Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 191: A 50-year-old HIV-positive male presents with fever and breathlessness, diagnosed with Pneumocystis jiroveci pneumonia (PCP). At what CD4 T cell count is primary prophylaxis for PCP recommended?

A. < 200 cells/mm³ (Correct Answer)
B. < 50 cells/mm³
C. < 150 cells/mm³
D. < 100 cells/mm³

Explanation: Pneumocystis jiroveci pneumonia (PCP) is the most common opportunistic infection in patients with HIV/AIDS. The risk of developing PCP increases significantly as the immune system weakens, specifically when the CD4+ T-lymphocyte count falls below 200 cells/mm³ [1]. Therefore, primary prophylaxis is initiated at this threshold to prevent the first occurrence of the disease. * Option A (Correct): Guidelines (CDC/WHO) recommend starting prophylaxis with Trimethoprim-Sulfamethoxazole (TMP-SMX) when CD4 < 200 cells/mm³ or if the patient has a history of oropharyngeal candidiasis [1]. * Option B (< 50 cells/mm³): This is the threshold for prophylaxis against Mycobacterium avium complex (MAC) (using Azithromycin) and is associated with increased risk for CMV retinitis. * Option C (< 150 cells/mm³): This threshold is used in specific endemic areas for prophylaxis against Histoplasma capsulatum. * Option D (< 100 cells/mm³): This is the threshold for starting prophylaxis against Toxoplasma gondii (in IgG-positive patients) and Cryptococcus neoformans (pre-emptive screening/treatment). Clinical Pearls for NEET-PG: 1. Drug of Choice: TMP-SMX (Double strength, once daily) is the gold standard for both prophylaxis and treatment [1]. 2. Alternative: If the patient is allergic to Sulfa drugs, use Dapsone or Atovaquone [1]. 3. Steroid Indication: In active PCP treatment, add corticosteroids if PaO₂ < 70 mmHg or A-a gradient > 35 mmHg to prevent respiratory failure [1]. 4. Discontinuation: Prophylaxis can be safely stopped when CD4 counts rise above 200 cells/mm³ for at least 3 months in response to ART.

Question 192: Regarding chronic hepatitis B, all of the following are true EXCEPT:

A. There is a 90% chance for chronic infection if infected at birth.
B. Mild chronic hepatitis B has a 5-year survival of 97%.
C. Adult infection is usually symptomatic.
D. Chronicity if infected in adulthood is about 10%. (Correct Answer)

Explanation: The risk of developing chronic Hepatitis B (HBV) is inversely proportional to the age at which the infection is acquired. This is due to the maturity of the host’s immune system. **1. Why Option D is the Correct Answer (The False Statement):** In immunocompetent adults, the risk of chronicity following an acute HBV infection is actually **less than 5%** (typically 1–3%) [1]. A 10% figure is an overestimation for healthy adults. The adult immune system is usually robust enough to mount a vigorous T-cell response, leading to viral clearance in the vast majority of cases. **2. Analysis of Other Options:** * **Option A:** Perinatal transmission (at birth) carries the highest risk of chronicity, approximately **90%**, because the neonatal immune system is immature and develops "immune tolerance" to the virus [1]. * **Option B:** Patients with mild chronic hepatitis B (compensated) have an excellent prognosis, with a **5-year survival rate of approximately 97%**. Survival drops significantly once cirrhosis or hepatocellular carcinoma (HCC) develops. * **Option C:** Unlike childhood infections which are mostly asymptomatic, **adult-acquired HBV is usually symptomatic** (jaundice, malaise, nausea) in about 30–50% of cases, reflecting the active immune-mediated destruction of infected hepatocytes. **Clinical Pearls for NEET-PG:** * **Serology:** The hallmark of chronic HBV is the persistence of **HBsAg for >6 months** [1]. * **Transmission:** Globally, the most common route is perinatal [1]; in low-prevalence areas, it is sexual or percutaneous. * **Ground Glass Hepatocytes:** The characteristic histopathological finding in chronic HBV due to HBsAg accumulation in the endoplasmic reticulum. * **Extrahepatic Manifestation:** Polyarteritis Nodosa (PAN) and Membranous Glomerulonephritis are strongly associated with chronic HBV.

Question 193: What is the most appropriate initial management for a traumatic street wound?

A. Immediate suturing
B. Cleaning with saline and debridement (Correct Answer)
C. Oral antibiotics
D. No intervention

Explanation: **Explanation:** The primary goal in managing a traumatic street wound is to minimize the risk of infection and promote healthy tissue healing. Street wounds are inherently contaminated with soil, debris, and polymicrobial flora. In cases of accidental injuries or cuts, the wound should be immediately washed thoroughly under running water [1]. **Why Option B is Correct:** The cornerstone of management is **thorough irrigation and debridement**. Cleaning with normal saline (or tap water) mechanically removes foreign bodies and reduces the bacterial load. Debridement involves removing devitalized or necrotic tissue [2], which otherwise acts as a culture medium for bacteria (especially anaerobes like *Clostridium tetani*). This "mechanical prophylaxis" is the most effective step in preventing wound sepsis. **Why Other Options are Incorrect:** * **Option A (Immediate suturing):** Traumatic street wounds are considered "dirty" or "contaminated." Primary closure (immediate suturing) traps bacteria inside, leading to abscess formation or gas gangrene. These wounds are often left open for **delayed primary closure**. * **Option C (Oral antibiotics):** While antibiotics may be indicated later based on wound severity or patient comorbidities, they cannot replace mechanical cleaning [2]. Antibiotics cannot penetrate necrotic tissue or remove foreign debris. * **Option D (No intervention):** This leads to a high risk of cellulitis, sepsis, and tetanus. **NEET-PG High-Yield Pearls:** * **Tetanus Prophylaxis:** Always assess the patient’s immunization status. For a dirty wound in a person with uncertain/incomplete vaccination, give both Tetanus Toxoid (TT) and Tetanus Immune Globulin (TIG). All staff involved in wound care should also be vaccinated [3]. * **Golden Period:** Wounds treated within 6–8 hours have a lower infection risk. * **Irrigation Pressure:** High-pressure irrigation (7–15 psi) is ideal for removing bacteria without damaging healthy tissue. * **Dog/Human Bites:** These are also managed by irrigation and are generally not sutured (except for certain facial wounds).

Question 194: Multidrug-resistant tuberculosis (MDRTB) must be treated for at least how many months?

A. 12 months
B. 18 months
C. 20 months (Correct Answer)
D. 36 months

Explanation: Explanation: 1. Why Option C is Correct: Multidrug-resistant tuberculosis (MDR-TB) is defined as resistance to at least Isoniazid (H) and Rifampicin (R). Because these two most potent bactericidal drugs are ineffective, treatment requires a combination of second-line drugs which are less potent and have slower sterilization rates. According to the WHO and NTEP (National Tuberculosis Elimination Program) guidelines for the conventional (longer) regimen, MDR-TB must be treated for a total duration of 18 to 24 months. The standard duration often cited in exams and clinical practice is 20 months (typically 6–9 months of Intensive Phase and 18 months of Continuation Phase). 2. Why Other Options are Incorrect: * Option A (12 months): This is too short for conventional MDR-TB treatment. While a "Shorter MDR-TB Regimen" (9–11 months) exists for specific eligible patients, it is not the standard answer for the general duration of MDR-TB treatment in traditional MCQ formats. * Option B (18 months): While 18 months is the minimum duration for the continuation phase, the total duration including the intensive phase usually extends to 20 months or more. * Option D (36 months): This is excessively long and is not supported by standard protocols, though Extensively Drug-Resistant TB (XDR-TB) may occasionally require longer durations. 3. High-Yield Clinical Pearls for NEET-PG: * Definition: MDR-TB = Resistance to H + R. * XDR-TB: MDR-TB + resistance to any Fluoroquinolone + at least one Group A drug (Bedaquiline or Linezolid) as per the new 2021 WHO definition. * Drug of Choice: Bedaquiline is now the backbone of MDR-TB regimens (inhibits mycobacterial ATP synthase). * NTEP Update: India is moving towards an all-oral H-mono/poly resistant regimen and shorter BPaL/BPaLM regimens (6 months) for specific cases, but for standard exam questions, the 20-month conventional regimen remains the classic benchmark [1].

Question 195: What is the most common complication of Typhoid fever?

A. Paralytic ileus (Correct Answer)
B. Otitis media
C. Oophoritis
D. Rheumatic fever

Explanation: **Explanation:** **Typhoid fever (Enteric fever)**, caused by *Salmonella Typhi*, primarily affects the gastrointestinal tract, specifically the Peyer's patches in the terminal ileum. **Why Paralytic Ileus is the correct answer:** During the third week of untreated typhoid fever, the inflammatory process in the Peyer's patches leads to necrosis and ulceration [1]. This intense inflammation and toxemia often result in **paralytic ileus** (adynamic ileus), which is considered the **most common gastrointestinal complication**. It presents with abdominal distension and absent bowel sounds [1]. If the ulceration progresses deeper, it can lead to more severe (but statistically less frequent) complications like intestinal perforation or hemorrhage [1]. **Analysis of Incorrect Options:** * **B. Otitis media:** While a common complication of respiratory infections (like Measles or Streptococcal infections), it is not a characteristic feature of Typhoid fever. * **C. Oophoritis:** This is a classic complication of **Mumps** in post-pubertal females, not Typhoid. * **D. Rheumatic fever:** This is a non-suppurative sequela of **Group A Streptococcal (GAS)** pharyngitis, involving an autoimmune cross-reactivity. **High-Yield Clinical Pearls for NEET-PG:** * **Most common complication overall:** Paralytic ileus. * **Most serious/dreaded complications:** Intestinal perforation and hemorrhage (typically occur in the 3rd week) [1]. * **Pathognomonic finding:** Rose spots (faint pink macules on the trunk, seen in the 2nd week). * **Temperature-Pulse Dissociation:** Also known as **Faget’s sign** (relative bradycardia despite high fever). * **Investigation of choice:** * 1st week: Blood culture (highest sensitivity). * 2nd week: Widal test (though non-specific). * 3rd week: Stool/Urine culture. * **Overall most sensitive:** Bone marrow culture.

Question 196: A 30-year-old man with AIDS complains of severe pain on swallowing. Upper GI endoscopy shows elevated, white plaques on a hyperemic and edematous esophageal mucosa. Which of the following is the most likely diagnosis?

A. Barrett esophagus
B. Candida esophagitis (Correct Answer)
C. Herpetic esophagitis
D. Reflux esophagitis

Explanation: ### Explanation **Correct Answer: B. Candida esophagitis** **Medical Concept:** In patients with HIV/AIDS, **Candida esophagitis** is the most common cause of infectious esophagitis and is an AIDS-defining illness [1]. The clinical hallmark is **odynophagia** (painful swallowing). Endoscopically, it presents as characteristic **adherent, elevated white plaques** (pseudomembranes) on an erythematous (hyperemic) and friable mucosa. These plaques cannot be easily washed away, and scraping them often reveals a raw, bleeding base. **Analysis of Incorrect Options:** * **A. Barrett esophagus:** This is a premalignant condition resulting from chronic GERD where squamous epithelium undergoes metaplasia to columnar epithelium. Endoscopy typically shows "salmon-pink" velvety mucosa, not white plaques. * **C. Herpetic esophagitis (HSV):** While common in AIDS, HSV typically presents with small, discrete, **"punched-out" stellate ulcers** (volcano-like). It does not present with elevated white plaques. * **D. Reflux esophagitis:** This is caused by gastric acid reflux. Endoscopic findings usually include linear erosions, streaks of erythema, or ulcerations in the distal esophagus, rather than diffuse white plaques. **NEET-PG High-Yield Pearls:** * **Most common cause of esophagitis in AIDS:** *Candida albicans*. * **Endoscopy vs. Symptoms:** If an AIDS patient has oral thrush and esophageal symptoms, empirical antifungal therapy (Fluconazole) is often started. Endoscopy is indicated if there is no response. * **Viral Differentials:** * **CMV Esophagitis:** Large, shallow, **linear ulcers** (Treatment: Ganciclovir). * **HSV Esophagitis:** Small, deep, **punched-out ulcers** (Treatment: Acyclovir). * **Microscopy:** Look for pseudohyphae and budding yeast on PAS or GMS stain.

Question 197: Which of the following is commonly associated with respiratory system infections in HIV patients?

A. Streptococcus
B. Haemophilus influenzae
C. Pneumocystis
D. All of the above (Correct Answer)

Explanation: **Explanation:** In patients with HIV, the risk of respiratory infections is significantly increased due to progressive depletion of CD4+ T-lymphocytes and impaired humoral immunity. **1. Why "All of the above" is correct:** HIV-infected individuals are susceptible to both **common bacterial pathogens** and **opportunistic infections**. While opportunistic infections like *Pneumocystis jirovecii* are classic hallmarks of advanced AIDS, **bacterial pneumonia** remains the most frequent cause of pulmonary disease in HIV patients across all CD4 counts [1]. * **Streptococcus pneumoniae (Option A):** This is the **most common cause of community-acquired pneumonia (CAP)** in HIV patients. The risk of invasive pneumococcal disease is nearly 100 times higher in HIV-positive individuals compared to the general population. * **Haemophilus influenzae (Option B):** This is the second most common bacterial cause of pneumonia in this population. Both encapsulated and non-encapsulated strains are prevalent. * **Pneumocystis jirovecii (Option C):** Formerly known as *P. carinii*, this is the most common **opportunistic** respiratory infection. It typically occurs when the CD4 count drops below **200 cells/µL** [1]. **Clinical Pearls for NEET-PG:** * **Most common cause of pneumonia in HIV:** *Streptococcus pneumoniae*. * **Most common opportunistic infection (OI):** *Pneumocystis jirovecii* (PCP) [1]. * **Radiology of PCP:** Classic bilateral perihilar ground-glass opacities (bat-wing appearance) [1]. * **Diagnosis of PCP:** Induced sputum or Bronchoalveolar Lavage (BAL) using Silver stain (Gomori Methenamine Silver) [1]. * **Prophylaxis:** Trimethoprim-Sulfamethoxazole (TMP-SMX) is started when CD4 < 200 cells/µL to prevent PCP.

Question 198: What is the most dreadful complication of meningococcal infection?

A. Waterhouse-Friderichsen syndrome
B. Fitz-Hugh-Curtis syndrome
C. Polyarthritis
D. Waterhouse-Friderichsen syndrome (Correct Answer)

Explanation: **Explanation:** **Waterhouse-Friderichsen Syndrome (WFS)** is the most dreaded and lethal complication of meningococcemia (caused by *Neisseria meningitidis*). It is characterized by **adrenal gland failure due to massive bilateral adrenal hemorrhage**. This occurs as a result of severe septicemia leading to Disseminated Intravascular Coagulation (DIC), widespread purpura, and profound septic shock. The rapid destruction of the adrenal cortex leads to acute adrenal insufficiency, which is often fatal if not treated emergently with aggressive fluid resuscitation, antibiotics, and steroid replacement. **Analysis of Options:** * **Fitz-Hugh-Curtis Syndrome:** This is a complication of Pelvic Inflammatory Disease (PID), typically caused by *Chlamydia trachomatis* or *Neisseria gonorrhoeae*. It involves perihepatitis (inflammation of the liver capsule) leading to "violin-string" adhesions. It is not associated with meningococcal infection. * **Polyarthritis:** While immune-mediated arthritis can occur as a late complication of meningococcal disease (Type III hypersensitivity), it is generally non-destructive and self-limiting, making it far less "dreadful" than WFS. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Endotoxin-mediated vascular damage leads to DIC and subsequent adrenal hemorrhage. * **Clinical Triad:** Rapidly spreading petechial/purpuric rash (Purpura fulminans), shock, and acute adrenal crisis [1]. * **Diagnosis:** Primarily clinical in an acute setting; CT may show bilateral adrenal enlargement/hemorrhage. * **Drug of Choice:** Ceftriaxone is the empirical treatment for meningococcal meningitis/sepsis [1]. Chemoprophylaxis for close contacts is Rifampicin (standard) or Ciprofloxacin/Ceftriaxone [1].

Question 199: Which of the following viruses is notorious for increased mortality in pregnant patients?

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

Explanation: **Explanation:** **Hepatitis E Virus (HEV)** is a single-stranded RNA virus transmitted primarily via the feco-oral route. While it typically causes a self-limiting acute viral hepatitis in the general population, it is notorious for causing **Fulminant Hepatic Failure (FHF)** in pregnant women, particularly during the **third trimester**. The mortality rate in pregnant patients infected with HEV can reach as high as **20–25%**, compared to <1% in the general population. The exact pathogenesis is linked to hormonal shifts and an altered immune response (Th2 over Th1) during pregnancy, which leads to high viral loads and severe liver necrosis. **Analysis of Incorrect Options:** * **Hepatitis A:** Also transmitted via the feco-oral route, it causes acute hepatitis but does not show a predilection for increased severity or mortality in pregnancy. * **Hepatitis B & C:** These are parenterally transmitted viruses. While they carry a significant risk of **vertical transmission** (mother-to-child) and chronic carrier states, they do not typically cause an increased rate of acute fulminant hepatic failure specifically due to the pregnant state. **High-Yield Clinical Pearls for NEET-PG:** * **HEV Genotypes:** Genotypes 1 and 2 are associated with waterborne epidemics in developing countries (including India) and high maternal mortality. * **Serology:** Diagnosis is confirmed by detecting **IgM anti-HEV** [1]. * **Prognosis:** HEV is the most common cause of sporadic and epidemic acute viral hepatitis in India. * **Prevention:** Since there is no widely available vaccine in many regions (except China), management focuses on clean water supply and sanitation.

Question 200: Which of the following is a contraindication to receiving the live rubella vaccine?

A. Children between 1 year old and puberty
B. Infants less than 1 year old
C. All adults
D. Pregnant women (Correct Answer)

Explanation: **Explanation:** The rubella vaccine is a **live-attenuated virus vaccine** (RA 27/3 strain). The primary contraindication for any live vaccine is pregnancy, due to the theoretical risk of the attenuated virus crossing the placenta and causing **Congenital Rubella Syndrome (CRS)** in the fetus [1]. While no cases of CRS have been documented from the vaccine itself, the risk remains a medical concern. **Analysis of Options:** * **D (Correct):** Pregnant women should not receive the vaccine. Furthermore, women are advised to avoid pregnancy for at least **4 weeks (28 days)** after receiving the rubella or MMR vaccine. * **A & B:** Rubella vaccination is routinely indicated for children. In India’s National Immunization Schedule, the MR/MMR vaccine is given at **9 months** and **16–24 months**. It is not given to infants under 6–9 months because maternal antibodies can interfere with the immune response. * **C:** Vaccination is recommended for non-pregnant adults who lack evidence of immunity, particularly healthcare workers and women of childbearing age (pre-conception), to prevent future outbreaks and CRS. **High-Yield Clinical Pearls for NEET-PG:** * **Post-partum Vaccination:** If a woman is found to be seronegative during pregnancy, she should be vaccinated immediately in the **immediate postpartum period**. Breastfeeding is *not* a contraindication. * **Egg Allergy:** Unlike the influenza vaccine, MMR is grown in chick embryo fibroblast cultures, not eggs; therefore, a history of egg allergy is **not** a contraindication. * **Immunocompromised states:** Like all live vaccines, it is contraindicated in severely immunocompromised individuals (e.g., HIV with CD4 <200), except for household contacts of such patients. [1]

Practice by Chapter

Principles of Antimicrobial Therapy

Practice Questions

Fever of Unknown Origin

Practice Questions

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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