Infectious Diseases Practice Questions

Q: Ileocecal tuberculosis presents with all the following findings except:

Longitudinal ulcers are more common. 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).

Q: Which of the following is a feature of Giardiasis?

Malabsorption. **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.

Q: 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?

Staphylococcus aureus. ### 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].

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

Pneumonia. 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 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**.

Q: Full blown immunodeficiency syndrome is characterized by?

High viral titres with low CD4 count. **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].

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

Anidulafungin. **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.

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

Nephritis. **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.

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

Pregnant women. **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.

Question 1

Ileocecal tuberculosis presents with all the following findings except:

Accepted Answer

Longitudinal ulcers are more common

Answer

Rapid emptying of narrowed terminal ileum

Answer

Inverted umbrella sign

Answer

Stellate ulcer with elevated margins

Question 2

Which of the following is a feature of Giardiasis?

Accepted Answer

Malabsorption

Answer

Cyst with 4 nuclei

Answer

Trophozoite with four nuclei

Answer

Common in hypogammaglobulinemia

Question 3

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?

Accepted Answer

Staphylococcus aureus

Answer

Bacteroides fragilis

Answer

Clostridium perfringens

Answer

Escherichia coli

Question 4

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

Accepted Answer

Pneumonia

Answer

Lymphadenopathy

Answer

Myelopathy

Answer

Encephalitis

Question 5

What is true about Tuberculosis in HIV patients?

Accepted Answer

Increased sputum positivity

Answer

INH prophylaxis prevents the development of Tuberculosis

Answer

Lack characteristic features of Tuberculosis

Answer

Highly positive PPD reaction

Question 6

Full blown immunodeficiency syndrome is characterized by?

Accepted Answer

High viral titres with low CD4 count

Answer

Low viral titres with low CD4 count

Answer

High viral titres with high CD4 count

Answer

High CD4 and high CD8 count

Question 7

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

Accepted Answer

Anidulafungin

Answer

Amphotericin B

Answer

Caspofungin

Answer

Micafungin

Question 8

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

Accepted Answer

Nephritis

Answer

Endocarditis

Answer

Meningitis

Answer

Arthritis

Question 9

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

Accepted Answer

White cell infusion

Answer

Repeated hand washing by hospital personnel

Answer

Prophylactic antibiotics

Answer

Colony-stimulating factor for macrophages

Question 10

Fulminant Hepatitis E is typically seen in which demographic group?

Accepted Answer

Pregnant women

Answer

Infants

Answer

Adolescents

Answer

Malnourished males

Infectious Diseases — MCQs

Infectious Diseases — MCQs

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