Infectious Diseases — MCQs
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Which of the following is true regarding Tuberculosis (TB) in HIV infection?
A 51-year-old cancer patient undergoing chemotherapy presents with clinical features of a urinary tract infection, including fever with rigors and flank pain. Urine examination reveals variable amounts of protein, leukocytes, and a few RBCs. Urine culture shows E. coli. Bladder wash shows characteristic polygonal granular cells and Michaelis-Gutmann bodies. Which of the following conditions is associated with these features?
Resistant kala-azar is defined by the persistence of which of the following features despite adequate therapy?
Plasmodium falciparum does not typically present with which of the following clinical manifestations?
Tuberculosis in HIV infection causes pulmonary disease resembling post-primary disease in normal individuals when it occurs during which stage of HIV infection?
A 50-year-old diabetic and hypertensive male presented with diplopia for 1 day, along with facial swelling and difficulty in speaking. The patient was in distress. On examination, he was febrile, hypertensive, and tachycardic, with right-sided proptosis, facial edema, and facial palsy. Laboratory findings revealed leukocytosis, increased serum glucose, and deranged RFTs. Cytopathology was taken on site. All of the following can be used in the management of the above condition except?
All of the following are known complications of tuberculous meningitis except?
A 35-year-old pet shop worker developed progressively spreading nodular lesions. He was afebrile. What is the most likely causative organism?
Diarrhoea in AIDS can be caused by all of the following organisms, EXCEPT:
Which of the following is NOT an opportunistic infection in HIV patients?
Infectious Diseases Indian Medical PG Practice Questions and MCQs
Question 371: Which of the following is true regarding Tuberculosis (TB) in HIV infection?
- A. Less susceptibility to Anti-TB therapy (ATT)
- B. Same susceptibility to ATT
- C. Faster progression of ATT (Correct Answer)
- D. TB is more common in AIDS
Explanation: **Explanation:** The relationship between HIV and Tuberculosis (TB) is synergistic and lethal [2]. In patients with HIV, the depletion of CD4+ T-lymphocytes impairs the body’s ability to form organized granulomas, which are essential for containing *Mycobacterium tuberculosis*. **Why the correct answer is right:** Option C refers to the clinical course of the disease rather than the drug efficacy. In HIV-positive individuals, the **progression of the disease is significantly accelerated** [2]. Latent TB infection (LTBI) progresses to active disease much faster, and the clinical deterioration is more rapid compared to immunocompetent patients. Furthermore, the response to treatment can be complicated by malabsorption of drugs or Immune Reconstitution Inflammatory Syndrome (IRIS), often necessitating a more vigilant monitoring of the "progression" and response to Anti-TB Therapy (ATT). **Analysis of incorrect options:** * **Options A & B:** HIV-positive patients generally show the **same susceptibility** to standard ATT as HIV-negative patients, provided the strain is not drug-resistant (MDR/XDR). The drugs work effectively on the bacteria; the challenge lies in the host's immune response and drug interactions (e.g., Rifampicin and Protease Inhibitors). * **Option D:** While TB is the most common opportunistic infection in HIV patients worldwide, the phrasing "TB is more common in AIDS" is a general epidemiological observation. However, in the context of clinical board exams, the **accelerated clinical progression** (Option C) is a more specific pathological hallmark of the co-infection. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** HIV patients often have **sputum-negative** TB and atypical chest X-ray findings (lower lobe infiltrates, hilar lymphadenopathy, and lack of cavitation) [1]. * **Extrapulmonary TB:** The incidence of disseminated and extrapulmonary TB (EPTB) increases as the CD4 count drops. * **Treatment:** Start ATT first, followed by ART (Antiretroviral Therapy) within 2 weeks if CD4 <50 cells/mm³ or within 8 weeks for others, to balance the risk of death and IRIS.
Question 372: A 51-year-old cancer patient undergoing chemotherapy presents with clinical features of a urinary tract infection, including fever with rigors and flank pain. Urine examination reveals variable amounts of protein, leukocytes, and a few RBCs. Urine culture shows E. coli. Bladder wash shows characteristic polygonal granular cells and Michaelis-Gutmann bodies. Which of the following conditions is associated with these features?
- A. Malakoplakia (Correct Answer)
- B. Xanthogranulomatous pyelonephritis
- C. Nail-patella syndrome
- D. Xanthelasma
Explanation: Explanation: 1. Why Malakoplakia is Correct: Malakoplakia is a rare chronic inflammatory condition, most commonly affecting the urinary bladder, often in immunocompromised patients (like those on chemotherapy). It results from the defective phagocytic killing of bacteria (usually E. coli) by macrophages. The hallmark histological finding is the presence of von Hansemann cells (large, polygonal granular macrophages) containing Michaelis-Gutmann bodies. These bodies are pathognomonic laminated calcified inclusions (iron and calcium deposits) formed due to the incomplete digestion of bacterial components. 2. Why Other Options are Incorrect: * Xanthogranulomatous pyelonephritis (XPN): While also a chronic inflammatory response to infection (often Proteus or E. coli), it is characterized by "foamy" lipid-laden macrophages and is typically associated with staghorn calculi and a "bear paw" appearance on CT. It lacks Michaelis-Gutmann bodies. * Nail-patella syndrome: A genetic disorder (LMX1B mutation) characterized by nail dysplasia, absent/hypoplastic patellae, and iliac horns. Renal involvement manifests as nephrotic syndrome with basement membrane thickening, not inflammatory bodies. * Xanthelasma: These are localized lipid deposits (xanthomas) typically found on the eyelids, associated with hyperlipidemia, and have no relation to urinary tract pathology. Clinical Pearls for NEET-PG: * Pathognomonic sign: Michaelis-Gutmann bodies (PAS positive, Von Kossa positive for calcium). * Common Organism: Escherichia coli (80% of cases). * Key Association: Immunosuppression or chronic debilitating diseases. * Staining: Michaelis-Gutmann bodies stain positive for Iron (Prussian blue) and Calcium (Von Kossa).
Question 373: Resistant kala-azar is defined by the persistence of which of the following features despite adequate therapy?
- A. Fever
- B. Non-regression of splenomegaly
- C. L.D. bodies in more than 5% of cells in bone marrow (Correct Answer)
- D. Hyperglobulinaemia
Explanation: The diagnosis of **Resistant Kala-azar** (Visceral Leishmaniasis) is primarily a parasitological diagnosis rather than a clinical one [1]. While clinical improvement (subsidence of fever and reduction in spleen size) usually mirrors therapeutic success, these signs can be misleading due to slow clinical recovery or secondary infections. **Why Option C is Correct:** The gold standard for defining resistance or treatment failure is the **persistence of Leishmania Donovani (L.D.) bodies** in tissue smears (bone marrow or splenic aspirate) after a full course of standard treatment [1]. Specifically, a parasite density where L.D. bodies are found in more than 5% of cells (or a high parasite grade) signifies that the drug has failed to achieve parasitological clearance. **Why Other Options are Incorrect:** * **A. Fever:** Fever may persist due to secondary bacterial infections (common in immunocompromised Kala-azar patients) or drug reactions, and does not exclusively indicate the failure of anti-leishmanial drugs. * **B. Non-regression of splenomegaly:** Splenomegaly takes weeks to months to resolve even after successful parasite clearance. A "hard" spleen may persist for a long duration post-cure. * **D. Hyperglobulinaemia:** Polyclonal hypergammaglobulinemia is a hallmark of the disease; however, antibody levels remain high for months after a clinical cure, making it an unreliable marker for acute resistance [1]. **NEET-PG High-Yield Pearls:** * **Drug of Choice:** Liposomal Amphotericin B is currently the preferred treatment for Kala-azar in India due to widespread resistance to Sodium Stibogluconate (SSG). * **Post-Kala-azar Dermal Leishmaniasis (PKDL):** Occurs in 5-10% of cases after apparent "cure." It presents as non-hypopigmented macules or nodules and serves as a reservoir for infection. * **Diagnostic Gold Standard:** Splenic aspirate is more sensitive (>95%) than bone marrow (60-85%) for detecting L.D. bodies [1].
Question 374: Plasmodium falciparum does not typically present with which of the following clinical manifestations?
- A. Hyperglycaemia (Correct Answer)
- B. Hypoglycaemia
- C. Hypotension
- D. Fever
Explanation: The correct answer is **A. Hyperglycaemia**. Severe *Plasmodium falciparum* malaria is classically associated with **hypoglycaemia**, not hyperglycaemia. [1] **1. Why Hyperglycaemia is the Correct Answer:** In falciparum malaria, blood glucose levels typically drop due to several synergistic mechanisms: * **Parasite Consumption:** The malaria parasites consume host glucose at a high rate for their metabolic needs. * **Inhibition of Gluconeogenesis:** Cytokine release (especially TNF-α) and liver dysfunction impair the liver's ability to produce glucose. * **Hyperinsulinemia:** Quinine/Quinidine therapy (common treatments) stimulates pancreatic beta cells to secrete insulin, further lowering blood sugar. [1] **2. Analysis of Incorrect Options:** * **B. Hypoglycaemia:** As explained above, this is a hallmark metabolic complication of severe malaria, particularly in children and pregnant women. [1] * **C. Hypotension:** Known as **"Algid Malaria,"** this occurs due to secondary bacterial septicaemia (often Gram-negative), dehydration, or splenic rupture, leading to circulatory collapse. * **D. Fever:** Fever is the most common clinical manifestation of all malaria species, resulting from the rupture of schizonts and the release of pyrogens into the bloodstream. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Blackwater Fever:** Intravascular haemolysis leading to haemoglobinuria (dark urine) caused by *P. falciparum*. * **Cerebral Malaria:** Defined by unarousable coma (Glasgow Coma Scale <11) not attributable to other causes. [1] * **Sequestration:** *P. falciparum* causes infected RBCs to stick to capillary endothelium (via PfEMP-1 protein), leading to microvascular obstruction and organ failure. * **Drug of Choice:** Artesunate is the current WHO-recommended treatment for severe malaria. [1]
Question 375: Tuberculosis in HIV infection causes pulmonary disease resembling post-primary disease in normal individuals when it occurs during which stage of HIV infection?
- A. Stage of viraemia (Correct Answer)
- B. Middle third of window period
- C. Last third of window period
- D. Full blown AIDS
Explanation: The clinical presentation of Tuberculosis (TB) in HIV-infected patients is directly dependent on the patient's degree of immunosuppression (CD4 count). [1] **1. Why "Stage of Viraemia" is correct:** The "Stage of Viraemia" refers to the early phase of HIV infection (Acute HIV Syndrome) where the CD4 count is still relatively high (usually >500 cells/mm³). At this stage, the body’s cell-mediated immunity is sufficiently intact to mount a typical granulomatous response. Consequently, TB presents as **Post-Primary (Reactivation) disease**, characterized by: * Upper lobe infiltrates. [1] * Cavitary lesions. [1] * Positive sputum smears (high bacterial load). **2. Why the incorrect options are wrong:** * **Full-blown AIDS:** In late-stage HIV (CD4 <200 cells/mm³), the immune system cannot form organized granulomas or cavities. TB here resembles **Primary Disease**, presenting with lower lobe infiltrates, mediastinal lymphadenopathy, miliary spread, and frequent extrapulmonary involvement. [1] Sputum smears are often negative despite high severity. * **Window Period (Middle/Last Third):** The window period refers to the time between infection and the appearance of detectable antibodies. While viraemia occurs here, the term "Stage of Viraemia" specifically denotes the clinical phase where the immune system is still robust enough to mimic immunocompetent TB patterns. **Clinical Pearls for NEET-PG:** * **CD4 >500:** Post-primary pattern (Cavitation, Upper lobe). [1] * **CD4 <200:** Primary pattern (Lymphadenopathy, Miliary, Extrapulmonary). [1] * **Most common extrapulmonary site in HIV:** Lymph nodes (Scrofula). [2] * **IRIS (Immune Reconstitution Inflammatory Syndrome):** Paradoxical worsening of TB symptoms after starting ART due to a recovering immune system. Always start TB treatment *before* ART to reduce this risk.
Question 376: A 50-year-old diabetic and hypertensive male presented with diplopia for 1 day, along with facial swelling and difficulty in speaking. The patient was in distress. On examination, he was febrile, hypertensive, and tachycardic, with right-sided proptosis, facial edema, and facial palsy. Laboratory findings revealed leukocytosis, increased serum glucose, and deranged RFTs. Cytopathology was taken on site. All of the following can be used in the management of the above condition except?
- A. Insulin
- B. Hemodialysis
- C. Voriconazole (Correct Answer)
- D. Amphotericin B
Explanation: ### **Explanation** **Diagnosis: Rhino-orbital-cerebral Mucormycosis (ROCM)** The clinical presentation of a **diabetic patient** with acute onset **proptosis, facial swelling, diplopia, and cranial nerve involvement** (facial palsy) is classic for **Mucormycosis**. The laboratory findings of hyperglycemia and deranged renal function tests (RFTs) further support this, as uncontrolled diabetes is the most significant risk factor for this invasive fungal infection [1]. #### **Why Voriconazole is the Correct Answer (The "Except"):** * **Voriconazole** is the drug of choice for *Aspergillus* species. However, **Mucorales (the causative agents of Mucormycosis) are intrinsically resistant to Voriconazole.** Using it in this scenario would result in treatment failure. #### **Analysis of Other Options:** * **Amphotericin B (Option D):** This is the **gold standard** medical treatment for Mucormycosis [1]. Liposomal Amphotericin B is preferred due to its better CNS penetration and lower nephrotoxicity. * **Insulin (Option A):** Aggressive management of the underlying predisposing factor is mandatory [1]. In this case, correcting hyperglycemia and ketoacidosis with insulin is a cornerstone of therapy to stop fungal proliferation. * **Hemodialysis (Option B):** The patient has deranged RFTs. Management of acute kidney injury (AKI) or metabolic acidosis via hemodialysis may be necessary to stabilize the patient for surgery or to manage the toxicity of conventional Amphotericin B. --- ### **NEET-PG High-Yield Pearls** * **Hallmark Pathology:** Mucormycosis is characterized by **angioinvasion**, leading to tissue necrosis and black eschar formation [1]. * **Microscopy:** Look for **broad, ribbon-like, aseptate hyphae** with **right-angled (90°) branching**. (Contrast with *Aspergillus*: thin, septate hyphae with acute-angled branching). * **Risk Factors:** Uncontrolled Diabetes (DKA), Neutropenia, Iron overload (Deferoxamine use), and Post-transplant immunosuppression [1]. * **Management Triad:** 1. Surgical debridement (most critical) [1]. 2. Intravenous Liposomal Amphotericin B [1]. 3. Control of underlying metabolic derangements (e.g., Hyperglycemia) [1]. * **Alternative Antifungals:** Isavuconazole and Posaconazole can be used as step-down or salvage therapy.
Question 377: All of the following are known complications of tuberculous meningitis except?
- A. Cranial nerve palsy
- B. Cerebral infarction
- C. Ptosis
- D. Parkinsonism (Correct Answer)
Explanation: **Explanation:** Tuberculous Meningitis (TBM) is characterized by a thick, gelatinous **exudate** that accumulates primarily at the **base of the brain** (basal cisterns). This unique pathology explains most of its clinical complications. **Why Parkinsonism is the correct answer:** While TBM can affect the basal ganglia via infarcts, **Parkinsonism** is not a recognized or classic complication of the disease. Movement disorders in TBM are rare; when they occur, they more commonly manifest as chorea or tremors in pediatric populations rather than true Parkinsonism. **Analysis of other options:** * **Cranial Nerve Palsy:** The dense basal exudates entrap and compress cranial nerves as they exit the brainstem. The **6th cranial nerve** (Abducens) is most commonly affected due to its long intracranial course, followed by the 3rd and 4th nerves. * **Ptosis:** This is a direct clinical manifestation of **3rd cranial nerve (Oculomotor) palsy**, which is a frequent result of the basal inflammatory process. * **Cerebral Infarction:** TBM causes **vasculitis** of the small and medium-sized arteries (especially the Circle of Willis and Middle Cerebral Artery). This leads to luminal narrowing and thrombosis, resulting in "tubercular zone" infarcts, typically in the basal ganglia and internal capsule. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hydrocephalus** is the most common complication of TBM (usually communicating type) [1]. 2. **Hyponatremia** in TBM is frequently caused by SIADH or Cerebral Salt Wasting Syndrome. 3. **Stage of TBM:** Medical management is most effective in Stage I (conscious, no focal deficits); prognosis worsens significantly by Stage III (coma/dense paraplegia). 4. **Diagnosis:** CSF typically shows high protein, low glucose, and **lymphocytic pleocytosis**.
Question 378: A 35-year-old pet shop worker developed progressively spreading nodular lesions. He was afebrile. What is the most likely causative organism?
- A. Acinetobacter baumannii
- B. Erysipelothrix rhusiopathiae
- C. Mycobacterium marinum (Correct Answer)
- D. Pasteurella multocida
Explanation: The clinical presentation of **progressively spreading nodular lesions** in a patient with occupational exposure to aquatic environments (pet shop worker/aquarium handler) is classic for **"Fish Tank Granuloma,"** caused by **Mycobacterium marinum**. **Why Mycobacterium marinum is correct:** * **Pathogenesis:** It is a non-tuberculous mycobacterium (NTM) found in fresh and salt water. It enters through minor skin abrasions. * **Clinical Presentation:** It typically presents as a localized granuloma or a series of nodules that follow a **sporotrichoid distribution** (spreading proximally along lymphatic drainage). * **Key Feature:** Patients are usually **afebrile**, and the lesions are chronic and slow-growing, matching the "progressive" nature described. **Why other options are incorrect:** * **Acinetobacter baumannii:** Typically causes opportunistic nosocomial infections (ventilator-associated pneumonia or UTIs), not chronic nodular skin lesions. * **Erysipelothrix rhusiopathiae:** Causes **Erysipeloid**, usually seen in fishermen or butchers. However, it presents as a well-demarcated, painful, purplish-red **erythematous plaque** (not nodules) and is often more acute. * **Pasteurella multocida:** Associated with **cat or dog bites**. It causes rapid-onset cellulitis (within 24 hours) with intense pain and swelling, rather than slow-spreading nodules. **NEET-PG High-Yield Pearls:** * **Sporotrichoid Spread:** Differential diagnosis includes *Sporothrix schenckii* (Rose gardener’s disease), *Mycobacterium marinum*, *Nocardia*, and *Leishmania*. * **Culture:** *M. marinum* grows best at a cooler temperature (**30-32°C**), explaining its predilection for the skin (extremities) rather than internal organs. * **Treatment:** Clarithromycin, ethambutol, or rifampin for several months.
Question 379: Diarrhoea in AIDS can be caused by all of the following organisms, EXCEPT:
- A. Mycobacterium
- B. Cryptosporidium
- C. Cytomegalovirus
- D. None of the above (Correct Answer)
Explanation: Diarrhea is one of the most common clinical manifestations of HIV/AIDS, often occurring when CD4 counts fall below 200 cells/mm³. The correct answer is **"None of the above"** because all three listed organisms—*Mycobacterium*, *Cryptosporidium*, and *Cytomegalovirus*—are well-recognized causes of HIV-associated diarrhea. 1. **Mycobacterium (Option A):** Specifically, *Mycobacterium avium complex* (MAC) is a common cause of chronic diarrhea and malabsorption in patients with advanced AIDS (CD4 < 50) [1]. It typically presents with fever, weight loss, and abdominal pain. 2. **Cryptosporidium (Option B):** This protozoan parasite causes severe, voluminous, watery diarrhea in immunocompromised hosts [1]. While it causes self-limiting illness in healthy individuals, it leads to chronic, life-threatening dehydration in AIDS patients [1]. 3. **Cytomegalovirus (Option C):** CMV is a major cause of serious colonic disease in AIDS (usually CD4 < 50). It causes CMV colitis, characterized by bloody diarrhea, tenesmus, and mucosal ulcerations visible on colonoscopy. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of diarrhea in AIDS:** Overall, it is often *Cryptosporidium* or *Isospora belli* [1]. * **Bloody diarrhea in AIDS:** Think **CMV** or enteric pathogens like *Salmonella* and *Shigella*. * **CD4 Count Correlations:** * **CD4 < 200:** *Cryptosporidium*, *Microsporidia*, *Giardia* [1]. * **CD4 < 50:** *CMV*, *Mycobacterium avium complex* (MAC) [1]. * **Diagnosis:** Acid-fast staining (Modified Kinyoun) is used to identify *Cryptosporidium*, *Isospora*, and *Cyclospora* [1].
Question 380: Which of the following is NOT an opportunistic infection in HIV patients?
- A. Toxoplasmosis
- B. Malaria (Correct Answer)
- C. Varicella
- D. Cytomegalovirus (CMV)
Explanation: **Explanation:** The core concept behind **Opportunistic Infections (OIs)** in HIV/AIDS is that they are caused by pathogens that typically do not cause disease in a host with a healthy immune system but take advantage of a compromised immune response (specifically low CD4+ T-cell counts). [1] **Why Malaria is the correct answer:** Malaria is considered an **endemic infection**, not an opportunistic one. While HIV-infected individuals (especially pregnant women) may experience more severe clinical manifestations or higher parasite densities due to impaired immunity, malaria occurs frequently in immunocompetent individuals living in endemic regions. It does not require an immunocompromised state to establish infection, nor is it listed in the CDC or WHO classification of AIDS-defining illnesses. [2] **Analysis of Incorrect Options:** * **Toxoplasmosis:** A classic OI caused by *Toxoplasma gondii*. It typically presents as ring-enhancing lesions on brain imaging when CD4 counts drop below **100 cells/mm³**. [1] * **Varicella (VZV):** While primary varicella occurs in healthy children, HIV patients are at a significantly higher risk for severe, disseminated primary infection or multidermatomal **Herpes Zoster (Shingles)** reactivation. [2] * **Cytomegalovirus (CMV):** A major OI that usually manifests when CD4 counts are **<50 cells/mm³**, commonly presenting as retinitis, esophagitis, or colitis. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Most common OI in India:** Tuberculosis (TB). * **Most common fungal OI:** Candidiasis (Oral thrush). [1] * **CD4 <200:** Prophylaxis for *Pneumocystis jirovecii* (PCP) using TMP-SMX. * **CD4 <100:** Prophylaxis for Toxoplasmosis. * **CD4 <50:** High risk for CMV and *Mycobacterium avium* complex (MAC).
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Principles of Antimicrobial Therapy
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Fever of Unknown Origin
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Viral Infections (Hepatitis, Herpes, etc.)
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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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