Infectious Diseases — MCQs

A 42-year-old man presents with a constant bad taste in his mouth for the past month. Physical examination reveals white, fluffy patches on the sides of his tongue that cannot be scraped off. A biopsy shows squamous epithelial hyperkeratosis, parakeratosis, and koilocytosis. Immunohistochemical staining for Epstein-Barr virus (EBV) is positive. Which of the following is the most likely risk factor for his oral lesions?

Q37Medium

A 52-year-old man presents with fever and cough productive of thick, gelatinous sputum that has worsened over 4 days. Physical examination reveals a temperature of 38.2°C. Auscultation of the chest shows diffuse crackles at the right lung base. Laboratory studies show a WBC count of 13,240/mm³ with 71% segmented neutrophils, 8% bands, 15% lymphocytes, and 6% monocytes. A sputum Gram stain reveals Gram-negative bacilli with mucoid capsules. His condition improves after a course of gentamicin therapy. Which of the following complications of this infection is he most likely to develop?

Q38Easy

Rasmussen's aneurysm involves which of the following?

Q39Easy

Warthin-Finkeldey giant cells are seen in which of the following conditions?

Q40Easy

All of the following organisms can cause serious infection in chronic granulomatous disease except?

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 31: What is the most common tumor associated with AIDS?

A. Carcinoma
B. Kaposi's sarcoma (Correct Answer)
C. Melanoma
D. Ewing's sarcoma

Explanation: **Explanation:** **Kaposi’s Sarcoma (KS)** is the most common neoplasm associated with AIDS [1], occurring in approximately 15–20% of untreated HIV-infected individuals. It is a vascular tumor caused by **Human Herpesvirus 8 (HHV-8)** [4], also known as Kaposi Sarcoma-associated Herpesvirus (KSHV). In the context of AIDS, it is classified as an "AIDS-defining illness." The pathogenesis involves the virus infecting spindle cells (of endothelial origin), leading to proliferation, angiogenesis, and inflammation, typically presenting as purple-red cutaneous nodules or plaques [2]. **Analysis of Incorrect Options:** * **A. Carcinoma:** While certain carcinomas (like invasive cervical cancer and anal cancer) are increased in frequency due to HPV co-infection in AIDS patients, they are not as classically associated or as frequent as Kaposi’s Sarcoma [1]. * **C. Melanoma:** There is no direct causal link between HIV/AIDS and melanoma. While immunosuppression can increase the risk of skin cancers, melanoma is not the most common tumor in this population. * **D. Ewing’s Sarcoma:** This is a primary bone tumor typically seen in children and adolescents. It is not associated with viral infections or immunodeficiency states like AIDS. **High-Yield Clinical Pearls for NEET-PG:** * **Second most common tumor in AIDS:** Non-Hodgkin Lymphoma (specifically Diffuse Large B-Cell Lymphoma and Burkitt Lymphoma) [3]. * **Histology of KS:** Characterized by slit-like vascular spaces containing extravasated red blood cells and spindle-shaped stromal cells [2]. * **CD4 Count:** KS can occur at various stages but is most prevalent when CD4 counts drop below 200 cells/mm³. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) often leads to the regression of KS lesions by improving immune function. **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. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 526-527. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 262-263. [4] 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. 219-220.

Question 32: A 24-year-old man is infected with HIV during a sexual encounter. During the asymptomatic latent phase of his infection, the virus is actively proliferating and can be found in association with which of the following?

A. B lymphocytes
B. Follicular dendritic cells in lymph nodes (Correct Answer)
C. Ganglion cells
D. Oligodendrocytes

Explanation: ### Explanation **Correct Option: B. Follicular dendritic cells in lymph nodes** During the **asymptomatic latent phase** of HIV infection, while the viral load in the peripheral blood is low, the virus is not truly "latent." It is actively replicating within the lymphoid tissues [2]. **Follicular Dendritic Cells (FDCs)** in the germinal centers of lymph nodes play a critical role here. They trap HIV particles coated with antibodies and complement on their surface via Fc and complement receptors [1]. These trapped virions serve as a continuous reservoir, infecting passing CD4+ T cells. This persistent viral replication eventually leads to the gradual attrition of the CD4+ T cell population [2]. **Analysis of Incorrect Options:** * **A. B lymphocytes:** While B cell follicles are the site of viral sequestration, B cells themselves are not the primary reservoirs or hosts for HIV replication. HIV primarily infects cells expressing CD4 and coreceptors (CCR5/CXCR4). * **C. Ganglion cells:** These are associated with the latency of the Herpes Simplex Virus (HSV), not HIV. HIV can enter the CNS via macrophages (Trojan horse mechanism), but it does not reside in ganglion cells. * **D. Oligodendrocytes:** These cells are the target of the **JC virus**, which causes Progressive Multifocal Leukoencephalopathy (PML) in immunocompromised HIV patients. HIV itself primarily infects microglia and macrophages in the brain. **NEET-PG High-Yield Pearls:** * **The "Trojan Horse" Theory:** Macrophages are the primary vehicles for HIV entry into the CNS and serve as a reservoir in late stages. * **Coreceptor Switch:** Early in the disease, the virus is **M-tropic** (uses **CCR5**); in later stages, it often switches to **T-tropic** (uses **CXCR4**). * **Diagnosis of Latency:** The clinical latency period is characterized by high viral turnover in lymphoid organs despite low plasma viremia [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 555-556. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 258-259.

Question 33: In a granuloma, from which cell type are the epithelioid and giant cells derived?

A. T cells
B. B cells
C. Plasma cells
D. Monocytes (Correct Answer)

Explanation: **Explanation:** The formation of a **granuloma** is a hallmark of Type IV (delayed-type) hypersensitivity reactions, typically seen in chronic infections like Tuberculosis or Sarcoidosis. **1. Why Monocytes are correct:** The central cell of a granuloma is the **activated macrophage**. When an offending agent (like *M. tuberculosis*) cannot be easily eliminated, T-helper 1 (Th1) cells secrete **Interferon-gamma (IFN-̳)** [1]. This cytokine activates circulating **monocytes**, which migrate into the tissue and transform into: * **Epithelioid cells:** Macrophages that have gained increased secretory capacity but lost phagocytic ability [1]. They resemble epithelial cells with abundant pink cytoplasm and slipper-shaped nuclei. * **Giant cells:** Formed by the fusion of multiple activated macrophages (e.g., Langhans giant cells with peripheral nuclei or Foreign body giant cells with disorganized nuclei) [1]. **2. Why other options are incorrect:** * **T cells (A):** While Th1 cells are essential for *initiating* the granuloma by secreting IFN-̳, they do not physically transform into epithelioid or giant cells [1]. * **B cells (B) & Plasma cells (C):** These are involved in humoral immunity. While they may be found in the "lymphocytic rim" surrounding a granuloma, they do not differentiate into the characteristic epithelioid cells [1]. **High-Yield Facts for NEET-PG:** * **Key Cytokine:** IFN-̳ is the most important cytokine for macrophage activation and granuloma formation. * **TNF-̑:** Essential for *maintaining* the structural integrity of a granuloma (Anti-TNF drugs can cause breakdown of granulomas and reactivation of TB). * **Langhans Giant Cell:** Characteristic of "immune" granulomas (TB); nuclei are arranged in a **horseshoe pattern** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Question 34: Which disease is transmitted by all components of blood?

A. Malaria (Correct Answer)
B. Syphilis
C. Toxoplasma
D. H. pylori

Explanation: **Explanation:** **Malaria (Option A)** is the correct answer because the *Plasmodium* parasite resides within erythrocytes (RBCs). However, during the erythrocytic cycle, parasites are also present in the plasma during merozoite release [1]. Since blood transfusion involves the transfer of RBCs, WBCs, platelets, and plasma, malaria can be transmitted through **whole blood** as well as any **individual blood component** (packed RBCs, fresh frozen plasma, or cryopreserved platelets) [2]. It is one of the most common transfusion-transmitted infections (TTI) in endemic regions [2]. **Why the other options are incorrect:** * **Syphilis (Option B):** While *Treponema pallidum* can be transmitted via fresh blood, it is highly sensitive to cold. It cannot survive at standard blood bank storage temperatures ($4^\circ\text{C}$) for more than 72 hours. Therefore, stored blood components pose a negligible risk. * **Toxoplasma (Option C):** *Toxoplasma gondii* is primarily an intracellular parasite of nucleated cells (WBCs) [2]. While transmission via leukocyte-rich components is theoretically possible, it is not transmitted by all components (like cell-free plasma) and is an extremely rare TTI. * **H. pylori (Option D):** This is a gastrointestinal pathogen colonizing the stomach lining. It is transmitted via the fecal-oral or oral-oral route, not through blood transfusion. **NEET-PG High-Yield Pearls:** * **Storage Lesion:** Malaria parasites can survive in stored blood at $4^\circ\text{C}$ for up to 3 weeks. * **Incubation Period:** Transfusion-induced malaria has a shorter incubation period because it bypasses the pre-erythrocytic (hepatic) stage. * **Screening:** In India, mandatory screening of donor blood includes HIV I & II, Hepatitis B (HBsAg), Hepatitis C (HCV), Syphilis (VDRL), and Malaria. * **TTI Risk:** HIV and Hepatitis B/C are the most clinically significant viral TTIs, but Malaria remains the classic answer for transmission via "all components." **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 398-400. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 628-631.

Question 35: The Maltese cross morphology is characteristic of which of the following parasitic infections?

A. Pneumocystis carinii
B. Leishmaniasis
C. Cryptococcosis
D. Babesiosis (Correct Answer)

Explanation: **Explanation:** The **Maltese cross** appearance is a pathognomonic finding in **Babesiosis**, a tick-borne zoonosis caused by *Babesia microti*. This morphology occurs when the parasite undergoes asexual reproduction (merogony) within host erythrocytes, resulting in a **tetrad of merozoites** joined at their bases. **Why the other options are incorrect:** * **Pneumocystis carinii (jirovecii):** On silver stains (GMS), these appear as crushed ping-pong balls or cup-shaped cysts with a central dark spot, but they do not form tetrads. * **Leishmaniasis:** Characterized by **LD bodies** (amastigotes) within macrophages. These are oval bodies with a distinct nucleus and a rod-shaped kinetoplast, not a cross shape. * **Cryptococcosis:** While *Cryptococcus neoformans* exhibits a "Maltese cross" appearance under **polarized light** when stained with specific dyes (due to the birefringence of its capsule), it is a fungus, not a parasite. In the context of parasitic morphology on a standard blood smear, the term specifically refers to Babesia. **NEET-PG High-Yield Pearls:** * **Vector:** *Ixodes scapularis* tick (the same vector as Lyme disease). * **Diagnosis:** Thick and thin peripheral blood smears (Giemsa/Wright stain). * **Distinction from Malaria:** Unlike *Plasmodium falciparum*, Babesia lacks hemozoin pigment and does not have a gametocyte stage [1]. * **Clinical Presentation:** Fever, hemolytic anemia, and hemoglobinuria. It is particularly severe in asplenic patients. * **Treatment:** Atovaquone + Azithromycin (preferred) or Clindamycin + Quinine. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 400.

Question 36: A 42-year-old man presents with a constant bad taste in his mouth for the past month. Physical examination reveals white, fluffy patches on the sides of his tongue that cannot be scraped off. A biopsy shows squamous epithelial hyperkeratosis, parakeratosis, and koilocytosis. Immunohistochemical staining for Epstein-Barr virus (EBV) is positive. Which of the following is the most likely risk factor for his oral lesions?

A. Chronic alcohol abuse
B. Diabetes mellitus
C. HIV infection (Correct Answer)
D. Pernicious anemia

Explanation: ### Explanation The clinical presentation and histopathology describe **Oral Hairy Leukoplakia (OHL)**. **1. Why HIV infection is the correct answer:** Oral Hairy Leukoplakia is a benign, white, corrugated (fluffy) lesion typically found on the **lateral borders of the tongue** [1]. Key diagnostic features include: * **Clinical:** Unlike Oral Candidiasis, OHL **cannot be scraped off** [1]. * **Etiology:** It is caused by the **Epstein-Barr Virus (EBV)** [1]. * **Histopathology:** Shows hyperkeratosis, parakeratosis (nuclei in the stratum corneum), and **koilocytosis** (balloon cells in the upper stratum spinosum) [1]. * **Association:** OHL is highly specific for **HIV infection** or other states of profound immunosuppression [1]. In an otherwise healthy-appearing patient, it is often the first clinical sign of HIV/AIDS. **2. Why the incorrect options are wrong:** * **A. Chronic alcohol abuse:** This is a risk factor for squamous cell carcinoma and traditional leukoplakia (a premalignant lesion), but not specifically for EBV-mediated OHL [3]. * **B. Diabetes mellitus:** While diabetics are prone to *Oral Candidiasis* (thrush), those lesions are easily scraped off and show fungal hyphae, not EBV-positive koilocytosis [1], [4]. * **D. Pernicious anemia:** This typically presents with **Atrophic Glossitis** (a smooth, red "beefy" tongue) due to Vitamin B12 deficiency, rather than white hyperkeratotic patches. **3. NEET-PG High-Yield Pearls:** * **OHL vs. Candidiasis:** OHL = Cannot be scraped off; Candidiasis = Can be scraped off (leaving an erythematous base) [1], [4]. * **OHL vs. Leukoplakia:** OHL is **not** premalignant; traditional Leukoplakia is a premalignant condition [3]. * **EBV Associations:** OHL, Burkitt Lymphoma, Nasopharyngeal Carcinoma, and Infectious Mononucleosis [2]. * **Koilocytes:** While usually associated with HPV (Cervical cancer/Warts), in the specific context of the lateral tongue and EBV positivity, they indicate OHL [1]. **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. Diseases of the Immune System, pp. 261-262. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 344-345. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 736-737.

Question 37: A 52-year-old man presents with fever and cough productive of thick, gelatinous sputum that has worsened over 4 days. Physical examination reveals a temperature of 38.2°C. Auscultation of the chest shows diffuse crackles at the right lung base. Laboratory studies show a WBC count of 13,240/mm³ with 71% segmented neutrophils, 8% bands, 15% lymphocytes, and 6% monocytes. A sputum Gram stain reveals Gram-negative bacilli with mucoid capsules. His condition improves after a course of gentamicin therapy. Which of the following complications of this infection is he most likely to develop?

A. Abscess formation (Correct Answer)
B. Adenocarcinoma
C. Bullous emphysema
D. Cavitary granulomas

Explanation: The clinical presentation of fever, cough, and **thick, gelatinous (currant jelly) sputum** in an older patient, combined with a Gram stain showing **Gram-negative bacilli with mucoid capsules**, is pathognomonic for **Klebsiella pneumoniae** infection [1]. **1. Why the Correct Answer is Right:** *Klebsiella pneumoniae* is a common cause of community-acquired pneumonia, particularly in individuals with underlying conditions like alcoholism or diabetes [1]. Unlike *Streptococcus pneumoniae*, which typically causes lobar pneumonia with resolution of the alveolar architecture, *Klebsiella* is a **tissue-destroying organism**. It causes significant inflammation and necrosis of the lung parenchyma, which frequently leads to **abscess formation** and cavitation [2]. The "currant jelly" appearance of the sputum is due to the abundant capsular polysaccharide produced by the bacteria. **2. Why the Incorrect Options are Wrong:** * **B. Adenocarcinoma:** While chronic inflammation can sometimes predispose to malignancy (e.g., scar carcinoma), there is no direct or common link between acute *Klebsiella* pneumonia and lung cancer. * **C. Bullous emphysema:** This is a chronic obstructive pulmonary disease (COPD) finding characterized by permanent enlargement of airspaces, usually due to smoking or alpha-1 antitrypsin deficiency, not acute bacterial infection. * **D. Cavitary granulomas:** These are characteristic of **Mycobacterium tuberculosis** or fungal infections (like Histoplasmosis), which present with a more chronic course and distinct histopathology (Ghon complex/caseating necrosis). **Clinical Pearls for NEET-PG:** * **Organism:** *Klebsiella pneumoniae* (Friedländer's bacillus). * **Classic Patient:** Chronic alcoholic, diabetic, or elderly [1]. * **Key Sign:** "Currant jelly" sputum (due to thick mucoid capsule). * **Radiology:** Often involves the upper lobes; may show a "bulging fissure sign" due to heavy inflammatory exudate. * **Complication:** High incidence of lung abscess and permanent scarring [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 715. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 715-716.

Question 38: Rasmussen's aneurysm involves which of the following?

A. Bronchial artery aneurysm
B. Pulmonary artery aneurysm (Correct Answer)
C. Vertebral artery aneurysm
D. Posterior intercostal artery aneurysm

Explanation: **Explanation:** **Rasmussen’s aneurysm** is a clinical phenomenon associated with **chronic cavitary pulmonary tuberculosis**. It refers to an inflammatory pseudoaneurysm of a **pulmonary artery** branch located within the wall of a tuberculous cavity. 1. **Why the correct answer is right:** In chronic tuberculosis, the progressive inflammation and necrosis (caseation) of the lung parenchyma eventually erode the walls of adjacent pulmonary arteries. As the surrounding lung tissue is destroyed, the arterial wall thins and weakens, leading to a localized dilation or "aneurysm." If this aneurysm ruptures into the cavity, it results in massive, life-threatening **hemoptysis**. 2. **Why the incorrect options are wrong:** * **Option A (Bronchial artery):** While bronchial arteries are the most common source of *general* hemoptysis in TB (due to hypertrophy under high pressure), they do not form the specific "Rasmussen’s aneurysm." * **Option C & D (Vertebral/Posterior intercostal):** These are systemic arteries. While vertebral arteries can be involved in cervical trauma or connective tissue disorders, and intercostal arteries in Coarctation of the Aorta, they have no pathological link to pulmonary TB cavities. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Usually occurs in the upper lobes (where TB cavities are most common). * **Pathology:** It is technically a *pseudoaneurysm* because it lacks all three layers of the arterial wall. * **Radiology/Management:** Diagnosed via CT Angiography; the treatment of choice for an unstable patient is **Bronchial/Pulmonary Artery Embolization (BAE)**. * **Differential:** Do not confuse with **Dieulafoy’s lesion** (a vascular malformation in the bronchus) which can also cause massive hemoptysis.

Question 39: Warthin-Finkeldey giant cells are seen in which of the following conditions?

A. Mumps
B. Rubella
C. Measles (Correct Answer)
D. Polio

Explanation: ### Explanation **Correct Answer: C. Measles** **Underlying Concept:** Warthin-Finkeldey giant cells are the pathognomonic histological hallmark of **Measles (Rubeola)** [1]. These are large, multinucleated giant cells formed by the fusion of infected lymphocytes or macrophages under the influence of the measles virus fusion (F) protein. Key features of these cells include: * **Location:** Found in lymphoid tissues such as the tonsils, adenoids, lymph nodes, and Peyer’s patches. * **Morphology:** They contain up to 50–100 nuclei and characteristic **eosinophilic inclusion bodies** in both the cytoplasm and the nucleus (Cowdry type A inclusions). --- **Analysis of Incorrect Options:** * **A. Mumps:** Characterized by interstitial edema and mononuclear cell infiltration of the parotid gland. It does not produce Warthin-Finkeldey cells. * **B. Rubella (German Measles):** While it presents with lymphadenopathy (typically post-auricular), the histology shows follicular hyperplasia without the specific giant cells seen in Rubeola. * **D. Polio:** Primarily affects the anterior horn cells of the spinal cord, leading to neuronal necrosis and microglial nodules, not lymphoid giant cells. --- **High-Yield Clinical Pearls for NEET-PG:** * **Koplik Spots:** Small white spots on the buccal mucosa (opposite the lower 2nd molar); these are the clinical pathognomonic sign of measles [1]. * **Inclusions:** Measles is unique for having **both** intracytoplasmic and intranuclear inclusions. * **Complications:** The most common cause of death in children with measles is **pneumonia** (Hecht’s giant cell pneumonia), while the most dreaded late neurological complication is **SSPE** (Subacute Sclerosing Panencephalitis) [1]. * **Vitamin A:** Supplementation reduces morbidity and mortality in measles-infected children. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 362-363.

Question 40: All of the following organisms can cause serious infection in chronic granulomatous disease except?

A. Streptococcus pneumoniae (Correct Answer)
B. Staphylococcus aureus
C. Pseudomonas
D. Haemophilus influenzae

Explanation: The core defect in **Chronic Granulomatous Disease (CGD)** is a deficiency in the **NADPH oxidase enzyme**, which prevents phagocytes (neutrophils and macrophages) from producing reactive oxygen species (ROS), specifically the superoxide radical. This leads to an inability to perform the "oxidative burst" necessary to kill certain pathogens. **Why Streptococcus pneumoniae is the correct answer:** *S. pneumoniae* is a **Catalase-negative** organism [1]. Catalase-negative bacteria produce their own hydrogen peroxide ($H_2O_2$) as a metabolic byproduct. Since CGD patients lack NADPH oxidase but have functional myeloperoxidase, they can "hijack" the $H_2O_2$ produced by the bacteria itself to create hypochlorite and kill the pathogen. Therefore, CGD patients are not at increased risk for serious infections from *S. pneumoniae* [3]. **Why the other options are incorrect:** * **Staphylococcus aureus, Pseudomonas, and Haemophilus influenzae** are all **Catalase-positive** organisms [1]. Catalase neutralizes the $H_2O_2$ produced by the bacteria. In CGD patients, who cannot produce their own ROS, there is no $H_2O_2$ available for the myeloperoxidase system to use. Consequently, these organisms survive and cause recurrent, severe infections [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most commonly **X-linked recessive** (CYBB gene mutation). * **Diagnosis:** The **Dihydrorhodamine (DHR) 123 flow cytometry** test is the current gold standard (replaces the older Nitroblue Tetrazolium/NBT slide test). * **Common Pathogens (The "Big 5"):** *Staphylococcus aureus, Burkholderia cepacia, Serratia marcescens, Nocardia,* and *Aspergillus*. * **Clinical Feature:** Recurrent pyogenic infections and granuloma formation in the skin, liver, and GI tract. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 709-711. [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. 64-65. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 714-715.

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