Immunology and Allergies — MCQs
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A previously healthy eight-year-old boy presented to the emergency department with high-grade fever, arthralgia, pruritic erythematous rash, and lymphadenopathy. He had completed 8 days of a 10-day course of cefaclor for an upper respiratory tract infection. Which of the following possibilities should be initially suspected?
In a 5-year-old boy with a history of recurrent pyogenic infections by bacteria with polysaccharide-rich capsules, which of the following investigations should be done?
Which of the following conditions is treated with Intravenous Immunoglobulin (IVIG)?
A patient presents with thrombocytopenia, eczema, and recurrent infections. What is the most probable diagnosis?
All of the following are true about Wiskott-Aldrich syndrome except:
Which of the following are true about Henoch-Schönlein purpura (HSP)?
A 4-month-old boy presented with spontaneous nose bleeds and bloody diarrhea. He has a history of recurrent chest and ear infections, leading to frequent hospitalizations. Examination revealed atopic dermatitis and petechiae all over the body. Laboratory findings suggested abnormally low platelet counts along with eosinophilia. The gene involved in this condition is located on which chromosome?
Wiskott-Aldrich syndrome is characterized by all of the following features except:
A 7-month-old boy has had multiple bouts of otitis media, sinusitis, bronchitis, oral candidiasis, and multiple viral infections. Cessation of the recurrent infections follows successful engraftment of a bone marrow transplant. What is the basis of the clinical improvement?
A full-term baby boy is delivered after an uneventful pregnancy and is well for the first 2 years of his life. He receives all his immunizations without any complications. Starting around his second birthday, the mother begins to note frequent upper respiratory tract infections, and the child is hospitalized three times for pneumonia. Laboratory testing would most likely reveal a deficiency of which of the following immunoglobulins in this child?
Immunology and Allergies Indian Medical PG Practice Questions and MCQs
Question 61: A previously healthy eight-year-old boy presented to the emergency department with high-grade fever, arthralgia, pruritic erythematous rash, and lymphadenopathy. He had completed 8 days of a 10-day course of cefaclor for an upper respiratory tract infection. Which of the following possibilities should be initially suspected?
- A. Kawasaki Disease
- B. Anaphylaxis
- C. Henoch-Schonlein purpura
- D. Type III Hypersensitivity Reaction (Correct Answer)
Explanation: **Explanation:** The clinical presentation of fever, arthralgia, lymphadenopathy, and a pruritic rash following the administration of a drug (specifically **Cefaclor**) is classic for **Serum Sickness-Like Reaction (SSLR)**, which is a **Type III Hypersensitivity Reaction**. **1. Why Type III Hypersensitivity is Correct:** Type III reactions involve the formation of **immune complexes** (antigen-antibody) that deposit in small blood vessels, activating the complement system and leading to tissue damage. In this case, the drug acts as the antigen. Symptoms typically appear **7–14 days** after exposure (matching the 8th day of Cefaclor treatment). Cefaclor is the most common antibiotic associated with SSLR in children. **2. Why Other Options are Incorrect:** * **A. Kawasaki Disease:** While it presents with fever and rash, it typically features non-purulent conjunctivitis, strawberry tongue, and extremity changes (edema/desquamation). It is not triggered by antibiotic completion. * **B. Anaphylaxis:** This is a Type I Hypersensitivity reaction. It occurs **minutes to hours** after exposure and is characterized by respiratory distress, hypotension, and angioedema, rather than delayed fever and arthralgia. * **C. Henoch-Schonlein Purpura (IgA Vasculitis):** Though it presents with arthralgia and rash, the rash is typically **palpable purpura** (non-pruritic) localized to the lower extremities and buttocks, often accompanied by abdominal pain or hematuria. **Clinical Pearls for NEET-PG:** * **Serum Sickness vs. SSLR:** True Serum Sickness involves heterologous proteins (e.g., antitoxins); SSLR is caused by drugs (Cefaclor, Penicillin, Sulfa) and lacks the vasculitis or renal lesions seen in true serum sickness. * **Treatment:** Discontinuation of the offending drug is the primary step. Supportive care with antihistamines and NSAIDs is usually sufficient. * **Mnemonic for Type III:** **"Immune Complex"** (e.g., SLE, Post-streptococcal glomerulonephritis, Arthus reaction).
Question 62: In a 5-year-old boy with a history of recurrent pyogenic infections by bacteria with polysaccharide-rich capsules, which of the following investigations should be done?
- A. IgA deficiency
- B. IgG1 deficiency
- C. IgG2 deficiency
- D. IgA and IgG2 deficiency (Correct Answer)
Explanation: **Explanation:** The correct answer is **D. IgA and IgG2 deficiency.** **Medical Concept:** The immune response to **encapsulated bacteria** (such as *Streptococcus pneumoniae*, *Haemophilus influenzae* type b, and *Neisseria meningitidis*) relies heavily on the production of antibodies against their **polysaccharide-rich capsules**. In humans, the antibody response to polysaccharide antigens is primarily mediated by the **IgG2 subclass**. Clinically, isolated IgG2 deficiency is rare; it most commonly occurs in association with **Selective IgA deficiency**. This combined deficiency significantly impairs the body's ability to opsonize and clear encapsulated organisms, leading to recurrent sinopulmonary and pyogenic infections. **Analysis of Options:** * **Option A (IgA deficiency):** While IgA deficiency is the most common primary immunodeficiency, it is often asymptomatic. Recurrent pyogenic infections specifically by encapsulated bacteria point more strongly toward a defect in the IgG subclass responsible for polysaccharide antigens. * **Option B (IgG1 deficiency):** IgG1 is the most abundant subclass and primarily responds to protein antigens (e.g., toxoids). Deficiency usually leads to a decrease in total IgG levels. * **Option C (IgG2 deficiency):** While IgG2 deficiency explains the susceptibility to encapsulated bacteria, it is frequently associated with IgA deficiency in clinical practice, making Option D the more comprehensive and clinically accurate choice. **High-Yield Pearls for NEET-PG:** * **IgG1 & IgG3:** Respond to **protein** antigens (e.g., viral proteins, tetanus toxoid). * **IgG2 & IgG4:** Respond to **polysaccharide** antigens. * **Selective IgA Deficiency:** Patients are at risk of **anaphylaxis** during blood transfusions due to anti-IgA antibodies. * **Wiskott-Aldrich Syndrome:** Another high-yield condition featuring low IgM and poor response to polysaccharide antigens.
Question 63: Which of the following conditions is treated with Intravenous Immunoglobulin (IVIG)?
- A. Kawasaki disease, Polyarteritis nodosa, Wegener's granulomatosis
- B. Kawasaki disease, Bruton's disease, Guillain-Barré syndrome (Correct Answer)
- C. Wegener's granulomatosis, Bruton's disease, Guillain-Barré syndrome
- D. Kawasaki disease, Wegener's granulomatosis, Bruton's disease
Explanation: **Explanation:** Intravenous Immunoglobulin (IVIG) is a blood product containing pooled IgG antibodies from thousands of donors. It functions through multiple mechanisms: providing passive immunity in immunodeficiency and exerting anti-inflammatory/immunomodulatory effects in autoimmune and neurological disorders. **Why Option B is Correct:** * **Kawasaki Disease:** IVIG is the gold standard treatment (along with Aspirin) to prevent coronary artery aneurysms. It reduces systemic inflammation by neutralizing bacterial superantigens and inhibiting cytokine production. * **Bruton’s Agammaglobulinemia (X-linked Agammaglobulinemia):** Since these patients lack B-cells and cannot produce their own antibodies, lifelong IVIG replacement is essential to prevent recurrent pyogenic infections. * **Guillain-Barré Syndrome (GBS):** IVIG acts as an immunomodulator that neutralizes pathogenic autoantibodies attacking the peripheral nerves, accelerating recovery. **Why Other Options are Incorrect:** * **Wegener’s Granulomatosis (Granulomatosis with Polyangiitis) & Polyarteritis Nodosa (PAN):** These are systemic vasculitides primarily managed with **Corticosteroids** and cytotoxic agents like **Cyclophosphamide** or Rituximab. While IVIG is occasionally used in refractory cases, it is not the primary or standard treatment. Options A, C, and D are incorrect because they include these conditions as primary indications. **NEET-PG High-Yield Pearls:** * **Kawasaki Dose:** 2 g/kg as a single infusion. Most effective if given within the first 10 days of fever. * **ITP Connection:** IVIG is also a first-line treatment for acute Immune Thrombocytopenic Purpura (ITP) to rapidly increase platelet counts by blocking Fc receptors on splenic macrophages. * **Contraindication:** IVIG is contraindicated in patients with **Selective IgA deficiency** due to the risk of anaphylaxis (anti-IgA antibodies).
Question 64: A patient presents with thrombocytopenia, eczema, and recurrent infections. What is the most probable diagnosis?
- A. Wiskott Aldrich syndrome (Correct Answer)
- B. Alpha-beta-gamma-globulinemia
- C. Chediak-Higashi syndrome
- D. Lazy leukocyte syndrome
Explanation: ### Explanation **Correct Option: A. Wiskott-Aldrich Syndrome (WAS)** Wiskott-Aldrich Syndrome is an **X-linked recessive** primary immunodeficiency caused by a mutation in the **WASp gene**, which leads to defects in the actin cytoskeleton of hematopoietic cells. The classic clinical triad presented in the question is: 1. **Thrombocytopenia:** Characteristically presents with **micro-thrombocytes** (small platelets) and bleeding tendencies (e.g., petechiae, epistaxis). 2. **Eczema:** Typically develops in early infancy. 3. **Recurrent Infections:** Due to combined B-cell and T-cell dysfunction (predisposing to encapsulated bacteria and opportunistic infections). **Why Incorrect Options are Wrong:** * **B. Agammaglobulinemia (Bruton’s):** Presents with recurrent sinopulmonary infections starting after 6 months of age (when maternal IgG wanes). It does not feature eczema or thrombocytopenia. * **C. Chediak-Higashi Syndrome:** Characterized by **oculocutaneous albinism**, peripheral neuropathy, and giant cytoplasmic granules in neutrophils. While it involves infections, the classic triad of WAS is absent. * **D. Lazy Leukocyte Syndrome:** A defect in neutrophil chemotaxis and mobility. Patients present with recurrent skin infections and gingivitis, but not with eczema or small-platelet thrombocytopenia. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked Recessive (mostly affects males). * **Lab Findings:** Low IgM, normal/low IgG, and **elevated IgA and IgE**. * **Platelet Morphology:** WAS is the only condition where **small platelets** are a hallmark feature. * **Mnemonic (WATER):** **W**iskott **A**ldrich, **T**hrombocytopenia, **E**czema, **R**ecurrent infections. * **Complications:** Increased risk of autoimmune diseases and **B-cell lymphomas**. * **Treatment:** Hematopoietic stem cell transplant is the definitive cure.
Question 65: All of the following are true about Wiskott-Aldrich syndrome except:
- A. Bloody diarrhea during infancy
- B. Low IgM and elevated IgA and IgE
- C. Large size platelets (Correct Answer)
- D. Atopic dermatitis
Explanation: **Explanation:** Wiskott-Aldrich Syndrome (WAS) is an X-linked recessive disorder caused by a mutation in the **WASp gene**, which is critical for actin cytoskeleton remodeling in hematopoietic cells. **Why Option C is the correct answer (The Exception):** In WAS, the hallmark hematological finding is **microthrombocytopenia**. Patients have a low platelet count and, characteristically, **small-sized platelets**. Finding large platelets (megathrombocytes) would instead point toward conditions like Bernard-Soulier Syndrome or ITP. **Analysis of Incorrect Options (True statements about WAS):** * **A. Bloody diarrhea:** This is often the earliest clinical manifestation in infancy due to severe thrombocytopenia and platelet dysfunction. * **B. Immunoglobulin profile:** The classic pattern is **low IgM**, normal to low IgG, and **elevated IgA and IgE**. This imbalance contributes to the underlying immunodeficiency. * **D. Atopic dermatitis:** Eczema is a core component of the clinical triad and is typically severe and difficult to manage. **Clinical Pearls for NEET-PG:** * **The Classic Triad:** 1. Thrombocytopenia (Microplatelets), 2. Eczema, 3. Recurrent Infections (especially encapsulated organisms like *S. pneumoniae*). * **Mnemonic:** **TIE** (Thrombocytopenia, Infections, Eczema). * **Inheritance:** X-linked Recessive (affects males). * **Complications:** High risk of **Non-Hodgkin Lymphoma** and autoimmune hemolytic anemia. * **Definitive Treatment:** Hematopoietic stem cell transplant (HSCT).
Question 66: Which of the following are true about Henoch-Schönlein purpura (HSP)?
- A. Palpable purpura and C-ANCA positivity
- B. Palpable purpura
- C. Palpable purpura and Thrombocytopenia
- D. Palpable purpura and Kidneys commonly affected (Correct Answer)
Explanation: **Explanation:** Henoch-Schönlein Purpura (HSP), now commonly referred to as **IgA Vasculitis**, is the most common systemic vasculitis in children. It is a small-vessel vasculitis characterized by the deposition of **IgA-dominant immune complexes**. **Why Option D is Correct:** The classic clinical tetrad of HSP includes **palpable purpura** (without thrombocytopenia), arthritis/arthralgia, abdominal pain, and **renal involvement**. Renal involvement (HSP Nephritis) occurs in approximately 30-50% of patients and is a major determinant of long-term prognosis. It typically manifests as hematuria or proteinuria. **Analysis of Incorrect Options:** * **Option A:** HSP is an immune-complex-mediated vasculitis, not a Pauci-immune vasculitis. **C-ANCA** is specifically associated with Granulomatosis with Polyangiitis (Wegener's), not HSP. * **Option B:** While palpable purpura is the hallmark sign, this option is incomplete compared to Option D, as renal involvement is a critical systemic feature of the disease. * **Option C:** This is a common distractor. In HSP, the purpura is **non-thrombocytopenic**. The platelet count is typically normal or even elevated (as an acute phase reactant). If a patient has purpura with a low platelet count, the diagnosis is more likely Immune Thrombocytopenic Purpura (ITP). **High-Yield Clinical Pearls for NEET-PG:** * **Trigger:** Often follows an Upper Respiratory Tract Infection (URTI). * **Biopsy:** Skin biopsy shows **Leukocytoclastic vasculitis** with IgA deposition on immunofluorescence. * **Gastrointestinal:** Can lead to **Intussusception** (characteristically ileo-ileal). * **Treatment:** Mainly supportive; steroids are used for severe GI symptoms or renal involvement but do not prevent chronic kidney disease.
Question 67: A 4-month-old boy presented with spontaneous nose bleeds and bloody diarrhea. He has a history of recurrent chest and ear infections, leading to frequent hospitalizations. Examination revealed atopic dermatitis and petechiae all over the body. Laboratory findings suggested abnormally low platelet counts along with eosinophilia. The gene involved in this condition is located on which chromosome?
- A. Chromosome 21
- B. Chromosome 23
- C. X-chromosome (Correct Answer)
- D. Chromosome 1
Explanation: ### Explanation The clinical presentation of the 4-month-old boy—characterized by the triad of **thrombocytopenia** (petechiae, nose bleeds, bloody diarrhea), **recurrent infections** (chest and ear), and **atopic dermatitis** (eczema)—is classic for **Wiskott-Aldrich Syndrome (WAS)**. **1. Why the Correct Answer is Right:** Wiskott-Aldrich Syndrome is an **X-linked recessive** immunodeficiency. It is caused by a mutation in the **WAS gene**, which is located on the short arm of the **X-chromosome (Xp11.22)**. The WAS protein (WASP) is crucial for actin cytoskeleton remodeling in hematopoietic cells. Its deficiency leads to defective T-cell function and impaired platelet production/size (microthrombocytopenia). **2. Why the Incorrect Options are Wrong:** * **Chromosome 21:** Associated with Down Syndrome. While Down Syndrome patients have increased susceptibility to infections and leukemia, they do not typically present with this specific triad of eczema and thrombocytopenia. * **Chromosome 23:** This is a misnomer in clinical genetics; humans have 22 pairs of autosomes and one pair of sex chromosomes (X and Y). While the X-chromosome is technically the 23rd pair, medical exams specifically refer to it as the "X-chromosome." * **Chromosome 1:** Associated with various conditions (e.g., Gaucher disease, Factor V Leiden), but not with the primary immunodeficiency described here. **3. Clinical Pearls for NEET-PG:** * **Triad Mnemonic:** **W**iskott-**A**ldrich: **W**atery diarrhea (bloody), **A**dema (Eczema), **T**hrombocytopenia, **I**nfections. * **Platelet Morphology:** A high-yield finding in WAS is **small platelets** (low Mean Platelet Volume - MPV), unlike ITP where platelets are large. * **Laboratory Findings:** Low IgM, normal/high IgA and IgE, and variable IgG. Eosinophilia is common. * **Complications:** High risk of autoimmune diseases and B-cell lymphomas. * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the definitive cure.
Question 68: Wiskott-Aldrich syndrome is characterized by all of the following features except:
- A. X-linked recessive mode of inheritance
- B. Atopic dermatitis and eczema during infancy
- C. Thrombocytopenia
- D. Increased IgM levels (Correct Answer)
Explanation: **Explanation:** Wiskott-Aldrich Syndrome (WAS) is a rare primary immunodeficiency caused by a mutation in the **WAS gene**, which encodes the **WASP protein**. This protein is crucial for actin cytoskeleton remodeling in hematopoietic cells, affecting both platelet formation and immune cell function. **Why Option D is correct:** In Wiskott-Aldrich Syndrome, the characteristic immunoglobulin profile is **decreased IgM**, with **elevated IgA and IgE** levels. IgG levels are typically normal or slightly low. The defect in the WASP protein leads to a poor polysaccharide antibody response, resulting in low IgM. Therefore, "Increased IgM levels" is the incorrect feature. **Analysis of incorrect options:** * **Option A (X-linked recessive):** This is the classic mode of inheritance for WAS. It primarily affects males. * **Option B (Atopic dermatitis/Eczema):** Eczema is a hallmark clinical feature, usually appearing in early infancy and resembling atopic dermatitis. * **Option C (Thrombocytopenia):** This is often the earliest sign. Patients present with **microthrombocytopenia** (small, few platelets), leading to mucosal bleeding, petechiae, or bloody diarrhea. **NEET-PG High-Yield Pearls:** * **Classic Triad:** "TIE" — **T**hrombocytopenia (micro-platelets), **I**mmunodeficiency (recurrent infections), and **E**czema. * **Platelet Morphology:** It is the only condition characterized by **small platelets** (low Mean Platelet Volume). * **Malignancy Risk:** Patients have a significantly increased risk of developing Non-Hodgkin Lymphoma and autoimmune diseases. * **Definitive Treatment:** Hematopoietic stem cell transplant (HSCT).
Question 69: A 7-month-old boy has had multiple bouts of otitis media, sinusitis, bronchitis, oral candidiasis, and multiple viral infections. Cessation of the recurrent infections follows successful engraftment of a bone marrow transplant. What is the basis of the clinical improvement?
- A. Direct transfusion of antibody-producing B cells.
- B. Direct transfusion of donor CD4+ and CD8+ lymphocytes.
- C. Donor suppression of recipient cytotoxic T cells.
- D. Maturation of donor lymphoid progenitor cells. (Correct Answer)
Explanation: **Explanation:** The clinical presentation of recurrent bacterial (otitis media, sinusitis), fungal (oral candidiasis), and viral infections in a 7-month-old infant is highly suggestive of **Severe Combined Immunodeficiency (SCID)**. SCID is a pediatric emergency characterized by a defect in both humoral (B-cell) and cell-mediated (T-cell) immunity. **1. Why Option D is Correct:** The definitive treatment for SCID is a **Hematopoietic Stem Cell Transplant (HSCT)**. The "engraftment" mentioned in the question refers to the donor's hematopoietic stem cells (lymphoid progenitors) successfully nesting in the recipient's bone marrow. These progenitor cells then undergo **maturation and differentiation** into functional T, B, and NK cells within the recipient’s microenvironment (e.g., the thymus). This restores the entire immune cascade, leading to clinical improvement. **2. Why Other Options are Incorrect:** * **Options A & B:** Transfusing mature B or T cells provides only transient, passive immunity. These mature cells have a limited lifespan and do not provide the lifelong, self-renewing immune reconstitution required to cure the disease. * **Option C:** The pathology in SCID is an *absence* or *dysfunction* of T cells, not an overactivity of recipient cytotoxic T cells. Suppressing the recipient's immune system is a part of the transplant conditioning process, but it is not the *basis* for the long-term clinical cure. **Clinical Pearls for NEET-PG:** * **SCID Inheritance:** Most common is **X-linked** (IL-2 receptor gamma chain mutation); second most common is **Adenosine Deaminase (ADA) deficiency** (Autosomal Recessive). * **Classic Sign:** Absence of a thymic shadow on chest X-ray. * **Contraindication:** Live vaccines (e.g., BCG, OPV) are strictly contraindicated as they can cause fatal disseminated infections. * **Diagnosis:** Low Absolute Lymphocyte Count (ALC) and low T-cell receptor excision circles (TRECs) on newborn screening.
Question 70: A full-term baby boy is delivered after an uneventful pregnancy and is well for the first 2 years of his life. He receives all his immunizations without any complications. Starting around his second birthday, the mother begins to note frequent upper respiratory tract infections, and the child is hospitalized three times for pneumonia. Laboratory testing would most likely reveal a deficiency of which of the following immunoglobulins in this child?
- A. IgA (Correct Answer)
- B. IgD
- C. IgG
- D. IgM
Explanation: **Explanation:** The clinical presentation is characteristic of **Selective IgA Deficiency**, the most common primary immunodeficiency. **Why IgA is the correct answer:** IgA is the primary immunoglobulin found in mucosal secretions (respiratory, GI, and urogenital tracts). It acts as the first line of defense against pathogens. A deficiency leads to recurrent sinopulmonary infections (sinusitis, pneumonia) and gastrointestinal infections (e.g., *Giardia*). The child remained healthy for the first two years because IgA deficiency often presents later in childhood, and many patients remain asymptomatic. Crucially, the patient tolerated **vaccinations** (which are mostly systemic/IM) without complications, indicating that his humoral (IgG/IgM) and cellular immunity are intact. **Why other options are incorrect:** * **IgG Deficiency (C):** IgG is the most abundant serum antibody. A deficiency (like X-linked Agammaglobulinemia) usually presents after 6 months of age (once maternal IgG wanes) with severe, systemic pyogenic infections. These patients also react poorly to live vaccines. * **IgM Deficiency (D):** Isolated IgM deficiency is rare. IgM is the first antibody produced in response to an antigen; its absence would lead to severe disseminated infections early in life. * **IgD (B):** IgD functions primarily as an antigen receptor on B-cell surfaces; its isolated deficiency is not a recognized cause of recurrent respiratory infections. **NEET-PG High-Yield Pearls:** * **Most Common:** Selective IgA Deficiency is the most common primary immunodeficiency. * **Associated Conditions:** High association with **Celiac disease**, autoimmune disorders, and atopy. * **The "Anaphylaxis" Rule:** Patients with IgA deficiency are at high risk of **anaphylaxis during blood transfusions** because they develop anti-IgA antibodies. * **Diagnosis:** Serum IgA levels < 7 mg/dL with normal IgG and IgM levels.
Practice by Chapter
Development of Immune System
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Primary Immunodeficiency Disorders
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Secondary Immunodeficiency Disorders
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Allergic Rhinitis
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Asthma in Children
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Atopic Dermatitis
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Food Allergies
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Drug Allergies
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Anaphylaxis
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Urticaria and Angioedema
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Autoimmune Disorders
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Immunotherapy
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