Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 61: Torres bodies are seen in which of the following conditions?

A. Kala azar
B. Yellow fever (Correct Answer)
C. HSV
D. EBV

Explanation: **Explanation:** **Yellow Fever (Correct Answer):** Torres bodies are characteristic **intranuclear eosinophilic inclusion bodies** found in the hepatocytes of patients with Yellow Fever. They represent viral nucleocapsids and are often seen alongside **Councilman bodies**, which are eosinophilic globules representing apoptotic hepatocytes (acidophilic degeneration). These findings are hallmark pathological features of the mid-zonal necrosis typically seen in the liver during Yellow Fever infection. **Analysis of Incorrect Options:** * **Kala-azar (Visceral Leishmaniasis):** Characterized by **LD bodies** (Leishman-Donovan bodies), which are amastigote forms of the parasite found within the macrophages of the reticuloendothelial system (spleen, liver, bone marrow). * **HSV (Herpes Simplex Virus):** Characterized by **Cowdry Type A** inclusions (intranuclear eosinophilic bodies surrounded by a clear halo) and "ground-glass" nuclei. * **EBV (Epstein-Barr Virus):** Associated with **atypical lymphocytes** [2] (Downey cells) in the peripheral blood smear. It does not produce Torres bodies. **High-Yield Clinical Pearls for NEET-PG:** * **Yellow Fever Triad:** Mid-zonal necrosis, Councilman bodies, and Torres bodies. * **Councilman bodies** are not pathognomonic for Yellow Fever; they can be seen in other forms of viral hepatitis [1], but **Torres bodies** are more specific. * **Negri bodies:** Seen in Rabies (intracytoplasmic, Hippocampus/Purkinje cells). * **Guarnieri bodies:** Seen in Smallpox (intracytoplasmic). * **Henderson-Paterson bodies:** Seen in Molluscum Contagiosum. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 390-391. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 369-370.

Question 62: Which of the following conditions is characterized by caseating necrosis?

A. Leprosy
B. Tuberculosis (Correct Answer)
C. Sarcoidosis
D. Infarct

Explanation: **Explanation:** **Caseating necrosis** is a unique form of cell death characterized by a "cheese-like" (caseous) appearance [1][3]. Microscopically, it presents as a structureless, eosinophilic, granular area of debris surrounded by a granulomatous inflammatory border [1]. * **Tuberculosis (Correct Answer):** This is the classic example of caseating necrosis [1][2][3]. It is caused by *Mycobacterium tuberculosis*. The lipid-rich cell wall of the organism (containing mycolic acid) contributes to the friable, yellowish-white appearance of the necrotic tissue [1][2]. * **Leprosy (Incorrect):** While leprosy is caused by *Mycobacterium leprae*, it typically presents with **non-caseating** granulomas (especially in the tuberculoid form). Caseation is rare in leprosy. * **Sarcoidosis (Incorrect):** This is a multisystem disorder characterized by the formation of **non-caseating** granulomas. The absence of necrosis is a key histological feature used to differentiate it from tuberculosis. * **Infarct (Incorrect):** Ischemic cell death in most solid organs (except the brain) leads to **coagulative necrosis**, where the basic structural outline of the cell is preserved for several days. **High-Yield NEET-PG Pearls:** 1. **Mnemonic:** "Caseating = Cheese." If the granuloma has a "soft" center, think TB or Fungal infections (like Histoplasmosis) [3]. 2. **Non-caseating granulomas** are also seen in Crohn’s disease, Cat-scratch disease (early stages), and Berylliosis. 3. **Liquefactive necrosis** is seen in brain infarcts and abscesses. 4. **Fat necrosis** is characteristic of acute pancreatitis (enzymatic) or breast trauma (non-enzymatic) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 55. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 741-742.

Question 63: Which virus is implicated in Burkitt's lymphoma?

A. HTLV
B. HPV
C. EBV (Correct Answer)
D. HHV8

Explanation: **Explanation:** **Epstein-Barr Virus (EBV)**, also known as Human Herpesvirus 4 (HHV-4), is the correct answer [1]. It is a potent oncogenic virus that infects B-lymphocytes via the **CD21 receptor** [4]. In Burkitt’s lymphoma, EBV infection leads to the immortalization of B-cells [2]. This process is characterized by a pathognomonic **t(8;14) translocation**, which results in the overexpression of the **c-MYC oncogene**, driving rapid cellular proliferation. Histologically, this appears as a "starry-sky" pattern. **Analysis of Incorrect Options:** * **HTLV-1 (Human T-cell Lymphotropic Virus):** Associated with Adult T-cell Leukemia/Lymphoma (ATLL), characterized by "flower cells" on peripheral smear [1]. * **HPV (Human Papillomavirus):** Primarily linked to squamous cell carcinomas of the cervix, anogenital region, and oropharynx (Types 16 and 18) [1]. * **HHV-8 (Human Herpesvirus 8):** Also known as KSHV, it is the causative agent of Kaposi Sarcoma and Primary Effusion Lymphoma (PEL), typically seen in HIV-infected patients [1], [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Burkitt’s Variants:** EBV is found in 100% of **Endemic (African)** cases (usually involving the jaw) but only 15-20% of Sporadic cases (usually involving the ileocecum) [2]. * **Other EBV Associations:** Nasopharyngeal carcinoma, Hodgkin Lymphoma (Mixed Cellularity subtype), and Oral Hairy Leukoplakia [1], [2]. * **Diagnostic Hallmark:** Translocation **t(8;14)** is most common; variants include t(2;8) and t(8;22). All involve the *MYC* gene on chromosome 8. **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. 219-221. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 368-369.

Question 64: What is septicemia?

A. Bacteria in the blood
B. Toxins in the blood
C. Pus in the blood
D. Multiplication of bacteria and toxins in the blood (Correct Answer)

Explanation: **Explanation:** **Septicemia** is a systemic clinical syndrome characterized by the active **multiplication of pathogenic microorganisms and the presence of their toxins** within the bloodstream. Unlike transient states, septicemia implies a severe, overwhelming infection where the body's immune response is triggered systemically, often leading to systemic inflammatory response syndrome (SIRS) and potential multi-organ dysfunction [2]. **Analysis of Options:** * **Option A (Bacteremia):** This refers simply to the presence of viable bacteria in the blood (e.g., after vigorous tooth brushing). It is often transient and does not necessarily involve multiplication or clinical symptoms [1]. * **Option B (Toxemia):** This is the presence of bacterial toxins (like tetanus or diphtheria toxins) in the blood, without the bacteria themselves necessarily circulating or multiplying in the bloodstream. * **Option C (Pyemia):** This refers to "pus in the blood," specifically the circulation of septic emboli (clumps of bacteria and pus) that settle in various organs to form secondary metastatic abscesses. **High-Yield NEET-PG Clinical Pearls:** 1. **Sepsis vs. Septicemia:** While "septicemia" is a classic pathological term, modern clinical practice uses the **Sepsis-3 definition**: Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection (measured by a change in **SOFA score** $\geq$ 2) [2]. 2. **Septic Shock:** Defined as sepsis requiring vasopressors to maintain a MAP $\geq$ 65 mmHg AND having a serum lactate level > 2 mmol/L despite adequate fluid resuscitation [2]. 3. **Common Triggers:** Gram-negative bacteria (due to Endotoxin/LPS) are frequent causes, but Gram-positive organisms are now equally prevalent in clinical settings [2]. **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. 64-65. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 142-143.

Question 65: Reactivation of TB is most commonly located near which anatomical area?

A. Apex (Correct Answer)
B. Bronchus
C. Subpleural space
D. Base

Explanation: **Explanation:** **Correct Answer: A. Apex** The hallmark of **Secondary (Reactivation) Tuberculosis** is its predilection for the **apical and posterior segments of the upper lobes** [1]. This localization occurs because *Mycobacterium tuberculosis* is an **obligate aerobe** that thrives in environments with high oxygen tension. In an upright individual, the apex of the lung has the highest ventilation-perfusion (V/Q) ratio, resulting in the highest alveolar oxygen concentration ($P_AO_2$), which favors the proliferation of the bacilli. **Analysis of Incorrect Options:** * **B. Bronchus:** While TB can spread via the endobronchial route (leading to endobronchial TB), the bronchus is a site of dissemination rather than the primary site of reactivation. * **C. Subpleural space:** This is the characteristic location for the **Ghon focus** in **Primary TB**, which typically occurs in the lower part of the upper lobe or upper part of the lower lobe [1]. * **D. Base:** The lung bases have higher perfusion but lower oxygen tension compared to the apices. Primary TB may involve the bases, but reactivation rarely begins here unless the patient is chronically recumbent. **Clinical Pearls for NEET-PG:** * **Simon’s Focus:** These are apical nodules representing healed secondary TB. * **Cavitation:** Unlike primary TB, reactivation TB is characterized by **cavitation** due to a brisk delayed-type hypersensitivity (Type IV) immune response [1]. * **Rasmussen Aneurysm:** A high-yield complication where a pulmonary artery aneurysm forms in a TB cavity; its rupture leads to massive hemoptysis. * **Miliary TB:** Occurs when bacilli drain through lymphatics into the venous return, seeding the entire lung or distant organs (liver, spleen, bone marrow) [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 319-320. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321.

Question 66: Which of the following conditions is characterized by granulomas with stellate abscesses?

A. Tuberculosis
B. Tularemia
C. Sarcoidosis
D. All of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **D. All of the above**. **Understanding Stellate Abscesses** A **stellate abscess** is a specific histological pattern characterized by a central area of necrosis (often containing neutrophils/pus) surrounded by a rim of palisading epithelioid histiocytes and multinucleated giant cells (a granuloma) [4]. While many students associate stellate abscesses exclusively with **Cat-Scratch Disease** (*Bartonella henselae*), they are a hallmark of several infectious and non-infectious granulomatous conditions. **Breakdown of Options:** * **Tularemia:** Caused by *Francisella tularensis*, this zoonotic infection typically presents with ulceroglandular disease. Histologically, the lymph nodes show necrotizing granulomas that frequently coalesce into star-shaped (stellate) abscesses. * **Tuberculosis (TB):** While the classic description of TB is "caseating granuloma," atypical presentations or specific stages of nodal TB can manifest with suppurative centers and stellate configurations, especially in primary progressive disease [3]. * **Sarcoidosis:** Although sarcoidosis is the prototype for "non-caseating granulomas," rare variants or specific organ involvements (like the skin or late-stage nodes) can occasionally show central fibrinoid necrosis or stellate patterns, though this is less common than in the infectious causes listed [2]. **High-Yield NEET-PG Pearls:** * **The "Big Four" for Stellate Abscesses:** 1. Cat-Scratch Disease (Most common association), 2. Lymphogranuloma Venereum (LGV), 3. Tularemia, 4. Fungal infections (e.g., Sporotrichosis). * **Differentiating Tip:** If the question asks for the *most common* cause of stellate abscesses in a child with lymphadenopathy, think **Cat-Scratch Disease**. If it involves a painful inguinal bubo, think **LGV**. * **Histology Note:** The presence of neutrophils within a granuloma is the key feature that transforms a standard granuloma into a "suppurative granuloma" or stellate abscess [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360. [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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Question 67: Cachectin is produced by which of the following cells?

A. Neutrophils
B. Eosinophils
C. Macrophages (Correct Answer)
D. Basophils

Explanation: **Explanation:** The correct answer is **Macrophages**. **Cachectin** is another name for **Tumor Necrosis Factor-alpha (TNF-α)**. It is a potent pro-inflammatory cytokine primarily produced by activated **macrophages** and monocytes, though it can also be secreted by T-cells and NK cells [1]. It earned the name "cachectin" because of its role in causing **cachexia**—a state of profound weight loss, muscle wasting, and anorexia seen in chronic infections and malignancies. It achieves this by suppressing lipoprotein lipase (LPL) activity, thereby inhibiting lipid storage and promoting the mobilization of fatty acids. **Analysis of Incorrect Options:** * **Neutrophils:** While neutrophils are the first responders in acute inflammation and release various enzymes (like myeloperoxidase) and cytokines, they are not the primary source of TNF-α/Cachectin. * **Eosinophils:** These cells are primarily involved in parasitic infections and Type I hypersensitivity reactions (allergic diseases). Their main products include Major Basic Protein (MBP) and Eosinophil Cationic Protein (ECP). * **Basophils:** These are circulating granulocytes involved in allergic responses and contain histamine and heparin; they do not produce significant amounts of cachectin. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Cachexia:** TNF-α causes wasting by suppressing appetite (via the hypothalamus) and inhibiting **Lipoprotein Lipase (LPL)**, which prevents adipocytes from taking up circulating triglycerides. * **Key Functions of TNF-α:** It mediates the acute phase response, induces fever (endogenous pyrogen), stimulates the expression of adhesion molecules (E-selectin) on endothelium, and is the key mediator of **septic shock**. * **Granuloma Formation:** TNF-α is essential for the formation and maintenance of granulomas in Tuberculosis. This is why patients on Anti-TNF therapy (e.g., Infliximab) are at high risk for TB reactivation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.

Question 68: Intranuclear viral inclusions are seen in tissue specimens of which of the following conditions?

A. Solar cheilitis
B. Minor aphthous ulcers
C. Geographic tongue
D. Hairy leukoplakia (Correct Answer)

Explanation: **Explanation:** **Oral Hairy Leukoplakia (OHL)** is a condition caused by the **Epstein-Barr Virus (EBV)**, typically occurring in immunocompromised individuals (especially those with HIV/AIDS) [1]. The virus replicates within the squamous epithelial cells of the tongue. Histologically, OHL is characterized by hyperparakeratosis, acanthosis, and "balloon cells" in the upper stratum spinosum [1]. The hallmark finding is the presence of **intranuclear viral inclusions** (Cowdry type A or "ground-glass" nuclei) representing active EBV replication. **Analysis of Incorrect Options:** * **Solar cheilitis:** This is a premalignant condition caused by chronic sun exposure (actinic damage) to the lips. Histology shows epithelial atrophy and **basophilic degeneration of collagen (solar elastosis)**, not viral inclusions. * **Minor aphthous ulcers:** These are common, painful ulcers of unknown etiology (likely T-cell mediated immune response). Histology shows a non-specific inflammatory fibrinopurulent membrane covering granulation tissue. * **Geographic tongue (Benign Migratory Glossitis):** This is an inflammatory condition characterized by the loss of filiform papillae. Histology shows **Munro’s microabscesses** (neutrophils in the keratin layer), similar to psoriasis, but no viral inclusions. **High-Yield Pearls for NEET-PG:** * **OHL Location:** Almost always occurs on the **lateral borders** of the tongue [1]. * **Clinical Significance:** It is often the first clinical sign of HIV infection or progression to AIDS [1]. * **Distinction:** Unlike Candidiasis, OHL **cannot be scraped off** [1]. * **Other Viral Inclusions:** Remember **Cowdry Type A** (HSV, VZV), **Cowdry Type B** (Polio), and **Owl’s Eye** appearance (CMV) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 737-738. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 366-367.

Question 69: Which of the following is NOT an example of a granulomatous disease?

A. Tuberculosis
B. Leprosy
C. Sarcoidosis
D. Mycoplasma infection (Correct Answer)

Explanation: **Explanation:** The core concept tested here is the distinction between **granulomatous inflammation** (a specific pattern of chronic inflammation) and acute/non-specific inflammation. [4] **Why Mycoplasma infection is the correct answer:** *Mycoplasma pneumoniae* typically causes **atypical pneumonia**, characterized by an interstitial inflammatory infiltrate consisting primarily of **lymphocytes and plasma cells**, not granulomas. It lacks the persistent, indigestible antigenic stimulus required to trigger a Type IV hypersensitivity reaction and subsequent granuloma formation. [1] **Why the other options are incorrect:** * **Tuberculosis (A):** The prototype of granulomatous disease. It features **caseating granulomas** with Langhans giant cells, driven by the cell wall lipids of *M. tuberculosis*. [4] * **Leprosy (B):** Caused by *M. leprae*. Depending on the immune response, it presents as **tuberculoid leprosy** (well-formed granulomas) or **lepromatous leprosy** (foamy macrophages/histiocytes). * **Sarcoidosis (C):** A multisystem disease of unknown etiology characterized by **non-caseating granulomas**. [1] A key histological feature is the presence of Schaumann bodies and Asteroid bodies. **NEET-PG High-Yield Pearls:** 1. **Definition:** A granuloma is a microscopic aggregation of **epithelioid histiocytes** (activated macrophages) surrounded by a collar of lymphocytes. [3] 2. **Caseating vs. Non-caseating:** TB is the classic cause of caseating necrosis. [4] Sarcoidosis, Crohn’s disease, and Berylliosis typically present with non-caseating granulomas. [1] 3. **Giant Cells:** Look for **Langhans giant cells** (peripheral nuclei) in TB and **Foreign body giant cells** (disorganized nuclei) in response to sutures or talc. [2][3] 4. **Cat-Scratch Disease:** Notable for causing **stellate (star-shaped) necrotizing granulomas**. **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] 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. 196-197. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.

Question 70: HIV infection is known to cause which of the following renal pathologies?

A. Membranous glomerulonephritis
B. Fibrillary glomerulopathy
C. Collapsing glomerulonephritis (Correct Answer)
D. Rapidly progressive glomerulonephritis (RPGN)

Explanation: **Explanation:** **HIV-Associated Nephropathy (HIVAN)** is a classic manifestation of renal involvement in HIV patients, particularly those of African descent. The hallmark pathological finding is **Collapsing Glomerulonephritis**, which is a severe variant of Focal Segmental Glomerulosclerosis (FSGS) [1]. 1. **Why Option C is Correct:** In HIVAN, the virus directly or indirectly (via cytokines) infects glomerular visceral epithelial cells (podocytes). This leads to the characteristic **"collapsing"** of the glomerular tuft, accompanied by podocyte hypertrophy and hyperplasia [2]. Other typical features include microcystic dilation of tubules and prominent tubuloreticular inclusions (seen on electron microscopy), which are induced by high levels of interferon-alpha. 2. **Why Other Options are Incorrect:** * **Option A (Membranous GN):** This is more commonly associated with Hepatitis B, Hepatitis C, and certain malignancies, but not typically the primary lesion of HIV [2]. * **Option B (Fibrillary Glomerulopathy):** This is a rare condition characterized by extracellular deposits of non-amyloid fibrils. It is not specifically linked to HIV infection. * **Option D (RPGN):** While HIV patients can develop various forms of glomerulonephritis (like IgA nephropathy or Lupus-like GN), RPGN is a clinical syndrome of rapid renal decline with "crescents" on biopsy, not the characteristic pathology of HIVAN. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Link:** HIVAN is strongly associated with **APOL1 gene** variants on chromosome 22 [1]. * **Morphology:** Look for "wrinkling" of the basement membrane and "global collapse" of the capillary loops [2]. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) has significantly reduced the incidence and progression of HIVAN. * **Differential:** While HIV causes the "Collapsing" variant, **Heroin-associated nephropathy** also presents as FSGS but usually lacks the collapsing feature. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 923-925. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 531-532.

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Infectious Disease Pathology in Immunocompromised Hosts

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