Infectious Diseases — MCQs

A young butcher cuts his forearm with a knife. Over the next week, he notices swelling, redness, and warmth at the site. Four days later, he presents to the emergency department with fever, shaking chills, and severe lower back pain. Physical examination reveals a temperature of 39.4 C (102.9 F), swelling in his forearm with an area of central softness, and tenderness to pressure over his lower spine. Laboratory data show a leukocyte count of 14,000/mm3 with 81% polymorphonuclear leukocytes. Blood cultures grew a gram-positive cocci in clusters on blood agar; colonies show a yellow pigment, and the organism is positive on mannitol/salt agar. The organism is catalase and coagulase positive. Which of the following is the most likely pathogen?

Q54Medium

Which of the following is NOT seen in acute HIV syndrome?

Q55Medium

What is true about Tuberculosis in HIV patients?

Q56Easy

Full blown immunodeficiency syndrome is characterized by?

Q57Medium

Which antifungal medication is safe in patients with both renal failure and hepatic failure?

Q58Medium

Which of the following is NOT a metastatic complication of gonococci?

Q59Medium

Which of the following is NOT essential when managing a febrile neutropenic patient?

Q60Easy

Fulminant Hepatitis E is typically seen in which demographic group?

Infectious Diseases Indian Medical PG Practice Questions and MCQs

Question 51: Ileocecal tuberculosis presents with all the following findings except:

A. Rapid emptying of narrowed terminal ileum
B. Inverted umbrella sign
C. Stellate ulcer with elevated margins
D. Longitudinal ulcers are more common (Correct Answer)

Explanation: Explanation: In **Ileocecal Tuberculosis**, the characteristic pathological finding is **transverse (circumferential) ulcers**, not longitudinal ones. This occurs because the tubercle bacilli travel via the lymphatics, which are arranged circumferentially around the bowel wall. As these transverse ulcers heal, they often lead to significant fibrosis and stricture formation. * **Why Option D is the correct answer (False statement):** Longitudinal ulcers are the hallmark of **Crohn’s Disease**, not Tuberculosis. In Crohn’s, ulcers follow the long axis of the bowel, often leading to a "cobblestone" appearance. * **Option A (Rapid emptying):** Known as **Stierlin’s Sign**, this is a classic radiological finding where the inflamed, irritable terminal ileum empties rapidly into the cecum, appearing narrow or empty on a barium meal. * **Option B (Inverted umbrella sign):** Also called the **Fleischner sign**, this refers to the thickening of the ileocecal valve and narrowing of the terminal ileum, giving the appearance of an inverted umbrella or a "T-shaped" junction. * **Option C (Stellate ulcers):** Early tubercular lesions present as small, stellate (star-shaped) ulcers with elevated, shaggy margins due to lymphoid hyperplasia in Peyer's patches. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Ileocecal region (due to high density of lymphoid tissue and physiological stasis). * **Sterling Sign:** Rapid emptying of the terminal ileum. * **Goose-neck deformity:** Shortening and straightening of the terminal ileum. * **Conical Cecum:** Fibrosis causing the cecum to become shrunken and pulled up. * **Differential Diagnosis:** Always differentiate from Crohn’s Disease (Longitudinal ulcers, transmural involvement, non-caseating granulomas).

Question 52: Which of the following is a feature of Giardiasis?

A. Malabsorption (Correct Answer)
B. Cyst with 4 nuclei
C. Trophozoite with four nuclei
D. Common in hypogammaglobulinemia

Explanation: **Explanation:** **Giardiasis**, caused by the flagellated protozoan *Giardia lamblia* (also known as *G. duodenalis* or *G. intestinalis*), primarily affects the proximal small intestine (duodenum and jejunum) [1]. 1. **Why Malabsorption is Correct:** *Giardia* trophozoites attach to the intestinal villi using a ventral sucking disc [1]. This leads to **villous atrophy**, blunting of microvilli, and damage to the brush border. This mechanical and inflammatory disruption results in **malabsorption** [3], particularly of fats (leading to foul-smelling, greasy **steatorrhea**) and fat-soluble vitamins. It also causes secondary lactose intolerance due to disaccharidase deficiency [2]. 2. **Analysis of Other Options:** * **B & C (Cyst vs. Trophozoite nuclei):** This is a common point of confusion. The **Cyst** (infective stage) is oval and contains **4 nuclei** when mature. The **Trophozoite** (pathogenic stage) is pear-shaped and contains **2 nuclei** (giving it a characteristic "owl’s eye" appearance). Therefore, Option B is technically a feature, but in the context of clinical pathology and NEET-PG patterns, Malabsorption is the hallmark functional consequence. * **D (Hypogammaglobulinemia):** While *Giardia* is indeed more common and severe in patients with **Common Variable Immunodeficiency (CVID)** or IgA deficiency [1], the option as phrased is a predisposing condition rather than a "feature" of the disease itself. **High-Yield Clinical Pearls for NEET-PG:** * **Transmission:** Fecal-oral route; often associated with contaminated water (hikers/campers) or daycare centers [1]. * **Diagnosis:** Stool microscopy (cysts/trophozoites) or **String Test (Entero-test)**. * **Morphology:** Trophozoites have 4 pairs of flagella and a "falling leaf" motility. * **Treatment:** Drug of choice is **Tinidazole** (single dose) or Metronidazole. Nitazoxanide is an alternative.

Question 53: A young butcher cuts his forearm with a knife. Over the next week, he notices swelling, redness, and warmth at the site. Four days later, he presents to the emergency department with fever, shaking chills, and severe lower back pain. Physical examination reveals a temperature of 39.4 C (102.9 F), swelling in his forearm with an area of central softness, and tenderness to pressure over his lower spine. Laboratory data show a leukocyte count of 14,000/mm3 with 81% polymorphonuclear leukocytes. Blood cultures grew a gram-positive cocci in clusters on blood agar; colonies show a yellow pigment, and the organism is positive on mannitol/salt agar. The organism is catalase and coagulase positive. Which of the following is the most likely pathogen?

A. Bacteroides fragilis
B. Clostridium perfringens
C. Escherichia coli
D. Staphylococcus aureus (Correct Answer)

Explanation: ### Explanation **1. Why Staphylococcus aureus is Correct:** The clinical presentation describes a classic case of **Staphylococcus aureus** skin and soft tissue infection (SSTI) leading to hematogenous spread [1]. The patient’s occupation (butcher) increases the risk of skin trauma. The subsequent development of fever, chills, and spinal tenderness suggests **vertebral osteomyelitis** via hematogenous seeding [1]. The laboratory findings are definitive for *S. aureus*: * **Morphology:** Gram-positive cocci in clusters. * **Biochemical tests:** Catalase positive (differentiates from Streptococcus) and **Coagulase positive** (differentiates from Coagulase-negative Staphylococci like *S. epidermidis*) [1]. * **Culture:** Yellow pigment (hence the name *aureus*) and growth on **Mannitol Salt Agar (MSA)**, where it ferments mannitol to produce yellow colonies. **2. Why the Other Options are Incorrect:** * **Bacteroides fragilis (A):** An anaerobic Gram-negative rod, typically associated with intra-abdominal infections, not primary skin trauma in a butcher. * **Clostridium perfringens (B):** An anaerobic Gram-positive rod that causes gas gangrene (crepitus on exam). It does not present as cocci in clusters or grow on MSA. * **Escherichia coli (C):** A Gram-negative rod. While it can cause osteomyelitis (especially post-UTI), it would not be catalase/coagulase positive or show the described Gram stain morphology. **3. Clinical Pearls for NEET-PG:** * **S. aureus** is the most common cause of **acute osteomyelitis** and **pyogenic spinal infections** in adults. * **Mannitol Salt Agar** is both selective (high salt inhibits most bacteria) and differential (only *S. aureus* ferments mannitol) for this pathogen. * In intravenous drug users (IVDU), *S. aureus* is the most common cause of **tricuspid valve endocarditis**, which can also lead to hematogenous seeding of the spine [1].

Question 54: Which of the following is NOT seen in acute HIV syndrome?

A. Pneumonia (Correct Answer)
B. Lymphadenopathy
C. Myelopathy
D. Encephalitis

Explanation: Explanation: Acute HIV Syndrome (Acute Retroviral Syndrome) occurs 2 to 4 weeks after initial infection, representing a burst of viral replication and a robust host immune response. It typically presents as a mononucleosis-like illness [1]. Why Option A (Pneumonia) is the correct answer: Pneumonia is **not** a feature of Acute HIV Syndrome. Pneumonia in HIV patients (such as *Pneumocystis jirovecii* or bacterial pneumonia) is an **opportunistic infection** that typically occurs during the advanced stage (AIDS), when the CD4+ T-cell count has significantly declined (usually <200 cells/µL) [1]. In the acute phase, the immune system is still relatively intact despite a transient dip in CD4 counts. Why the other options are incorrect: * **B. Lymphadenopathy:** This is one of the most common findings (seen in >70% of cases), typically involving the axillary, cervical, and occipital nodes [1]. * **C & D. Myelopathy and Encephalitis:** Neurological manifestations occur in about 10–15% of patients during the acute phase. These include aseptic meningitis, encephalitis, peripheral neuropathy, and transverse myelopathy, caused by the direct neurotropic nature of the virus during primary seeding [1]. High-Yield Clinical Pearls for NEET-PG: * **Most common symptom:** Fever (96%), followed by lymphadenopathy and pharyngitis [1]. * **Dermatological finding:** A maculopapular rash involving the trunk and face is characteristic [1]. * **Laboratory findings:** High viral load (HIV-RNA), negative or indeterminate ELISA/Western Blot (the "window period"), and a high CD8+ T-cell count. * **Diagnosis:** Best confirmed by **HIV-RNA levels (NAT)** or **p24 antigen assay**.

Question 55: What is true about Tuberculosis in HIV patients?

A. Increased sputum positivity (Correct Answer)
B. INH prophylaxis prevents the development of Tuberculosis
C. Lack characteristic features of Tuberculosis
D. Highly positive PPD reaction

Explanation: Explanation: Tuberculosis (TB) is the most common opportunistic infection in HIV patients [1]. The clinical presentation depends heavily on the patient's immune status (CD4 count) [1]. Why Option A is Correct: In HIV-infected individuals, there is a higher risk of cavitary disease during the early stages of HIV (when immunity is relatively preserved) [1]. Cavitary lesions contain high bacterial loads, leading to increased sputum positivity. Even in advanced stages, while atypical features occur, sputum smear and molecular tests (CBNAAT) remain the primary diagnostic tools, though sensitivity may decrease as CD4 counts drop. Why the other options are Incorrect: * Option B: While Isoniazid Preventive Therapy (IPT) significantly reduces the risk of active TB, it does not guarantee prevention [2]. It reduces the risk by about 33–60%, but the risk of reactivation or new infection remains higher than in the general population. * Option C: HIV patients do not "lack" features; rather, they present with atypical features [1]. As CD4 counts fall (<200 cells/µL), classic apical cavitary lesions are replaced by lower lobe infiltrates, hilar lymphadenopathy, and a higher incidence of extrapulmonary and disseminated TB (e.g., miliary TB) [1]. * Option D: HIV patients often show a diminished or negative PPD (Mantoux) reaction due to anergy (loss of delayed-type hypersensitivity). In HIV patients, an induration of ≥5 mm is considered positive, unlike the 10 mm threshold for the general population [2]. High-Yield Clinical Pearls for NEET-PG: * Most common extrapulmonary site in HIV: Lymph nodes (TB Lymphadenitis). * IRIS (Immune Reconstitution Inflammatory Syndrome): A paradoxical worsening of TB symptoms after starting ART. * Treatment: Rifampicin-based regimens are standard, but watch for drug-drug interactions with Protease Inhibitors (PIs). Use Rifabutin as an alternative if necessary. * Diagnosis: CBNAAT (GeneXpert) is the preferred initial diagnostic test for TB in HIV patients.

Question 56: Full blown immunodeficiency syndrome is characterized by?

A. High viral titres with low CD4 count (Correct Answer)
B. Low viral titres with low CD4 count
C. High viral titres with high CD4 count
D. High CD4 and high CD8 count

Explanation: **Explanation:** The progression of HIV infection to **Full-blown AIDS (Stage 3)** is defined by the catastrophic failure of the cell-mediated immune system. The hallmark of this stage is the inverse relationship between viral replication and immune competence [1]. **1. Why Option A is Correct:** In the advanced stage of the disease, the virus undergoes rapid, unchecked replication because the body’s immune surveillance is exhausted. This leads to **high viral titers** (high viral load) [1]. Concurrently, HIV selectively infects and destroys T-helper cells via the gp120-CD4 interaction, resulting in a **profoundly low CD4 count**, typically <200 cells/mm³ [1]. This combination creates the "window of vulnerability" for opportunistic infections and malignancies. **2. Why the other options are incorrect:** * **Option B:** Low viral titers are seen during the "Clinical Latency" phase (where the immune system partially controls the virus) or in patients on successful ART. * **Option C:** High CD4 counts are found in the early stages of infection or in healthy individuals; they are never characteristic of immunodeficiency [1]. * **Option D:** In AIDS, both CD4 and CD8 counts eventually decline, though the CD4 drop is more pathognomonic. A high CD8 count is often seen during the acute seroconversion phase as the body attempts to fight the initial viremia. **NEET-PG High-Yield Pearls:** * **Normal CD4/CD8 Ratio:** 2:1. In AIDS, this ratio is **inverted** (<1:1). * **Indicator of Prognosis:** Viral load (RNA levels) is the best predictor of disease progression. * **Indicator of Immune Status:** CD4+ T-cell count is the best indicator of immediate risk for opportunistic infections [1]. * **AIDS Definition:** CD4 count **<200 cells/mm³** or the presence of an AIDS-defining illness (e.g., Esophageal Candidiasis, PCP pneumonia, Kaposi Sarcoma) [1].

Question 57: Which antifungal medication is safe in patients with both renal failure and hepatic failure?

A. Amphotericin B
B. Caspofungin
C. Micafungin
D. Anidulafungin (Correct Answer)

Explanation: **Explanation:** The correct answer is **Anidulafungin**. The underlying medical concept is its unique metabolic pathway, which makes it the safest echinocandin (and antifungal) in the setting of multi-organ failure. **1. Why Anidulafungin is correct:** Anidulafungin undergoes **slow chemical degradation** in the plasma (spontaneous hydrolysis) rather than being metabolized by the liver or excreted by the kidneys. Because it does not rely on the cytochrome P450 system or renal clearance, its half-life remains unchanged in patients with any degree of hepatic or renal impairment. No dose adjustment is required for either condition. **2. Why the other options are incorrect:** * **Amphotericin B:** Highly **nephrotoxic**. It causes renal vasoconstriction and direct tubular damage, making it contraindicated or requiring extreme caution in renal failure. * **Caspofungin:** It undergoes hepatic metabolism. While safe in renal failure, it **requires dose reduction** in patients with moderate-to-severe hepatic impairment (Child-Pugh Class B and C). * **Micafungin:** Like Caspofungin, it is metabolized by the liver. Although it requires less frequent dose adjustments than Caspofungin, it is still primarily cleared hepatically, making Anidulafungin the superior choice for combined failure. **High-Yield Clinical Pearls for NEET-PG:** * **Echinocandins Mechanism:** Inhibit **1,3-beta-D-glucan synthase**, disrupting the fungal cell wall. * **Drug of Choice:** Echinocandins are the first-line treatment for invasive Candidiasis and Candidemia [1]. * **Anidulafungin "Unique Selling Point":** It has **zero** significant drug-drug interactions because it bypasses the CYP450 system entirely. * **Amphotericin B Toxicity:** To reduce nephrotoxicity, use **Liposomal Amphotericin B** or pre-infusion saline loading.

Question 58: Which of the following is NOT a metastatic complication of gonococci?

A. Endocarditis
B. Meningitis
C. Nephritis (Correct Answer)
D. Arthritis

Explanation: **Explanation:** Disseminated Gonococcal Infection (DGI) occurs when *Neisseria gonorrhoeae* spreads hematogenously from a primary mucosal site (e.g., endocervix, urethra, or pharynx). This leads to "metastatic" complications where the bacteria seed distant organs. **Why Nephritis is the correct answer:** Nephritis is **not** a recognized metastatic complication of gonococci. While *N. gonorrhoeae* can cause local genitourinary inflammation, it does not typically seed the renal parenchyma or cause glomerulonephritis. In contrast, other Neisseria species or post-streptococcal sequelae are associated with renal pathology, but not the gonococcus. **Analysis of Incorrect Options:** * **Arthritis:** This is the most common manifestation of DGI. It typically presents in two forms: a triad of tenosynovitis, dermatitis, and polyarthralgia, or a purulent monoarticular septic arthritis. * **Endocarditis:** Though rare (<1% of DGI cases), gonococcal endocarditis is a classic metastatic complication. It often affects the aortic valve and can be rapidly destructive if not treated aggressively. * **Meningitis:** Another rare but documented metastatic complication resulting from the hematogenous spread of the bacteria to the central nervous system. **NEET-PG High-Yield Pearls:** * **DGI Triad:** Tenosynovitis, Dermatitis (painless maculopapular or pustular lesions), and Polyarthralgia. * **Risk Factor:** Patients with **deficiencies in late complement components (C5–C9)** are at a significantly higher risk for disseminated gonococcal and meningococcal infections. * **Diagnosis:** Synovial fluid cultures are positive in less than 50% of cases; mucosal swabs (NAAT) often provide the diagnosis. * **Treatment:** Ceftriaxone (1g IV/IM) is the drug of choice for DGI.

Question 59: Which of the following is NOT essential when managing a febrile neutropenic patient?

A. Repeated hand washing by hospital personnel
B. White cell infusion (Correct Answer)
C. Prophylactic antibiotics
D. Colony-stimulating factor for macrophages

Explanation: **Explanation:** **Febrile Neutropenia** is a medical emergency defined as a single oral temperature of >38.3°C (101°F) or >38.0°C (100.4°F) sustained over one hour in a patient with an Absolute Neutrophil Count (ANC) <500 cells/microL [1]. **Why White Cell Infusion is NOT essential:** Granulocyte (white cell) transfusions are **not** a standard or essential part of management. While theoretically beneficial, clinical trials have failed to show a significant survival benefit. They are associated with severe adverse effects, including pulmonary toxicity (TRALI), alloimmunization, and transmission of CMV [3]. They are reserved only as a "last resort" for patients with profound neutropenia and life-threatening infections not responding to optimal antimicrobial therapy. **Analysis of Incorrect Options:** * **Repeated hand washing:** This is the **most effective** way to prevent nosocomial transmission of pathogens. Since most infections in neutropenic patients arise from colonizing flora or healthcare workers, strict hand hygiene is mandatory. * **Prophylactic antibiotics:** Immediate empirical administration of broad-spectrum bactericidal antibiotics (e.g., Piperacillin-Tazobactam or Carbapenems) is the cornerstone of management to prevent rapid clinical deterioration and sepsis. * **Colony-stimulating factors (G-CSF/GM-CSF):** These are used to reduce the duration and severity of neutropenia. While not always mandatory for every patient, they are essential components of management protocols to accelerate myeloid recovery. **NEET-PG High-Yield Pearls:** * **MASCC Score:** Used to identify low-risk patients who can be managed with oral antibiotics (Ciprofloxacin + Amoxicillin-Clavulanate) as outpatients. * **Initial Choice:** Monotherapy with an anti-pseudomonal beta-lactam (Cefepime, Meropenem, or Pip-Taz) is the standard first-line treatment. * **Vancomycin:** Not routinely included unless there is suspicion of catheter-related infection, skin/soft tissue infection, or hemodynamic instability [2].

Question 60: Fulminant Hepatitis E is typically seen in which demographic group?

A. Pregnant women (Correct Answer)
B. Infants
C. Adolescents
D. Malnourished males

Explanation: **Explanation:** Hepatitis E Virus (HEV) is a single-stranded RNA virus primarily transmitted via the fecal-oral route. While it usually causes a self-limiting illness in the general population, it is notorious for causing **Fulminant Hepatic Failure (FHF)** in **pregnant women**, particularly during the second and third trimesters. **1. Why Pregnant Women?** The mortality rate for HEV in the general population is low (0.5–4%), but in pregnant women, it skyrockets to **15–25%**. The exact pathogenesis is multifactorial, involving a shift in the Th1/Th2 cytokine balance, high levels of progesterone and estrogen (which may promote viral replication), and a diminished cell-mediated immune response. This leads to rapid hepatic necrosis and liver failure. **2. Analysis of Incorrect Options:** * **Infants:** While infants can contract HEV, they do not show a specific predisposition to fulminant failure compared to the high-risk profile of pregnancy. * **Adolescents:** In this age group, HEV is typically subclinical or presents as a mild, self-limiting icteric hepatitis. * **Malnourished males:** While malnutrition can worsen the prognosis of any infectious disease, there is no specific epidemiological link between malnourishment in males and the fulminant presentation of HEV. **3. NEET-PG High-Yield Pearls:** * **Virus Family:** Hepeviridae (Non-enveloped RNA virus). * **Genotypes:** Genotypes 1 and 2 are associated with waterborne epidemics in humans; Genotypes 3 and 4 are zoonotic (pork/deer meat). * **Chronic HEV:** Can occur in **immunocompromised** patients (e.g., organ transplant recipients), usually associated with Genotype 3. * **Extra-hepatic manifestations:** Guillain-Barré syndrome and Neuralgic amyotrophy. * **Prophylaxis:** The Hecolin vaccine is available in some countries (China) but not yet globally widespread.

Practice by Chapter

Principles of Antimicrobial Therapy

Practice Questions

Fever of Unknown Origin

Practice Questions

HIV/AIDS and Related Infections

Practice Questions

Tuberculosis and Mycobacterial Diseases

Practice Questions

Tropical and Parasitic Infections

Practice Questions

Viral Infections (Hepatitis, Herpes, etc.)

Practice Questions

Healthcare-Associated Infections

Practice Questions

Fungal Infections

Practice Questions

Sepsis and Septic Shock

Practice Questions

Infection in Immunocompromised Hosts

Practice Questions

Emerging and Re-emerging Infections

Practice Questions

Antimicrobial Resistance

Practice Questions

Vaccination Principles

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free