowdry bodies* - **Cowdry bodies** are also intranuclear inclusion bodies but are classified into **Type A and Type B**. - **Type A Cowdry bodies** are acidophilic inclusions surrounded by a clear halo, seen in herpes and varicella-zoster infections [1], [2]. - Unlike Lipschutz bodies which are ovoid and eosinophilic, Cowdry A bodies have a characteristic halo and different morphology [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 366-367. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 365-366.

Question 145: Characteristic histopathological finding in Whipple's disease is?

A. Mononuclear infiltration at base of crypts
B. Shortened thickened villi with increased crypt depth
C. Blunting and flattening of mucosal surface and absent villi
D. PAS positive macrophages and rod shaped bacilli in lamina propria (Correct Answer)

Explanation: ***PAS positive macrophages and rod shaped bacilli in lamina propria*** - Whipple's disease is caused by the bacterium ***Tropheryma whipplei***, which accumulates in **macrophages** within the lamina propria. [1] - These macrophages stain **positive with Periodic Acid-Schiff (PAS)** due to the presence of bacterial glycoproteins, and **rod-shaped bacilli** can be visualized on electron microscopy. [1] *Mononuclear infiltration at base of crypts* - This finding is more characteristic of **inflammatory bowel disease**, particularly **Crohn's disease** or **ulcerative colitis**, rather than Whipple's disease. - It does not involve the specific PAS-positive macrophages or bacteria seen in Whipple's. *Shortened thickened villi with increased crypt depth* - This histological pattern can be seen in various conditions causing **malabsorption**, such as **celiac disease** post-treatment or certain infectious enteropathies. - It lacks the distinct features of **macrophage accumulation** and **bacterial presence** specific to Whipple's disease. *Blunting and flattening of mucosal surface and absent villi* - This describes **severe villous atrophy**, a hallmark of **untreated celiac disease**, where immune-mediated damage leads to extensive loss of villi. - While it indicates significant malabsorption, it does not involve the specific **PAS-positive macrophages** or the bacterial etiology found in Whipple's. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 798-799.

Question 146: What is the primary reason why pre-transfusion testing does not completely eliminate the risk of hepatitis transmission?

A. Present screening test is not sensitive for HBsAg
B. Post transfusions hepatitis is caused by CMV
C. HCV not screened
D. Some carriers may not have detectable HBsAg (Correct Answer)

Explanation: ***Most carriers do not have HBsAg*** - Some carriers may not have detectable **HBsAg** during the **window period** of acute infection or in **chronic carriers** with very low viral loads [1]. - This creates a gap in screening where infectious individuals can donate blood despite negative **HBsAg** testing, leading to potential transmission [1]. *Present screening test is not sensitive for HBsAg* - Modern **HBsAg screening tests** are highly sensitive and can detect very low levels of the antigen using **enzyme immunoassays** and **chemiluminescent assays**. - The issue is not test sensitivity but rather the **biological absence** of HBsAg during certain phases of hepatitis B infection. *Post transfusions hepatitis is caused by CMV* - **Cytomegalovirus (CMV)** can be transmitted through transfusion but typically causes **mononucleosis-like symptoms** rather than classic hepatitis. - Post-transfusion hepatitis is primarily caused by **hepatitis viruses (B, C)** that specifically target liver cells and cause hepatocellular damage. *HCV not screened* - **Hepatitis C virus (HCV)** is routinely screened in blood donations using **anti-HCV antibody testing** and **nucleic acid testing (NAT)**. - Modern comprehensive screening has dramatically reduced the risk of **HCV transmission** from approximately 1 in 100 to less than 1 in 2 million units. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 838.

Question 147: Lipschutz bodies are seen in ?

A. Herpes (Correct Answer)
B. Yellow fever
C. Hodgkin's disease
D. Viral hepatitis

Explanation: ***Herpes*** - **Lipschutz bodies**, also known as **intranuclear eosinophilic inclusion bodies**, are characteristic cytopathic effects seen in cells infected with the **Herpes Simplex Virus (HSV)** [1]. - These inclusions are visible within the nucleus of epithelial cells, indicating active viral replication and aiding in the histological diagnosis of herpes infections [1]. *Yellow fever* - Yellow fever is caused by a **flavivirus** and does not typically present with Lipschutz bodies. - Histological findings in yellow fever include **Councilman bodies** (apoptotic hepatocytes) and fatty degeneration in the liver. *Hodgkin's disease* - Hodgkin's disease is a **lymphoma**, a type of cancer, and is characterized by the presence of large, often multinucleated **Reed-Sternberg cells**. - It is a neoplastic condition and not an infectious disease associated with viral inclusions like Lipschutz bodies. *Viral hepatitis* - Viral hepatitis, caused by various hepatitis viruses (e.g., HAV, HBV, HCV), primarily affects the **liver** [2]. - Histological changes in viral hepatitis include **hepatocyte necrosis**, inflammation, and immune cell infiltration, but not Lipschutz bodies [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 365-366. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 390-391.

Question 148: Giant cells in measles are called as:

A. Weinberger bodies
B. HP bodies
C. Koplik spots
D. Warthin-Finkeldey cells (Correct Answer)

Explanation: ***Warthin-Finkeldey cells*** - **Warthin-Finkeldey cells** are multinucleated giant cells characteristic of **measles virus infection**. [1] - They are formed by the fusion of infected cells and are found in lymphoid tissues, such as the **lymph nodes**, tonsils, and appendix, during the acute phase of measles. [1] *Weinberger bodies* - **Weinberger bodies** are not a recognized term for giant cells in measles or any other medical condition. - This term does not correspond to any known pathological finding. *Koplik spots* - **Koplik spots** are **pathognomonic enanthem** of measles, appearing as small, white spots with erythematous halos on the buccal mucosa. [1] - While characteristic of measles, they are clinical lesions, not giant cells. *HP bodies* - **HP bodies** (also known as **Henderson-Paterson bodies**) are cytoplasmic inclusion bodies seen in cells infected with **molluscum contagiosum virus**. [2] - These are indicative of molluscum contagiosum, not measles. [2] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 362-363. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1177-1178.

Question 149: Which of the following agents causing acute infectious diarrhea can be paired with the pathogenic mechanism of destruction limited to the mature villus cells of small intestine?

A. Rotavirus (Correct Answer)
B. E. coli
C. Vibrio cholerae
D. Shigella

Explanation: ***Correct: Rotavirus*** - **Rotavirus** infection primarily targets and destroys the mature **villus cells (enterocytes)** at the tips of villi in the small intestine, leading to villus blunting, malabsorption, and secretory diarrhea - The **NSP4 enterotoxin** produced by rotavirus specifically damages mature absorptive cells, resulting in reduced surface area for absorption - This destruction leads to decreased **disaccharidase activity** (particularly lactase), causing osmotic diarrhea from carbohydrate malabsorption - The pathogenic mechanism is **cytolytic destruction limited to mature villus cells**, making this the correct pairing *Incorrect: E. coli* - **Enterotoxigenic E. coli (ETEC)** produces heat-labile (LT) and heat-stable (ST) toxins that stimulate intestinal secretion through cAMP/cGMP pathways **without cellular destruction** - **Enterohemorrhagic E. coli (EHEC)**, particularly O157:H7, produces Shiga toxin that primarily affects the **colon** and causes microvascular damage, not villus cell destruction in the small intestine - **Enteropathogenic E. coli (EPEC)** causes attaching-effacing lesions but affects both mature and immature cells, not selectively mature villus cells *Incorrect: Vibrio cholerae* - **Vibrio cholerae** produces cholera toxin that activates adenylate cyclase in **crypt cells** of the small intestine, leading to massive secretion of fluid and electrolytes [1] - The mechanism is **purely toxin-mediated** with **no cellular destruction** - the epithelium remains intact [1] - Causes profuse watery "rice-water" diarrhea through hypersecretion, not through villus cell damage [1] *Incorrect: Shigella* - **Shigella** species invade and destroy epithelial cells of the **colon** (large intestine), not the small intestine [2], [3] - Causes inflammatory colitis with ulceration, leading to dysentery with bloody diarrhea, mucus, and pus [3] - The pathogenic mechanism involves **bacterial invasion, intracellular multiplication**, and **inflammatory response** - distinct from selective mature villus cell destruction in the small intestine [3] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 792-793. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 793. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 794-795.

Question 150: Virchow Lepra cells are seen in:

A. Tuberculoid leprosy
B. Indeterminate leprosy
C. Lepromatous Leprosy (Correct Answer)
D. Borderline tuberculoid leprosy

Explanation: ***Lepromatous Leprosy*** - **Virchow cells** (also known as **foamy macrophages** or **lepra cells**) are characteristic histological findings in **lepromatous leprosy** [1]. - These cells are macrophages distended with numerous **Mycobacterium leprae bacilli**, forming a foamy or vacuolated appearance due to the stored lipids and bacteria [1]. *Tuberculoid leprosy* - Characterized by a strong cell-mediated immune response, leading to few bacilli and often well-formed **granulomas** [1], [2]. - **Virchow cells** are typically absent because macrophages effectively clear the bacteria [1]. *Indeterminate leprosy* - This is an early, unstable form of leprosy with a low bacterial load and non-specific histological features. - It often lacks the distinct **Virchow cells** seen in lepromatous leprosy or the granulomas of tuberculoid leprosy. *Borderline tuberculoid leprosy* - This form lies between tuberculoid and lepromatous leprosy, with some features of both but leaning towards a more effective immune response than lepromatous. - While lymphocytes and some granuloma formation may be present, it generally does not show the prominent **Virchow cells** characteristic of lepromatous 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. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 638-639.

Practice by Chapter

Host-Pathogen Interactions

Practice Questions

Bacterial Infections

Practice Questions

Viral Infections

Practice Questions

Fungal Infections

Practice Questions

Parasitic Diseases

Practice Questions

Emerging Infections

Practice Questions

Healthcare-Associated Infections

Practice Questions

Infectious Disease Pathology in Immunocompromised Hosts

Practice Questions

Laboratory Diagnosis of Infections

Practice Questions

Antimicrobial Resistance

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free