Inflammation: complement deficiencies: 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 · Inflammation: complement deficiencies

Sample item

A 19-year-old man has his second episode of meningococcal meningitis within two years. He has no splenic abnormality and normal immunoglobulin levels, but total haemolytic complement activity (CH50) is nearly absent. Which deficiency best explains this?

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

The answer and the reasoning

C. Terminal complement components (C5 to C9) forming the membrane attack complex

Deficiency of the terminal components C5 to C9 prevents formation of the membrane attack complex, which is needed to lyse Neisseria. The patients have recurrent meningococcal or disseminated gonococcal infection and a low CH50. Deficiency of C3 causes severe recurrent infections by many encapsulated pyogenic bacteria from early childhood.

Option by option

  • A. Decay-accelerating factor (CD55)

    Decay-accelerating factor deficiency causes complement-mediated lysis of red cells in paroxysmal nocturnal haemoglobinuria.

  • B. Mannose-binding lectin, with an intact classical pathway

    Mannose-binding lectin deficiency leaves the classical pathway and CH50 normal, and gives at most a mild infection tendency in infancy.

  • C. Terminal complement components (C5 to C9) forming the membrane attack complex (correct)

    Correct. Without the membrane attack complex Neisseria species escape complement-mediated killing, giving recurrent infection.

  • D. C1 esterase inhibitor

    C1 inhibitor deficiency causes hereditary angioedema, not recurrent meningitis.

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, Terminal complement components (C5 to C9) forming the membrane attack complex. Deficiency of the terminal components C5 to C9 prevents formation of the membrane attack complex, which is needed to lyse Neisseria.

Why is "Decay-accelerating factor (CD55)" not the answer?

Decay-accelerating factor deficiency causes complement-mediated lysis of red cells in paroxysmal nocturnal haemoglobinuria.

Why is "Mannose-binding lectin, with an intact classical pathway" not the answer?

Mannose-binding lectin deficiency leaves the classical pathway and CH50 normal, and gives at most a mild infection tendency in infancy.

Why is "C1 esterase inhibitor" not the answer?

C1 inhibitor deficiency causes hereditary angioedema, not recurrent meningitis.

What concept does this question test?

It tests Inflammation: complement deficiencies in Pathology. The patients have recurrent meningococcal or disseminated gonococcal infection and a low CH50. Deficiency of C3 causes severe recurrent infections by many encapsulated pyogenic bacteria from early childhood.

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 Inflammation: complement deficiencies?

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.