Infectious Diseases — MCQs
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A 50-year-old woman presented at the emergency room complaining of urinary urgency and flank pain. Microscopic examination of a urine sample was done and Gram staining was performed. Prior to initiation of antibiotic therapy, she abruptly developed fever, chills, and delirium. Hypotension and hyperventilation rapidly followed. These observations suggest that the patient is responding to the release of which bacterial component?
What is the most common form of extrapulmonary tuberculosis?
A 31-year-old Haitian woman is evaluated for infertility. Pelvic examination shows a markedly enlarged vulva, inguinal lymph node enlargement, and rectal stricture. Biopsy of an inguinal lymph node reveals necrotizing granulomas, neutrophilic infiltrates, and inclusion bodies within macrophages. Which of the following is the most likely etiology of infertility in this patient?
Which of the following subtypes of Hodgkin lymphoma has the strongest association with HIV?
A 45-year-old male patient presents with cough and diarrhea for the past 3 weeks. He is diagnosed as HIV positive with Tuberculosis. What should be the next line of management?
In fever of unknown origin, how many blood samples should ideally be drawn?
What is the commonest site of involvement in herpes zoster?
A 19-year-old intravenous drug user has regularly sought human immunodeficiency virus (HIV) testing, always with negative results. He admits to carelessly sharing needles on multiple occasions with individuals later found to be HIV-positive. He has heard that there is an inherited genetic basis for some people to be relatively "immune" to HIV infection. The genetic change that he is referring to is a mutation in a gene coding for which of the following proteins?
Trophic ulcers are seen in which of the following conditions?
What is occult hepatitis B?
Infectious Diseases Indian Medical PG Practice Questions and MCQs
Question 351: A 50-year-old woman presented at the emergency room complaining of urinary urgency and flank pain. Microscopic examination of a urine sample was done and Gram staining was performed. Prior to initiation of antibiotic therapy, she abruptly developed fever, chills, and delirium. Hypotension and hyperventilation rapidly followed. These observations suggest that the patient is responding to the release of which bacterial component?
- A. Collagenase
- B. Exotoxin
- C. Hyaluronidase
- D. Lipopolysaccharide (Correct Answer)
Explanation: ### Explanation The clinical presentation describes a classic progression from a **Urinary Tract Infection (UTI)/Pyelonephritis** to **Septic Shock**. The rapid onset of fever, chills [2], delirium, hypotension, and hyperventilation (compensatory for metabolic acidosis) indicates a systemic inflammatory response triggered by bacterial components entering the bloodstream [1]. **1. Why Lipopolysaccharide (LPS) is correct:** LPS, also known as **Endotoxin**, is a structural component of the outer membrane of **Gram-negative bacteria** (the most common cause of UTIs, e.g., *E. coli*). When these bacteria multiply or die, LPS is released. The **Lipid A** moiety of LPS binds to CD14 and **Toll-like Receptor 4 (TLR4)** on macrophages. This triggers a massive release of pro-inflammatory cytokines like **TNF-α, IL-1, and IL-6**, leading to systemic vasodilation, endothelial damage, and multi-organ failure (Septic Shock). **2. Why the other options are incorrect:** * **Exotoxins (B):** These are proteins secreted by living bacteria (e.g., Tetanus or Diphtheria toxin). While some exotoxins (Superantigens) can cause shock, the clinical context of a UTI strongly points toward Gram-negative endotoxemia. * **Collagenase (A) and Hyaluronidase (C):** These are "spreading factors" or enzymes that degrade the extracellular matrix to help bacteria invade tissues. They do not directly trigger the systemic inflammatory cascade leading to acute hypotension and shock. **3. NEET-PG High-Yield Pearls:** * **Lipid A:** The toxic component of LPS responsible for septic shock. * **Cytokine Triad of Sepsis:** TNF-α (most important), IL-1, and IL-6. * **Gram-negative Sepsis:** Most commonly associated with the urinary tract, biliary tract, or GI tract. * **Warm vs. Cold Shock:** Early septic shock often presents with warm extremities (vasodilation), unlike cardiogenic or hypovolemic shock. * **Monitoring:** Respiratory rate and depth are increased in metabolic acidosis associated with renal or systemic complications [3].
Question 352: What is the most common form of extrapulmonary tuberculosis?
- A. Tuberculous meningitis (TB CNS)
- B. Tuberculous lymphadenitis (Correct Answer)
- C. Genitourinary tuberculosis (TB Genito-urinary)
- D. Tuberculous spondylitis (Potts spine)
Explanation: **Explanation:** **Tuberculous lymphadenitis** is the most common form of extrapulmonary tuberculosis (EPTB) worldwide [1], accounting for approximately 30–40% of all EPTB cases. In clinical practice, the most frequent presentation is involvement of the cervical lymph nodes [1], historically referred to as **Scrofula**. The infection typically occurs via lymphohematogenous spread from a primary focus in the lungs [3]. **Analysis of Options:** * **Tuberculous lymphadenitis (Correct):** It remains the leading site of EPTB across all age groups, particularly in children and young adults [1]. It is characterized by painless, "matted" lymphadenopathy [1]. * **Tuberculous meningitis (Incorrect):** While it is the most *severe* and life-threatening form of EPTB due to high morbidity and mortality [2], it is significantly less common than lymph node involvement. * **Genitourinary tuberculosis (Incorrect):** This was historically the second most common form in some Western populations, but globally, it ranks lower than lymphadenitis and pleural TB. * **Tuberculous spondylitis (Incorrect):** Also known as Pott’s disease, this is the most common form of *skeletal* TB [2], but skeletal TB as a whole accounts for only about 10% of EPTB cases. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common site of EPTB:** Lymph nodes (specifically Cervical nodes) [1]. 2. **Most common site of Skeletal TB:** Spine (Pott’s Spine), specifically the lower thoracic and upper lumbar vertebrae [2]. 3. **Cold Abscess:** A classic feature of TB lymphadenitis/spine where there is swelling without the typical signs of inflammation (redness/heat) [1]. 4. **Diagnosis:** Fine Needle Aspiration Cytology (FNAC) showing granulomatous inflammation and Ziehl-Neelsen (ZN) staining for AFB is the initial investigation of choice for lymphadenitis.
Question 353: A 31-year-old Haitian woman is evaluated for infertility. Pelvic examination shows a markedly enlarged vulva, inguinal lymph node enlargement, and rectal stricture. Biopsy of an inguinal lymph node reveals necrotizing granulomas, neutrophilic infiltrates, and inclusion bodies within macrophages. Which of the following is the most likely etiology of infertility in this patient?
- A. Chlamydia trachomatis (Correct Answer)
- B. Gardnerella vaginalis
- C. Molluscum contagiosum
- D. Mycobacterium tuberculosis
Explanation: ### Explanation The clinical presentation of a markedly enlarged vulva (esthiomene), inguinal lymphadenopathy, and rectal strictures in a patient from an endemic region (Haiti) is classic for **Lymphogranuloma Venereum (LGV)**, caused by **_Chlamydia trachomatis_ serotypes L1, L2, and L3**. **1. Why Chlamydia trachomatis is correct:** LGV progresses through three stages. The primary stage involves a painless papule/ulcer. The secondary stage (inguinal syndrome) presents with painful "buboes" and the "Groove sign." The tertiary stage (anogenital syndrome) leads to chronic inflammation, resulting in lymphatic obstruction (elephantiasis of the vulva/esthiomene) and rectal strictures. Histopathology typically shows **necrotizing granulomas** and **stellate abscesses**. The inclusion bodies mentioned are characteristic of *Chlamydia*. Infertility in this patient results from chronic pelvic inflammatory disease (PID) and tubal scarring associated with the infection. **2. Why incorrect options are wrong:** * **Gardnerella vaginalis:** Causes Bacterial Vaginosis, characterized by a "fishy" odor and Clue cells, but does not cause granulomas, elephantiasis, or strictures. * **Molluscum contagiosum:** A viral infection (Poxvirus) presenting as umbilicated papules. Histology shows Henderson-Patterson bodies, not necrotizing granulomas. * **Mycobacterium tuberculosis:** While it causes necrotizing granulomas and infertility (via tuberculous salpingitis), it does not typically present with the specific triad of esthiomene, inguinal buboes, and rectal strictures seen in LGV. **Clinical Pearls for NEET-PG:** * **Esthiomene:** Chronic hypertrophic ulceration and edema of the female external genitalia seen in late-stage LGV. * **Groove Sign:** Inguinal and femoral lymph nodes separated by the inguinal ligament (pathognomonic for LGV). * **Drug of Choice:** Doxycycline (100 mg BID for 21 days). * **Donovanosis (Granuloma Inguinale):** Often confused with LGV but caused by *Klebsiella granulomatis*; it features "beefy red" ulcers and **Donovan bodies** (safety-pin appearance) without significant lymphadenopathy.
Question 354: Which of the following subtypes of Hodgkin lymphoma has the strongest association with HIV?
- A. Lymphocyte-rich
- B. Lymphocyte-depleted (Correct Answer)
- C. Nodular lymphocyte-predominant
- D. Nodular sclerosis
Explanation: The association between HIV and Hodgkin Lymphoma (HL) is unique. Unlike non-Hodgkin lymphoma, HL is not an AIDS-defining illness, but its incidence is significantly higher in HIV-positive individuals [1]. **Why Lymphocyte-depleted is correct:** In the setting of advanced HIV/AIDS, patients typically have severe immunosuppression and low CD4 counts. The **Lymphocyte-depleted (LD)** subtype is the rarest form of HL in the general population but is the **most strongly associated with HIV**. It is characterized by a paucity of lymphocytes and an abundance of Reed-Sternberg (RS) cells [1]. In HIV patients, HL often presents at an advanced stage (Stage III/IV), involves extranodal sites (bone marrow, liver), and is almost 100% associated with **Epstein-Barr Virus (EBV)**. Mixed Cellularity is the second most common subtype in HIV. **Analysis of Incorrect Options:** * **Nodular sclerosis:** This is the most common subtype of HL in the general population (especially young females). While it can occur in HIV patients, it does not have the strongest specific association with the virus. * **Lymphocyte-rich:** This subtype has a very good prognosis and is characterized by many reactive lymphocytes; it is rarely seen in the immunodeficient state of HIV. * **Nodular lymphocyte-predominant (NLPHL):** This is a distinct clinical entity (CD20+) and is generally not associated with EBV or HIV infection. **High-Yield Pearls for NEET-PG:** * **Most common HL subtype in HIV:** Mixed Cellularity (historically) or Nodular Sclerosis (in the HAART era), but **LD** has the strongest *relative* association. * **EBV Association:** Nearly all HL cases in HIV patients are EBV-positive. * **Prognosis:** HL in HIV patients is more aggressive, presents with B-symptoms, and has a poorer prognosis compared to HIV-negative patients. * **CD4 Count:** Unlike NHL, HL often occurs when CD4 counts are relatively preserved (often >200 cells/mm³).
Question 355: A 45-year-old male patient presents with cough and diarrhea for the past 3 weeks. He is diagnosed as HIV positive with Tuberculosis. What should be the next line of management?
- A. Start ATT followed by A (Correct Answer)
- B. Start A followed by ATT
- C. Start ATT
- D. Start A then start ATT after 6-8 weeks
Explanation: **Explanation:** The management of HIV-TB co-infection is a high-yield topic for NEET-PG. The primary goal is to treat the life-threatening opportunistic infection (TB) first while minimizing the risk of **Immune Reconstitution Inflammatory Syndrome (IRIS)** [1]. **1. Why Option A is Correct:** According to WHO and National Guidelines (NACO), **Anti-Tubercular Therapy (ATT)** should always be initiated first [3]. **Antiretroviral Therapy (ART)** is then added after a short interval (usually 2 weeks to 2 months). Starting ATT first reduces the mycobacterial load, which significantly lowers the risk and severity of IRIS once the immune system begins to recover under ART [1]. **2. Why Other Options are Incorrect:** * **Option B:** Starting ART before ATT is contraindicated. It increases the risk of severe IRIS and high pill burden, leading to poor compliance and potential drug-drug interactions (e.g., between Rifampicin and Protease Inhibitors) [2]. * **Option C:** Starting ATT alone is insufficient. Without ART, the patient remains severely immunocompromised, leading to further opportunistic infections and increased mortality [4]. * **Option D:** While waiting 6–8 weeks was previously common for patients with high CD4 counts, current guidelines emphasize starting ART as soon as ATT is tolerated (within 2 weeks if CD4 <50 cells/mm³ and within 8 weeks for others) to improve survival [3]. **Clinical Pearls for NEET-PG:** * **Timing:** If CD4 <50/mm³, start ART within **2 weeks** of ATT. If CD4 >50/mm³, start ART within **8 weeks** [3]. * **Exception:** In **TB Meningitis**, ART should be delayed for 4–8 weeks regardless of CD4 count to prevent life-threatening intracranial IRIS. * **Drug Choice:** Efavirenz is the preferred NNRTI with Rifampicin-based ATT, though Dolutegravir (standard in current regimens) requires a dose increase to 50mg twice daily due to enzyme induction by Rifampicin [2].
Question 356: In fever of unknown origin, how many blood samples should ideally be drawn?
- A. 2
- B. 3 (Correct Answer)
- C. 4
- D. 5
Explanation: In the evaluation of **Fever of Unknown Origin (FUO)**, the goal of blood cultures is to maximize the sensitivity for detecting intermittent or low-grade bacteremia while minimizing the risk of contamination. [1] ### **Why 3 is the Correct Answer** According to standard clinical guidelines (including Harrison’s Principles of Internal Medicine), **three sets of blood cultures** (each consisting of an aerobic and anaerobic bottle) should be drawn over a 24-hour period. * **Sensitivity:** A single set has a sensitivity of approximately 70-80%. Two sets increase this to ~90%. Drawing **three sets** achieves a cumulative sensitivity of **>95-98%**, which is the clinical gold standard for excluding or confirming bacteremia in complex febrile cases. * **Timing:** These should be drawn from different venipuncture sites to help differentiate true pathogens from skin contaminants (like Coagulase-negative Staphylococci). [1] ### **Explanation of Incorrect Options** * **A (2 samples):** While two sets are often sufficient for routine infections (like pneumonia), they are inadequate for FUO or suspected Endocarditis, as they may miss low-density bacteremia. * **C & D (4 or 5 samples):** Drawing more than three sets provides **diminishing returns**. The incremental increase in sensitivity is negligible (<1%), while the risk of "culture-positive" results due to contamination increases, leading to diagnostic confusion and unnecessary antibiotic use. ### **High-Yield Clinical Pearls for NEET-PG** * **Volume Matters:** For adults, each bottle should ideally contain **8-10 mL** of blood. Under-filling is the most common cause of false-negative cultures. * **Culture-Negative FUO:** If three sets are negative but suspicion remains high, consider "Culture-Negative Endocarditis" (HACEK group) or fastidious organisms (e.g., *Brucella*, *Coxiella*), which may require extended incubation or serology. [2] * **Timing:** In FUO, cultures do not need to be timed with "fever spikes," as bacteremia in these cases is often continuous or frequent enough to be captured at any time.
Question 357: What is the commonest site of involvement in herpes zoster?
- A. Thoracic region (Correct Answer)
- B. Cranial nerve
- C. Face
- D. Lumbar region
Explanation: **Explanation:** **Herpes Zoster (Shingles)** is caused by the reactivation of the latent Varicella-Zoster Virus (VZV) within the sensory ganglia. The virus remains dormant in the dorsal root ganglia after a primary chickenpox infection and reactivates when cell-mediated immunity declines. **Why Thoracic region is correct:** The distribution of the rash follows specific dermatomes. The **thoracic dermatomes (T3 to L2)** are the most frequently involved sites, accounting for over **50-60% of all cases** [1]. This is because the primary infection (chickenpox) often features a high density of lesions on the trunk, leading to a higher viral load seeding the corresponding thoracic sensory ganglia. **Analysis of Incorrect Options:** * **Cranial nerve & Face:** While the Trigeminal nerve (especially the ophthalmic division, leading to *Herpes Zoster Ophthalmicus*) is the most common cranial nerve involved, it occurs less frequently than thoracic involvement (approx. 10-20% of cases). * **Lumbar region:** Though common, lumbar involvement occurs less frequently than thoracic involvement. The frequency of reactivation generally correlates with the density of the original varicella rash in that area. **High-Yield Clinical Pearls for NEET-PG:** * **Hutchinson’s Sign:** Vesicles on the tip or side of the nose indicate involvement of the nasociliary branch of the trigeminal nerve and predict a high risk of ocular complications. * **Ramsay Hunt Syndrome:** Reactivation in the geniculate ganglion involving CN VII and VIII, presenting with facial palsy and vesicles in the external auditory canal. * **Post-Herpetic Neuralgia (PHN):** The most common complication, defined as pain persisting >90 days after the rash onset [1]. * **Treatment:** Oral Acyclovir, Valacyclovir, or Famciclovir is most effective when started within **72 hours** of rash onset [1].
Question 358: A 19-year-old intravenous drug user has regularly sought human immunodeficiency virus (HIV) testing, always with negative results. He admits to carelessly sharing needles on multiple occasions with individuals later found to be HIV-positive. He has heard that there is an inherited genetic basis for some people to be relatively "immune" to HIV infection. The genetic change that he is referring to is a mutation in a gene coding for which of the following proteins?
- A. CCR5 (Correct Answer)
- B. CD4
- C. gp120
- D. gp41
Explanation: ### Explanation **Correct Answer: A. CCR5** The entry of HIV-1 into host cells is a multi-step process requiring the binding of the viral envelope to specific host cell receptors. [1] The primary receptor is the **CD4 molecule**, but a **co-receptor** is essential for successful viral entry. In the early stages of infection (and in most transmissions), the virus is **M-tropic** (Macrophage-tropic) and utilizes the **CCR5** chemokine receptor as its co-receptor. [1] A specific genetic mutation known as the **CCR5-Δ32 (delta 32) mutation** results in a truncated, non-functional protein that does not reach the cell surface. Individuals who are **homozygous** for this mutation are highly resistant to HIV infection despite repeated exposure, as the virus cannot fuse with the host cell membrane. Heterozygotes typically show a slower progression to AIDS. --- ### Why the other options are incorrect: * **B. CD4:** This is the primary receptor for HIV. [1] While it is necessary for infection, there are no common genetic mutations in the CD4 gene that confer immunity to HIV in humans. * **C. gp120:** This is a **viral** glycoprotein (encoded by the HIV *env* gene) that mediates initial attachment to the CD4 receptor. It is not a human protein. * **D. gp41:** This is also a **viral** glycoprotein (transmembrane unit) responsible for the fusion of the viral envelope with the host cell membrane. It is the target of the drug **Enfuvirtide**. --- ### NEET-PG High-Yield Pearls: * **CCR5 vs. CXCR4:** Early-stage/transmitted HIV uses **CCR5** (M-tropic). Late-stage HIV often switches to **CXCR4** (T-tropic), which is associated with rapid CD4+ T-cell decline. * **Maraviroc:** A CCR5 antagonist (entry inhibitor) used in HIV treatment; it is only effective against CCR5-tropic strains. * **Berlin Patient:** The first person "cured" of HIV (Timothy Ray Brown) received a bone marrow transplant from a donor homozygous for the **CCR5-Δ32** mutation.
Question 359: Trophic ulcers are seen in which of the following conditions?
- A. Poliomyelitis
- B. Syringomyelia
- C. Leprosy (Correct Answer)
- D. Tuberculous Meningitis
Explanation: **Explanation:** **Trophic ulcers** (also known as neuropathic ulcers) occur primarily due to the loss of protective sensation (anesthesia) and autonomic dysfunction [1]. In **Leprosy** (Hansen’s Disease), the *Mycobacterium leprae* bacilli have a predilection for peripheral nerves. Damage to sensory fibers leads to unrecognized repetitive trauma, while damage to autonomic fibers causes anhidrosis (dry skin), leading to fissures and secondary infections. These ulcers typically occur at pressure points on the soles of the feet (e.g., the metatarsal heads) [1]. **Analysis of Options:** * **Leprosy (Correct):** It is the most common cause of trophic ulcers in India. The combination of sensory loss, motor weakness (leading to foot drop/deformity), and autonomic dysfunction creates the perfect environment for chronic non-healing ulcers [1]. * **Poliomyelitis:** This is a pure **lower motor neuron (LMN)** disease affecting the anterior horn cells. While it causes muscle wasting and paralysis, **sensory perception remains intact**; therefore, trophic ulcers are not a feature. * **Syringomyelia:** While this condition causes "dissociated sensory loss" and can lead to painless burns or injuries (especially in the hands), the term "trophic ulcer" is classically associated with the weight-bearing areas affected in peripheral neuropathies like Leprosy or Diabetes [1]. * **Tuberculous Meningitis:** This is an infection of the CNS (meninges). While it can cause cranial nerve palsies or hydrocephalus, it does not typically cause peripheral sensory loss leading to trophic ulcers. **Clinical Pearls for NEET-PG:** * **Common causes of Trophic Ulcers:** Leprosy (most common), Diabetes Mellitus, Tabes Dorsalis (Syphilis), and Spina Bifida [1]. * **Management:** The mainstay is "off-loading" the pressure using specialized footwear (e.g., Microcellular Rubber - MCR soles). * **Squamous Cell Carcinoma:** A long-standing, neglected trophic ulcer in Leprosy can undergo malignant transformation (Marjolin’s ulcer).
Question 360: What is occult hepatitis B?
- A. HBV DNA < 104 copies/ml with HBsAg negative (Correct Answer)
- B. HBV DNA < 104 copies/ml with HBsAg positive
- C. HBV DNA < 104 copies/ml with HBeAg negative
- D. HBV DNA < 104 copies/ml with HBeAg positive
Explanation: **Explanation:** **Occult Hepatitis B Infection (OBI)** is defined by the presence of replication-competent HBV DNA in the liver (and sometimes the serum) of individuals who test **negative for Hepatitis B surface antigen (HBsAg)** using routine assays. 1. **Why Option A is correct:** The hallmark of occult HBV is the absence of HBsAg despite the presence of HBV DNA [1]. In OBI, the viral load is typically very low, usually **<200 IU/ml** (roughly equivalent to **<10⁴ copies/ml**) [1]. This occurs because the virus persists in the hepatocytes as covalently closed circular DNA (cccDNA), but viral gene expression is suppressed by the host immune system, keeping HBsAg levels below the detection threshold. 2. **Why the other options are incorrect:** * **Option B:** If HBsAg is positive, the infection is by definition "Overt" rather than "Occult." This would be classified as chronic HBV infection or an inactive carrier state depending on other markers. * **Options C & D:** The status of HBeAg (envelope antigen) does not define occult hepatitis. While OBI is almost always HBeAg negative, the defining criteria must involve the absence of HBsAg. **High-Yield Clinical Pearls for NEET-PG:** * **Serology:** Most OBI patients are **anti-HBc positive** (indicating past exposure), but "seronegative" OBI (anti-HBc negative) can also occur. * **Clinical Significance:** OBI is a significant risk factor for **Hepatocellular Carcinoma (HCC)** and can lead to **reactivation** (fulminant hepatitis) in patients undergoing chemotherapy or immunosuppression (especially Anti-CD20 therapy like Rituximab). * **Transmission:** OBI can be transmitted via blood transfusion or liver transplantation; hence, nucleic acid testing (NAT) is used in blood banks to screen donors.
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
Practice Questions
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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