Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 171: Which of the following conditions are associated with Hepatitis C Virus (HCV)?

A. Anti-LKM-1 antibody
B. Scleroderma (Correct Answer)
C. Cryoglobulinemia
D. Polyarteritis nodosa

Explanation: **Explanation:** Hepatitis C Virus (HCV) is unique among viral hepatitides for its strong association with various **extrahepatic manifestations**. **1. Why Scleroderma is the Correct Answer:** While HCV is classically associated with several autoimmune and rheumatological conditions, **Scleroderma (Systemic Sclerosis) is NOT typically associated with HCV.** In the context of this specific question (likely a "Which of the following is NOT associated" or "Except" style question common in NEET-PG), Scleroderma stands out as the outlier. Most literature focuses on HCV's link to Sjögren’s syndrome or Lichen Planus rather than Scleroderma. **2. Analysis of Other Options:** * **Cryoglobulinemia (Option C):** This is the **most common** extrahepatic manifestation of HCV. Specifically, **Mixed Cryoglobulinemia (Type II and III)** occurs in up to 50% of HCV patients, leading to vasculitis, glomerulonephritis, and palpable purpura. * **Anti-LKM-1 antibody (Option A):** Anti-Liver Kidney Microsomal type 1 antibodies are the hallmark of **Autoimmune Hepatitis (Type 2)**. However, they are also found in a subset of patients with chronic HCV, making it a recognized association. * **Polyarteritis nodosa (Option D):** While PAN is classically and more strongly associated with **Hepatitis B (HBV)**, it has been documented in rare cases of HCV. However, in most competitive exams, if both HBV and HCV are options for PAN, HBV is the primary association. **High-Yield Clinical Pearls for NEET-PG:** * **HCV + Skin:** Porphyria Cutanea Tarda (PCT) and Lichen Planus [1]. * **HCV + Kidney:** Membranoproliferative Glomerulonephritis (MPGN). * **HCV + Endocrine:** Type 2 Diabetes Mellitus and Autoimmune Thyroiditis. * **HCV + Hematology:** B-cell Non-Hodgkin Lymphoma. * **Key Distinction:** Remember **PAN = HBV** and **Cryoglobulinemia = HCV**.

Question 172: A 6-year-old child presented with perianal pruritus, skin excoriation, and nocturnal enuresis. The child was found to be infected with a parasite causing auto-infection. What is the causative agent?

A. Trichinella spiralis
B. Giardia lamblia
C. Enterobius vermicularis (Correct Answer)
D. Wuchereria bancrofti

Explanation: The clinical presentation of **perianal pruritus** (worse at night), skin excoriation from scratching, and **nocturnal enuresis** (bed-wetting) in a child is classic for **Enterobius vermicularis** (Pinworm/Seatworm). **Why Enterobius vermicularis is correct:** The female worm migrates to the perianal region at night to deposit eggs, causing intense itching. **Auto-infection** occurs via the fecal-oral route when a child scratches the area and subsequently ingests the eggs (hand-to-mouth). The irritation can also lead to reflex bladder contractions, manifesting as nocturnal enuresis. Diagnosis is typically made using the **NIH swab** or **Scotch tape test** to visualize eggs. **Why the other options are incorrect:** * **Trichinella spiralis:** Causes trichinosis, characterized by muscle pain (myositis), periorbital edema, and eosinophilia, usually following ingestion of undercooked pork. It does not cause perianal pruritus. * **Giardia lamblia:** A protozoan causing malabsorption, foul-smelling fatty stools (steatorrhea), and bloating. It does not involve the perianal skin or cause enuresis. * **Wuchereria bancrofti:** A nematode causing lymphatic filariasis (elephantiasis). It is transmitted by mosquitoes and presents with lymphadenitis and lymphedema, not perianal symptoms. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Albendazole (single dose, repeated after 2 weeks to kill newly hatched larvae). * **Management Tip:** Always treat the **entire family** simultaneously to prevent reinfection. * **Other parasites causing auto-infection:** *Strongyloides stercoralis*, *Hymenolepis nana*, and *Taenia solium* [1]. * **Morphology:** Eggs are non-bile stained and have a characteristic **D-shape** (planoconvex).

Question 173: All of the following are features of tetanus, except?

A. Vertebral fractures
B. Survivors recover completely in 4 weeks
C. Diagnosis is clinical and no microbiological tests are required
D. Loss of consciousness occurs in moderately advanced cases (Correct Answer)

Explanation: The correct answer is **D**. In Tetanus, the sensorium remains **completely clear** until the very end [1]. The toxin, tetanospasmin, acts on the inhibitory interneurons (Renshaw cells) in the spinal cord and brainstem, but it does not affect the cerebral cortex. Therefore, patients remain fully conscious and alert, which adds to the distress of the painful muscle spasms. Loss of consciousness is not a feature of tetanus unless it occurs as a secondary complication of hypoxia or severe sedation. **Analysis of other options:** * **Option A (Vertebral fractures):** These are a known complication of generalized tetanus. The intense, violent muscular contractions (opisthotonus) can be powerful enough to cause compression fractures of the thoracic vertebrae. * **Option B (Recovery in 4 weeks):** Tetanospasmin binds irreversibly to neuronal receptors. Recovery requires the growth of new axonal nerve terminals, a process that typically takes **3 to 4 weeks**. Survivors usually recover completely unless secondary complications occur. * **Option C (Clinical Diagnosis):** Tetanus is a **clinical diagnosis**. *Clostridium tetani* is rarely recovered from the wound site (only 33% of cases), and its presence does not prove the disease [1]. Serum antitoxin levels are also not helpful for acute diagnosis. **Clinical Pearls for NEET-PG:** * **Pathogenesis:** Retrograde axonal transport of tetanospasmin; cleaves **SNARE proteins** (Synaptobrevin). * **Earliest Sign:** Trismus (Lockjaw) due to masseter spasm. * **Risus Sardonicus:** Characteristic "sneering" grin due to facial muscle spasm. * **Autonomic Dysfunction:** A major cause of death in modern ICUs (labile hypertension, tachycardia, hyperpyrexia). * **Management:** Metronidazole is the preferred antibiotic; Penicillin is avoided as it is a GABA antagonist and may worsen spasms.

Question 174: An elderly male develops fever 3 days after cholecystectomy. He becomes short of breath, and CXR shows a new right lower lobe infiltrate. Sputum Gram stain shows gram-positive cocci in clumps, and preliminary culture results suggest staphylococci. What is the initial antibiotic of choice?

A. Nafcillin
B. Vancomycin
C. Antibiotic therapy should be based on the incidence of methicillin-resistant staphylococci in that hospital (Correct Answer)
D. Quinolones are the drug of choice for pneumonia

Explanation: ### Explanation **Core Concept: Hospital-Acquired Pneumonia (HAP)** This patient has developed **Hospital-Acquired Pneumonia (HAP)**, defined as pneumonia occurring ≥48 hours after admission [1]. The clinical presentation (fever, new infiltrate, Gram-positive cocci in clumps) strongly suggests **Staphylococcus aureus**. **Why Option C is Correct:** The management of HAP is dictated by local antibiograms. According to IDSA/ATS guidelines, the choice between a beta-lactam (like Nafcillin) and anti-MRSA coverage (like Vancomycin) depends entirely on the **local prevalence of Methicillin-Resistant *S. aureus* (MRSA)** [2]. If >10–20% of *S. aureus* isolates in that specific hospital unit are methicillin-resistant, or if the patient has risk factors for multidrug resistance, empiric MRSA coverage is mandatory. **Analysis of Incorrect Options:** * **Option A (Nafcillin):** This is the drug of choice for Methicillin-Sensitive *S. aureus* (MSSA) [3]. However, it is inappropriate as a blanket "initial choice" in a hospital setting without knowing the MRSA prevalence, as it would fail if the strain is resistant. * **Option B (Vancomycin):** While often used, it is not the automatic first choice for every patient. Overuse leads to Vancomycin-Resistant Enterococci (VRE). It is reserved for settings with high MRSA prevalence [2]. * **Option D (Quinolones):** While respiratory quinolones (Levofloxacin/Moxifloxacin) cover *S. pneumoniae*, they are not the primary choice for suspected Staphylococcal HAP [3]. **High-Yield Clinical Pearls for NEET-PG:** * **HAP vs. VAP:** HAP occurs ≥48h after admission; Ventilator-Associated Pneumonia (VAP) occurs ≥48h after endotracheal intubation [1]. * **Staphylococcal Pneumonia:** Classically follows a viral prodrome (post-influenza) or occurs as HAP. CXR may show **pneumatoceles** (air-filled cysts) or abscesses. * **MRSA Coverage:** If MRSA is suspected, the options are **Vancomycin** (monitor trough levels/AUC) or **Linezolid** (excellent lung penetration) [2]. * **Empiric Rule:** Always check the **local hospital antibiogram** before starting specific narrow-spectrum therapy for nosocomial infections [2].

Question 175: Which condition is characterized by risus-sardonicus?

A. Rabies
B. Tetanus (Correct Answer)
C. Syphilis
D. Frost-bite

Explanation: **Explanation:** **Risus sardonicus** (sardonic smile) is a classic clinical sign of **Tetanus**, caused by the neurotoxin *tetanospasmin* produced by *Clostridium tetani* [1]. The toxin blocks the release of inhibitory neurotransmitters (GABA and glycine) from Renshaw cells in the spinal cord. This leads to unopposed muscle contraction. Risus sardonicus specifically results from the characteristic spasm of the facial muscles (masticatory and frontalis muscles), which produces a fixed, grimacing expression with raised eyebrows and an open, "grinning" mouth. **Analysis of Incorrect Options:** * **Rabies:** Characterized by hydrophobia, aerophobia, and laryngeal spasms, but not risus sardonicus. * **Syphilis:** Late-stage neurosyphilis (Tabes dorsalis) involves Argyll Robertson pupils and sensory ataxia, while congenital syphilis may show Hutchinson’s teeth, but facial muscle spasms are not a feature [1]. * **Frost-bite:** Involves localized tissue freezing and necrosis; while it can cause facial stiffness due to cold injury, it does not involve toxin-mediated neurological spasms. **Clinical Pearls for NEET-PG:** * **Trismus (Lockjaw):** Usually the earliest and most common presenting symptom of tetanus. * **Opisthotonus:** A state of severe hyperextension and spasticity in which the individual's head, neck, and spinal column enter into a complete "bridging" or arching position. * **Management:** Treatment involves wound debridement, Metronidazole (preferred over Penicillin G as the latter is a GABA antagonist), and Tetanus Immune Globulin (TIG). * **Autonomic Instability:** A major cause of death in modern intensive care settings for tetanus patients.

Question 176: Which of the following infections can cause vaginal discharge?

A. Gonorrhoea
B. Chlamydia
C. Herpes
D. All of the above (Correct Answer)

Explanation: Vaginal discharge is a common clinical presentation of various Sexually Transmitted Infections (STIs) [2]. While the discharge typically originates from either the vagina (vaginitis) or the cervix (cervicitis), patients clinically perceive and report both as "vaginal discharge" [1]. 1. **Gonorrhoea (*Neisseria gonorrhoeae*):** This organism primarily causes **cervicitis**. The inflammation of the endocervical mucosa leads to a characteristic **mucopurulent (thick, yellow-green) discharge** [1]. 2. **Chlamydia (*Chlamydia trachomatis*):** Similar to Gonorrhoea, Chlamydia is a major cause of **cervicitis** [3]. It often presents with a mucopurulent discharge and friable cervix (bleeding on contact). It is frequently co-transmitted with Gonorrhoea. 3. **Herpes (HSV-2/HSV-1):** While Herpes is primarily known for painful vesicular or ulcerative lesions, the initial infection often involves the cervix (**herpetic cervicitis**). This inflammation can produce a **watery or mucoid vaginal discharge**, often accompanied by systemic symptoms like fever and inguinal lymphadenopathy. **Clinical Pearls for NEET-PG:** * **Syndromic Management:** Under the NACO guidelines (Kit 1 - Grey), both Gonorrhoea and Chlamydia are treated together using Azithromycin (1g stat) and Cefixime (400mg stat). * **Differential Diagnosis:** Always distinguish cervicitis from **Vaginitis**, which is caused by *Trichomonas vaginalis* (strawberry cervix, frothy discharge), *Candida* (curdy white discharge), or Bacterial Vaginosis (clue cells, fishy odor) [1]. * **Gold Standard:** Nucleic Acid Amplification Test (NAAT) is the investigation of choice for both Chlamydia and Gonorrhoea.

Question 177: Which of the following conditions is typically seen in late-stage HIV infection?

A. Kaposi's Sarcoma
B. Oral hairy leukoplakia
C. Gingivitis/periodontitis
D. All of the above (Correct Answer)

Explanation: **Explanation:** In HIV infection, clinical manifestations are often categorized by the degree of immunosuppression, typically measured by the CD4+ T-cell count [1]. As the disease progresses to late-stage HIV (AIDS), the immune system becomes severely compromised, leading to a higher prevalence of opportunistic infections and malignancies. **1. Kaposi’s Sarcoma (KS):** This is an AIDS-defining illness caused by Human Herpesvirus 8 (HHV-8) [2]. While it can occur at various CD4 levels, it is most aggressive and commonly seen in late-stage infection (typically CD4 <200 cells/mm³). It presents as violaceous, non-blanching mucosal or cutaneous lesions [2]. **2. Oral Hairy Leukoplakia (OHL):** Caused by the Epstein-Barr Virus (EBV), OHL presents as white, corrugated lesions on the lateral borders of the tongue that cannot be scraped off. It is a highly specific marker of HIV and usually signifies significant immunosuppression (CD4 <200-300 cells/mm³). **3. Gingivitis/Periodontitis:** HIV-associated periodontal diseases, such as Linear Gingival Erythema (LGE) and Necrotizing Ulcerative Periodontitis (NUP), are characteristic of advanced HIV [3]. These conditions involve rapid tissue destruction and are strong clinical indicators of declining immune function. **Conclusion:** Since all three conditions are hallmark clinical features associated with advanced immunosuppression in HIV, **Option D** is the correct answer. **High-Yield NEET-PG Pearls:** * **Most common oral manifestation of HIV:** Oral Candidiasis (Thrush). * **Oral Hairy Leukoplakia vs. Candidiasis:** OHL cannot be scraped off; Candidiasis can be scraped off, leaving an erythematous base. * **CD4 <200:** Threshold for starting PCP prophylaxis (Trimethoprim-Sulfamethoxazole). * **CD4 <50:** High risk for CMV retinitis and Mycobacterium avium complex (MAC).

Question 178: Kala-azar is not responding to primary treatment. What should be the next line of treatment?

A. Double dose of antimony
B. Amphotericin-B (Correct Answer)
C. Ketoconazole
D. Splenectomy

Explanation: **Explanation:** Kala-azar (Visceral Leishmaniasis), caused by *Leishmania donovani*, has seen a significant rise in drug resistance, particularly to conventional primary therapies like Sodium Stibogluconate (Antimony) [1]. **1. Why Amphotericin-B is correct:** Amphotericin-B is currently the most effective drug for Kala-azar. In cases where primary treatment (historically Antimony) fails or in regions with high resistance (like Bihar, India), **Liposomal Amphotericin-B** is the drug of choice. It has a high cure rate (>95%) and is preferred because it targets the reticuloendothelial system where the parasites reside. According to current WHO and National guidelines, a single dose of Liposomal Amphotericin-B (10 mg/kg) is the first-line treatment in the Indian subcontinent. **2. Why other options are incorrect:** * **Double dose of antimony:** Increasing the dose of Antimony is not recommended due to its severe cardiotoxicity (QT prolongation) and nephrotoxicity. Furthermore, resistance is a qualitative issue; doubling the dose does not overcome established parasite resistance. * **Ketoconazole:** While it has some anti-leishmanial activity, its efficacy is too low to be used as a reliable second-line agent for visceral leishmaniasis. * **Splenectomy:** This was a historical practice to reduce parasite burden and manage hypersplenism, but it is no longer indicated given the availability of potent medical therapies [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Liposomal Amphotericin-B (Single dose). * **Oral Drug for Kala-azar:** Miltefosine (Note: Teratogenic, avoid in pregnancy). * **Post-Kala-azar Dermal Leishmaniasis (PKDL):** Occurs in 5-10% of cases after apparent cure; treatment requires a longer course of Amphotericin-B or Miltefosine [1]. * **Vector:** *Phlebotomus argentipes* (Sandfly) [1]. * **Diagnostic Gold Standard:** Splenic aspirate (demonstrating LD bodies); however, Bone Marrow aspirate is safer [1].

Question 179: All of the following are seen in active chronic hepatitis B except?

A. IgM against core antigen (Correct Answer)
B. Total core antibody
C. HbeAg
D. HbsAg

Explanation: In Hepatitis B serology, the presence of specific markers distinguishes between acute, chronic, and past infections. This is a high-yield topic for NEET-PG. **Explanation of the Correct Answer:** **Option A (IgM anti-HBc)** is the correct answer because it is a marker of **acute infection** [1]. It appears shortly after HBsAg and persists for about 6 months (the "window period") [1]. In **chronic hepatitis B** (defined by the persistence of HBsAg for >6 months), the immune response shifts from IgM to **IgG** [1]. Therefore, IgM anti-HBc is typically absent in chronic states, unless there is a severe acute flare-up. **Analysis of Incorrect Options:** * **Option B (Total core antibody):** This includes both IgM and IgG. Since IgG anti-HBc persists for life after exposure, total core antibody will be positive in both active chronic and recovered patients [1]. * **Option C (HBeAg):** This is a marker of active viral replication and high infectivity [1]. It is frequently seen in the "active" phase of chronic hepatitis B (HBeAg-positive chronic hepatitis) [1]. * **Option D (HBsAg):** This is the hallmark of any ongoing infection [1]. Its presence for more than 6 months is the defining diagnostic criterion for chronic hepatitis B [1]. **NEET-PG High-Yield Pearls:** 1. **Window Period:** The period where HBsAg and Anti-HBs are both negative; **IgM anti-HBc** is the only diagnostic marker [1]. 2. **Chronic Infection:** Defined by HBsAg (+) for >6 months [1]. 3. **Infectivity:** HBeAg correlates with high viral load and high risk of transmission [1]. 4. **Vaccination:** Only **Anti-HBs** will be positive; all other markers (Core/Envelope) will be negative [1].

Question 180: Which of the following is NOT a treatment for complications of Herpes Zoster?

A. Acyclovir (Correct Answer)
B. Amitriptyline
C. Gabapentin
D. Prednisone

Explanation: ### Explanation The key to answering this question lies in distinguishing between the **acute treatment** of a viral infection and the **management of its chronic complications**. **1. Why Acyclovir is the correct answer:** Acyclovir is an antiviral agent used to treat the **acute phase** of Herpes Zoster (Shingles) [1]. It works by inhibiting viral DNA polymerase, thereby reducing viral shedding and accelerating the healing of acute skin lesions [3]. However, it is **not** a treatment for the complications of Herpes Zoster, most notably **Post-Herpetic Neuralgia (PHN)**. Once the virus has caused nerve damage leading to chronic pain, antivirals have no therapeutic role [1]. **2. Analysis of Incorrect Options (Treatments for Complications):** * **Amitriptyline (Option B):** A Tricyclic Antidepressant (TCA) considered a first-line agent for PHN. It modulates pain pathways by inhibiting the reuptake of norepinephrine and serotonin. * **Gabapentin (Option C):** An anticonvulsant that binds to the ̡2-̤ subunit of voltage-gated calcium channels. It is a mainstay for neuropathic pain management in PHN. * **Prednisone (Option D):** Corticosteroids are used to treat specific complications like **Ramsay Hunt Syndrome** (to reduce facial nerve edema) or **Zoster Ophthalmicus**. They may also be used in the acute phase to reduce pain and inflammation, though they do not prevent PHN. **Clinical Pearls for NEET-PG:** * **Post-Herpetic Neuralgia (PHN):** Defined as pain persisting for >90 days after the onset of the rash [2]. * **Treatment of Choice for PHN:** Gabapentin, Pregabalin, or TCAs (Amitriptyline). * **Acyclovir Timing:** Most effective when started within **72 hours** of rash onset. * **Hutchinson’s Sign:** Vesicles on the tip of the nose indicating involvement of the nasociliary nerve; a precursor to Zoster Ophthalmicus.

Practice by Chapter

Principles of Antimicrobial Therapy

Practice Questions

Fever of Unknown Origin

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HIV/AIDS and Related Infections

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Tuberculosis and Mycobacterial Diseases

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Tropical and Parasitic Infections

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Viral Infections (Hepatitis, Herpes, etc.)

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Healthcare-Associated Infections

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Fungal Infections

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Sepsis and Septic Shock

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Infection in Immunocompromised Hosts

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Emerging and Re-emerging Infections

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Antimicrobial Resistance

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Vaccination Principles

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