Infectious Diseases — MCQs

A 25-year-old male student presents with a rash. He denies headache, fever, or myalgia. A slightly pruritic maculopapular rash is noted over the abdomen, trunk, palms of the hands, and soles of the feet. Inguinal, occipital, and cervical lymphadenopathy is also noted. Hypertrophic, flat, wart-like lesions are noted around the anal area. Laboratory studies show: Hct: 40%, Hgb: 14 g/dL, WBC: 13,000/mL with a differential of 50% segmented neutrophils and 50% lymphocytes. Which of the following is the most useful laboratory test in this patient?

Q508Easy

Which of the following is a new oral drug used in the treatment of chronic Hepatitis C?

Q509Easy

Hyperbaric oxygen is useful in which of the following conditions?

Q510Medium

A patient with AIDS and a CD4 cell count of 100/µL presents with persistent fever and weight loss associated with invasive pulmonary disease due to Mycobacterium avium complex. What is the optimal management for this case?

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 501: A patient with dengue hemorrhagic fever presents with myalgia and spontaneous skin bleeds. Laboratory tests show thrombocytopenia and a raised hematocrit. What is the Dengue Hemorrhagic Fever grade of the disease in this patient?

A. Grade I
B. Grade II (Correct Answer)
C. Grade III
D. Grade IV

Explanation: ### Explanation The classification of Dengue Hemorrhagic Fever (DHF) is based on the severity of clinical manifestations and hemodynamic stability. The hallmark of DHF is **plasma leakage** (evidenced here by raised hematocrit) along with thrombocytopenia and hemorrhagic tendencies [1]. **Why Grade II is correct:** According to the WHO classification, DHF is divided into four grades: * **Grade I:** Fever with non-specific constitutional symptoms; the only hemorrhagic manifestation is a **positive tourniquet test** and/or easy bruising [1]. * **Grade II:** All signs of Grade I plus **spontaneous bleeding** (e.g., skin bleeds like petechiae/ecchymosis, epistaxis, or gum bleeding). [1] Since this patient presents with spontaneous skin bleeds and evidence of plasma leakage (raised hematocrit), they are classified as **Grade II**. **Why other options are incorrect:** * **Grade I:** Incorrect because the patient has spontaneous bleeding, which exceeds the criteria for Grade I (where bleeding is only induced/provoked). * **Grade III:** Incorrect because Grade III represents **Dengue Shock Syndrome (DSS)**, characterized by circulatory failure (rapid/weak pulse, narrowing of pulse pressure <20 mmHg, or hypotension) [1]. This patient is currently hemodynamically stable. * **Grade IV:** Incorrect because Grade IV is **profound shock** with undetectable blood pressure or pulse. **High-Yield Clinical Pearls for NEET-PG:** * **Critical Phase:** Usually occurs during defervescence (days 3–7). This is when plasma leakage is most prominent [1]. * **Warning Signs:** Abdominal pain, persistent vomiting, mucosal bleed, lethargy, and sudden increase in hematocrit with a rapid decrease in platelet count. * **Fluid Management:** Isotonic crystalloids (like Normal Saline or Ringer's Lactate) are the gold standard for resuscitation in DHF. * **Hematocrit:** A rise of $\geq 20\%$ from the baseline is a definitive objective sign of plasma leakage.

Question 502: Plasmapheresis is the treatment of choice for which of the following conditions?

A. Henoch-Schönlein purpura
B. Wegener's granulomatosis
C. Goodpasture's syndrome (Correct Answer)
D. Acute renal transplant rejection

Explanation: **Explanation:** **Goodpasture’s Syndrome (Anti-GBM Disease)** is the correct answer because its pathogenesis involves circulating pathogenic autoantibodies directed against the alpha-3 chain of Type IV collagen in the glomerular and alveolar basement membranes [1]. **Plasmapheresis** is the treatment of choice because it directly and rapidly removes these circulating anti-GBM antibodies from the plasma, preventing further tissue damage [1]. It is typically combined with corticosteroids and cyclophosphamide to suppress further antibody production [1]. **Analysis of Incorrect Options:** * **Henoch-Schönlein Purpura (IgA Vasculitis):** This is usually a self-limiting condition, especially in children. Treatment is primarily supportive; steroids are used for severe abdominal or renal involvement, but plasmapheresis is not standard therapy. * **Wegener's Granulomatosis (GPA):** The mainstay of treatment is induction with corticosteroids and immunosuppressants (Cyclophosphamide or Rituximab). While plasmapheresis may be considered in severe cases with rapidly progressive glomerulonephritis (RPGN) or pulmonary hemorrhage, it is not the primary "treatment of choice." * **Acute Renal Transplant Rejection:** Cellular rejection is treated with high-dose steroids or anti-thymocyte globulin. Plasmapheresis is reserved only for antibody-mediated rejection (AMR), not all acute rejections. **High-Yield Clinical Pearls for NEET-PG:** * **Goodpasture’s Triad:** Glomerulonephritis (hematuria), Pulmonary hemorrhage (hemoptysis), and Anti-GBM antibodies. * **Immunofluorescence Pattern:** Characterized by **linear** IgG deposits along the glomerular basement membrane [1]. * **Other Indications for Plasmapheresis:** TTP (Treatment of choice), Guillain-Barré Syndrome, Myasthenia Gravis (crisis), and Hyperviscosity syndrome.

Question 503: Which of the following statements is NOT TRUE regarding infective endocarditis caused by HACEK organisms?

A. The clinical course of HACEK endocarditis tends to be acute and fulminant. (Correct Answer)
B. Cultures of blood from patients with HACEK endocarditis may require up to 4 weeks to be positive.
C. Embolization is common and occurs in around 50% of cases of HACEK endocarditis.
D. Valvular vegetations are seen in up to 85% of patients.

Explanation: ### Explanation **1. Why Option A is the Correct Answer (The "Not True" Statement):** HACEK organisms (*Haemophilus* species, *Aggregatibacter*, *Cardiobacterium*, *Eikenella*, and *Kingella*) are small, fastidious Gram-negative bacilli that are part of the normal oropharyngeal flora [1]. Unlike *Staphylococcus aureus*, which causes acute, fulminant endocarditis [2], HACEK organisms are characterized by a **subacute, indolent clinical course**. Patients often present with symptoms lasting weeks to months before a diagnosis is made. **2. Analysis of Other Options:** * **Option B:** Historically, HACEK organisms were the leading cause of "culture-negative" endocarditis because they are slow-growing. While modern automated systems (like BACTEC) usually detect them within 5–7 days, standard teaching for exams remains that they may require **extended incubation (up to 2–4 weeks)** for definitive growth. * **Option C:** Embolization is a hallmark of HACEK endocarditis, occurring in approximately **28% to 50%** of cases [2]. These emboli often involve the central nervous system or systemic arteries. * **Option D:** Echocardiography reveals valvular vegetations in the majority of patients (**up to 85%**) [1]. These vegetations are often large and friable, contributing to the high risk of embolization mentioned above. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most Common HACEK:** *Aggregatibacter* (formerly *Actinobacillus*) is the most frequently isolated genus. * **Risk Factor:** Often associated with prior dental procedures or periodontal disease [2]. * **Treatment of Choice:** **Ceftriaxone** (3rd generation cephalosporin) is the preferred treatment due to increasing beta-lactamase production among these strains. * **Culture-Negative IE:** If cultures remain negative at 48-72 hours in a patient with suspected IE, HACEK and *Coxiella burnetii* should be high on the differential.

Question 504: Which of the following is a common cause of chronic liver disease?

A. Hepatitis B
B. Hepatitis A
C. Hepatitis C (Correct Answer)
D. Hepatitis E

Explanation: The correct answer is **Hepatitis C**. The primary medical concept here is the **rate of chronicity**. Hepatitis C Virus (HCV) is notorious for its high propensity to cause persistent infection; approximately **75%–85%** of individuals infected with HCV fail to clear the virus and progress to chronic hepatitis [1]. Over decades, this chronic inflammation leads to cirrhosis and hepatocellular carcinoma (HCC), making it a leading cause of chronic liver disease (CLD) and liver transplantation worldwide [1]. **Analysis of Incorrect Options:** * **Hepatitis A and E:** These are transmitted via the **fecal-oral route** and typically cause acute, self-limiting hepatitis [2]. They **do not** cause chronic liver disease. (Exception: Hepatitis E can cause chronicity in severely immunocompromised individuals/transplant recipients, but this is not the "common" presentation). * **Hepatitis B:** While HBV is a major cause of CLD globally, its rate of chronicity in adults is relatively low (**<5%**) [3]. In contrast, HCV has a much higher transition rate from acute to chronic states [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Chronicity Rates:** HCV (75-85%) > HBV in neonates (90%) > HBV in adults (<5%) [3]. * **Screening:** Anti-HCV antibody is the initial screening test; **HCV RNA (PCR)** is the gold standard for confirming active infection [1]. * **Treatment:** Unlike HBV, which is usually managed with long-term suppression, HCV is now considered **curable** with Direct-Acting Antivirals (DAAs) like Sofosbuvir. * **Hepatitis D:** Requires the presence of HBsAg to replicate; it can significantly accelerate the progression of CLD in HBV-infected patients.

Question 505: In AIDS, Kaposi sarcoma may respond to which of the following treatments?

A. Interleukin-2 infusion
B. Azathioprine
C. Alpha interferon (Correct Answer)
D. Any of the above

Explanation: **Explanation:** **1. Why Alpha Interferon is Correct:** Kaposi Sarcoma (KS) is a multicentric angioproliferative tumor caused by **Human Herpesvirus 8 (HHV-8)**, typically occurring in HIV patients with low CD4 counts [1], [2]. **Interferon-alpha (IFN-α)** is an FDA-approved systemic therapy for AIDS-related KS. It works through a triple mechanism: * **Antiviral:** Inhibits the replication of HHV-8. * **Antiproliferative:** Directly inhibits the growth of tumor cells. * **Immunomodulatory:** Enhances the host’s immune response against the tumor. It is most effective in patients with relatively preserved immune function (CD4 count >200 cells/µL) and no systemic symptoms. **2. Why Other Options are Incorrect:** * **Interleukin-2 (IL-2):** While IL-2 is used to boost T-cell counts in some research settings, it is not a standard or effective treatment for the vascular lesions of Kaposi Sarcoma. * **Azathioprine:** This is an immunosuppressant. Since KS is an opportunistic malignancy driven by immunosuppression, giving Azathioprine would worsen the underlying immunodeficiency and potentially accelerate the progression of the tumor [2]. **3. NEET-PG High-Yield Pearls:** * **First-line Management:** The most important initial step in treating AIDS-related KS is the initiation of **Highly Active Antiretroviral Therapy (HAART)**. Many lesions regress simply by restoring the CD4 count. * **Chemotherapy of Choice:** For advanced or symptomatic visceral KS, **Liposomal Doxorubicin** is the first-line systemic chemotherapy. * **Histology:** Look for "spindle-shaped cells" and "slit-like vascular spaces" containing extravasated RBCs. * **Classic Association:** KS is the most common neoplasm associated with HIV/AIDS [2].

Question 506: Exanthemas are caused by all of the following EXCEPT:

A. Malaria (Correct Answer)
B. Typhoid
C. Measles
D. Rubella

Explanation: An **exanthema** is defined as a widespread skin rash that occurs as a symptom of a systemic disease, usually infectious in nature. **Why Malaria is the Correct Answer:** Malaria is a protozoal infection caused by *Plasmodium* species. Its clinical hallmark is the "malarial paroxysm" (chills, high fever, and sweating) and systemic features like splenomegaly and anemia. Crucially, **Malaria does not cause a skin rash (exanthema).** Any rash seen in a patient with malaria is likely due to a co-infection or a drug reaction [1]. **Why the other options are incorrect:** * **Typhoid (Enteric Fever):** Caused by *Salmonella typhi*, it classically presents with **"Rose Spots"**—faint, salmon-colored, blanching macules typically found on the chest and abdomen during the second week of illness [1]. * **Measles (Rubeola):** A viral infection characterized by a high-grade fever and a **maculopapular rash** that begins behind the ears and spreads cephalocaudally (downward) [1, 2]. It is also associated with Koplik spots [2]. * **Rubella (German Measles):** Presents with a similar but milder maculopapular rash compared to measles, often starting on the face and spreading rapidly [3]. It is famously associated with **Forchheimer spots** on the soft palate. **High-Yield Clinical Pearls for NEET-PG:** * **Rose Spots:** Pathognomonic for Typhoid; they are transient and often disappear within 2–5 days [1]. * **Koplik Spots:** Precede the Measles rash; located on the buccal mucosa opposite the lower molars [2]. * **Common Exanthematous Diseases:** Remember the "Classical Six" (Measles, Scarlet Fever, Rubella, Duke’s Disease, Erythema Infectiosum, and Roseola Infantum) [1]. * **Dengue:** Often presents with a "white islands in a sea of red" rash during the recovery phase [1].

Question 507: A 25-year-old male student presents with a rash. He denies headache, fever, or myalgia. A slightly pruritic maculopapular rash is noted over the abdomen, trunk, palms of the hands, and soles of the feet. Inguinal, occipital, and cervical lymphadenopathy is also noted. Hypertrophic, flat, wart-like lesions are noted around the anal area. Laboratory studies show: Hct: 40%, Hgb: 14 g/dL, WBC: 13,000/mL with a differential of 50% segmented neutrophils and 50% lymphocytes. Which of the following is the most useful laboratory test in this patient?

A. Human papillomavirus (HPV) serology
B. Rapid Plasma Reagin (RPR) test (Correct Answer)
C. Nucleic acid amplification test for Chlamydia
D. Blood cultures

Explanation: ### Explanation The clinical presentation is classic for **Secondary Syphilis**, caused by the spirochete *Treponema pallidum*. The hallmark features in this case include a generalized maculopapular rash involving the **palms and soles** [1], generalized lymphadenopathy (including occipital nodes), and **condyloma lata** (hypertrophic, flat, wart-like lesions in the anogenital region). **1. Why RPR is the correct answer:** The **Rapid Plasma Reagin (RPR)** and VDRL are non-treponemal screening tests used to detect biomarkers (reagin antibodies) released during active infection. In secondary syphilis, these tests have nearly **100% sensitivity**. Diagnosis is typically confirmed with treponemal-specific tests (e.g., FTA-ABS or TP-PA) [1]. **2. Why other options are incorrect:** * **A. HPV serology:** While HPV causes *Condyloma acuminata* (genital warts), those lesions are typically "cauliflower-like" and pedunculated, not flat. HPV does not cause a palm/sole rash or generalized lymphadenopathy. * **C. NAAT for Chlamydia:** Chlamydia (LGV strain) causes painful inguinal lymphadenopathy (buboes) and proctitis, but it does not present with a diffuse maculopapular rash or condyloma lata. * **D. Blood cultures:** *T. pallidum* cannot be cultured on standard blood agar or broth. Diagnosis relies on serology or dark-field microscopy. ### NEET-PG High-Yield Pearls: * **Condyloma Lata vs. Acuminata:** *Lata* is flat/broad-based (Syphilis); *Acuminata* is pointed/verrucous (HPV). * **Rash on Palms and Soles:** Differential includes Secondary Syphilis, Rocky Mountain Spotted Fever (RMSF), Hand-Foot-Mouth Disease (Coxsackie A), and Erythema Multiforme. * **Prozone Phenomenon:** In secondary syphilis, very high antibody titers can lead to a **false-negative** RPR [1]. If clinical suspicion is high, the lab should dilute the specimen. * **Treatment:** The drug of choice for secondary syphilis is a single IM dose of **Benzathine Penicillin G** (2.4 million units).

Question 508: Which of the following is a new oral drug used in the treatment of chronic Hepatitis C?

A. Interferon alpha
B. Ledipasvir (Correct Answer)
C. Oseltamivir
D. Lamivudine

Explanation: **Explanation:** The treatment of Chronic Hepatitis C (HCV) has been revolutionized by the introduction of **Direct-Acting Antivirals (DAAs)**. These are oral drugs that target specific non-structural proteins of the virus, leading to high cure rates (SVR >95%) with minimal side effects. **Why Ledipasvir is correct:** Ledipasvir is a potent inhibitor of the **NS5A protein**, which is essential for HCV viral replication and assembly. It is typically used in a fixed-dose combination with Sofosbuvir (an NS5B polymerase inhibitor) for the treatment of HCV Genotype 1. Unlike older therapies, it is administered orally and does not require co-administration with Interferon. **Analysis of Incorrect Options:** * **Interferon-alpha (A):** This was the historical mainstay of HCV treatment. However, it is an **injectable** drug associated with significant systemic side effects (flu-like symptoms, depression, cytopenias) and is no longer the first-line choice in the DAA era. * **Oseltamivir (C):** This is a neuraminidase inhibitor used specifically for the treatment and prophylaxis of **Influenza A and B**. It has no activity against the Hepatitis C virus. * **Lamivudine (D):** This is a nucleoside reverse transcriptase inhibitor (NRTI) used in the treatment of **Hepatitis B (HBV)** and HIV. It is not effective against HCV. **NEET-PG High-Yield Pearls:** * **DAA Classification by Target:** * **NS3/4A Protease Inhibitors:** End in “-previr” (e.g., Telaprevir, Simeprevir). * **NS5A Inhibitors:** End in “-asvir” (e.g., Ledipasvir, Daclatasvir, Velpatasvir). * **NS5B Polymerase Inhibitors:** End in “-buvir” (e.g., Sofosbuvir). * **Pangenotypic Regimens:** Combinations like **Sofosbuvir + Velpatasvir** are now preferred as they work across all HCV genotypes. [1] * **Goal of Therapy:** To achieve **SVR12** (Sustained Virologic Response), defined as undetectable HCV RNA 12 weeks after completing treatment. [1] **Diagnosis Context:** Active infection is confirmed by the presence of serum hepatitis C RNA in anyone who is antibody-positive. [1]

Question 509: Hyperbaric oxygen is useful in which of the following conditions?

A. Tetanus
B. Gas gangrene (Correct Answer)
C. Frostbite
D. Vincent's angina

Explanation: Explanation: Hyperbaric Oxygen Therapy (HBOT) involves breathing 100% oxygen at pressures greater than atmospheric pressure. It is a cornerstone adjunct treatment for Gas Gangrene (Clostridial Myonecrosis) [1]. Why Gas Gangrene is the correct answer: Gas gangrene is caused by Clostridium perfringens, an obligate anaerobe. HBOT works through two primary mechanisms: 1. Bactericidal/Bacteriostatic effect: High partial pressures of oxygen are directly toxic to anaerobic bacteria. 2. Inhibition of Alpha-toxin: HBOT halts the production of the alpha-toxin (lecithinase), which is the primary virulence factor responsible for tissue necrosis and systemic toxicity. This helps demarcate the wound and reduces the extent of surgical debridement required. Analysis of Incorrect Options: * Tetanus: While caused by an anaerobe (C. tetani), the pathology is driven by a fixed neurotoxin (tetanospasmin). HBOT does not neutralize the toxin or improve outcomes in clinical trials. * Frostbite: The primary treatment is rapid rewarming in water (37-39°C). While HBOT is occasionally studied for microvascular salvage, it is not a standard or first-line indication compared to gas gangrene. * Vincent’s Angina: Also known as "Trench Mouth" (necrotizing ulcerative gingivitis), it is treated with oral hygiene, saline rinses, and antibiotics (Metronidazole). HBOT is not indicated for this localized oral infection. Clinical Pearls for NEET-PG: * Absolute Contraindication for HBOT: Untreated tension pneumothorax. * Other High-Yield Indications: Carbon monoxide poisoning, Decompression sickness (The Bends), Air/Gas embolism, and refractory Chronic Osteomyelitis. * Most common side effect: Middle ear barotrauma (due to pressure changes).

Question 510: A patient with AIDS and a CD4 cell count of 100/µL presents with persistent fever and weight loss associated with invasive pulmonary disease due to Mycobacterium avium complex. What is the optimal management for this case?

A. Select an antibiotic regimen based on drug susceptibility testing of the cultured organism.
B. Initiate treatment with isoniazid and rifampicin.
C. Treat the patient with clarithromycin, ethambutol, and rifabutin. (Correct Answer)
D. Treat with trimethoprim-sulfamethoxazole.

Explanation: **Explanation:** **1. Why Option C is Correct:** In patients with AIDS and low CD4 counts (<50–100/µL), *Mycobacterium avium* complex (MAC) typically presents as a disseminated or invasive pulmonary disease. The standard of care for treatment involves a multi-drug regimen to prevent the emergence of resistance. **Clarithromycin** (or Azithromycin) is the cornerstone of therapy. It must be combined with **Ethambutol**. The addition of a third drug, **Rifabutin**, is recommended for patients with high mycobacterial loads or advanced immunosuppression to improve clinical outcomes and reduce the risk of relapse. **2. Why Other Options are Incorrect:** * **Option A:** Unlike *M. tuberculosis*, the clinical response to MAC treatment does not correlate well with *in vitro* susceptibility testing for most drugs, except for macrolides and amikacin. Treatment is initiated empirically based on established guidelines rather than waiting for extensive sensitivity panels. * **Option B:** Isoniazid and Rifampicin are the backbone of treatment for *Mycobacterium tuberculosis*. [1] MAC is intrinsically resistant to standard doses of Isoniazid and Pyrazinamide. * **Option D:** Trimethoprim-sulfamethoxazole (TMP-SMX) is the drug of choice for prophylaxis and treatment of *Pneumocystis jirovecii* pneumonia (PCP) and Toxoplasmosis, but it has no activity against MAC. [2] **3. Clinical Pearls for NEET-PG:** * **Prophylaxis:** Primary prophylaxis for MAC is indicated when CD4 <50/µL (usually with Azithromycin 1200 mg once weekly). However, current guidelines suggest deferring prophylaxis if ART is started immediately. * **Diagnosis:** Definitive diagnosis of disseminated MAC is made via **blood culture** (using BACTEC systems) or tissue biopsy. * **Drug Interaction:** Rifabutin is preferred over Rifampicin in HIV patients because it is a less potent inducer of the Cytochrome P450 system, leading to fewer interactions with Protease Inhibitors (PIs).

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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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