Infectious Diseases — MCQs

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 1011: A patient comes to ED with fever and headache. On examination he has neck stiffness. CSF analysis was done: Glucose 55 mg/dl (normal 50-80), Protein 0.50 g/L (normal 0.18-0.45), ICT 35 cmH2O (normal 5-20), WBC 25 (predominantly lymphocytes). Most likely diagnosis is:

A. Cryptococcus
B. TB
C. N. Gonorrhea
D. Coxsackie (Correct Answer)

Explanation: ***Coxsackie*** - The CSF analysis shows **normal glucose**, **mildly elevated protein**, **moderately elevated opening pressure**, and a **淋巴细胞主导** pleocytosis, which are characteristic findings in **viral meningitis**, commonly caused by enteroviruses such as Coxsackie virus [1]. - The combination of **fever, headache, neck stiffness**, and the specific CSF profile strongly points towards a viral etiology [1]. *Cryptococcus* - While fungal meningitis can present with similar symptoms and lymphocyte-dominant pleocytosis, it typically causes **markedly low CSF glucose** and **higher protein levels** than observed here. - Diagnosis usually requires specific tests like **India ink stain** or **cryptococcal antigen detection**, which are not indicated by these CSF findings. *TB* - Tuberculous meningitis usually presents with **very low CSF glucose** (often <40 mg/dl), **markedly elevated protein** (>1 g/L), and predominantly **lymphocytic pleocytosis**, often with a very slow onset [2]. - The CSF profile in this case, particularly the normal glucose, makes TB less likely [2]. *N. Gonorrhea* - *Neisseria gonorrhoeae* can cause **meningitis**, but it is generally a rare presentation and usually results in **neutrophilic pleocytosis** in the CSF, similar to other bacterial meningitides. - The **lymphocytic predominance** in this patient's CSF makes *N. gonorrhoeae* an unlikely cause.

Question 1012: Pulmonary manifestation for inhalational anthrax is:

A. Hemorrhagic mediastinitis (Correct Answer)
B. Lobar consolidation
C. Bronchopneumonia with type two respiratory failure
D. Can cause pneumonia

Explanation: ***Hemorrhagic mediastinitis*** - Inhalational anthrax is characterized by the rapid development of **hemorrhagic mediastinitis** due to direct bacterial infection and subsequent toxin-induced vascular damage in the mediastinal lymph nodes. - This leads to a widened mediastinum on chest imaging, often with **pleural effusions** and surrounding edema. *Lobar consolidation* - **Lobar consolidation** is more typical of common bacterial pneumonias, such as those caused by *Streptococcus pneumoniae* or *Klebsiella pneumoniae* [1]. - While pulmonary symptoms occur in anthrax, it is not primarily a direct lobar parenchymal infection but rather an infection of the **mediastinal lymph nodes**. *Bronchopneumonia with type two respiratory failure* - **Bronchopneumonia** involves patchy inflammation centered around bronchioles, which is not the primary pattern of lung involvement in inhalational anthrax. - **Type 2 respiratory failure** (hypercapnic respiratory failure) results from ventilation-perfusion mismatch or hypoventilation, but its direct association with this specific anthrax manifestation is less characteristic compared to the hemorrhagic mediastinitis. *Can cause pneumonia* - While inhalational anthrax can lead to severe pulmonary symptoms and acute respiratory failure, describing it simply as "pneumonia" is insufficient as it fails to capture the unique and critical finding of **hemorrhagic mediastinitis**. - The disease's characteristic features, such as mediastinal widening and hemorrhage, differentiate it from typical bacterial pneumonias.

Question 1013: Cerebrospinal fluid analysis shows lymphocytic pleocytosis, elevated protein, and low glucose. AFB stain positive. Likely diagnosis?

A. Bacterial meningitis
B. Viral meningitis
C. TB meningitis (Correct Answer)
D. Fungal meningitis

Explanation: ***TB meningitis*** - The combination of **lymphocytic pleocytosis**, **elevated protein**, and **low glucose** in CSF, along with a **positive AFB stain**, is highly indicative of **tuberculous meningitis** [1]. - **Mycobacterium tuberculosis** is an acid-fast bacillus (AFB) and causes a chronic inflammatory response in the meninges, leading to characteristic CSF changes [2]. *Bacterial meningitis* - Typically presents with **neutrophilic pleocytosis**, **markedly elevated protein**, and **very low glucose**, which differs from the lymphocytic predominance seen here [3]. - While bacteria can cause low glucose, the positive AFB stain rules out common bacterial causes. *Viral meningitis* - Characterized by **lymphocytic pleocytosis** and normal to mildly elevated protein, but usually has **normal glucose levels** [4]. - No specific staining like AFB would be positive in viral meningitis. *Fungal meningitis* - May show **lymphocytic pleocytosis**, elevated protein, and low glucose, similar to TB meningitis. - However, **AFB stain** would be **negative**, and diagnosis would rely on fungal stains or cultures.

Question 1014: A 50-year-old diabetic presents with facial palsy, ear pain, and vesicles in EAC. Best initial treatment is:

A. IV acyclovir (Correct Answer)
B. Antibiotics
C. Oral steroids
D. Oral acyclovir

Explanation: ***IV acyclovir*** - The constellation of **facial palsy**, **ear pain**, and **vesicles in the external auditory canal** (EAC) in a diabetic patient is highly suggestive of **Herpes Zoster Oticus** (Ramsay Hunt Syndrome). - Given the patient's age and diabetes (an immunocompromised state), **intravenous acyclovir** is the best initial treatment to achieve higher drug concentrations quickly and prevent complications such as permanent facial paralysis or postherpetic neuralgia [1]. *Antibiotics* - Antibiotics are indicated for **bacterial infections**, but Ramsay Hunt Syndrome is caused by **Varicella-Zoster virus reactivation**, not bacteria. - Using antibiotics would be ineffective and could contribute to **antibiotic resistance**. *Oral steroids* - While steroids like prednisone are often used in conjunction with antivirals for Ramsay Hunt Syndrome to reduce inflammation and improve outcomes, they are not the **primary initial treatment** as they do not address the viral cause directly. - Steroids alone, especially in an immunocompromised diabetic patient, could potentially worsen the viral infection. *Oral acyclovir* - **Oral acyclovir** is used for Ramsay Hunt Syndrome, but **intravenous administration** is preferred as the initial treatment in patients with severe symptoms, immunocompromised states (like diabetes), or extensive disease to ensure better bioavailability and faster viral suppression [1]. - Oral acyclovir might be considered for milder cases or as a follow-up after initial IV treatment, but its absorption and efficacy are often lower compared to IV.

Question 1015: Which of the following markers persists in chronic hepatitis B and recurrent hepatitis B?

A. IgG Anti HbcAg (Correct Answer)
B. Anti Hbs
C. HBsAg
D. Anti-HBs

Explanation: ### IgG Anti HbcAg - **IgG anti-HBc** (antibody to hepatitis B core antigen) persists throughout chronic hepatitis B infection and is also present during recurrent hepatitis B after liver transplantation, indicating past or ongoing infection [1]. - This antibody targets the **viral core antigen**, which is present in infected hepatocytes and is not circulating, thus the presence of IgM anti-HBc indicates an acute infection, while IgG anti-HBc indicates chronic or past infection [1]. ### Anti Hbs - **Anti-HBs** (antibody to hepatitis B surface antigen) indicates **immunity** to hepatitis B, either from vaccination or successful resolution of a past infection [1]. - It would typically be present in someone who has cleared the virus or been vaccinated, not in chronic or recurrent active infection. ### HBsAg - **HBsAg** (hepatitis B surface antigen) indicates an active hepatitis B infection, either acute or chronic [1]. While present in chronic hepatitis, its persistence alone doesn't specifically define recurrence, as it's the primary marker of chronic infection. - In recurrent hepatitis B after liver transplant, HBsAg would reappear, but **IgG anti-HBc** is also crucial for confirming the presence of the virus [1]. ### Anti-HBs - **Anti-HBs** (antibody to hepatitis B surface antigen) is a marker of **immunity** and indicates successful resolution of an infection or vaccination [1]. - Its presence signifies protection against the virus and would not be consistently high in the setting of persistent chronic or recurrent active infection.

Question 1016: Episodes of repeated thin stools with mucus, subjective feeling of fever and lower abdominal pain, with leukocytes in stool. Which of the following is likely?

A. Clostridium perfringens
B. Staphylococcus aureus
C. Giardia
D. Entamoeba (Correct Answer)

Explanation: ***Entamoeba*** - The presence of **leukocytes in stool** along with symptoms like repeated thin stools with mucus, subjective fever, and lower abdominal pain are characteristic of **invasive amoebiasis** caused by *Entamoeba histolytica* [1]. - *Entamoeba histolytica* is known to cause **amoebic dysentery**, which involves inflammation and ulceration of the colon, leading to the presence of inflammatory cells in the stool [1]. *Clostridium perfringens* - This bacterium typically causes **food poisoning** with symptoms of abdominal cramps and watery diarrhea, which is usually **self-limiting** and does not typically involve significant inflammation or leukocytes in stool. - While it can cause necrotizing enteritis in severe cases, the more common presentation does not align with the description of mucosal stools and leukocytes. *Staphylococcus aureus* - *S. aureus* causes **food poisoning** through the ingestion of preformed toxins, leading to rapid onset of nausea, vomiting, and non-bloody diarrhea. - This condition is typically **short-lived** and does not usually involve leukocytes in the stool or significant inflammation, primarily affecting the upper gastrointestinal tract. *Giardia* - *Giardia lamblia* causes **giardiasis**, characterized by chronic diarrhea, malabsorption, bloating, and foul-smelling stools, but generally **does not cause invasive disease** or significant inflammation in the intestinal lining [2]. - Stool analysis in giardiasis typically shows **no leukocytes** or red blood cells, as the parasite does not invade the intestinal wall [2].

Question 1017: Dengue discharge protocol includes:

A. Return of normal appetite (Correct Answer)
B. Urine output > 0.5 ml/kg/hr
C. 24 hours after Recovery from shock
D. 24 hours after absence of fever without antipyretics

Explanation: ***Return of normal appetite*** - A **normal appetite** indicates that the patient's overall condition and gastrointestinal function are improving, suggesting recovery from the acute phase of dengue. - This is a key clinical sign that contributes to deciding whether a patient is stable enough for discharge. *Urine output > 0.5 ml/kg/hr* - While adequate **urine output** is important for assessing renal function and hydration status in dengue, a value of >0.5 ml/kg/hr is generally considered the *minimum adequate output* and is not, by itself, a specific discharge criterion. - Normal urine output is often cited as at least 1 mL/kg/hr, especially in children, and simply meeting the bare minimum does not guarantee full recovery. *24 hours after Recovery from shock* - Recovery from **shock** is a critical milestone, but discharge typically requires a longer period of observation and stability after the resolution of severe symptoms. - Patients are generally observed for at least **48 hours** after recovery from shock to ensure no relapse or complications before considering discharge. *24 hours after absence of fever without antipyretics* - The absence of **fever for 24 hours** without antipyretics is an important criterion for ruling out ongoing active infection, but for dengue, global guidelines often recommend a fever-free period of **48 hours** or more for discharge. - This longer observation period helps confirm that the patient has moved past the critical phase and is not at risk of re-developing complications.

Question 1018: A patient with HIV develops CMV retinitis at CD4 count of 75/µL. When can prophylaxis be stopped?

A. CD4 >100/µL
B. CD4 >200/µL for 3 months (Correct Answer)
C. After 6 months of treatment
D. Viral load undetectable

Explanation: Detailed guidance on managing opportunistic infections in HIV emphasizes that the best way to prevent such infections is to improve the CD4 count with antiretroviral therapy (ART) [1]. Prophylaxis for **CMV retinitis** can generally be safely discontinued in HIV-infected patients when they have received at least **3-6 months of ART** and their **CD4+ count increases to >100 or >150 cells/µL for at least 3-6 months**. Many guidelines, including those from the DHHS, suggest a CD4 count of **>100 cells/µL for 3-6 months** as the threshold for stopping therapy, but a higher threshold like **>200 cells/µL for 3 months** provides an even safer margin, especially given the severity of CMV retinitis. Because the CD4 count can vary by up to 20% due to intercurrent infections, major therapeutic decisions regarding the discontinuation of prophylaxis should not be based on a single measurement [1]. While a CD4 count of **>100/µL** is a common threshold for considering discontinuation of CMV prophylaxis, guidelines often recommend this count be sustained for at least **3 to 6 months** before stopping, emphasizing sustained immune recovery. Simply exceeding **100/µL** without a prolonged period of immune stability may not be sufficient to prevent relapse or development of drug resistance. The duration of treatment alone, without considering the patient's **immune status (CD4 count)**, is an insufficient criterion for stopping prophylaxis in **CMV retinitis**. Immune recovery, as indicated by a sustained increase in **CD4 count**, is critical for preventing CMV reactivation and recurrence, not just the passage of time on treatment. An **undetectable viral load** indicates successful **ART suppression of HIV**, which is essential for immune reconstitution. However, for conditions like **CMV retinitis**, a sustained increase in **CD4 count** is the primary marker of immune recovery necessary to discontinue specific prophylaxis, as it reflects the functional ability of the immune system to control opportunistic infections.

Question 1019: Most specific sign of secondary syphilis is:

A. Mucous patches
B. Condyloma lata (Correct Answer)
C. Copper colored rash
D. Palm/sole lesions

Explanation: ***Condyloma lata*** - These are **flat-topped, moist, wart-like lesions** that appear in warm, moist areas like the anogenital region or skin folds. They are highly contagious and are considered the most specific sign of secondary syphilis due to their unique appearance and association. - Their distinct morphology and location help differentiate them from other dermatological conditions, making them a key diagnostic feature. *Mucous patches* - While **mucous patches** are characteristic of secondary syphilis, appearing as painless, whitish lesions on mucous membranes, they are less specific as similar lesions can be seen in other conditions. - They are often overlooked or mistaken for other oral or genital lesions, making them less distinct than condyloma lata for specific diagnosis. *Copper colored rash* - A **diffuse, copper-colored macular or papular rash** is a common manifestation of secondary syphilis, often affecting the trunk and extremities. - However, similar rashes can be seen in various viral exanthems or drug reactions, making it less specific than condyloma lata. *Palm/sole lesions* - **Lesions on the palms and soles** are a highly suggestive, though not entirely specific, sign of secondary syphilis, presenting as macules or papules. - While very characteristic, other conditions like Rocky Mountain spotted fever or hand-foot-and-mouth disease can also cause palmoplantar lesions, reducing their specificity compared to condyloma lata.

Question 1020: A patient on steroids develops sudden onset painful vesicles in T4 dermatome. Best initial treatment is:

A. Oral Acyclovir
B. Oral Valacyclovir
C. Topical Acyclovir
D. IV Acyclovir (Correct Answer)

Explanation: ***IV Acyclovir*** - Patients on **steroids** are considered **immunocompromised**, and a sudden onset of painful vesicles in a dermatomal distribution strongly suggests **herpes zoster (shingles)** [1]. - In immunocompromised patients, **intravenous acyclovir** is the preferred initial treatment due to better bioavailability and more rapid systemic drug levels, helping to prevent complications like **postherpetic neuralgia** or disseminated disease [1]. *Oral Acyclovir* - While oral acyclovir is used for herpes zoster, it is generally less effective in **immunocompromised patients** due to lower bioavailability compared to IV administration. - The slower onset of action and lower peak plasma concentrations may not be sufficient to control the viral infection rapidly in this high-risk group. *Oral Valacyclovir* - **Valacyclovir** is a prodrug of acyclovir with improved oral bioavailability, making it a good option for immunocompetent patients with herpes zoster. - However, for **immunocompromised patients**, particularly those on steroids, **IV acyclovir** is still superior due to the need for rapid and high systemic drug levels to prevent severe complications [1]. *Topical Acyclovir* - **Topical acyclovir** is primarily used for **herpes simplex labialis (cold sores)** and has very limited efficacy for systemic viral infections like **herpes zoster**. - It does not achieve adequate systemic concentrations to treat the underlying viral replication or prevent complications in dermatomal zoster, especially in an immunocompromised individual.

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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