Infectious Diseases — MCQs
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Dengue shock syndrome occurs due to-
A patient requires antibiotic treatment for culture-positive infective enterococcal endocarditis involving an artificial valve. The patient has a history of a severe anaphylactic reaction to penicillin G within the past year. What is the recommended treatment approach?
A 20-year-old female swimmer presents with new-onset severe fatigue and left upper abdominal pain. She was recently treated for presumed typhoid fever. She has a past history of typhoid fever two years ago. On physical examination, her heart rate is 120 bpm and she has a palpable spleen. Stool is negative for heme. Laboratory investigations show a hemoglobin of 5 g/dL with normal TLC and platelets. Peripheral blood smear reveals an excess of spherocytes. Which of the following conditions can cause a similar presentation except?
Which of the following is NOT a complication of HIV infection?
What is currently the most common cause for chronic HCV infection?
Which of the following antitubercular drugs is safe in hepatitis?
What is the most common extranodal site of lymphoma in HIV-positive individuals?
Which of the following is a common oral lesion found in immunocompromised individuals?
A resident doctor sustained a needlestick injury while sampling blood of a patient who is HIV positive. A decision is taken to offer him post-exposure prophylaxis. Which one of the following would be the best recommendation?
Which of the following is/are clinical features of tetanus?
Infectious Diseases Indian Medical PG Practice Questions and MCQs
Question 181: Dengue shock syndrome occurs due to-
- A. Super-imposed bacterial infection
- B. Capillary leak (Correct Answer)
- C. Addison's crisis
- D. Myocarditis
Explanation: **Explanation:** **Dengue Shock Syndrome (DSS)** is primarily a result of **increased vascular permeability**, leading to a massive **capillary leak**. The underlying pathophysiology involves an intense immune response (often during a secondary infection with a different serotype) that triggers a "cytokine storm." This leads to the activation of the vascular endothelium and the leakage of plasma into extravascular spaces (pleural effusion, ascites). The resulting intravascular volume depletion leads to hemoconcentration and, ultimately, hypovolemic shock [1]. **Analysis of Options:** * **A. Super-imposed bacterial infection:** While secondary infections can occur in any debilitated patient, they are not the primary mechanism of shock in Dengue. * **C. Addison's crisis:** Adrenal insufficiency is not a standard feature of Dengue. While "Waterhouse-Friderichsen syndrome" (adrenal hemorrhage) is seen in Meningococcemia, it is rare in Dengue. * **D. Myocarditis:** Although Dengue can cause viral myocarditis and cardiac dysfunction, it is a rare complication [1]. The hallmark of DSS remains plasma leakage rather than primary pump failure. **High-Yield Clinical Pearls for NEET-PG:** * **Critical Phase:** DSS typically occurs during the transition from the febrile to the afebrile phase (usually days 3–7) [1]. * **Warning Signs:** Abdominal pain, persistent vomiting, mucosal bleed, and a rapid drop in platelet count with a **rising Hematocrit (Hct)**. * **Hct as a Marker:** A rise in Hct ≥20% is the most sensitive objective indicator of plasma leakage. * **WHO Classification:** DSS is defined as Dengue Hemorrhagic Fever (DHF) plus circulatory failure (narrow pulse pressure <20 mmHg, hypotension, or shock).
Question 182: A patient requires antibiotic treatment for culture-positive infective enterococcal endocarditis involving an artificial valve. The patient has a history of a severe anaphylactic reaction to penicillin G within the past year. What is the recommended treatment approach?
- A. Amoxicillin-clavulanic acid
- B. Aztreonam
- C. Cefazolin plus gentamicin
- D. Vancomycin (Correct Answer)
Explanation: ### Explanation **1. Why Vancomycin is the Correct Choice:** The standard treatment for Enterococcal Endocarditis typically involves a cell-wall active agent (like Penicillin or Ampicillin) combined with an aminoglycoside (Gentamicin) for synergy [3]. However, this patient has a history of **Type I hypersensitivity (anaphylaxis)** to Penicillin. In such cases, **Vancomycin** is the recommended alternative cell-wall active agent [1]. It provides coverage against most *Enterococcus faecalis* and *E. faecium* strains while avoiding the risk of cross-reactivity associated with beta-lactams [1]. **2. Analysis of Incorrect Options:** * **A. Amoxicillin-clavulanic acid:** This is a penicillin derivative. In a patient with a history of anaphylaxis to Penicillin G, all penicillins are strictly contraindicated due to the high risk of life-threatening recurrence. * **B. Aztreonam:** While Aztreonam (a monobactam) is safe in penicillin-allergic patients, it has **no activity** against Gram-positive organisms like *Enterococcus* [1]. It is exclusively used for Gram-negative infections. * **C. Cefazolin plus gentamicin:** Cefazolin is a 1st-generation cephalosporin. In patients with a history of **anaphylaxis** to penicillin, cephalosporins are generally avoided due to the risk of cross-reactivity [2]. Furthermore, cephalosporins have no inherent activity against *Enterococcus* species. **3. NEET-PG High-Yield Pearls:** * **Enterococcus Rule:** Cephalosporins are the "classic" drugs that have **zero** activity against *Enterococcus* (the "LAME" mnemonic: Listeria, Atypicals, MRSA, Enterococcus). * **Synergy:** For Enterococcal Endocarditis, monotherapy is insufficient; a combination of a cell-wall agent (Penicillin/Vancomycin) + Aminoglycoside (Gentamicin) is required for bactericidal action [3]. * **Alternative for HLAR:** If the strain shows High-Level Aminoglycoside Resistance (HLAR), the combination of **Ampicillin + Ceftriaxone** is used (specifically for *E. faecalis*), but only if the patient is not allergic to penicillin.
Question 183: A 20-year-old female swimmer presents with new-onset severe fatigue and left upper abdominal pain. She was recently treated for presumed typhoid fever. She has a past history of typhoid fever two years ago. On physical examination, her heart rate is 120 bpm and she has a palpable spleen. Stool is negative for heme. Laboratory investigations show a hemoglobin of 5 g/dL with normal TLC and platelets. Peripheral blood smear reveals an excess of spherocytes. Which of the following conditions can cause a similar presentation except?
- A. Systemic lupus erythematosus
- B. Methyldopa ingestion
- C. Quinidine
- D. Infectious mononucleosis (Correct Answer)
Explanation: ### **Explanation** The clinical presentation describes a 20-year-old with severe anemia (Hb 5 g/dL), tachycardia, left upper quadrant pain (splenomegaly), and **spherocytes** on peripheral smear. The key diagnostic clue is the history of "presumed typhoid" treated recently. In clinical vignettes, typhoid is often a distractor for **Infectious Mononucleosis (EBV)**, which presents with fever, pharyngitis, and lymphadenopathy. However, the presence of spherocytes and sudden severe anemia points toward **Autoimmune Hemolytic Anemia (AIHA)**. AIHA is classified into **Warm AIHA** (IgG-mediated) and **Cold AIHA** (IgM-mediated) [2]. * **Warm AIHA** is characterized by **spherocytes** on the peripheral smear (due to partial splenic macrophage ingestion of RBC membranes) [2]. * **Cold AIHA** is characterized by **RBC agglutination** [1]. **Why Infectious Mononucleosis is the correct answer:** Infectious Mononucleosis (EBV) is a classic cause of **Cold AIHA**. Therefore, the peripheral smear would typically show **clumping/agglutination** of RBCs rather than the **spherocytes** seen in this patient [1]. Spherocytes are the hallmark of Warm AIHA [2]. **Analysis of Incorrect Options (Causes of Warm AIHA):** * **A. Systemic Lupus Erythematosus (SLE):** The most common secondary cause of Warm AIHA [2]. * **B. Methyldopa:** A classic drug-induced cause of Warm AIHA (via true autoantibody production). * **C. Quinidine:** Can cause immune-mediated hemolysis (typically via the "innocent bystander" mechanism). ### **High-Yield Clinical Pearls for NEET-PG** 1. **Warm AIHA (IgG):** Associated with SLE, CLL, and drugs (Methyldopa, Penicillin). Shows **Spherocytes**. Treatment: Steroids (First-line), Splenectomy [2]. 2. **Cold AIHA (IgM):** Associated with *Mycoplasma pneumoniae* and **Infectious Mononucleosis**. Shows **Agglutination**. Treatment: Keep warm, Rituximab (Steroids/Splenectomy are ineffective) [1]. 3. **Direct Antiglobulin Test (Coombs):** The gold standard for diagnosing AIHA [2]. 4. **Spherocytes DDx:** Hereditary Spherocytosis (Negative Coombs) vs. Warm AIHA (Positive Coombs) [2].
Question 184: Which of the following is NOT a complication of HIV infection?
- A. Neurocognitive dysfunction
- B. Diabetes
- C. Thromboembolism (Correct Answer)
- D. Accelerated aging syndrome
Explanation: **Explanation:** The correct answer is **C. Thromboembolism**. While HIV is a pro-inflammatory state that can increase the risk of various vascular events, it is **not** traditionally classified as a direct "complication" of the virus in the same clinical category as neurocognitive decline or metabolic syndrome. In the context of standard medical examinations, thromboembolism is often considered a multifactorial event rather than a defining complication of the HIV disease process itself. **Analysis of Options:** * **A. Neurocognitive dysfunction:** HIV-associated neurocognitive disorders (HAND) range from asymptomatic impairment to **HIV-associated dementia (HAD)** [1]. The virus crosses the blood-brain barrier early, infecting microglia and macrophages, leading to chronic neuroinflammation. * **B. Diabetes:** HIV infection and long-term **Antiretroviral Therapy (ART)**—specifically older Protease Inhibitors (PIs) and Nucleoside Reverse Transcriptase Inhibitors (NRTIs)—are strongly associated with insulin resistance, lipodystrophy, and Type 2 Diabetes Mellitus [1]. * **D. Accelerated aging syndrome:** HIV causes "inflammaging"—a state of chronic immune activation and senescence. Patients often experience age-related comorbidities (cardiovascular disease, bone loss, frailty) approximately **10–15 years earlier** than HIV-negative individuals. **High-Yield NEET-PG Pearls:** * **HAND:** The most common cause of dementia in young adults worldwide before the widespread use of ART [1]. * **Metabolic Complications:** Always monitor lipid profiles and blood glucose in patients on ART (especially PIs like Lopinavir/Ritonavir) [1]. * **Malignancies:** HIV increases the risk of AIDS-defining cancers (Kaposi Sarcoma, Non-Hodgkin Lymphoma, Cervical Cancer) and non-AIDS-defining cancers (Lung, Anal, and Liver cancer) [1].
Question 185: What is currently the most common cause for chronic HCV infection?
- A. Blood product transfusion
- B. Anal sex with prostitutes
- C. IV drug abuse (Correct Answer)
- D. Blood product transfusion
Explanation: **Explanation:** The epidemiology of Hepatitis C Virus (HCV) has shifted significantly over the last few decades due to improved screening protocols. **1. Why IV Drug Abuse (IVDA) is the Correct Answer:** Currently, **Injection Drug Use (IDU)** is the most common risk factor and mode of transmission for HCV globally and in India [2]. The sharing of needles, syringes, and other drug paraphernalia provides a direct route for blood-to-blood transmission. Because HCV is highly stable in the environment, even microscopic amounts of blood can lead to infection. Approximately 60–80% of people who inject drugs become HCV-positive [2]. **2. Why the Other Options are Incorrect:** * **Blood Product Transfusion (Options A & D):** Historically, this was the leading cause of HCV. However, since the implementation of mandatory and highly sensitive screening (including Nucleic Acid Testing or NAT) of donor blood in the 1990s, the risk of post-transfusion hepatitis C has become extremely rare (less than 1 per 2 million units). * **Anal Sex (Option B):** While HCV can be transmitted sexually, it is inefficiently transmitted via this route compared to HIV or HBV. Sexual transmission is primarily seen in specific populations, such as HIV-positive men who have sex with men (MSM), but it is not the most common cause in the general population. **Clinical Pearls for NEET-PG:** * **The "Rule of 80s":** Approximately 80% of acute HCV cases become **chronic** [1]; 80% of chronic cases remain stable, while 20% progress to **cirrhosis** [1]. * **Screening:** Anti-HCV antibody is the initial screening test; **HCV RNA (PCR)** is the gold standard for confirming active infection [1]. * **Treatment:** The current standard of care involves **Direct-Acting Antivirals (DAAs)** like Sofosbuvir and Daclatasvir, which offer a cure rate (SVR) of >95%. * **Vaccine:** There is **no vaccine** available for HCV due to high antigenic variation in the E2 envelope glycoprotein.
Question 186: Which of the following antitubercular drugs is safe in hepatitis?
- A. Isoniazid
- B. Rifampicin
- C. Pyrazinamide
- D. Ethambutol (Correct Answer)
Explanation: ### Explanation The management of Tuberculosis in patients with pre-existing liver disease or drug-induced hepatitis requires a clear understanding of the metabolic pathways of Anti-Tubercular Treatment (ATT). [1] **1. Why Ethambutol is the Correct Answer:** Ethambutol is primarily excreted via the **kidneys (approx. 80%)** and does not undergo significant hepatic metabolism. Unlike other first-line drugs, it is **not hepatotoxic**. Therefore, it is considered the safest first-line agent to continue or initiate in patients with hepatitis or chronic liver disease. Streptomycin is the other first-line drug (injectable) that is safe in hepatitis as it is also renally excreted. **2. Why the Other Options are Incorrect:** The "Big Three" hepatotoxic drugs are: * **Pyrazinamide (C):** The **most hepatotoxic** drug among the first-line agents. It often causes prolonged or severe liver injury. * **Isoniazid (A):** Frequently causes a transient rise in transaminases; it is metabolized via acetylation in the liver. It is the second most hepatotoxic. [1] * **Rifampicin (B):** While it can cause hepatitis, it more commonly causes **asymptomatic cholestasis** (elevation of bilirubin) due to competition for excretion. It is the least hepatotoxic of these three but still contraindicated in acute hepatitis. **Clinical Pearls for NEET-PG:** * **Order of Hepatotoxicity:** Pyrazinamide > Isoniazid > Rifampicin. * **Safe Drugs in Liver Disease:** Ethambutol, Streptomycin, and Fluoroquinolones (like Levofloxacin). [1] * **Management Rule:** If AST/ALT levels are >3 times the upper limit of normal (with symptoms) or >5 times (without symptoms), hepatotoxic drugs must be stopped. [1] * **Reintroduction:** Once enzymes normalize, drugs are reintroduced one by one: Rifampicin first, followed by Isoniazid, and finally Pyrazinamide. [1]
Question 187: What is the most common extranodal site of lymphoma in HIV-positive individuals?
- A. Central Nervous System (CNS) (Correct Answer)
- B. Gastrointestinal Tract (GIT)
- C. Retroperitoneum
- D. Mediastinum
Explanation: **Explanation:** In the context of HIV/AIDS, the risk of developing Non-Hodgkin Lymphoma (NHL) is significantly elevated due to chronic B-cell stimulation and loss of T-cell surveillance [1]. While the **Gastrointestinal Tract (GIT)** is the most common extranodal site for lymphoma in the **general population**, the epidemiology shifts in HIV-positive individuals. **Why CNS is the Correct Answer:** In HIV-positive patients, the **Central Nervous System (CNS)** is the most common extranodal site for lymphoma. Primary CNS Lymphoma (PCNSL) is an AIDS-defining illness, typically occurring when CD4 counts drop below **50 cells/mm³**. It is almost universally associated with **Epstein-Barr Virus (EBV)** infection [1]. **Analysis of Incorrect Options:** * **B. Gastrointestinal Tract (GIT):** While frequently involved in systemic HIV-associated lymphomas (like Burkitt or DLBCL), it ranks second to the CNS in terms of primary extranodal frequency in this specific population. * **C. Retroperitoneum:** This is a common site for nodal involvement or late-stage spread but is not the primary extranodal site. * **D. Mediastinum:** Mediastinal involvement is more characteristic of Hodgkin Lymphoma or Primary Mediastinal B-cell Lymphoma, which are less common than CNS involvement in advanced AIDS. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogen Association:** PCNSL in HIV is >95% associated with **EBV** [1]. * **Imaging:** On MRI/CT, PCNSL typically presents as a **single, ring-enhancing lesion** (though it can be multiple) [1]. * **Differential Diagnosis:** The main differential is **Toxoplasmosis** (usually multiple lesions, eccentric target sign) [1]. * **Diagnostic Gold Standard:** Brain biopsy; however, detection of **EBV DNA in CSF** via PCR is a highly specific non-invasive marker.
Question 188: Which of the following is a common oral lesion found in immunocompromised individuals?
- A. Lichen planus
- B. Lichenoid eruption
- C. Oral hairy leukoplakia (Correct Answer)
- D. Erythroplakia
Explanation: **Explanation:** **Oral Hairy Leukoplakia (OHL)** is the correct answer because it is a classic opportunistic manifestation strongly associated with immunocompromised states, particularly **HIV/AIDS** (often occurring when CD4 counts fall below 200-300 cells/mm³). It is caused by the **Epstein-Barr Virus (EBV)**, which leads to benign epithelial hyperplasia [1]. Clinically, it presents as white, corrugated (hairy), non-scrapable patches, typically on the lateral borders of the tongue. **Analysis of Incorrect Options:** * **Lichen Planus (A):** An idiopathic inflammatory condition mediated by T-cells. While it involves the oral mucosa (Wickham striae), it is not specifically an opportunistic infection of the immunocompromised. * **Lichenoid Eruption (B):** These are drug-induced or hypersensitivity reactions (e.g., to NSAIDs or dental amalgam) that mimic lichen planus clinically but are not related to immune suppression. * **Erythroplakia (D):** A red, velvety patch on the oral mucosa [2]. It is highly concerning for **premalignancy** or carcinoma in situ and is primarily associated with tobacco and alcohol use rather than immunosuppression. **High-Yield Clinical Pearls for NEET-PG:** * **Differentiating Feature:** Unlike Oral Candidiasis (Thrush), OHL **cannot be scraped off** with a tongue depressor [1]. * **Diagnostic Association:** OHL is often the first clinical sign of HIV infection; its presence warrants immediate HIV testing [1]. * **Treatment:** Usually asymptomatic and requires no treatment, but responds to systemic antivirals (Acyclovir) or HAART (by improving immune status). * **Histology:** Look for "balloon cells" (koilocytosis) in the upper layers of the epithelium. **Note on other oral lesions:** While OHL is the classic EBV-related lesion, other conditions like oropharyngeal candidiasis (thrush) and Kaposi's sarcoma are also common oral manifestations of HIV [1][2].
Question 189: A resident doctor sustained a needlestick injury while sampling blood of a patient who is HIV positive. A decision is taken to offer him post-exposure prophylaxis. Which one of the following would be the best recommendation?
- A. Zidovudine + Lamivudine for 4 weeks
- B. Zidovudine + Lamivudine + Nevirapine for 4 weeks
- C. Zidovudine + Lamivudine + Indinavir for 4 weeks (Correct Answer)
- D. Zidovudine + Stavudine + Nevirapine for 4 weeks
Explanation: The management of occupational exposure to HIV (Post-Exposure Prophylaxis - PEP) is a high-yield topic for NEET-PG. The goal of PEP is to prevent viral replication immediately after exposure [1]. **1. Why Option C is Correct:** According to the classic guidelines (NACO/WHO) reflected in this question, PEP for a "high-risk" exposure (e.g., a hollow-bore needle stick from a known HIV-positive patient) requires an **Expanded Regimen**. This consists of **two NRTIs plus a Protease Inhibitor (PI)** [3]. * **Zidovudine + Lamivudine** (NRTIs) form the backbone. * **Indinavir** (or Lopinavir/Ritonavir) is added as the third drug to increase potency [3]. * The duration for all PEP regimens is strictly **4 weeks (28 days)**. **2. Why Other Options are Incorrect:** * **Option A:** This is a "Basic Regimen." While used for low-risk exposures (e.g., solid needle, superficial injury), it is not the "best" recommendation for a needle stick from a confirmed HIV-positive source. * **Option B & D:** These include **Nevirapine** (an NNRTI). Nevirapine is strictly **contraindicated** in PEP because it carries a high risk of severe hepatotoxicity and Stevens-Johnson Syndrome (SJS) in HIV-negative individuals. **Stavudine** (in Option D) is also avoided due to high toxicity. **3. Clinical Pearls for NEET-PG:** * **Timing:** PEP should ideally be started within **2 hours**, and definitely within **72 hours** of exposure. * **Current Update:** While this question reflects the classic PI-based exam pattern, current WHO/NACO guidelines now prefer **Tenofovir + Lamivudine + Dolutegravir (TLD)** as the single preferred regimen for all exposures. * **Testing Schedule:** Follow-up HIV testing for the healthcare worker should be done at baseline, 6 weeks, 12 weeks, and 6 months [1]. * **Risk of Transmission:** The average risk of HIV transmission after a percutaneous skin puncture is approximately **0.3%** [2].
Question 190: Which of the following is/are clinical features of tetanus?
- A. Dysphagia
- B. Risus sardonicus
- C. Opisthotonus
- D. All of the above (Correct Answer)
Explanation: Tetanus is caused by the neurotoxin **tetanospasmin**, released by *Clostridium tetani*. The toxin acts by blocking the release of inhibitory neurotransmitters (GABA and glycine) from Renshaw cells in the spinal cord [1]. This leads to unchecked excitatory impulses, resulting in generalized muscle rigidity and reflex spasms [1]. **Breakdown of Clinical Features:** * **Dysphagia (Option A):** This occurs due to the involvement of the pharyngeal muscles. Early in the disease, spasm of the jaw muscles (**Trismus** or "lockjaw") is often followed by stiffness in the neck and difficulty swallowing [1]. * **Risus Sardonicus (Option B):** This is a characteristic "sardonic smile" caused by the sustained contraction of the facial muscles (specifically the *frontalis* and *orbicularis oculi* muscles) and the muscles at the angles of the mouth. * **Opisthotonus (Option C):** This refers to a profound backward arching of the spine caused by the powerful contraction of the paravertebral (extensor) muscles, which overpower the weaker flexor muscles. Since all three features are classic manifestations of generalized tetanus, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Trismus (Lockjaw) is the most common presenting symptom. * **Autonomic Instability:** A major cause of death in modern ICUs, manifesting as labile hypertension, tachycardia, and hyperpyrexia. * **Diagnosis:** Primarily **clinical**. Wound cultures for *C. tetani* are positive in only about 30% of cases [1]. * **Spatula Test:** A high-yield bedside test; touching the posterior pharyngeal wall triggers a reflex bite (positive) instead of a gag reflex (negative). * **Management:** Includes wound debridement, Metronidazole (preferred over Penicillin G), and Human Tetanus Immune Globulin (HTIG).
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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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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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