Infectious Diseases — MCQs

A 30-year-old male with a history of high-grade fever with rigors followed by profuse sweating is admitted to the ICU after an episode of generalized tonic-clonic seizure. The patient was comatose with no focal neurological deficit or signs of meningeal irritation. The eyes were divergent, and the pout reflex was present. What is an important cause of death in this setting?

Q124Medium

Which of the following is NOT true of kala-azar?

Q125Medium

An 18-year-old woman presents with a 2-day history of sore throat. Which of the following constellation of symptoms and signs is most consistent with group-A streptococcal pharyngitis?

Q126Medium

In falciparum malaria, which of the following is NOT a cause of anemia?

Q127Easy

Massive myoclonus is a hallmark of which stage of Subacute Sclerosing Panencephalitis (SSPE)?

Q128Medium

A 45-year-old woman is undergoing chemotherapy for breast cancer and presents 10 days after her last treatment with fever (temperature >38.5°C) and a sore throat. On examination, she has oral mucositis, and her WBC count is 800/mL with an absolute neutrophil count below 500/mL. Other investigations, including CXR, urinalysis, and biochemistry, are normal. What is the most appropriate next step in management?

Q129Easy

What is the most common malignancy in patients with HIV?

Q130Easy

Antiretroviral drugs are started for HIV/AIDS patients if the CD4 count is:

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 121: In the management of complications of falciparum malaria, which of the following is generally avoided?

A. Phenobarbitone
B. Dexamethasone (Correct Answer)
C. Quinine
D. Blood transfusion

Explanation: In the management of severe falciparum malaria (specifically cerebral malaria), **Dexamethasone** is strictly contraindicated. ### Why Dexamethasone is Avoided Historically, steroids were used to reduce suspected cerebral edema in malaria. However, landmark clinical trials demonstrated that Dexamethasone is not only **ineffective** in reducing mortality but is actually **harmful**. It is associated with an increased risk of secondary infections, gastrointestinal bleeding, and prolonged duration of coma. Current WHO guidelines explicitly state that corticosteroids should not be used in cerebral malaria [1]. ### Analysis of Other Options * **Phenobarbitone (A):** While high prophylactic doses are avoided due to respiratory depression, it remains a standard treatment for controlling active seizures in cerebral malaria. * **Quinine (C):** Although Artesunate is now the first-line drug for severe malaria, Quinine remains an effective alternative and a mainstay of treatment in many protocols, especially when parenteral artesunate is unavailable [1]. * **Blood Transfusion (D):** This is a life-saving intervention in severe malaria complicated by severe anemia (Hemoglobin <5 g/dL or Hematocrit <15%) or hyperparasitemia [1]. ### NEET-PG High-Yield Pearls * **Drug of Choice (DOC):** IV Artesunate is the DOC for all cases of severe malaria (including cerebral malaria and pregnancy) [1]. * **Other Avoided Adjuvants:** Besides steroids, osmotic diuretics (like Mannitol), Heparin, and Adrenaline are generally avoided in cerebral malaria unless specific indications exist. * **Blackwater Fever:** This is a complication of falciparum malaria (often associated with irregular Quinine use) characterized by massive intravascular hemolysis and hemoglobinuria [2].

Question 122: Which type of cell is present in large numbers in the peritoneal fluid of patients with tuberculous peritonitis?

A. Eosinophils
B. Polymorphs
C. Lymphocytes (Correct Answer)
D. Monocytes

Explanation: **Explanation:** Tuberculous peritonitis is a form of chronic granulomatous inflammation caused by *Mycobacterium tuberculosis*. The correct answer is **Lymphocytes** because the body’s immune response to TB is a **Type IV hypersensitivity reaction** (delayed-type), which is primarily cell-mediated [1]. 1. **Why Lymphocytes are correct:** In TB peritonitis, the peritoneal fluid is typically an **exudate** (protein >3g/dL). The inflammatory process triggers a massive influx of mononuclear cells, specifically T-lymphocytes, to the site of infection to form granulomas [2]. A lymphocyte count exceeding **70%** of the total white cell count in the ascitic fluid is a hallmark finding. 2. **Why other options are incorrect:** * **Polymorphs (Neutrophils):** These are characteristic of acute bacterial infections, such as Spontaneous Bacterial Peritonitis (SBP). In TB, they may only be seen in the very early acute phase. * **Eosinophils:** These are associated with parasitic infections, allergic reactions, or continuous ambulatory peritoneal dialysis (CAPD). * **Monocytes:** While part of the mononuclear family, they are not the predominant cell type compared to the overwhelming lymphocytic response in TB. **High-Yield Clinical Pearls for NEET-PG:** * **SAAG (Serum-Ascites Albumin Gradient):** In TB peritonitis, the SAAG is typically **low (<1.1 g/dL)**, indicating a non-portal hypertensive etiology. * **Gold Standard Diagnosis:** Peritoneal biopsy showing caseating granulomas (highest sensitivity). * **Biochemical Marker:** Elevated **Adenosine Deaminase (ADA)** levels in ascitic fluid (usually >30-40 U/L) is a highly sensitive screening tool for TB peritonitis. * **Appearance:** The fluid is often "straw-colored" or turbid.

Question 123: A 30-year-old male with a history of high-grade fever with rigors followed by profuse sweating is admitted to the ICU after an episode of generalized tonic-clonic seizure. The patient was comatose with no focal neurological deficit or signs of meningeal irritation. The eyes were divergent, and the pout reflex was present. What is an important cause of death in this setting?

A. Acidosis (Correct Answer)
B. Aspiration
C. Hypoglycemia
D. Anemia

Explanation: ### Explanation The clinical presentation of high-grade fever with rigors followed by sweating, coupled with a seizure and coma (without meningeal signs), is classic for **Cerebral Malaria** caused by *Plasmodium falciparum*. **1. Why Acidosis is the Correct Answer:** In severe malaria, **Metabolic Acidosis** (specifically lactic acidosis) is the most important independent predictor of mortality [2]. It occurs due to several factors: * **Microvascular Obstruction:** Cytoadherence of parasitized RBCs to vascular endothelium leads to tissue hypoxia. * **Anaerobic Metabolism:** Hypoxia forces tissues to switch to anaerobic glycolysis, producing lactate [2]. * **Reduced Clearance:** Impaired hepatic and renal clearance of lactate further exacerbates the condition. Acidosis often manifests clinically as "Kussmaul breathing" (air hunger) and is a terminal event in many cases. **2. Why the Other Options are Incorrect:** * **B. Aspiration:** While a risk in comatose patients [1], it is a complication of the state rather than the primary pathophysiological driver of death in severe malaria. * **C. Hypoglycemia:** Common in severe malaria (especially in children and pregnant women or due to quinine therapy), it can cause seizures and coma [1]. However, when compared to acidosis, acidosis carries a higher prognostic weight for mortality. * **D. Anemia:** Severe malarial anemia is a major cause of morbidity and mortality, particularly in children, but in an adult presenting with acute encephalopathy (Cerebral Malaria), metabolic derangements like acidosis are more immediate causes of death. **Clinical Pearls for NEET-PG:** * **Cerebral Malaria Definition:** Coma (GCS <11) persisting >6 hours after a seizure, with *P. falciparum* parasitemia, after excluding other encephalopathies [1]. * **Retinopathy:** Malarial retinopathy (hemorrhages, vessel whitening) is the most specific diagnostic sign for cerebral malaria. * **Pout Reflex:** Presence of primitive reflexes (like the pout reflex) indicates diffuse cortical dysfunction in cerebral malaria. * **Drug of Choice:** IV Artesunate is the preferred treatment for severe malaria, regardless of the species.

Question 124: Which of the following is NOT true of kala-azar?

A. Persistent hypergammaglobulinemia
B. Pancytopenia
C. Cancrum oris can occur
D. Full treatment prevents post-kala-azar dermal leishmaniasis (Correct Answer)

Explanation: The correct answer is **D**. Post-Kala-azar Dermal Leishmaniasis (PKDL) is a sequela of visceral leishmaniasis (Kala-azar) that typically appears months to years after the initial infection [4]. Crucially, **full treatment of the primary visceral disease does not guarantee the prevention of PKDL.** In fact, PKDL is considered an immunopathological reaction where the parasite persists in the skin despite clinical cure of the systemic visceral infection. In the Indian subcontinent, approximately 5-10% of treated patients develop PKDL. **Analysis of other options:** * **A. Persistent hypergammaglobulinemia:** This is a hallmark of Kala-azar. There is a massive, polyclonal stimulation of B-cells leading to a reversal of the Albumin-Globulin (A:G) ratio. * **B. Pancytopenia:** Parasitization of the reticuloendothelial system, particularly the bone marrow, along with hypersplenism (due to massive splenomegaly), leads to anemia, leucopenia, and thrombocytopenia [1]. * **C. Cancrum oris:** In severe, malnourished, or immunocompromised cases of Kala-azar, secondary bacterial infections can lead to "Cancrum oris" (noma), a destructive gangrenous stomatitis. **NEET-PG High-Yield Pearls:** * **Vector:** *Phlebotomus argentipes* (Sandfly) [2]. * **Gold Standard Diagnosis:** Bone marrow aspiration (most common) or Splenic aspiration (highest sensitivity) showing **LD bodies** (amastigotes) [3]. * **Drug of Choice:** Liposomal Amphotericin B (single dose 10mg/kg is the current WHO recommendation for India). * **PKDL Presentation:** Characterized by hypopigmented macules, papules, or nodules; it serves as a major reservoir for transmission in the community [4].

Question 125: An 18-year-old woman presents with a 2-day history of sore throat. Which of the following constellation of symptoms and signs is most consistent with group-A streptococcal pharyngitis?

A. Fever, anorexia, dysphagia, and hoarseness
B. Fever, runny nose, cough, myalgia, and poor appetite
C. Fever, no cough, tonsillar exudates, and tender anterior cervical lymphadenopathy (Correct Answer)
D. Fever, cough, pharyngeal erythema, and dysphagia

Explanation: ### Explanation The diagnosis of **Group A Streptococcal (GAS) pharyngitis** is clinically guided by the **Centor Criteria** (or the modified McIsaac score). This scoring system helps clinicians differentiate between bacterial and viral etiologies of a sore throat. **1. Why Option C is Correct:** The constellation of **fever, absence of cough, tonsillar exudates, and tender anterior cervical lymphadenopathy** represents the classic four components of the Centor Criteria. * **Absence of cough** is a highly specific predictor for bacterial infection. * **Tender anterior cervical nodes** and **tonsillar exudates** are hallmark signs of local pyogenic inflammation caused by *Streptococcus pyogenes*. **2. Why Other Options are Incorrect:** * **Option A & D:** The presence of **hoarseness** or a significant **cough** strongly suggests a viral etiology (like Rhinovirus or Adenovirus) or irritation of the larynx/trachea, which is uncommon in isolated GAS pharyngitis. * **Option B:** Symptoms like **runny nose (coryza)**, **cough**, and generalized **myalgia** are classic indicators of a viral upper respiratory tract infection (URTI) or Influenza. GAS pharyngitis is typically a localized infection of the oropharynx without prominent nasal symptoms. **3. NEET-PG High-Yield Pearls:** * **Centor Criteria:** 1 point each for: (1) Fever, (2) Tonsillar exudates, (3) Tender anterior cervical adenopathy, (4) Absence of cough. (Age <15 adds 1 point; Age >45 subtracts 1 point). * **Gold Standard Diagnosis:** Throat culture (though Rapid Antigen Detection Test - RADT is used for immediate results). * **Treatment of Choice:** Penicillin V or Amoxicillin for 10 days. This is primarily done to prevent **Acute Rheumatic Fever**, though it only minimally shortens the duration of symptoms. * **Complication Note:** Antibiotics prevent Rheumatic Fever but do **not** prevent Post-Streptococcal Glomerulonephritis (PSGN).

Question 126: In falciparum malaria, which of the following is NOT a cause of anemia?

A. Hemolysis
B. Malabsorption (Correct Answer)
C. Spleen sequestration
D. Bone marrow depression

Explanation: Anemia is a hallmark of severe *Plasmodium falciparum* malaria, resulting from a multifactorial process involving the destruction and underproduction of red blood cells (RBCs) [1]. **Explanation of the Correct Answer:** **B. Malabsorption:** This is **not** a recognized mechanism of anemia in malaria. While malaria can cause gastrointestinal symptoms like vomiting or diarrhea, it does not lead to the chronic malabsorption of nutrients (like Vitamin B12 or Iron) required to cause acute or subacute malarial anemia. **Explanation of Incorrect Options:** * **A. Hemolysis:** This is the primary cause [2]. It occurs via two mechanisms: **Direct lysis** of RBCs by the parasite during the erythrocytic cycle [1] and **Immune-mediated destruction** of non-parasitized RBCs (bystander hemolysis) due to oxidative stress and antibody coating. * **C. Spleen sequestration:** The spleen filters damaged or less deformable parasitized RBCs [2]. In malaria, splenomegaly occurs as the splenic macrophages hyper-function to remove these cells from circulation, leading to increased sequestration and destruction [1]. * **D. Bone marrow depression:** Malaria causes "dyserythropoiesis." Inflammatory cytokines (like TNF-̑) released during infection suppress erythropoiesis and interfere with the effective utilization of iron, leading to a temporary state of bone marrow hypofunction [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Blackwater Fever:** Severe intravascular hemolysis leading to hemoglobinuria (dark urine) and acute renal failure, often associated with *P. falciparum* and quinine use [2]. * **Cerebral Malaria:** Characterized by the sequestration of parasitized RBCs in cerebral microvasculature via **cytoadherence** (mediated by PfEMP-1 protein). * **Hemozoin:** The "malaria pigment" found in monocytes and neutrophils on a peripheral smear, indicating recent or heavy parasite burden.

Question 127: Massive myoclonus is a hallmark of which stage of Subacute Sclerosing Panencephalitis (SSPE)?

A. Stage 1
B. Stage 2 (Correct Answer)
C. Stage 3
D. Stage 4

Explanation: Subacute Sclerosing Panencephalitis (SSPE) is a progressive, fatal neurodegenerative disease caused by a persistent infection with a mutant Measles virus. The clinical progression is classically divided into four stages [1]: * **Stage 1 (Behavioral):** Characterized by subtle changes including irritability, social withdrawal, and declining school performance. * **Stage 2 (Motor Regression):** This is the stage where **massive myoclonus** (periodic, synchronous muscle jerks) occurs. It is the hallmark of this stage, often accompanied by worsening motor coordination and seizures. * **Stage 3 (Extrapyramidal):** Myoclonus disappears and is replaced by severe extrapyramidal symptoms, including choreoathetosis, dystonia, and spasticity. * **Stage 4 (Terminal):** The patient enters a vegetative state, characterized by akinetic mutism, decorticate/decerebrate rigidity, and eventually death. **Why Stage 2 is correct:** Massive myoclonus is the defining clinical feature of Stage 2. These jerks are typically "slow," lasting 1–3 seconds, and involve the head, trunk, and limbs. **High-Yield Clinical Pearls for NEET-PG:** * **EEG Finding:** Characterized by **Radermecker complexes** (periodic, high-voltage, generalized slow-wave complexes). * **Diagnosis:** Elevated titers of **anti-measles antibodies** in both serum and CSF (intrathecal synthesis) [1]. * **CSF Analysis:** Shows a normal cell count but significantly elevated **gamma globulin** levels (oligoclonal bands). * **Risk Factor:** Early-age measles infection (usually <2 years old) with a latency period of 5–10 years.

Question 128: A 45-year-old woman is undergoing chemotherapy for breast cancer and presents 10 days after her last treatment with fever (temperature >38.5°C) and a sore throat. On examination, she has oral mucositis, and her WBC count is 800/mL with an absolute neutrophil count below 500/mL. Other investigations, including CXR, urinalysis, and biochemistry, are normal. What is the most appropriate next step in management?

A. Start empiric bacterial antibiotics. (Correct Answer)
B. Start empiric antifungal and bacterial antibiotics.
C. Administer acetaminophen until culture results are available.
D. Start antiviral medications for HSV-1.

Explanation: This patient presents with **Febrile Neutropenia**, defined as a single oral temperature of >38.3°C (or >38.0°C sustained for 1 hour) and an Absolute Neutrophil Count (ANC) <500 cells/mm³. This is a medical emergency in oncology patients [1]. **1. Why Option A is Correct:** In neutropenic patients, the inflammatory response is blunted, making fever often the only sign of a life-threatening infection [1]. The most common pathogens are skin and gut flora (e.g., *Pseudomonas aeruginosa*, *Staphylococcus aureus*). Because these infections can progress to septic shock within hours, **immediate empiric broad-spectrum intravenous antibiotics** (e.g., Piperacillin-Tazobactam, Cefepime, or Meropenem) must be started after blood cultures are drawn, without waiting for results [2]. **2. Why Other Options are Incorrect:** * **Option B:** Empiric antifungal therapy is typically reserved for patients who remain febrile after 4–7 days of broad-spectrum antibiotics and have no identified source. * **Option C:** Delaying antibiotics to wait for cultures is dangerous and associated with high mortality in neutropenic sepsis. * **Option D:** While mucositis can be associated with HSV, the primary threat to life is bacterial translocation; antivirals are not the first-line empiric treatment for fever unless specific lesions are present. **Clinical Pearls for NEET-PG:** * **ANC Calculation:** Total WBC × (% Neutrophils + % Bands). * **MASCC Score:** Used to determine if a patient is low-risk (eligible for oral antibiotics) or high-risk (requires IV admission). * **Monotherapy:** For most cases, anti-pseudomonal beta-lactam monotherapy is sufficient. Vancomycin is added only if there is clinical suspicion of MRSA, catheter infection, or skin/soft tissue edition.

Question 129: What is the most common malignancy in patients with HIV?

A. Lymphoma (Correct Answer)
B. Squamous Cell Carcinoma (SCC)
C. Adenocarcinoma
D. Fibroma

Explanation: **Explanation:** In the era of **Highly Active Antiretroviral Therapy (HAART)**, the epidemiology of malignancies in HIV patients has shifted. While Kaposi Sarcoma (KS) was historically the most common, **Non-Hodgkin Lymphoma (NHL)** is now recognized as the most common malignancy overall in HIV-infected individuals [2]. **Why Lymphoma is Correct:** HIV-associated lymphomas are primarily B-cell in origin (e.g., Diffuse Large B-cell Lymphoma and Burkitt Lymphoma). The underlying mechanism involves chronic B-cell activation, immune dysregulation, and the oncogenic role of co-infections like **Epstein-Barr Virus (EBV)** and **HHV-8** [2]. These are classified as "AIDS-Defining Illnesses." **Analysis of Incorrect Options:** * **B. Squamous Cell Carcinoma (SCC):** While HIV patients have a higher risk of SCC (particularly anal and cervical due to HPV co-infection), it is not as prevalent as lymphoma. * **C. Adenocarcinoma:** Though the risk of lung adenocarcinoma is increased in HIV patients (often due to high smoking rates), it is not the most common malignancy. * **D. Fibroma:** These are benign connective tissue tumors and are not specifically associated with or common in HIV. **High-Yield Clinical Pearls for NEET-PG:** * **Most common AIDS-defining malignancy:** Non-Hodgkin Lymphoma (specifically DLBCL). * **Most common "Non-AIDS Defining" malignancy:** Lung Cancer. * **Primary CNS Lymphoma:** Strongly associated with **EBV**; it is a critical differential for ring-enhancing lesions on MRI (alongside Toxoplasmosis). * **Kaposi Sarcoma:** Caused by **HHV-8**; it presents as violaceous skin lesions and was the most common malignancy *before* the widespread use of HAART [1].

Question 130: Antiretroviral drugs are started for HIV/AIDS patients if the CD4 count is:

A. < 500 cells/mm
B. < 350 cells/mm
C. < 200 cells/mm
D. Any CD4 count (Correct Answer)

Explanation: **Explanation:** The management of HIV has evolved significantly over the last decade. The correct answer is **D (Any CD4 count)**, reflecting the current **"Test and Treat"** policy. **1. Why "Any CD4 count" is correct:** Current WHO and National AIDS Control Organization (NACO) guidelines recommend that Antiretroviral Therapy (ART) should be initiated in **all** individuals living with HIV, regardless of their clinical stage or CD4 cell count [1]. This shift is based on the **START (Strategic Timing of AntiRetroviral Treatment) trial**, which demonstrated that early initiation of ART significantly reduces the risk of AIDS-defining events, non-AIDS-related complications (like cardiovascular or renal disease), and prevents horizontal transmission of the virus (U=U: Undetectable = Untransmittable). **2. Why other options are incorrect:** * **Options A, B, and C:** Historically, ART was deferred until the immune system showed signs of failure to avoid drug toxicity and preserve future options. Previous thresholds were <200 (1990s), <350 (2010), and <500 (2013) [3]. These are now considered outdated as the benefits of early viral suppression far outweigh the risks of early drug exposure. **High-Yield Clinical Pearls for NEET-PG:** * **First-line ART Regimen (NACO):** TLD regimen — **T**enofovir (TDF) + **L**amivudine (3TC) + **D**olutegravir (DTG) [1]. * **Exception to Immediate Start:** In cases of **Cryptococcal Meningitis** or **Tubercular Meningitis**, ART is typically delayed by 4–6 weeks to prevent a life-threatening Immune Reconstitution Inflammatory Syndrome (IRIS) [4]. * **Monitoring:** Viral load is the preferred tool for monitoring ART response (Target: <50 copies/ml). CD4 count is used primarily to assess the need for opportunistic infection prophylaxis (e.g., Co-trimoxazole if CD4 <200) [2].

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Principles of Antimicrobial Therapy

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Fever of Unknown Origin

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HIV/AIDS and Related Infections

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Tuberculosis and Mycobacterial Diseases

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Tropical and Parasitic Infections

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Viral Infections (Hepatitis, Herpes, etc.)

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Healthcare-Associated Infections

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Fungal Infections

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Sepsis and Septic Shock

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Infection in Immunocompromised Hosts

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Emerging and Re-emerging Infections

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Antimicrobial Resistance

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Vaccination Principles

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