Infectious Diseases — MCQs

A 31-year-old man with AIDS complains of difficulty in swallowing. Examination of his oral cavity demonstrates whitish membranes covering much of his tongue and palate. Endoscopy also reveals several whitish, ulcerated lesions in the esophagus. These pathologic findings are fundamentally caused by loss of which of the following immune cells?

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 141: An HIV patient developed goiter. On examination, there was non-tender diffuse enlargement of the thyroid. All of the following can be causes of this condition, except:

A. Toxoplasma
B. Cryptococcus
C. Aspergillus (Correct Answer)
D. Pneumocystis

Explanation: In HIV-infected individuals, the thyroid gland can be a site for opportunistic infections, typically presenting as a **painless, diffuse goiter** or localized nodules. **Explanation of the Correct Answer:** * **C. Aspergillus:** This is the correct answer because *Aspergillus* species typically cause **acute, painful thyroiditis** rather than non-tender diffuse enlargement. In immunocompromised patients, *Aspergillus* is angioinvasive, leading to infarction, necrosis, and abscess formation [1]. This clinical presentation is characterized by rapid onset, localized pain, and fever, which contradicts the "non-tender diffuse enlargement" described in the question. **Explanation of Incorrect Options:** * **D. Pneumocystis jirovecii:** This is the **most common** opportunistic infection of the thyroid in AIDS patients. It typically presents as a painless, diffuse goiter or a slowly enlarging thyroid mass. It often occurs in patients receiving aerosolized pentamidine (which doesn't provide systemic protection). * **B. Cryptococcus neoformans:** This is a well-documented cause of subacute, non-tender thyroid involvement in advanced HIV/AIDS, usually occurring during disseminated disease. * **A. Toxoplasma gondii:** While rarer than *Pneumocystis*, *Toxoplasma* can involve the thyroid in disseminated cases, often presenting as asymptomatic or non-tender enlargement. **High-Yield Clinical Pearls for NEET-PG:** * **Most common thyroid opportunistic infection in HIV:** *Pneumocystis jirovecii*. * **Thyroid Function:** Most patients with opportunistic thyroid infections remain **euthyroid**, although destructive thyroiditis can occasionally cause transient hyperthyroidism followed by hypothyroidism. * **Kaposi Sarcoma:** Aside from infections, Kaposi Sarcoma and Lymphoma can also cause non-tender thyroid enlargement in HIV patients. * **Drug Interaction:** Remember that **Rifampin** (used for TB in HIV) can induce hepatic enzymes, leading to increased clearance of T4 and potentially worsening hypothyroidism in patients with pre-existing thyroid disease.

Question 142: All of the following are seen in Legionnaire's disease except?

A. Fever
B. Mental confusion
C. Diarrhoea
D. Unilateral pneumonitis (Correct Answer)

Explanation: Legionnaire’s disease, caused by *Legionella pneumophila*, is a multisystem illness characterized by atypical pneumonia. The correct answer is **Unilateral pneumonitis** because the radiological hallmark of Legionnaire’s disease is typically **patchy, rapidly progressive, and often bilateral infiltrates**, rather than localized unilateral involvement. **Why Option D is correct:** While the disease may start as a focal infiltrate, it characteristically progresses to involve multiple lobes or both lungs [1]. Pleural effusions are also common. Therefore, "unilateral pneumonitis" is the least characteristic feature among the choices. **Why other options are incorrect:** * **Fever (A):** High-grade fever (often >40°C) is a classic feature. A key diagnostic clue is **Faget’s sign** (relative bradycardia), where the heart rate does not increase proportionally with the fever. * **Mental Confusion (B):** Neurological symptoms, particularly headache and confusion/encephalopathy, are common extrapulmonary manifestations that distinguish Legionella from other bacterial pneumonias [1]. * **Diarrhoea (C):** Gastrointestinal symptoms are highly characteristic. Watery, non-bloody diarrhea often precedes the respiratory symptoms. **High-Yield Clinical Pearls for NEET-PG:** * **Hyponatremia:** This is the most characteristic laboratory finding in Legionnaire’s disease (due to SIADH or renal loss). * **Diagnosis:** The **Urinary Antigen Test** is the most common rapid diagnostic tool (detects Serogroup 1). * **Culture:** Requires **BCYE (Buffered Charcoal Yeast Extract) agar** supplemented with L-cysteine and iron. * **Treatment:** Macrolides (Azithromycin) or Respiratory Fluoroquinolones (Levofloxacin) are the drugs of choice. Beta-lactams are ineffective as the organism is intracellular.

Question 143: What is an early manifestation of a patient infected with HIV virus?

A. Elevation of p16
B. Unexplained fear and weight loss (Correct Answer)
C. Kaposi's sarcoma
D. Hairy cell leukoplakia

Explanation: ### Explanation The clinical progression of HIV is divided into stages: Acute HIV infection, Clinical Latency, and AIDS. Understanding the timeline of symptoms is crucial for NEET-PG. **1. Why "Unexplained fear and weight loss" is correct:** Early HIV infection (Acute Retroviral Syndrome) typically occurs 2–4 weeks after exposure [1]. It often presents as a **mononucleosis-like illness** [1]. Constitutional symptoms such as **unexplained weight loss**, fever, and fatigue are hallmark early signs [1]. "Unexplained fear" or anxiety is frequently documented in early stages due to neuropsychiatric involvement or the psychological stress of the prodromal illness. Weight loss (even if not meeting the "Wasting Syndrome" criteria of AIDS) starts early due to the high metabolic demand of rapid viral replication. **2. Analysis of Incorrect Options:** * **Elevation of p16:** This is incorrect. The diagnostic marker for early HIV is the **p24 antigen** (part of the 4th generation ELISA). p16 is a tumor suppressor protein associated with HPV-related cancers, not HIV diagnosis. * **Kaposi’s Sarcoma (KS):** This is an **AIDS-defining illness** caused by HHV-8. It typically occurs when the CD4 count falls below 200 cells/mm³, marking a late stage of infection. * **Hairy Cell Leukoplakia:** Caused by the Epstein-Barr Virus (EBV), this is an intermediate manifestation. While it occurs earlier than KS, it usually signifies significant immunosuppression (CD4 < 300–400 cells/mm³) and is not part of the acute/initial infection phase. **3. NEET-PG High-Yield Pearls:** * **Window Period:** The time between infection and detectable antibodies. The **p24 antigen** is the first virological marker to appear (approx. 14 days). * **Best Initial Test:** 4th Generation ELISA (detects p24 antigen + HIV 1/2 antibodies). * **Most Common Initial Symptom:** Fever (96%), followed by lymphadenopathy and pharyngitis [1]. * **Dermatology Link:** Seborrheic dermatitis can be one of the earliest cutaneous clues to HIV infection [1].

Question 144: What is the diagnostic test for Zollinger-Ellison syndrome?

A. Secretin test (Correct Answer)
B. Standard test meal
C. ACTH infusion
D. Calcium infusion

Explanation: Zollinger-Ellison Syndrome (ZES) is caused by a gastrin-secreting tumor (gastrinoma), leading to hypergastrinemia and severe peptic ulcer disease [1]. **Why Secretin Test is the Correct Answer:** The **Secretin Stimulation Test** is the most sensitive and specific provocative test for ZES. Under normal physiological conditions, secretin inhibits gastrin release from G-cells. However, in gastrinoma cells, secretin paradoxically stimulates the release of gastrin. A positive test is defined as an increase in serum gastrin levels of **>200 pg/mL** above the baseline after secretin injection. **Analysis of Incorrect Options:** * **Standard Test Meal:** In ZES, gastrin levels do not significantly increase after a meal because the secretion is autonomous. This test is more useful in diagnosing G-cell hyperplasia, where gastrin levels rise by >50%. * **ACTH Infusion:** This is used to evaluate adrenal function (e.g., Addison’s disease or Cushing’s syndrome [2]) and has no role in diagnosing gastrinomas. * **Calcium Infusion:** While calcium can stimulate gastrin release from a gastrinoma, it is less sensitive and more hazardous (due to hypercalcemia) than the secretin test. It is reserved for cases where ZES is strongly suspected but the secretin test is negative. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Most gastrinomas are found in the **"Gastrinoma Triangle"** (bounded by the cystic duct, junction of the 2nd and 3rd parts of the duodenum, and the neck of the pancreas). * **Association:** Approximately 25% of ZES cases are associated with **Multiple Endocrine Neoplasia type 1 (MEN1)**. * **Initial Screening:** The first step in diagnosis is measuring **Fasting Serum Gastrin (FSG)** levels (usually >1000 pg/mL) while the patient is off Proton Pump Inhibitors (PPIs) [1]. * **Localization:** Somatostatin Receptor Scintigraphy (Octreotide scan) is the preferred imaging modality to locate the tumor [3].

Question 145: A patient presents with lower gastrointestinal bleeding. Sigmoidoscopy shows ulcers in the sigmoid. Biopsy from this area shows flask-shaped ulcers. Which of the following is the most appropriate treatment?

A. Intravenous ceftriaxone
B. Intravenous metronidazole (Correct Answer)
C. Intravenous steroids and sulphasalazine
D. Hydrocortisone enemas

Explanation: **Explanation:** The clinical presentation of lower gastrointestinal bleeding combined with the pathognomonic finding of **flask-shaped ulcers** on biopsy is diagnostic of **Amoebic Colitis**, caused by *Entamoeba histolytica* [1]. 1. **Why Option B is correct:** *Entamoeba histolytica* trophozoites invade the intestinal mucosa, causing lateral spread in the submucosa, which creates the classic "flask-shaped" appearance. **Metronidazole** (or Tinidazole) is the drug of choice for invasive amoebiasis as it is a potent tissue amoebicide. In cases of severe colitis or systemic symptoms, intravenous administration is preferred to ensure rapid therapeutic levels. 2. **Why the other options are incorrect:** * **Option A (Ceftriaxone):** This is a third-generation cephalosporin used for bacterial infections like Enteric fever or Shigellosis. It has no activity against protozoa like *E. histolytica*. * **Options C & D (Steroids/Sulphasalazine):** These are used to treat Inflammatory Bowel Disease (IBD), specifically Ulcerative Colitis [2]. While IBD also presents with bloody diarrhea and ulcers, the biopsy would show crypt abscesses rather than flask-shaped ulcers. Importantly, giving steroids in a case of amoebiasis can lead to toxic megacolon or perforation. **Clinical Pearls for NEET-PG:** * **Pathology:** The "flask shape" occurs because the organism cannot easily penetrate the muscularis propria, leading to lateral expansion in the submucosa. * **Diagnosis:** Stool microscopy may show trophozoites with ingested RBCs (erythrophagocytosis) [1]. * **Treatment Protocol:** Always follow a tissue amoebicide (Metronidazole) with a **luminal amoebicide** (e.g., Diloxanide furoate or Paromomycin) to eradicate the cyst stage and prevent relapse/transmission. * **Complication:** The most common extra-intestinal manifestation is an Amoebic Liver Abscess (anchovy sauce pus) [1].

Question 146: What is the recommended duration of treatment for multidrug-resistant tuberculosis (MDR-TB)?

A. 8-12 months
B. 12-16 months
C. 16-24 months (Correct Answer)
D. 2-3 years

Explanation: ### Explanation **Correct Answer: C. 16-24 months** **Understanding the Concept:** Multidrug-resistant tuberculosis (MDR-TB) is defined as resistance to at least **Isoniazid (H) and Rifampicin (R)**, the two most potent first-line drugs. Because these primary bactericidal agents are ineffective, treatment must rely on second-line drugs (such as Fluoroquinolones and Aminoglycosides/Bedaquiline), which are generally less potent and have slower bactericidal activity. To ensure complete sterilization of the dormant bacilli and prevent relapse, a significantly longer duration of therapy is required compared to drug-susceptible TB. According to WHO and NTEP guidelines, the conventional (longer) regimen for MDR-TB typically lasts **18 to 24 months**, consisting of an Intensive Phase (IP) of 6–9 months and a Continuation Phase (CP) of 18 months. Treatment failure is defined as any patient with a multidrug resistant strain, regardless of whether they are smear-positive or negative [1]. **Analysis of Incorrect Options:** * **A & B (8–16 months):** These durations are too short for conventional MDR-TB treatment. While the "Shorter MDR-TB Regimen" (Bangladesh Regimen) lasts 9–11 months, it is only indicated for specific patients without resistance to second-line drugs. Standard MDR-TB management exceeds this timeframe. * **D (2–3 years):** While XDR-TB (Extensively Drug-Resistant TB) or complicated cases might occasionally require prolonged therapy, 24 months is the standard upper limit for most MDR-TB protocols. Treatment beyond 24 months increases the risk of severe drug toxicity without significant clinical benefit. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** MDR-TB = Resistance to H + R. * **XDR-TB (New Definition):** MDR-TB plus resistance to any **Fluoroquinolone** AND at least one additional Group A drug (**Bedaquiline or Linezolid**). * **Bedaquiline:** Now a cornerstone of MDR-TB treatment; it inhibits mycobacterial **ATP synthase**. * **Site of Action:** The primary reason for long treatment is the "persister" bacilli located within caseous necrosis/granulomas.

Question 147: Which of the following is NOT a characteristic feature of cerebral malaria?

A. Bloody cerebrospinal fluid (Correct Answer)
B. Retinal hemorrhages
C. Extensor plantar reflex
D. Absent abdominal reflex

Explanation: **Explanation:** Cerebral malaria is a severe neurological complication of *Plasmodium falciparum* infection, characterized by unarousable coma (Glasgow Coma Scale <11) in the absence of other identifiable causes [2]. **Why "Bloody Cerebrospinal Fluid" is the correct answer:** In cerebral malaria, the cerebrospinal fluid (CSF) is typically **clear and colorless**. While there may be a mild increase in opening pressure and a slight elevation in protein levels (<100 mg/dL), the CSF cell count is usually normal (pleocytosis is rare). The presence of bloody or xanthochromic CSF suggests an alternative diagnosis, such as subarachnoid hemorrhage or a traumatic tap, and is **not** a feature of malaria [1]. **Analysis of Incorrect Options:** * **Retinal Hemorrhages:** This is a key diagnostic and prognostic marker. "Malarial retinopathy" (including retinal whitening, vessel changes, and hemorrhages) is highly specific for cerebral malaria and correlates with the severity of brain sequestration. * **Extensor Plantar Reflex:** Upper motor neuron signs are common. Patients often exhibit decerebrate or decorticate posturing, hyperreflexia, and a positive Babinski sign (extensor plantar response) due to diffuse encephalopathy. * **Absent Abdominal Reflex:** This is a classic clinical finding in cerebral malaria, reflecting the involvement of the corticospinal tracts. **High-Yield NEET-PG Pearls:** * **Pathogenesis:** Sequestration of parasitized RBCs in cerebral microvasculature (cytoadherence via PfEMP-1) [3]. * **Drug of Choice:** Intravenous **Artesunate** is the gold standard (preferred over Quinine). * **Hypoglycemia:** Always check blood glucose, as both the disease and Quinine treatment can cause severe hypoglycemia [2]. * **Mortality:** Even with treatment, mortality remains 15–20%.

Question 148: Hemolysis is most severe with Plasmodium falciparum infection compared to other malarial parasites because of which of the following?

A. Associated gram-negative bacteremia
B. Ability of the parasite to infect red blood cells of all ages (Correct Answer)
C. Ability of the organism to infect selectively reticulocytes
D. Ability of the organism to escape immune recognition by the immune system

Explanation: **Explanation:** The severity of anemia and hemolysis in malaria is directly proportional to the level of parasitemia (the percentage of infected red blood cells). **Why Option B is Correct:** *Plasmodium falciparum* is the most virulent species because it lacks selectivity regarding the age of the erythrocyte. It can invade **RBCs of all ages** (young reticulocytes, mature cells, and old cells) [1]. This leads to unrestricted multiplication, resulting in high-density parasitemia (often >5-10%), massive hemolysis, and life-threatening complications like "Blackwater fever." **Analysis of Incorrect Options:** * **Option C:** This describes ***Plasmodium vivax* and *Plasmodium ovale***, which selectively infect only **reticulocytes** (young RBCs) [1]. Since reticulocytes make up only ~1-2% of total circulating RBCs, the parasitemia remains low, and hemolysis is less severe. * **Option D:** While *P. falciparum* uses antigenic variation (via *pfEMP-1*) to evade the immune system, this mechanism primarily facilitates **sequestration** (cytoadherence) rather than being the primary driver of the *severity of hemolysis*. * **Option A:** Gram-negative bacteremia (often *Salmonella*) can occur as a complication of severe malaria due to increased gut permeability, but it is a consequence/comorbidity rather than the underlying cause of the hemolysis itself. **NEET-PG High-Yield Pearls:** 1. **Selectivity:** *P. falciparum* (All ages), *P. vivax/ovale* (Reticulocytes/Duffy antigen), *P. malariae* (Senescent/Old RBCs) [1]. 2. **Sequestration:** Only *P. falciparum* exhibits sequestration; therefore, only ring forms and gametocytes are typically seen in peripheral smears (schizonts stay in deep capillaries). 3. **Maurer’s Clefts:** Coarse granulations seen in *P. falciparum* infected RBCs. 4. **Blackwater Fever:** Severe intravascular hemolysis leading to hemoglobinuria, caused by *P. falciparum* (often associated with irregular Quinine use) [1], [2].

Question 149: What is the least common cause of sporadic encephalitis?

A. Herpes Simplex Virus (HSV)
B. Varicella-Zoster Virus (VZV)
C. Arbovirus
D. Rhinovirus (Correct Answer)

Explanation: The correct answer is **D. Rhinovirus**. **Medical Concept:** Sporadic encephalitis refers to isolated cases of brain inflammation occurring year-round, independent of seasonal outbreaks. While many viruses are neurotropic (capable of infecting nerve tissue), **Rhinovirus** is primarily restricted to the upper respiratory tract. It thrives at temperatures slightly below core body temperature (33–35°C) and lacks the typical mechanisms to cross the blood-brain barrier. While extremely rare case reports exist in immunocompromised individuals, it is not considered a standard or recognized cause of sporadic encephalitis in clinical practice. **Analysis of Options:** * **HSV (Option A):** Herpes Simplex Virus-1 is the **most common cause** of sporadic fatal encephalitis worldwide [1]. It typically involves the temporal lobes [1]. * **VZV (Option B):** Varicella-Zoster Virus is a significant cause of sporadic encephalitis, often occurring during primary infection (chickenpox) or reactivation (shingles), frequently associated with vasculopathy. * **Arboviruses (Option C):** While many arboviruses (like Japanese Encephalitis) are epidemic/seasonal, several can present sporadically depending on geographic location and vector prevalence. They are well-established neurotropic pathogens. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of sporadic encephalitis:** HSV-1. * **Most common cause of epidemic encephalitis in India:** Japanese Encephalitis (JE) virus. * **Gold Standard Diagnosis:** CSF PCR for viral DNA/RNA. * **Imaging Choice:** MRI is superior to CT; look for temporal lobe involvement in HSV [1]. * **Treatment:** Empiric Acyclovir should be started immediately if encephalitis is suspected.

Question 150: A 31-year-old man with AIDS complains of difficulty in swallowing. Examination of his oral cavity demonstrates whitish membranes covering much of his tongue and palate. Endoscopy also reveals several whitish, ulcerated lesions in the esophagus. These pathologic findings are fundamentally caused by loss of which of the following immune cells?

A. B lymphocytes
B. Helper T lymphocytes (Correct Answer)
C. Killer T lymphocytes
D. Monocytes/macrophages

Explanation: ### Explanation **Correct Answer: B. Helper T lymphocytes** **1. Why Helper T lymphocytes is correct:** The clinical presentation describes **Oral Candidiasis (Thrush)** and **Candida Esophagitis** in a patient with AIDS [1]. *Candida albicans* is a dimorphic fungus that is normally kept in check by the immune system. * **Cell-Mediated Immunity (CMI)** is the primary defense against localized mucosal fungal infections. * In HIV/AIDS, the virus selectively infects and destroys **CD4+ Helper T lymphocytes** [2]. * When CD4+ counts drop (typically below 200 cells/mm³), the loss of T-cell-mediated cytokine signaling prevents the activation of macrophages and neutrophils, leading to opportunistic mucosal infections like esophageal candidiasis (an AIDS-defining illness) [2]. **2. Why the other options are incorrect:** * **A. B lymphocytes:** These are responsible for humoral immunity (antibody production). While HIV can cause B-cell dysfunction, B-cells are not the primary defense against *Candida*. * **C. Killer T lymphocytes (CD8+):** These cells are responsible for destroying virally infected cells and tumor cells. While they play a role in the overall immune response, the hallmark of HIV pathogenesis and the specific susceptibility to fungal infections is the depletion of CD4+ cells. * **D. Monocytes/macrophages:** While these cells can be infected by HIV (acting as reservoirs), their loss is not the fundamental driver of the immunodeficiency seen in AIDS. The quantitative depletion of CD4+ T cells is the primary mechanism. **3. NEET-PG High-Yield Pearls:** * **CD4+ vs. Neutrophils:** CD4+ T cells protect against **mucosal** candidiasis (thrush, esophagitis). Neutrophils protect against **systemic/disseminated** candidiasis (candidemia). * **AIDS-Defining Illness:** Esophageal candidiasis is an AIDS-defining condition, whereas oral thrush is not (though it is highly predictive of progression) [1]. * **Treatment:** The first-line treatment for esophageal candidiasis is oral **Fluconazole**. * **Endoscopy:** Characterized by "cottage-cheese" like white plaques that, when scraped, reveal an erythematous, friable base.

Practice by Chapter

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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