Infectious Diseases — MCQs

A 36-year-old man with AIDS develops right-sided weakness involving the lower, but not the upper, limb. MRI scans reveal a ring-enhancing lesion within the white matter of the left frontal lobe. A biopsy showed coagulative necrosis of brain parenchyma with macrophage-rich chronic inflammatory infiltration admixed with microscopic cysts that contain characteristic bradyzoites. What is the most common source of this type of infection?

Q440Easy

Which parasite causes 'River blindness'?

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 431: A 30-year-old HIV positive patient presents with fever, dyspnoea and non-productive cough. The patient is cyanosed. His chest X-ray reveals bilateral, symmetrical interstitial infiltrates. What is the most likely diagnosis?

A. Tuberculosis
B. Cryptococcosis
C. Pneumocystis jirovecii pneumonia (Correct Answer)
D. Toxoplasmosis

Explanation: ### Explanation **Pneumocystis jirovecii Pneumonia (PCP)** is the most common opportunistic infection in HIV patients with a CD4 count <200 cells/µL. **Why Option C is Correct:** The clinical triad of **fever, progressive dyspnoea, and non-productive cough** in an HIV-positive patient is classic for PCP [1]. The presence of **cyanosis** and exercise-induced desaturation is common due to significant alveolar-capillary block. Radiologically, the hallmark is **bilateral, symmetrical perihilar interstitial infiltrates** (ground-glass opacities), which matches the description provided [1]. **Why Other Options are Incorrect:** * **A. Tuberculosis:** Usually presents with a productive cough, hemoptysis, and weight loss. Radiologically, it typically shows focal infiltrates, cavitary lesions (in the upper lobes), or miliary patterns rather than symmetrical interstitial infiltrates [1]. * **B. Cryptococcosis:** Primarily presents as meningitis in HIV patients. Pulmonary involvement is less common and usually manifests as well-defined nodules or pleural effusions . * **C. Toxoplasmosis:** Most commonly affects the CNS, presenting with seizures or focal neurological deficits and "ring-enhancing lesions" on MRI. Pulmonary toxoplasmosis is rare and clinically indistinguishable from PCP, but PCP is statistically much more likely . **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Definitive diagnosis is made via **Gomori Methenamine Silver (GMS) stain** of induced sputum or Bronchoalveolar Lavage (BAL), showing "crushed ping-pong ball" cysts [1]. * **Lab Marker:** Elevated **Serum LDH** levels are highly sensitive but non-specific for PCP. * **Treatment:** **DOC is IV Trimethoprim-Sulfamethoxazole (TMP-SMX)** [1]. * **Steroid Indication:** Add Prednisone if $PaO_2 < 70$ mmHg or A-a gradient $> 35$ mmHg to prevent respiratory failure triggered by dying organisms [1].

Question 432: A patient with undulating fever presents with features of encephalitis. He is treated successfully with doxycycline and rifampicin. What is the most probable diagnosis?

A. Brucellosis (Correct Answer)
B. Bordetella pertussis
C. Francisella tularensis
D. Mycoplasma

Explanation: ### Explanation **Correct Answer: A. Brucellosis** The clinical triad of **undulating fever** (fever that rises and falls like a wave), neurological involvement (**neurobrucellosis** presenting as encephalitis), and a dramatic response to **Doxycycline and Rifampicin** is classic for Brucellosis. Brucellosis is a zoonotic infection caused by *Brucella* species (e.g., *B. melitensis* from goats/sheep). It is an intracellular pathogen, necessitating drugs with good intracellular penetration. While osteoarticular involvement is the most common complication, neurobrucellosis occurs in 5–10% of cases and can manifest as meningitis or encephalitis [1]. The WHO-recommended regimen for uncomplicated brucellosis is Doxycycline + Rifampicin for 6 weeks; however, for neurobrucellosis, treatment is often extended and may include a third drug like Ceftriaxone [1]. **Why other options are incorrect:** * **B. Bordetella pertussis:** Causes "Whooping Cough." It presents with paroxysmal cough and post-tussive vomiting, not undulating fever or encephalitis. The treatment of choice is Macrolides (Azithromycin). * **C. Francisella tularensis:** Causes Tularemia. While it is zoonotic, it typically presents with ulceroglandular disease or oculoglandular syndromes. The drug of choice is Streptomycin or Gentamicin. * **D. Mycoplasma:** Causes "Walking Pneumonia." While it can have extrapulmonary manifestations, it does not present with an undulating fever pattern. **High-Yield Clinical Pearls for NEET-PG:** * **Most common source:** Consumption of unpasteurized dairy products or contact with infected livestock. * **Gold Standard Diagnosis:** Bone marrow culture (more sensitive than blood culture) [1]. * **Serology:** Standard Agglutination Test (SAT); titers >1:160 are significant [1]. * **Rose Bengal Test:** Used as a rapid screening tool. * **Castaneda Medium:** A specialized biphasic medium used for culturing *Brucella*.

Question 433: Which of the following is NOT a characteristic of acute urinary tract infection?

A. Pus cells in urine
B. Elastase activity in urine (Correct Answer)
C. Nitrite positive
D. Leucocyte esterase positive

Explanation: ### Explanation The diagnosis of an acute Urinary Tract Infection (UTI) relies on clinical symptoms supported by urinalysis (dipstick and microscopy) and culture [1]. **Why "Elastase activity" is the correct answer:** **Elastase** is a proteolytic enzyme primarily associated with the degradation of elastin in connective tissues. While it is a marker for conditions like acute pancreatitis (fecal elastase) or certain pulmonary diseases, it is **not** a standard marker used to diagnose or characterize a UTI. There is no significant elastase activity in the urine during a typical acute urinary infection. **Analysis of Incorrect Options:** * **Pus cells in urine (Pyuria):** This is the hallmark of UTI. The presence of ≥10 white blood cells (WBCs) per high-power field (hpf) in centrifuged urine indicates an inflammatory response to infection in the urinary tract [1]. * **Nitrite positive:** Many common uropathogens (especially Enterobacteriaceae like *E. coli*) reduce dietary nitrates to nitrites. A positive nitrite test is highly specific for bacteriuria. * **Leucocyte esterase (LE) positive:** This enzyme is produced by neutrophils. A positive LE dipstick test indicates the presence of pyuria (pus cells), even if the cells have already lysed. **Clinical Pearls for NEET-PG:** * **Sterile Pyuria:** Presence of pus cells but negative routine culture [1]. Classic causes include *Mycobacterium tuberculosis* (Renal TB), Chlamydia, or recent antibiotic use [1]. * **Nitrite False Negatives:** Occur with organisms that do not produce nitrate reductase (e.g., *Enterococcus*, *Staphylococcus saprophyticus*, and *Pseudomonas*). * **Gold Standard:** The most definitive diagnosis for UTI remains a **urine culture** showing significant bacteriuria (traditionally ≥10⁵ CFU/mL). * **Most Common Organism:** *Uropathogenic E. coli* (UPEC) remains the leading cause of both uncomplicated and complicated UTIs [2].

Question 434: Diagnosis of acute viral hepatitis A is primarily established by which of the following findings?

A. Significant hepatic injury indicated by transaminase levels.
B. Variable increase in transaminase levels. (Correct Answer)
C. Detection of IgG anti-HAV antibodies.
D. Absence of any rise in transaminase levels.

Explanation: **Explanation:** The diagnosis of **Acute Viral Hepatitis A (HAV)** relies on a combination of clinical presentation, biochemical markers of liver injury, and serological confirmation. **Why the correct answer is right:** In acute viral hepatitis, the hallmark biochemical finding is a **variable increase in serum transaminases (ALT and AST)**. These enzymes are released into the bloodstream due to hepatocellular necrosis and inflammation. In symptomatic cases, these levels typically exceed 500 U/L and can often reach into the thousands. The degree of elevation is "variable" because it depends on the timing of the test relative to the onset of symptoms and the severity of the hepatic insult. **Analysis of Incorrect Options:** * **Option A:** While hepatic injury is present, "significant" is subjective. Transaminase levels do not always correlate linearly with the degree of liver cell necrosis or the ultimate prognosis. * **Option C:** **IgG anti-HAV** indicates past infection or immunity (post-vaccination). It is **not** used to diagnose acute infection. The gold standard serological marker for acute HAV is **IgM anti-HAV**. * **Option D:** An absence of a rise in transaminases would effectively rule out acute viral hepatitis, as these are the primary indicators of active liver inflammation. **NEET-PG High-Yield Pearls:** * **Route of Transmission:** Fecal-oral (most common). * **Incubation Period:** 15–45 days (Average: 4 weeks). * **Serology:** **IgM anti-HAV** is the diagnostic marker of choice for acute infection. It appears at the onset of symptoms and persists for 3–6 months. * **Prognosis:** HAV is typically self-limiting and **never** progresses to chronic hepatitis. * **Complication:** The most feared (though rare) complication is **Fulminant Hepatic Failure**, especially in patients with underlying chronic liver disease.

Question 435: Fresh water swimming can lead to which of the following infections?

A. Brucellosis
B. Leptospirosis (Correct Answer)
C. Babesiosis
D. Lassa fever

Explanation: **Explanation:** **Leptospirosis** is a zoonotic infection caused by the spirochete *Leptospira interrogans*. The bacteria are shed in the **urine of infected animals** (most commonly rodents, dogs, and livestock) [1]. These spirochetes can survive for weeks in **fresh water and moist soil** [1]. Human infection occurs through direct contact with contaminated water or soil via skin abrasions or mucous membranes. Activities like **freshwater swimming**, kayaking, or wading in floodwaters are classic risk factors frequently tested in exams [1]. **Analysis of Incorrect Options:** * **A. Brucellosis:** Primarily transmitted through the consumption of unpasteurized dairy products or direct contact with infected livestock (cattle, goats, sheep). It is an occupational hazard for veterinarians and slaughterhouse workers, not associated with swimming. * **C. Babesiosis:** A malaria-like illness caused by *Babesia microti*. It is transmitted by the bite of the **Ixodes tick** (the same vector for Lyme disease). * **D. Lassa Fever:** A viral hemorrhagic fever transmitted through contact with food or household items contaminated with the urine or feces of infected **Mastomys rats** (multimammate rats), primarily in West Africa. **High-Yield Clinical Pearls for NEET-PG:** * **Weil’s Disease:** The severe form of Leptospirosis characterized by the triad of **Jaundice, Renal failure, and Hemorrhage**. * **Clinical Feature:** Look for **conjunctival suffusion** (redness without exudate), which is a highly specific sign. * **Biphasic illness:** It typically presents with an initial septicemic phase followed by an immune phase (meningitis/uveitis). * **Treatment:** **Doxycycline** is the drug of choice for prophylaxis and mild cases; IV **Penicillin G** is preferred for severe disease.

Question 436: Which of the following hepatitis viruses can cause chronic liver disease?

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

Explanation: **Explanation:** The ability of a hepatitis virus to cause chronic liver disease depends on its potential for **persistence** within the host. Chronic hepatitis is defined as inflammation of the liver lasting for more than 6 months. **Why Hepatitis C is the Correct Answer:** Hepatitis C Virus (HCV) is notorious for its high rate of chronicity [1]. Approximately **75%–85%** of individuals infected with HCV fail to clear the virus and develop chronic infection. This persistence often leads to liver cirrhosis and hepatocellular carcinoma (HCC) over decades, making it a leading indication for liver transplantation worldwide [1]. **Analysis of Incorrect Options:** * **Hepatitis A (Option B):** This is an enterically transmitted virus (fecal-oral) that causes acute hepatitis only. It **never** leads to chronic infection or a carrier state. * **Hepatitis E (Option D):** Similar to Hep A, it is enterically transmitted and usually causes self-limiting acute disease. While it can cause chronic hepatitis in **immunocompromised** patients (e.g., organ transplant recipients), in the general population and for standard exam purposes, it is considered a cause of acute hepatitis. * **Hepatitis B (Option A):** While HBV *can* cause chronic liver disease, the question asks which virus "can" cause it, and often in MCQ formats, if both B and C are present, the one with the **highest chronicity rate** or the most definitive association is prioritized [2]. However, in a "Multiple Correct" scenario, both B and C would be right. In a single-choice format where C is marked correct, it highlights HCV's higher progression rate (80%) compared to adult-acquired HBV (only 5-10%). **NEET-PG High-Yield Pearls:** * **Chronicity Rates:** HCV (80%) > HBV (5-10% in adults, but 90% in neonates). * **Hepatitis E:** Associated with high mortality (up to 20%) in **pregnant women** due to fulminant hepatic failure. * **Hepatitis D:** Can only cause infection in the presence of HBV (Co-infection or Super-infection). * **DNA vs RNA:** HBV is the only **DNA** virus among the major hepatitis viruses; the rest are RNA viruses.

Question 437: All of the following are true regarding typhoid ulcers except:

A. Mainly affects the ileum
B. Multiple ulcers and transverse (Correct Answer)
C. Perforation occurs at the 3rd week
D. Perforation is treated by surgery

Explanation: In Typhoid fever (Enteric fever), the causative organism *Salmonella typhi* invades the **Peyer’s patches** (lymphoid tissue) located in the intestinal wall. ### **Explanation of the Correct Option** **Option B (Multiple ulcers and transverse) is the INCORRECT statement.** Typhoid ulcers are typically **longitudinal** (parallel to the long axis of the bowel). This is because Peyer’s patches are arranged longitudinally along the antimesenteric border of the ileum. In contrast, **Tubercular ulcers** are transverse (circumferential) because they follow the path of the lymphatics around the bowel wall. ### **Analysis of Other Options** * **Option A (Mainly affects the ileum):** This is true. Peyer’s patches are most numerous in the terminal ileum, making it the primary site for typhoid-induced inflammation and ulceration. * **Option C (Perforation occurs at the 3rd week):** This is true. The "Pathological Timetable" of Typhoid is: * Week 1: Hyperplasia of Peyer’s patches. * Week 2: Necrosis and sloughing [1]. * **Week 3: Ulceration and potential perforation/hemorrhage.** [1] * Week 4: Resolution/Healing. * **Option D (Perforation is treated by surgery):** This is true. Intestinal perforation is a surgical emergency. The standard treatment is resuscitation followed by primary closure of the perforation or resection-anastomosis. ### **High-Yield Clinical Pearls for NEET-PG** * **Shape:** Typhoid ulcers are oval/longitudinal; Tubercular ulcers are transverse. * **Complication:** The most common cause of death in Typhoid is intestinal perforation, which typically occurs at the end of the second week or during the third week [1]. * **Widal Test:** Becomes positive in the 2nd week. * **Culture Gold Standard:** Bone marrow culture is the most sensitive, but Blood culture is the standard in the 1st week (Mnemonic: **BASU** - **B**lood (Wk 1), **A**ntibody/Widal (Wk 2), **S**tool (Wk 3), **U**rine (Wk 4)).

Question 438: Opportunistic infections are seen in which of the following conditions?

A. AIDS
B. Autoimmune diseases
C. Organ transplantation
D. All of the above (Correct Answer)

Explanation: **Explanation:** Opportunistic infections (OIs) occur in individuals with compromised immune systems [2]. These pathogens, which typically do not cause disease in healthy hosts, take advantage of a weakened immune response (cellular or humoral). * **AIDS (Option A):** This is the classic example of profound immunosuppression. HIV targets and destroys **CD4+ T-lymphocytes**. When the CD4 count falls below 200 cells/mm³, the risk for OIs like *Pneumocystis jirovecii* pneumonia, Toxoplasmosis, and Cryptococcosis increases significantly [3]. * **Autoimmune Diseases (Option B):** While the diseases themselves involve immune dysregulation, the primary risk for OIs stems from **iatrogenic immunosuppression** [2]. Patients are often treated with long-term corticosteroids, Methotrexate, or Biologicals (e.g., TNF-alpha inhibitors), which suppress the body's ability to fight latent or environmental pathogens. * **Organ Transplantation (Option C):** To prevent graft rejection, transplant recipients must take lifelong **immunosuppressive therapy** (e.g., Cyclosporine, Tacrolimus, Mycophenolate) [1]. This creates a "window of vulnerability" where patients are highly susceptible to Cytomegalovirus (CMV), BK virus, and fungal infections [1]. **Conclusion:** Since all three conditions involve a state of immunosuppression (either primary or secondary), **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Most common OI in AIDS:** *Pneumocystis jirovecii* (PCP) [3]. * **Post-Transplant Period:** The first month is dominated by surgical/bacterial infections; months 1–6 are the peak period for OIs like CMV and *Nocardia*. * **TNF-alpha Inhibitors:** Always screen for **Latent Tuberculosis** before starting these drugs for autoimmune conditions (e.g., Rheumatoid Arthritis), as they significantly increase the risk of TB reactivation.

Question 439: A 36-year-old man with AIDS develops right-sided weakness involving the lower, but not the upper, limb. MRI scans reveal a ring-enhancing lesion within the white matter of the left frontal lobe. A biopsy showed coagulative necrosis of brain parenchyma with macrophage-rich chronic inflammatory infiltration admixed with microscopic cysts that contain characteristic bradyzoites. What is the most common source of this type of infection?

A. Anopheles mosquitoes
B. Bird droppings
C. Cats (Correct Answer)
D. Cooling systems

Explanation: **Explanation:** The clinical presentation and histopathology point to **Toxoplasmosis**, caused by the protozoan *Toxoplasma gondii*. In patients with AIDS (typically CD4 <100 cells/mm³), this is the most common cause of focal brain lesions [1]. **Why Cats are the Correct Answer:** The definitive hosts for *T. gondii* are members of the **Felidae family (cats)**. The parasite undergoes sexual reproduction in the feline gut, and infectious **oocysts** are shed in cat feces. Humans typically acquire the infection by accidental ingestion of these oocysts (e.g., cleaning litter boxes or contaminated soil) or by eating undercooked meat containing tissue cysts. The biopsy findings of **bradyzoites** (slow-growing forms within cysts) and **tachyzoites** (rapidly dividing forms) are pathognomonic for Toxoplasmosis. **Why Other Options are Incorrect:** * **Anopheles mosquitoes:** These are the vectors for *Plasmodium* species (Malaria), which presents with cyclical fevers and diffuse encephalopathy rather than focal ring-enhancing lesions. * **Bird droppings:** This is the classic transmission route for *Cryptococcus neoformans*. While common in AIDS, it typically presents as meningitis or "soap-bubble" lesions in the basal ganglia, not ring-enhancing necrotic masses. * **Cooling systems:** These are associated with *Legionella pneumophila*, which causes atypical pneumonia (Legionnaires' disease) and hyponatremia, not focal brain abscesses. **High-Yield Clinical Pearls for NEET-PG:** * **Imaging:** MRI typically shows **multiple** ring-enhancing lesions with a predilection for the **basal ganglia** and corticomedullary junction [1]. * **Differential Diagnosis:** The main differential for a ring-enhancing lesion in AIDS is **Primary CNS Lymphoma** [1] (usually a single lesion, EBV DNA positive in CSF). * **Treatment:** The first-line regimen is **Sulfadiazine + Pyrimethamine** (plus folinic acid to prevent bone marrow suppression) [1]. * **Prophylaxis:** Start **TMP-SMX** in HIV patients when CD4 count is <100 cells/mm³.

Question 440: Which parasite causes 'River blindness'?

A. Onchocerca volvulus (Correct Answer)
B. Schistosoma haematobium
C. Fasciola hepatica
D. Opisthorchis viverrini

Explanation: **Onchocerca volvulus** is the causative agent of **River Blindness** (Onchocerciasis). It is a filarial nematode transmitted to humans through the bite of an infected **Blackfly (*Simulium* genus)**, which breeds in fast-flowing rivers—hence the name. The pathology is primarily caused by the host's inflammatory response to dying **microfilariae**. These larvae migrate to the skin (causing severe pruritus and "leopard skin" appearance) and the eyes, where chronic inflammation leads to sclerosing keratitis and eventual blindness [1]. **Analysis of Incorrect Options:** * **Schistosoma haematobium:** A trematode (blood fluke) that causes urinary schistosomiasis [2]. It is associated with terminal hematuria and is a significant risk factor for **Squamous Cell Carcinoma of the bladder**. * **Fasciola hepatica:** Known as the "Sheep liver fluke," it causes hepatobiliary disease after ingestion of contaminated watercress. It typically presents with right upper quadrant pain and eosinophilia. * **Opisthorchis viverrini:** A Southeast Asian liver fluke associated with the consumption of raw fish. Chronic infection is a major risk factor for **Cholangiocarcinoma** (bile duct cancer). **High-Yield Clinical Pearls for NEET-PG:** * **Vector:** Blackfly (*Simulium*) [1]. * **Drug of Choice:** **Ivermectin** (kills microfilariae but not adults) [1]. * **Diagnosis:** Skin snip preparation to visualize microfilariae. * **Wolbachia:** *Onchocerca* harbors symbiotic *Wolbachia* bacteria; treating with Doxycycline can sterilize adult female worms [1]. * **Mazzotti Reaction:** A severe systemic reaction (fever, hypotension) that can occur after treating onchocerciasis with diethylcarbamazine (DEC).

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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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Antimicrobial Resistance

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