Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 151: Which antibodies are used to diagnose acute viral hepatitis A and E?

A. IgM anti-HAV and IgM anti-HEV (Correct Answer)
B. IgG anti-HAV and IgG anti-HEV
C. Liver biopsy
D. Virus detection in stool

Explanation: **Explanation:** The diagnosis of acute viral hepatitis relies on identifying markers of active infection. In clinical practice, **IgM (Immunoglobulin M)** is the hallmark of an **acute or recent infection**, whereas **IgG (Immunoglobulin G)** typically signifies **past exposure or immunity**. [1] 1. **Why Option A is correct:** Both Hepatitis A (HAV) and Hepatitis E (HEV) are transmitted via the fecal-oral route and cause acute, self-limiting hepatitis. **IgM anti-HAV** is the gold standard for diagnosing acute Hepatitis A [1]; it appears early in the course of the disease and usually becomes undetectable within 3 to 6 months. Similarly, **IgM anti-HEV** is the primary marker for diagnosing acute Hepatitis E. [1] 2. **Why other options are incorrect:** * **Option B:** IgG anti-HAV and IgG anti-HEV indicate past infection or long-term immunity (in the case of HAV, also post-vaccination). They do not differentiate a current acute illness from a previous one. [1] * **Option C:** Liver biopsy is rarely indicated for acute viral hepatitis. It is an invasive procedure reserved for cases of diagnostic uncertainty or chronic liver disease assessment. * **Option D:** While viruses are shed in the stool, this occurs during the late incubation period *before* the onset of clinical symptoms (jaundice). By the time a patient presents to a clinic, stool shedding has often ceased, making it a poor diagnostic tool. **High-Yield Clinical Pearls for NEET-PG:** * **Hepatitis E & Pregnancy:** HEV is notorious for causing **Fulminant Hepatic Failure** in pregnant women (especially in the 3rd trimester), with mortality rates reaching up to 20-25%. * **Hepatitis A:** It is the most common cause of acute viral hepatitis in children worldwide. It never progresses to chronicity. * **Window Period:** In Hepatitis B, the "window period" is diagnosed by **IgM anti-HBc**, as HBsAg and anti-HBs may both be negative.

Question 152: Black water fever is seen in which of the following conditions?

A. Leishmaniasis
B. Falciparum malaria (Correct Answer)
C. Trypanosomiasis
D. Leptospirosis

Explanation: **Explanation:** **Black Water Fever** is a severe and life-threatening complication of **Plasmodium falciparum** malaria [1]. It is characterized by sudden, massive intravascular hemolysis (destruction of red blood cells), leading to severe hemoglobinemia and subsequent **hemoglobinuria** [4]. The name "Black Water" refers to the dark, cola-colored, or blackish urine passed by the patient due to the presence of free hemoglobin. **Pathophysiology:** The condition is often associated with irregular treatment or repeated infections, particularly in patients treated with **Quinine**. The hemolysis leads to acute tubular necrosis, often resulting in acute renal failure, which is the primary cause of mortality in these cases. **Analysis of Options:** * **Falciparum malaria (Correct):** It is the specific causative agent. The high parasite load and immune-mediated destruction of both parasitized and non-parasitized RBCs trigger the syndrome [1]. * **Leishmaniasis (Incorrect):** Known for causing Kala-azar (Visceral Leishmaniasis), characterized by massive splenomegaly and pancytopenia, but not acute intravascular hemolysis [2]. * **Trypanosomiasis (Incorrect):** Causes Sleeping Sickness (African) or Chagas disease (American). It involves the CNS or heart but does not present with Black Water Fever. * **Leptospirosis (Incorrect):** While it causes **Weil’s syndrome** (jaundice, renal failure, and hemorrhage), the renal failure is not typically due to massive hemoglobinuria from RBC hemolysis [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of Black Water Fever:** Fever with chills, hemoglobinuria (dark urine), and rapidly progressing anemia. * **Drug Association:** Classically associated with **Quinine** therapy in sensitized individuals. * **Management:** Immediate cessation of Quinine (if applicable), aggressive fluid resuscitation, and renal replacement therapy (dialysis) if acute kidney injury occurs. * **G6PD Deficiency:** Must be differentiated from G6PD-induced hemolysis triggered by Primaquine.

Question 153: Anti-retroviral therapy is started when the CD4 count is less than which value?

A. 100
B. 350 (Correct Answer)
C. 200
D. 400

Explanation: The initiation of Anti-Retroviral Therapy (ART) has evolved significantly over the years. Historically, the threshold for starting ART was a **CD4 count of <350 cells/mm³**. This value was established based on evidence that starting treatment at this level significantly reduced morbidity and mortality from opportunistic infections. * **Why 350 is the correct answer (in the context of this question):** While current WHO and National AIDS Control Organization (NACO) guidelines now follow the **"Test and Treat"** policy (starting ART regardless of CD4 count), many medical examinations, including NEET-PG, still test on the classic threshold of 350 cells/mm³ as the traditional point of intervention [1]. * **Option A (100):** This is a state of severe immunosuppression. At this level, patients are at high risk for *Toxoplasmosis* and *Cryptococcosis* [1]. * **Option C (200):** This is the threshold for defining AIDS and the point where prophylaxis for *Pneumocystis jirovecii* pneumonia (PCP) must be started [1]. * **Option D (400):** This value is generally considered within the lower end of the "safe" range and was never a standard threshold for starting ART in asymptomatic patients [1]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Current Gold Standard:** The **"Treat All"** strategy (initiated in 2017 by NACO) recommends starting ART for all HIV-positive individuals, irrespective of CD4 count or clinical stage [1]. 2. **CD4 <200:** Start Cotrimoxazole Prophylaxis (CPT) to prevent PCP [1]. 3. **CD4 <100:** Start prophylaxis for Cryptococcal meningitis (if screening is positive) and Toxoplasmosis [1]. 4. **Pregnancy:** ART should be started immediately in all pregnant women regardless of CD4 count to prevent vertical transmission.

Question 154: Which of the human intestinal parasitic nematodes does not infest the small bowel?

A. Ascaris lumbricoides
B. Necator americanus
C. Strogyloides stercoralis
D. Trichuris trichiura (Correct Answer)

Explanation: ### Explanation The correct answer is **D. Trichuris trichiura**. The primary site of infestation for intestinal nematodes is determined by their life cycle and physiological requirements. Most common nematodes inhabit the small intestine, but **Trichuris trichiura (Whipworm)** is a notable exception [1]. **1. Why Trichuris trichiura is correct:** * **Habitat:** Unlike the other options, the adult whipworm resides in the **large intestine**, specifically the **cecum** and ascending colon [1]. * **Pathophysiology:** The anterior thin end of the worm embeds into the mucosal lining of the colon. Heavy infestations can lead to "Trichuris dysentery syndrome" and, classically, **rectal prolapse** in children [1]. **2. Why the other options are incorrect:** * **Ascaris lumbricoides (Roundworm):** Adult worms live in the lumen of the **jejunum** (upper small intestine). They are the largest nematodes and can cause intestinal obstruction at this site. * **Necator americanus (Hookworm):** These parasites inhabit the **upper small intestine**, where they attach to the villi of the duodenum and jejunum to suck blood, leading to iron-deficiency anemia [4]. * **Strongyloides stercoralis:** The adult female worms burrow into the mucosal epithelium of the **duodenum and jejunum** [2]. It is unique because it can cause autoinfection. **High-Yield NEET-PG Pearls:** * **Large Intestine Nematodes:** Remember the "Big Two"—*Trichuris trichiura* (Whipworm) and *Enterobius vermicularis* (Pinworm) [1]. * **Small Intestine Nematodes:** *Ascaris*, Hookworms (*Ancylostoma* and *Necator*), and *Strongyloides* [4]. * **Egg Morphology:** *Trichuris* eggs are characteristically **barrel-shaped with bipolar mucus plugs**. * **Treatment:** Albendazole or Mebendazole are the drugs of choice for most intestinal nematodes [3].

Question 155: Which of the following is NOT a manifestation of Cytomegalovirus (CMV) infection following lung transplant?

A. Bronchiolitis obliterans
B. CMV syndrome
C. CMV retinitis
D. Esophagitis (Correct Answer)

Explanation: Cytomegalovirus (CMV) is the most common opportunistic pathogen following lung transplantation, typically occurring within the first 6 months [1]. The correct answer is **Esophagitis** because, while CMV can affect the GI tract, it is a **rare** manifestation specifically in **lung transplant** recipients compared to other solid organ transplants. In lung transplant patients, CMV has a unique tropism for the allograft (the lungs) and systemic involvement. * **Option D (Esophagitis):** In the context of lung transplantation, CMV primarily manifests as pneumonitis or systemic syndrome. While GI involvement (like esophagitis or colitis) is common in HIV/AIDS patients, it is significantly less frequent than pulmonary complications in lung transplant recipients. * **Option A (Bronchiolitis Obliterans):** This is a critical association. CMV infection is a major risk factor for the development of **Bronchiolitis Obliterans Syndrome (BOS)**, which represents chronic allograft rejection. CMV-induced inflammation leads to airway injury and fibroproliferation. * **Option B (CMV Syndrome):** This is a common systemic manifestation characterized by fever, malaise, leukopenia, and thrombocytopenia without specific organ dysfunction [1]. * **Option C (CMV Retinitis):** Though more common in HIV, retinitis can occur in any severely immunocompromised state, including post-transplant patients on potent immunosuppression. **Clinical Pearls for NEET-PG:** * **Target Organ:** In lung transplants, the "vulnerable organ" for CMV is the lung itself (**CMV Pneumonitis**). * **Diagnosis:** Histopathology showing **"Owl’s Eye" intranuclear inclusions** is pathognomonic. * **Prophylaxis:** Valganciclovir is the drug of choice for prevention in high-risk (Donor+/Recipient-) patients [1]. * **Association:** Always link CMV infection with an increased risk of **Chronic Rejection (BOS)** in lung transplant questions.

Question 156: Which of the following organisms is known to cause endocarditis?

A. Coxiella
B. Chlamydia
C. HACEK (Correct Answer)
D. Salmonella

Explanation: Infective Endocarditis (IE) is primarily caused by Gram-positive cocci (Staphylococci and Streptococci) [1]. However, the **HACEK group** represents a significant cluster of fastidious Gram-negative bacilli that are well-recognized causes of **culture-negative endocarditis**. **Why HACEK is correct:** The HACEK group includes *Haemophilus species, Aggregatibacter, Cardiobacterium hominis, Eikenella corrodens,* and *Kingella kingae*. These organisms are part of the normal oropharyngeal flora. They are characterized by slow growth, often requiring specialized media or prolonged incubation. Clinically, HACEK endocarditis typically presents with large vegetations and a higher risk of embolic phenomena compared to other pathogens. **Analysis of Incorrect Options:** * **Coxiella burnetii:** While it is the most common cause of culture-negative endocarditis worldwide (Q fever), it is an obligate intracellular bacterium and is less frequently tested as a "standard" organism compared to the classic HACEK group in general medical exams unless specifically discussing Q fever [1]. In Coxiella infections, the spleen and the liver may be considerably enlarged [1]. * **Chlamydia:** While *Chlamydia psittaci* or *pneumoniae* are extremely rare causes of endocarditis, they are not considered standard or "known" causes in a clinical board context. * **Salmonella:** Salmonella typically causes endovascular infections (like mycotic aneurysms) rather than valvular endocarditis. **High-Yield Pearls for NEET-PG:** * **Most common cause of IE (Overall):** *Staphylococcus aureus* [1]. * **Most common cause in Subacute IE/Native Valve:** *Streptococcus viridans* [1]. * **Most common cause in IV Drug Users:** *Staphylococcus aureus* (Tricuspid valve) [1]. * **Culture-Negative IE:** Most commonly due to prior antibiotic use, followed by *Coxiella burnetii* and HACEK organisms [1]. * **Treatment for HACEK:** Ceftriaxone is the drug of choice due to increasing beta-lactamase production.

Question 157: What is the treatment of choice for seasonal influenza?

A. Oseltamivir (Correct Answer)
B. Zanamivir
C. Peramivir
D. Amantadine

Explanation: **Explanation:** **Oseltamivir (Option A)** is the treatment of choice for seasonal influenza (both Influenza A and B) [1]. It is a **Neuraminidase Inhibitor** [1] that works by preventing the release of new viral particles from infected host cells. For maximum clinical benefit, it should ideally be initiated within **48 hours** of symptom onset. It is preferred over other options due to its oral bioavailability, established safety profile in all age groups (including infants and pregnant women), and efficacy in preventing complications like pneumonia [1]. **Why other options are incorrect:** * **Zanamivir (Option B):** Also a neuraminidase inhibitor [1], but administered via **inhalation**. It is contraindicated in patients with underlying airway diseases (Asthma/COPD) due to the risk of bronchospasm, making it a second-line choice. * **Peramivir (Option C):** An **intravenous** neuraminidase inhibitor [1]. While effective, it is typically reserved for hospitalized patients who cannot tolerate oral or inhaled medications. * **Amantadine (Option D):** An M2 ion channel blocker. It is no longer recommended for seasonal influenza because it is only active against Influenza A and has high rates of viral resistance (>99%). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Neuraminidase inhibitors mimic sialic acid to competitively inhibit the viral neuraminidase enzyme [1]. * **Pregnancy:** Oseltamivir is the drug of choice for pregnant women with suspected or confirmed influenza. * **Prophylaxis:** Oseltamivir is also used for post-exposure prophylaxis (75 mg OD for 7-10 days). * **Newer Agent:** **Baloxavir marboxil** (a cap-dependent endonuclease inhibitor) is a single-dose oral alternative recently approved for uncomplicated influenza.

Question 158: A 20-year-old male presents with fever and chronic cough. His ESR is 35 mm. Sputum cytology is negative for AFB, and a tuberculin test shows indurations of 19 x 23 mm. What is the probable diagnosis?

A. Fungal pneumonia
B. Viral pneumonia
C. Pulmonary tuberculosis (Correct Answer)
D. Bacterial pneumonia

Explanation: ### Explanation The clinical presentation of a young male with a chronic cough, fever, and an elevated ESR (35 mm) strongly suggests a chronic granulomatous infection. The definitive clue in this case is the **Tuberculin Skin Test (Mantoux test)** result. **1. Why Pulmonary Tuberculosis is correct:** An induration of **19 x 23 mm** is considered a strongly positive (hyper-reactive) Mantoux test. In India (an endemic area), an induration of **≥10 mm** is generally considered positive. A very large induration (>15-20 mm) significantly increases the probability of active Tuberculosis (TB). While sputum cytology was negative for Acid-Fast Bacilli (AFB), this does not rule out TB [1]; "Sputum Negative Pulmonary TB" is a common clinical entity, especially in early stages or paucibacillary cases. The probability of detecting AFB in sputum is directly proportional to the bacillary burden [1]. **2. Why other options are incorrect:** * **Viral and Bacterial Pneumonia:** These typically present as acute illnesses (days, not weeks/months). Bacterial pneumonia usually shows high-grade fever and leukocytosis, while viral pneumonia often presents with interstitial patterns on X-ray. Neither would cause a strongly positive Tuberculin test. * **Fungal Pneumonia:** While it can be chronic, it is less common in immunocompetent 20-year-olds. It would not cause a positive Tuberculin test, which is specific to delayed hypersensitivity against *M. tuberculosis* antigens. **Clinical Pearls for NEET-PG:** * **Mantoux Interpretation:** ≥5 mm is positive in HIV+ or immunosuppressed; ≥10 mm is positive in endemic areas/high-risk groups; ≥15 mm is positive in those with no risk factors. The tuberculin test is usually strongly positive in cases of lymphadenitis [1]. * **False Negative Mantoux:** Can occur in miliary TB, malnutrition (anergy), sarcoidosis, and recent viral infections (e.g., Measles). * **Gold Standard:** Culture on **Lowenstein-Jensen (LJ) medium** remains the traditional gold standard, though **CBNAAT (GeneXpert)** is now the preferred initial diagnostic test under NTEP guidelines.

Question 159: Which of the following can occur due to meningococcal infection?

A. Meningitis
B. Waterhouse-friderichsen syndrome
C. Petechial hemorrhages
D. All of the above (Correct Answer)

Explanation: **Explanation:** Meningococcal infection, caused by the Gram-negative diplococcus *Neisseria meningitidis*, is a multisystemic disease characterized by rapid progression and high morbidity. The correct answer is **"All of the above"** because the pathogen can manifest in several distinct clinical forms: 1. **Meningitis (Option A):** This is the most common clinical presentation. The bacteria cross the blood-brain barrier, leading to inflammation of the meninges. Patients typically present with the classic triad of fever, headache, and nuchal rigidity. 2. **Waterhouse-Friderichsen Syndrome (Option B):** This is a catastrophic complication of fulminant meningococcemia. It involves severe septicemia leading to **bilateral adrenal hemorrhage**, resulting in acute adrenal insufficiency, profound shock, and disseminated intravascular coagulation (DIC). 3. **Petechial Hemorrhages (Option C):** A hallmark sign of meningococcemia is a non-blanching petechial or purpuric rash. This occurs due to bacterial endotoxin-mediated vascular damage, capillary leak, and thrombocytopenia. **Why other options are incorrect:** Since all three conditions (A, B, and C) are classic manifestations of *N. meningitidis* infection, selecting any single option would be incomplete. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** **Ceftriaxone** is the empirical treatment of choice. * **Chemoprophylaxis:** **Rifampicin** is the drug of choice for close contacts; Ciprofloxacin or Ceftriaxone (in pregnancy) are alternatives. * **Virulence Factor:** The **polysaccharide capsule** is the primary virulence factor (except for Serogroup B, which is poorly immunogenic). * **Deficiency Association:** Individuals with **terminal complement deficiencies (C5-C9)** are at a significantly higher risk for recurrent meningococcal infections.

Question 160: A patient develops hepatosplenomegaly and lymphadenopathy following sexual contact 3 weeks prior. What is the best test to rule out HIV infection?

A. ELISA
B. Western blot
C. P24 antigen test (Correct Answer)
D. Lymph node biopsy

Explanation: The clinical presentation of hepatosplenomegaly, lymphadenopathy, and fever following sexual contact 3 weeks prior is highly suggestive of **Acute Retroviral Syndrome (ARS)** [1]. **Why P24 Antigen Test is Correct:** The "Window Period" is the time between infection and the appearance of detectable antibodies. In HIV, this typically lasts 3–6 weeks. During this early phase, standard antibody tests (ELISA) will be negative [2]. The **p24 antigen**, a viral capsid protein, becomes detectable in the serum as early as **1–3 weeks** after exposure, coinciding with the peak of viremia. Therefore, it is the best test to diagnose or rule out early acute infection before seroconversion occurs [1]. **Analysis of Incorrect Options:** * **A. ELISA:** This is a screening test for HIV antibodies. Since it takes 3–12 weeks for antibodies to develop (seroconversion), an ELISA would likely yield a false negative at the 3-week mark [2]. * **B. Western Blot:** Historically used as a confirmatory test, it also detects antibodies against specific viral proteins (gp120, gp41, p24) [2]. Like ELISA, it is unreliable during the acute window period. * **C. Lymph Node Biopsy:** While it might show follicular hyperplasia, it is non-specific and not a standard diagnostic tool for HIV. **NEET-PG High-Yield Pearls:** * **Best Initial Test (Routine):** 4th Generation ELISA (detects both p24 antigen and HIV 1/2 antibodies). * **Earliest Test to become positive:** HIV RNA by PCR (detectable within 7–10 days). * **Confirmatory Test (Traditional):** Western Blot (though 4th Gen ELISA + Viral Load is now preferred) [2]. * **Diagnosis in Infants (<18 months):** DNA PCR (due to persistence of maternal IgG antibodies).

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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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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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