Hypersensitivity: Arthus reaction: practice question

A Pathology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Pathology · Hypersensitivity: Arthus reaction

Sample item

A farmer who has had several tetanus toxoid boosters is given another dose. Six hours later the injection site is red, indurated and painful, and over the next day it becomes necrotic. Histology shows fibrinoid necrosis of small vessels with neutrophils. What is the mechanism?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

C. Local formation of IgG-antigen complexes in vessel walls with complement activation and neutrophil recruitment

The Arthus reaction is a localised type III hypersensitivity. Antigen injected into an individual with high preformed IgG forms immune complexes in and around vessel walls, activating complement and attracting neutrophils, producing vasculitis, thrombosis and necrosis that peaks at 4 to 10 hours. Repeated booster doses are a classic precipitant.

Option by option

  • A. Antibody binding to a cell-surface antigen causing opsonisation

    Antibody to cell-surface antigens (type II) is not the explanation for local vessel wall necrosis at an injection site.

  • B. IgE-mediated mast cell degranulation within minutes

    A type I reaction appears within minutes and is not necrotising.

  • C. Local formation of IgG-antigen complexes in vessel walls with complement activation and neutrophil recruitment (correct)

    Correct. Immune complex deposition with complement and neutrophils explains the hours-long timing and fibrinoid necrosis.

  • D. Th1 cell sensitisation causing a delayed reaction peaking at 48 to 72 hours

    A Th1 mediated reaction (type IV) peaks at 48 to 72 hours and shows lymphocytes and macrophages.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is C, Local formation of IgG-antigen complexes in vessel walls with complement activation and neutrophil recruitment. The Arthus reaction is a localised type III hypersensitivity.

Why is "Antibody binding to a cell-surface antigen causing opsonisation" not the answer?

Antibody to cell-surface antigens (type II) is not the explanation for local vessel wall necrosis at an injection site.

Why is "IgE-mediated mast cell degranulation within minutes" not the answer?

A type I reaction appears within minutes and is not necrotising.

Why is "Th1 cell sensitisation causing a delayed reaction peaking at 48 to 72…" not the answer?

A Th1 mediated reaction (type IV) peaks at 48 to 72 hours and shows lymphocytes and macrophages.

What concept does this question test?

It tests Hypersensitivity: Arthus reaction in Pathology. Antigen injected into an individual with high preformed IgG forms immune complexes in and around vessel walls, activating complement and attracting neutrophils, producing vasculitis, thrombosis and necrosis that peaks at 4 to 10 hours. Repeated booster doses are a classic precipitant.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Hypersensitivity: Arthus reaction?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.