Immunology and Allergies — MCQs

A 9-year-old male child presented with a history of spiking fevers from the last 2 months, which have been as high as 104°F. On examination, he has spindle-shaped swelling of multiple finger joints and complains of upper sternal pain. When he had fever, his mother noticed a salmon-colored rash that resolves with the resolution of the fever. He had no conjunctivitis or any oral ulcers, but his heart sounds are muffled and he has pulsus paradoxus. Which of the following is the most likely diagnosis?

Q39Easy

Which one of the following is not a feature of DiGeorge syndrome?

Q40Medium

An 8-month-old boy is evaluated because of repeated episodes of pneumococcal pneumonia. Serum studies demonstrate very low levels of IgM, IgG, and IgA. This patient's condition is related to a deficiency of which of the following proteins?

Immunology and Allergies Indian Medical PG Practice Questions and MCQs

Question 31: A 3-year-old child presents with recurrent pneumonia, eczema, and thrombocytopenia. Which protein synthesis is abnormal in this child?

A. Wiskott-Aldrich syndrome protein (WASp) (Correct Answer)
B. Hamartin
C. Adenosine deaminase
D. HLA-A1

Explanation: ### Explanation The clinical triad of **recurrent infections (pneumonia), eczema, and thrombocytopenia** (classically with small-sized platelets) is the hallmark presentation of **Wiskott-Aldrich Syndrome (WAS)**. **1. Why the Correct Answer is Right:** Wiskott-Aldrich Syndrome is an **X-linked recessive** primary immunodeficiency caused by mutations in the **WAS gene**, which encodes the **Wiskott-Aldrich Syndrome protein (WASp)**. WASp is expressed exclusively in hematopoietic cells and is crucial for **actin cytoskeleton remodeling**. Defective WASp leads to: * **Thrombocytopenia:** Defective proplatelet formation and increased splenic clearance (microthrombocytes). * **Immunodeficiency:** Impaired T-cell function and defective migration of immune cells, leading to recurrent sinopulmonary infections. * **Eczema:** Likely due to immune dysregulation. **2. Why the Incorrect Options are Wrong:** * **Hamartin:** This protein (encoded by *TSC1*) is associated with **Tuberous Sclerosis**, characterized by seizures, mental retardation, and angiofibromas, not immunodeficiency. * **Adenosine deaminase (ADA):** Deficiency of ADA leads to **Severe Combined Immunodeficiency (SCID)**. While it causes recurrent infections, it does not typically present with thrombocytopenia or the specific triad of WAS. * **HLA-A1:** This is a Major Histocompatibility Complex (MHC) Class I molecule. While certain HLA types are associated with autoimmune diseases, they are not the primary cause of this clinical triad. **3. High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked Recessive (mostly affects males). * **Platelet Morphology:** WAS is unique because it features **small platelets** (low Mean Platelet Volume - MPV). * **Laboratory Findings:** Characteristically shows **Low IgM**, Normal/High IgA and IgG, and **High IgE**. * **Complications:** Increased risk of **autoimmune hemolytic anemia** and **B-cell lymphomas**. * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the definitive cure.

Question 32: Uveitis is most commonly associated with which of the following conditions?

A. Rheumatoid arthritis
B. Systemic juvenile idiopathic arthritis
C. Pauciarticular juvenile idiopathic arthritis (Correct Answer)
D. Polyarticular juvenile idiopathic arthritis

Explanation: **Explanation:** The association between Juvenile Idiopathic Arthritis (JIA) and uveitis is a high-yield topic in Pediatrics. Chronic non-granulomatous anterior uveitis (iridocyclitis) is most strongly associated with **Pauciarticular (Oligoarticular) JIA**. **1. Why Pauciarticular JIA is correct:** Pauciarticular JIA involves $\le$ 4 joints during the first 6 months of disease. It carries the highest risk for uveitis, especially in patients who are **ANA (Antinuclear Antibody) positive**. The uveitis is typically asymptomatic and "white," meaning it lacks the classic red-eye presentation, making regular slit-lamp examinations mandatory to prevent blindness. **2. Analysis of Incorrect Options:** * **Rheumatoid Arthritis (RA):** While RA in adults is associated with episcleritis and scleritis, it is rarely associated with anterior uveitis. * **Systemic JIA (Still’s Disease):** This subtype is characterized by high-grade fever, evanescent rash, and hepatosplenomegaly. Interestingly, uveitis is **extremely rare** in the systemic form. * **Polyarticular JIA:** This involves $\ge$ 5 joints. While uveitis can occur in this subtype, the incidence is significantly lower (approx. 5-10%) compared to the Pauciarticular subtype (approx. 20%). **Clinical Pearls for NEET-PG:** * **Risk Factors for Uveitis in JIA:** Pauciarticular onset, Female gender, and **ANA positivity** (the strongest predictor). * **Screening:** ANA-positive Pauciarticular JIA patients require slit-lamp exams every 3 months. * **Treatment:** First-line treatment for JIA-associated uveitis includes topical steroids and cycloplegics; Methotrexate is the preferred systemic DMARD for refractory cases. * **HLA Association:** Pauciarticular JIA is often associated with HLA-DR8, DR5, and DRw52.

Question 33: What is the most common cause of liver abscess in chronic granulomatous disease?

A. Klebsiella
B. Staphylococcus aureus (Correct Answer)
C. Peptostreptococcus
D. E.coli

Explanation: **Explanation:** **Chronic Granulomatous Disease (CGD)** is a primary immunodeficiency caused by a defect in the **NADPH oxidase enzyme complex**. This defect prevents phagocytes (neutrophils and macrophages) from generating a "respiratory burst" (superoxide radicals), rendering them unable to kill **catalase-positive organisms**. **Why Staphylococcus aureus is correct:** *S. aureus* is the most common cause of liver abscesses in CGD patients. Because *S. aureus* is catalase-positive, it neutralizes the small amount of hydrogen peroxide it produces. In CGD, since the host cannot produce its own reactive oxygen species, the bacteria survive and multiply within phagocytes, leading to granuloma formation and abscesses. Liver abscesses in CGD are often "cold" (lacking classic systemic inflammatory signs) and require prolonged treatment. **Why the other options are incorrect:** * **A. Klebsiella:** While it is a catalase-positive Gram-negative rod and can cause infections in CGD, it is less frequent than *S. aureus* for hepatic involvement. * **C. Peptostreptococcus:** This is an anaerobe. Anaerobes are generally not the primary pathogens in CGD because they do not produce catalase and are usually handled by other immune mechanisms. * **D. E. coli:** Although catalase-positive, *E. coli* is a more common cause of liver abscesses in the *general population* (often via biliary sources), but not specifically the hallmark pathogen for CGD. **NEET-PG High-Yield Pearls:** * **Inheritance:** Most common is **X-linked recessive** (CYBB gene mutation). * **Pathogens to remember:** *S. aureus*, *Burkholderia cepacia* (most common cause of death), *Serratia marcescens*, *Nocardia*, and *Aspergillus*. * **Diagnostic Test:** **Dihydrorhodamine (DHR) 123 flow cytometry** (Gold Standard) or the Nitroblue Tetrazolium (NBT) slide test (shows no blue color). * **Prophylaxis:** Trimethoprim-sulfamethoxazole and Itraconazole; Interferon-gamma is used for severe cases.

Question 34: A child with agammaglobulinemia presents with respiratory tract infection and diarrhea. What is the most likely infectious agent?

A. Cocksackie virus
B. Rotavirus (Correct Answer)
C. Shigella
D. None of the above

Explanation: **Explanation:** In patients with **X-linked Agammaglobulinemia (Bruton’s)**, there is a profound deficiency of B-cells and all classes of immunoglobulins (IgG, IgA, IgM). The lack of **Secretory IgA** at mucosal surfaces makes these children highly susceptible to specific gastrointestinal and respiratory pathogens. 1. **Why Rotavirus is correct:** While these patients are classically associated with *Giardia lamblia* (due to lack of IgA), **Rotavirus** is the most common viral cause of severe diarrhea in children with agammaglobulinemia. In the absence of neutralizing antibodies, viral clearance is impaired, leading to prolonged and severe gastroenteritis. 2. **Why other options are incorrect:** * **Coxsackievirus:** While patients with agammaglobulinemia are uniquely susceptible to **Enteroviruses** (like Polio, Echovirus, and Coxsackie), these typically manifest as chronic progressive **meningoencephalitis** or dermatomyositis-like syndromes rather than isolated diarrhea. * **Shigella:** This is an invasive bacterial pathogen. While humoral immunity plays a role, the primary defect in agammaglobulinemia predisposes more significantly to encapsulated bacteria (like *S. pneumoniae* and *H. influenzae*) and specific protozoa/viruses rather than typical bacillary dysentery. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Absent B-cells (CD19/20+), absent tonsils/lymph nodes, and recurrent pyogenic infections after 6 months of age (once maternal IgG wanes). * **Most common GI parasite:** *Giardia lamblia*. * **Most common CNS complication:** Chronic Enteroviral Encephalitis. * **Contraindication:** Live vaccines (OPV, Rotavirus vaccine, MMR) are strictly contraindicated. * **Treatment:** Intravenous Immunoglobulin (IVIG) replacement.

Question 35: What is the age criterion for Juvenile Rheumatoid Arthritis (JRA)?

A. Less than 10 years
B. Less than 12 years
C. Less than 14 years
D. Less than 16 years (Correct Answer)

Explanation: ### Explanation **Juvenile Idiopathic Arthritis (JIA)**, formerly known as Juvenile Rheumatoid Arthritis (JRA), is the most common chronic rheumatic disease of childhood. According to the International League of Associations for Rheumatology (ILAR) and the American College of Rheumatology (ACR), the diagnosis requires the onset of persistent arthritis in one or more joints for at least **6 weeks** in a child **less than 16 years of age**, after excluding other known conditions (e.g., trauma, infection, malignancy). **Why Option D is Correct:** The age cutoff of 16 years is the standard clinical definition used to differentiate pediatric inflammatory arthritides from adult-onset Rheumatoid Arthritis. This distinction is crucial because the clinical presentation, genetic associations (HLA types), and prognosis in children differ significantly from adults. **Why Other Options are Incorrect:** * **Options A, B, and C:** While JIA can certainly manifest at ages 10, 12, or 14, these are not the upper age limits for the diagnostic criteria. Setting the limit too low would misclassify adolescents (aged 14–15) who present with the same pediatric-specific pathophysiology. **High-Yield Clinical Pearls for NEET-PG:** * **Subtypes:** The most common subtype is **Oligoarticular JIA** (involving ≤4 joints), which carries a high risk of **asymptomatic chronic anterior uveitis**. * **Systemic JIA (Still’s Disease):** Characterized by daily "quotidian" fevers, evanescent salmon-pink rashes, and hepatosplenomegaly. It is often associated with **Macrophage Activation Syndrome (MAS)**. * **Markers:** Rheumatoid Factor (RF) is usually negative in children (only 5-10% are RF positive). **ANA positivity** is a strong predictor for the development of uveitis. * **First-line Treatment:** NSAIDs are the initial therapy; Methotrexate is the most common DMARD used for persistent disease.

Question 36: A two-year-old male child completed an 8-day course of cefaclor. He then developed low-grade fever, malaise, lymphadenopathy, irritability, and a generalized erythematous rash that is mildly pruritic. What is the most probable diagnosis?

A. Kawasaki disease
B. Partially treated meningitis
C. IMN
D. Type 3 hypersensitivity (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Type 3 Hypersensitivity (Serum Sickness-Like Reaction)** The clinical presentation describes a classic **Serum Sickness-Like Reaction (SSLR)**, which is a **Type 3 Hypersensitivity** reaction. * **Mechanism:** It involves the formation of immune complexes (antigen-antibody) that deposit in small blood vessels, activating the complement cascade and leading to systemic inflammation. * **Trigger:** Cefaclor is the most common antibiotic associated with SSLR in children. * **Clinical Features:** Typically occurs 7–21 days after drug exposure (or sooner if previously sensitized). It is characterized by the triad of **fever, rash (urticarial or multiforme-like), and polyarthralgia/arthritis**, often accompanied by lymphadenopathy and malaise. **Why other options are incorrect:** * **A. Kawasaki Disease:** While it presents with fever and rash, it typically requires high-grade fever for ≥5 days plus specific criteria like conjunctivitis, strawberry tongue, and extremity changes, which are absent here. * **B. Partially Treated Meningitis:** This would present with signs of meningeal irritation (neck stiffness, bulging fontanelle) and a more toxic appearance, rather than a generalized pruritic rash and lymphadenopathy following a completed antibiotic course. * **C. IMN (Infectious Mononucleosis):** While it causes fever, rash (especially after amoxicillin), and lymphadenopathy, the specific temporal relationship with **Cefaclor** and the nature of the irritability/malaise point more strongly toward a drug-induced hypersensitivity. **NEET-PG High-Yield Pearls:** * **Cefaclor** is the "classic" board-exam trigger for SSLR in pediatrics. * Unlike true Serum Sickness, SSLR does **not** typically involve immune complex-mediated nephritis or vasculitis. * **Treatment:** Withdrawal of the offending drug and supportive care (antihistamines/NSAIDs). Steroids are reserved for severe cases. * **Type 3 Hypersensitivity Examples:** SLE, Post-streptococcal glomerulonephritis (PSGN), and Arthus reaction.

Question 37: Which one of the following vaccines is contraindicated in children with egg allergy?

A. MMR
B. Yellow Fever (Correct Answer)
C. DPT
D. BCG

Explanation: **Explanation:** The correct answer is **Yellow Fever**. The underlying medical concept relates to the manufacturing process of vaccines. Certain vaccines are cultured in **embryonated chicken eggs** or chick embryo cell cultures. During the purification process, trace amounts of egg proteins (specifically **ovalbumin**) may remain in the final product, potentially triggering an anaphylactic reaction in sensitized individuals. **Why Yellow Fever is the correct answer:** The Yellow Fever vaccine is grown directly in chicken embryos. It contains a higher concentration of egg protein compared to other vaccines, making it strictly contraindicated in individuals with a history of severe egg allergy (anaphylaxis). **Analysis of Incorrect Options:** * **MMR (Measles, Mumps, Rubella):** Although the Measles and Mumps components are grown in chick embryo fibroblast cultures, the amount of egg protein is negligible. Large-scale studies have proven that MMR is **safe** for children with egg allergies, and it can be administered in a routine primary care setting. * **DPT (Diphtheria, Pertussis, Tetanus):** This is a toxoid/subunit vaccine produced using synthetic media; it contains no egg protein. * **BCG (Bacillus Calmette–Guérin):** This is a live attenuated bacterial vaccine (derived from *Mycobacterium bovis*) and does not involve egg-based cultivation. **High-Yield Clinical Pearls for NEET-PG:** * **Egg-containing vaccines:** Yellow Fever and Influenza (most formulations) are the primary concerns. * **Influenza Vaccine:** Most children with egg allergy can now receive the inactivated influenza vaccine (IIV) in a standard medical setting, but Yellow Fever remains the most "high-risk" in exams. * **Rabies Vaccine:** The Chick Embryo Cell Vaccine (PCECV) should be used with caution in egg-allergic patients; Human Diploid Cell Vaccine (HDCV) is the preferred alternative.

Question 38: A 9-year-old male child presented with a history of spiking fevers from the last 2 months, which have been as high as 104°F. On examination, he has spindle-shaped swelling of multiple finger joints and complains of upper sternal pain. When he had fever, his mother noticed a salmon-colored rash that resolves with the resolution of the fever. He had no conjunctivitis or any oral ulcers, but his heart sounds are muffled and he has pulsus paradoxus. Which of the following is the most likely diagnosis?

A. Toxic synovitis
B. Juvenile idiopathic arthritis (Correct Answer)
C. Rheumatic fever
D. Septic arthritis

Explanation: The clinical presentation is classic for **Systemic Juvenile Idiopathic Arthritis (sJIA)**, formerly known as Still’s disease. ### **Why Option B is Correct** The diagnosis is based on the following pathognomonic features: * **Quotidian Fever:** High-grade spiking fevers (up to 104°F) that return to baseline daily for at least 2 weeks. * **Evanescent Rash:** A characteristic salmon-pink, non-pruritic, macular rash that appears during fever spikes and disappears as the temperature drops. * **Arthritis:** Spindle-shaped swelling of the proximal interphalangeal (PIP) joints is a hallmark of small joint involvement in JIA. * **Extra-articular Involvement:** Upper sternal pain suggests **manubriosternal arthritis**, while muffled heart sounds and pulsus paradoxus indicate **pericarditis with effusion**, a known life-threatening complication of sJIA. ### **Why Other Options are Incorrect** * **A. Toxic Synovitis:** Usually follows a viral URI, typically affects the hip joint in younger children (3–6 years), and lacks systemic features like high fever or pericarditis. * **C. Rheumatic Fever:** While it presents with fever and carditis, the arthritis is typically **migratory** and affects large joints. The rash (Erythema marginatum) is persistent and has serpiginous borders, unlike the evanescent rash of sJIA. * **D. Septic Arthritis:** Usually presents as acute monoarthritis (single joint) with localized signs of inflammation and high fever, but does not cause a salmon-colored rash or pericardial effusion. ### **High-Yield Pearls for NEET-PG** * **Diagnosis of sJIA:** Requires arthritis in $\ge$1 joint with or preceded by fever of $\ge$2 weeks (daily/quotidian for 3 days) plus one of: evanescent rash, generalized lymphadenopathy, hepatosplenomegaly, or serositis. * **Laboratory:** Characterized by marked leukocytosis, thrombocytosis, and very high ESR/CRP. **Ferritin** is often massively elevated. * **Complication:** Watch for **Macrophage Activation Syndrome (MAS)**, a severe complication characterized by cytopenias and falling ESR.

Question 39: Which one of the following is not a feature of DiGeorge syndrome?

A. Congenital heart defects
B. Abnormalities of palate
C. Hypocalcemia
D. Rocker bottom feet (Correct Answer)

Explanation: **Explanation:** DiGeorge syndrome (22q11.2 deletion syndrome) is a primary immunodeficiency caused by the abnormal development of the **third and fourth pharyngeal pouches**. This results in a classic constellation of symptoms often remembered by the mnemonic **CATCH-22**. **Why "Rocker bottom feet" is the correct answer:** Rocker bottom feet (congenital vertical talus) is a classic dysmorphic feature associated with **Trisomy 18 (Edwards syndrome)** and **Trisomy 13 (Patau syndrome)**, but it is not a characteristic feature of DiGeorge syndrome. **Analysis of incorrect options:** * **A. Congenital heart defects:** These are present in ~75% of cases, most commonly **Conotruncal anomalies** such as Tetralogy of Fallot, Interrupted aortic arch, and Truncus arteriosus. * **B. Abnormalities of palate:** Velopharyngeal insufficiency and **Cleft palate** are common due to the maldevelopment of the pharyngeal arches. * **C. Hypocalcemia:** This occurs due to **Parathyroid hypoplasia/aplasia**. It typically presents as neonatal seizures or tetany in the first few days of life. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic CATCH-22:** **C**ardiac defects, **A**bnormal facies (low-set ears, hypertelorism), **T**hymic hypoplasia (leading to T-cell deficiency/infections), **C**left palate, **H**ypocalcemia, and **22**q11.2 deletion. * **Chest X-ray:** Look for the **absence of a thymic shadow** (also seen in SCID). * **Diagnosis:** Confirmed via **FISH** (Fluorescence In Situ Hybridization) or MLPA. * **Management:** Avoid live vaccines if T-cell count is low; irradiated blood products are preferred to prevent Graft-vs-Host Disease.

Question 40: An 8-month-old boy is evaluated because of repeated episodes of pneumococcal pneumonia. Serum studies demonstrate very low levels of IgM, IgG, and IgA. This patient's condition is related to a deficiency of which of the following proteins?

A. Adenosine deaminase
B. Class III MHC gene
C. Gamma chain of the IL-2 receptor
D. Tyrosine kinase (Correct Answer)

Explanation: **Explanation:** The clinical presentation of an 8-month-old boy with recurrent pyogenic infections (specifically *Streptococcus pneumoniae*) and pan-hypogammaglobulinemia (low IgM, IgG, and IgA) is classic for **X-linked Agammaglobulinemia (XLA)**, also known as Bruton’s Agammaglobulinemia. **1. Why Tyrosine Kinase is Correct:** XLA is caused by a mutation in the **Bruton Tyrosine Kinase (BTK) gene**. This cytoplasmic tyrosine kinase is essential for B-cell signal transduction. Without functional BTK, B-cell precursors (Pre-B cells) in the bone marrow fail to mature into mature B-cells. Consequently, there is a complete absence of B-cells in the peripheral blood, leading to a lack of plasma cells and a failure to produce all classes of antibodies. **2. Why the Incorrect Options are Wrong:** * **Adenosine deaminase (ADA):** Deficiency leads to **SCID** (Autosomal Recessive). It causes the accumulation of toxic metabolites that destroy both B and T lymphocytes. * **Class III MHC gene:** These genes encode components of the complement system (C2, C4) and TNF. Deficiencies do not typically present with pan-hypogammaglobulinemia. * **Gamma chain of the IL-2 receptor:** This is the most common cause of **X-linked SCID**. It results in a lack of T-cells and NK cells, with secondary B-cell dysfunction. **Clinical Pearls for NEET-PG:** * **Age of Onset:** Symptoms typically appear after **6 months** of age, once maternal IgG wanes. * **Physical Exam:** Look for **absent or hypoplastic tonsils** and lymph nodes (due to lack of germinal centers). * **Infections:** Increased susceptibility to encapsulated bacteria (*H. influenzae, S. pneumoniae*) and certain viruses/parasites (Enteroviruses, *Giardia*). * **Diagnosis:** Flow cytometry showing **CD19+ B-cell count <2%**.

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