Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 311: Relative bradycardia with fever is characteristic of which condition?

A. Typhoid (Correct Answer)
B. Malaria
C. Tuberculosis
D. Brucellosis

Explanation: **Explanation:** **Relative Bradycardia** (also known as **Faget’s Sign**) is a clinical phenomenon where the pulse rate does not increase commensurately with the rise in body temperature. Normally, for every 1°F rise in temperature, the heart rate increases by approximately 10 beats per minute. In relative bradycardia, the heart rate remains lower than expected. **1. Why Typhoid is Correct:** Typhoid fever (Enteric fever), caused by *Salmonella Typhi*, is the classic cause of relative bradycardia [1]. The underlying mechanism is attributed to the release of inflammatory cytokines and the direct effect of endotoxins on the sinoatrial (SA) node, or potentially increased vagal tone. It typically appears during the first and second weeks of the illness alongside the "step-ladder" pattern of fever [1]. **2. Why Other Options are Incorrect:** * **Malaria:** Characterized by high-grade fever with rigors and chills. It typically presents with **tachycardia** proportional to the fever. * **Tuberculosis:** Usually presents with a chronic low-grade evening rise of temperature. It is generally associated with a normal or slightly elevated heart rate, not relative bradycardia. * **Brucellosis:** While it causes an "undulant fever," it does not characteristically present with relative bradycardia (though it can occur in rare complications like endocarditis). **3. NEET-PG Clinical Pearls:** * **Differential Diagnosis of Relative Bradycardia:** Remember the mnemonic **"BRUCE"**: **B**rucellosis (rarely), **R**ickettsial infections [1], **U**nusual bacteria (Legionella, Psittacosis), **C**hlamydia, and **E**nteric fever (Typhoid) [1]. It is also seen in **Yellow Fever** and **Dengue**. * **Typhoid Triad:** Step-ladder fever, Relative bradycardia, and Rose spots (on the abdomen) [1]. * **Investigation of Choice:** Blood culture is most sensitive in the 1st week; Widal test becomes positive in the 2nd week.

Question 312: Which HIV subtype is predominantly seen in Africa?

A. Subtype A
B. Subtype B
C. Subtype C
D. Subtype D (Correct Answer)

Explanation: ### Explanation The genetic diversity of HIV-1 is categorized into groups (M, N, O, and P), with **Group M (Major)** being responsible for the global pandemic [1]. Group M is further divided into several clades or subtypes (A–L). **Correct Option: D (Subtype D)** While multiple subtypes circulate in Africa, **Subtype D** is highly prevalent in East and Central Africa (e.g., Uganda, Kenya, Tanzania). It is clinically significant because it is associated with a **faster rate of CD4+ T-cell decline** and more rapid progression to AIDS compared to other subtypes. **Analysis of Incorrect Options:** * **Subtype A:** Common in West and East Africa and parts of the former Soviet Union. While prevalent, it is not the "predominant" answer often tested in the context of specific African regional virulence. * **Subtype B:** This is the dominant subtype in **North America, Western Europe, and Australia**. It is the most studied subtype but is relatively rare in sub-Saharan Africa. * **Subtype C:** This is the most common subtype **worldwide** and is the predominant subtype in **India** and Southern Africa. (Note: If the question asks for the most common subtype in *India*, the answer is Subtype C). **High-Yield Clinical Pearls for NEET-PG:** * **Global Dominance:** Subtype C accounts for nearly 50% of all HIV infections globally. * **Indian Context:** **Subtype C** is the most common subtype in India. * **Transmission:** Subtype C is more efficiently transmitted heterosexually, whereas Subtype B was historically associated with MSM (men who have sex with men) and IV drug use populations [1]. * **Screening:** Current 4th generation ELISA tests (p24 antigen + antibodies) are effective at detecting all major HIV-1 subtypes.

Question 313: What is the drug of choice in herpes simplex encephalitis?

A. Acyclovir (Correct Answer)
B. Vidarabine
C. Interferon
D. Amantadine

Explanation: **Explanation:** **Acyclovir** is the gold-standard drug of choice for Herpes Simplex Encephalitis (HSE). HSE is a medical emergency, most commonly caused by HSV-1 in adults. Acyclovir acts as a nucleoside analog that inhibits viral DNA polymerase [1]. It is administered intravenously (10 mg/kg every 8 hours for 14–21 days) [1]. Early initiation is critical because it significantly reduces mortality (from 70% to ~20-30%) and improves neurological outcomes. **Why other options are incorrect:** * **Vidarabine:** This was the previous standard of care before the 1980s. However, it is less effective and significantly more toxic (bone marrow suppression, neurotoxicity) compared to Acyclovir. * **Interferon:** While interferons have antiviral properties and are used in chronic hepatitis, they have no proven efficacy in the acute management of HSE. * **Amantadine:** This is an anti-influenza A medication (M2 ion channel blocker) and is also used in Parkinson’s disease. It has no activity against the Herpesviridae family. **High-Yield Clinical Pearls for NEET-PG:** * **Site of involvement:** HSE characteristically affects the **temporal lobes** (look for "hemorrhagic necrosis" on pathology) [2]. * **Gold Standard Diagnosis:** **CSF PCR** for HSV DNA (highest sensitivity and specificity). * **EEG Finding:** Periodic lateralized epileptiform discharges (**PLEDs**) over the temporal lobes. * **MRI:** The most sensitive imaging modality, showing hyperintensities in the temporal lobes and insular cortex on T2/FLAIR sequences. * **Empiric Therapy:** Never delay Acyclovir while waiting for diagnostic confirmation if HSE is suspected.

Question 314: In what proportion of post-primary (adult-type) tuberculosis is hemoptysis seen?

A. 10-20%
B. 20-30% (Correct Answer)
C. 30-40%
D. 40-50%

Explanation: **Explanation:** **1. Understanding the Correct Answer (B: 20-30%)** Post-primary (adult-type) tuberculosis (TB) typically involves the reactivation of a latent infection, usually localized to the apical and posterior segments of the upper lobes. Hemoptysis is a hallmark clinical feature of this stage, occurring in approximately **20-30% of cases**. The underlying mechanism is usually the erosion of a small blood vessel within a tuberculous cavity or due to endobronchial erosion [1]. While many patients present with blood-streaked sputum, massive hemoptysis can occur if a **Rasmussen aneurysm** (dilatation of a pulmonary artery branch in a cavity wall) ruptures. **2. Why Other Options are Incorrect** * **A (10-20%):** This range is too low for post-primary TB. While constitutional symptoms like fever and weight loss are more frequent (occurring in up to 80% of patients), hemoptysis is common enough to exceed this threshold. * **C & D (30-50%):** These ranges overestimate the prevalence. While cough is present in nearly all patients (approx. 90%), frank hemoptysis or blood-streaking is not seen in the majority of cases. **3. NEET-PG High-Yield Clinical Pearls** * **Most common symptom of TB:** Cough (initially non-productive, later productive). * **Most common site of post-primary TB:** Apical and posterior segments of the upper lobes (due to high oxygen tension). * **Rasmussen Aneurysm:** A rare but life-threatening cause of massive hemoptysis in chronic cavitary TB [1]. * **Differential Diagnosis:** In a patient with "healed" TB presenting with new-onset hemoptysis, always consider an **Aspergilloma** (fungus ball) colonizing an old cavity [1]. * **Primary TB vs. Post-Primary:** Hemoptysis is significantly less common in primary TB, which more frequently presents with lymphadenopathy and pleural effusions.

Question 315: A 27-year-old male is incidentally HBsAg positive. DNA-PCR for hepatitis B revealed 1000 copies/ml. The patient is suffering from?

A. Active HBV carrier
B. Acute hepatitis B
C. Chronic hepatitis B
D. Inactive HBV carrier (Correct Answer)

Explanation: ### Explanation The correct answer is **D. Inactive HBV carrier**. **1. Why the Correct Answer is Right:** An **Inactive HBV Carrier** (also known as the HBeAg-negative chronic HBV infection phase) is characterized by the presence of HBsAg for >6 months, but with low viral replication and no active liver inflammation [1]. The diagnostic criteria include: * **HBsAg:** Positive * **HBeAg:** Negative (and Anti-HBe positive) * **HBV DNA levels:** Low (typically <2,000 IU/mL or <10,000 copies/mL) * **ALT/AST levels:** Persistently normal In this case, the DNA count of **1,000 copies/ml** is significantly low, pointing toward an inactive state rather than active disease [1]. **2. Why the Other Options are Wrong:** * **A. Active HBV Carrier:** This term is often used for "Chronic Hepatitis B." It involves high DNA levels (>20,000 IU/mL) and elevated ALT, indicating active liver damage. * **B. Acute Hepatitis B:** This presents with clinical symptoms (jaundice, fever) and markedly elevated transaminases (often >1000 U/L). An incidental finding in an asymptomatic patient makes this unlikely [1]. * **C. Chronic Hepatitis B:** While the patient has the virus, "Chronic Hepatitis" implies active necroinflammation [2]. With a DNA load as low as 1,000 copies/ml, the virus is not currently causing active hepatitis. **3. NEET-PG High-Yield Pearls:** * **Conversion Factor:** 1 IU/mL ≈ 5.2 copies/mL. * **Window Period:** The time between the disappearance of HBsAg and the appearance of Anti-HBs. The only marker present is **Anti-HBc IgM** [1]. * **Best Marker of Infectivity:** HBeAg (indicates high replication). * **First Marker to appear:** HBsAg [1]. * **Prognosis:** Inactive carriers have a low risk of cirrhosis or HCC but require lifelong monitoring of ALT every 6–12 months [1].

Question 316: Which of the following statements is NOT true about the clinical course of chickenpox?

A. Skin rash is maculopapular and vesicular in various stages of development.
B. Younger children tend to have more vesicles than elders. (Correct Answer)
C. Secondary and tertiary cases in the family tend to have a relatively larger number of vesicles.
D. Immunocompromised hosts have a higher chance of visceral complications.

Explanation: **Explanation:** The clinical course of Chickenpox (Varicella-Zoster Virus) is characterized by age-dependent severity [1]. **Why Option B is the correct (False) statement:** In chickenpox, the severity of the disease and the density of the rash are **directly proportional to age**. Younger children typically experience a milder clinical course with fewer vesicles and minimal systemic symptoms [1]. In contrast, adolescents and adults (elders) tend to have a more profuse rash, higher fever, and a significantly increased risk of complications like varicella pneumonia. **Analysis of other options:** * **Option A:** The hallmark of chickenpox is **pleomorphism**. The rash evolves rapidly from macules to papules to vesicles ("dewdrops on a rose petal") and finally crusts. Because new crops appear every 2–4 days, lesions in all stages of development are seen simultaneously in the same anatomical area. * **Option C:** Secondary and tertiary cases within a household often have a **higher viral load** exposure compared to the index case, leading to a more severe clinical presentation and a higher number of vesicles. * **Option D:** Immunocompromised individuals (e.g., HIV, malignancy, transplant recipients) are at high risk for **disseminated varicella**, which involves visceral organs such as the lungs (pneumonitis), liver (hepatitis), and CNS (encephalitis) [1]. **NEET-PG High-Yield Pearls:** * **Infectivity:** 1–2 days *before* the rash appears until all lesions have *crusted* (usually 5 days) [1]. * **Incubation Period:** 10–21 days (Average 14–15 days). * **Congenital Varicella Syndrome:** Highest risk if maternal infection occurs in the first 20 weeks of gestation (presents with cicatricial skin scarring and limb hypoplasia). * **Treatment:** Oral Acyclovir is indicated for those >12 years old, secondary household cases, or those with chronic skin/lung disease. IV Acyclovir is used for the immunocompromised [1].

Question 317: A patient with necrotizing fasciitis was treated with antibiotics and debridement and discharged on wound recovery. He presented 10 days later with diarrhea and fever. Which of the following investigations or interventions is NOT indicated?

A. Continue the same antibiotic (Correct Answer)
B. Stop loperamide
C. Oral Vancomycin is the drug of choice
D. Washing hands with alcohol-based hand sanitizers is superior to washing hands with soap to stop the spread of diarrhea.

Explanation: The clinical presentation of fever and diarrhea following recent broad-spectrum antibiotic therapy for necrotizing fasciitis is highly suggestive of **Clostridioides difficile Infection (CDI)** [1]. **Why "Continue the same antibiotic" is NOT indicated:** The primary step in managing CDI is the immediate cessation of the inciting antibiotic agent whenever possible. Continuing the same antibiotic further disrupts the normal colonic flora, allowing *C. difficile* to proliferate and produce toxins, thereby worsening the clinical condition. **Analysis of other options:** * **Stop loperamide:** Anti-motility agents like loperamide are contraindicated in CDI as they can precipitate toxic megacolon by slowing the clearance of toxins from the bowel. * **Oral Vancomycin:** According to current guidelines (IDSA/SHEA), oral Vancomycin (or Fidaxomicin) is the first-line treatment for CDI [2]. Intravenous vancomycin is ineffective as it does not reach therapeutic concentrations in the gut lumen. * **Hand Hygiene:** *C. difficile* produces spores that are resistant to alcohol-based sanitizers. **Mechanical handwashing with soap and water** is mandatory to physically remove spores and prevent nosocomial transmission. Therefore, the statement that alcohol sanitizers are superior is false (making it a potential distractor, though in this specific question format, stopping the offending drug is the most critical clinical intervention). **Clinical Pearls for NEET-PG:** * **Risk Factors:** Recent antibiotic use (Clindamycin, Fluoroquinolones, Cephalosporins), PPI use, and hospitalization [2]. * **Diagnosis:** Stool toxin assay (GDH/EIA) or PCR for toxin genes [1]. * **Complication:** Pseudomembranous colitis (visualized as yellow-white plaques on colonoscopy) [1]. * **Treatment:** Oral Vancomycin 125 mg QID for 10 days [2]. For fulminant cases, use high-dose oral Vancomycin plus IV Metronidazole.

Question 318: Which of the following is pathognomonic of miliary tuberculosis?

A. Snow storm appearance in CXR
B. Choroid tubercles on fundus examination (Correct Answer)
C. Pericardial TB
D. Peritoneal TB

Explanation: **Explanation:** **Miliary Tuberculosis (TB)** is a form of disseminated tuberculosis resulting from the hematogenous spread of *Mycobacterium tuberculosis* [1]. **Why Option B is Correct:** **Choroid tubercles** are considered **pathognomonic** of miliary TB [1]. These are small, yellowish-white, granulomatous lesions with ill-defined margins, typically seen on funduscopic examination. They represent direct hematogenous seeding of the choroid plexus. Their presence is highly specific; when seen in a patient with systemic symptoms, they confirm the diagnosis of miliary TB even before radiological or microbiological evidence is available. They are found in approximately 10–30% of cases. **Analysis of Incorrect Options:** * **Option A (Snow storm appearance):** While a "millet-seed" or "snow storm" appearance on Chest X-ray (CXR) is a classic finding of miliary TB, it is **not pathognomonic** [1]. Similar radiological patterns can be seen in silicosis, sarcoidosis, histoplasmosis, or metastatic deposits (e.g., thyroid or renal cell carcinoma). * **Options C & D (Pericardial and Peritoneal TB):** These are forms of extrapulmonary tuberculosis [2]. While they can occur concurrently with miliary spread, they are distinct clinical entities and do not serve as diagnostic hallmarks for miliary dissemination. **Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Sputum/body fluid culture or biopsy showing caseating granulomas. * **Most Sensitive Imaging:** High-Resolution CT (HRCT) is more sensitive than CXR for detecting early miliary nodules (1–2 mm). * **Hematological finding:** Leukopenia or leukemoid reaction can occur; hyponatremia (due to SIADH or adrenal involvement) is common. * **Anergetic response:** Up to 50% of patients with miliary TB may have a **negative Tuberculin Skin Test (Mantoux)** due to overwhelmed immunity.

Question 319: Which of the following is NOT a Bioterrorism group A organism?

A. Ebola
B. Botulism
C. Rickettsia (Correct Answer)
D. Yersinia

Explanation: The CDC classifies bioterrorism agents into three categories (A, B, and C) based on their potential for mass casualties, ease of dissemination, and public health impact [1]. **Explanation of the Correct Answer:** **Rickettsia** (specifically the species causing Q fever or Typhus) is classified as a **Category B** agent [1]. While these organisms are moderately easy to disseminate and result in moderate morbidity, they have low mortality rates compared to Category A agents. Therefore, Rickettsia does not meet the criteria for the highest priority group. **Analysis of Incorrect Options (Category A Agents):** * **Ebola:** Viral Hemorrhagic Fevers (including Ebola, Marburg, and Lassa) are Category A because they are highly infectious, carry high mortality rates, and can cause widespread social disruption [1]. * **Botulism (*Clostridium botulinum* toxin):** This is Category A due to its extreme potency; a very small amount of toxin can cause widespread respiratory failure and death [1]. * **Yersinia (*Yersinia pestis*):** The causative agent of Plague is Category A because it can be aerosolized (pneumonic plague), leading to rapid person-to-person spread and high fatality if not treated immediately [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Category A Mnemonic (6 Ps):** **P**lague (*Y. pestis*), **P**ox (Smallpox), **P**hyllo-viruses (Ebola/Marburg), **P**aralysis (Botulism), **P**asturella (*Tularemia*), and **P**ustule (Anthrax) [1]. * **Category B:** Includes *Coxiella burnetii* (Q fever), *Brucella* species, *Salmonella*, and *Vibrio cholerae* [1]. * **Category C:** Emerging pathogens with potential for future mass dissemination, such as **Hantavirus** and **Nipah virus** [1]. * **Anthrax (*B. anthracis*):** Often considered the #1 bioterrorism threat due to its highly resilient spores [1].

Question 320: All of the following should be included during the preliminary evaluation of a case of suspected acute viral hepatitis, except?

A. Hepatitis B surface antigen (HBsAg)
B. IgM antibody to Hepatitis B core antigen (IgM anti-HBc)
C. Antibody to Hepatitis C virus (Anti-HCV)
D. IgM antibody to Hepatitis B e antigen (IgM anti-HBe) (Correct Answer)

Explanation: Explanation: In the preliminary evaluation of acute viral hepatitis, the goal is to identify the specific viral etiology (A, B, C, or E) using markers that appear during the acute phase of infection [1]. Why Option D is the Correct Answer: IgM anti-HBe is not a standard clinical marker used in the diagnosis of acute hepatitis. While HBeAg (Hepatitis B e-antigen) indicates high viral replication and infectivity, the antibodies to it (Anti-HBe) typically appear during the "seroconversion" phase as HBeAg disappears. There is no clinical utility for an IgM-specific version of this antibody in routine diagnostic panels; its presence does not help differentiate acute from chronic infection or guide initial management. Analysis of Incorrect Options: * A. HBsAg: This is the first serological marker to appear in Hepatitis B [1]. It indicates the presence of the virus but cannot distinguish between acute infection and a chronic carrier state [1]. * B. IgM anti-HBc: This is the gold standard for diagnosing acute Hepatitis B [1]. It is particularly crucial during the "window period" when HBsAg may have disappeared but Anti-HBs has not yet appeared [1]. * C. Anti-HCV: This is the primary screening test for Hepatitis C. While it may take weeks to become positive (leading to a potential false negative in the very early acute phase), it remains a standard part of the initial workup for viral hepatitis. High-Yield Clinical Pearls for NEET-PG: * Best marker for acute HBV: IgM anti-HBc [1]. * Best marker for chronic HBV: HBsAg persisting for >6 months [1]. * Window Period: The interval where only IgM anti-HBc is detectable [1]. * Acute Hepatitis A/E: Diagnosed by IgM anti-HAV and IgM anti-HEV, respectively [1]. * HBeAg: Indicates high infectivity and active viral replication ("e" for envelope/extracellular) [1].

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Fungal Infections

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Infection in Immunocompromised Hosts

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