Late complement factor deficiency leads to?
Early complement deficiencies (like C1, C2, C4) are associated with autoimmune diseases, such as systemic lupus erythematosus (SLE), because these components are involved in the classical pathway's regulation. But the question is about late factors. Late complement factors include C5 to C9, which form the membrane attack complex (MAC). The MAC is responsible for cell lysis, so if these components are deficient, the body can't effectively kill certain pathogens.
Deficiency in late complement factors (C5-C9) is known to lead to recurrent infections, particularly with encapsulated bacteria like Neisseria species. Neisseria meningitidis and Neisseria gonorrhoeae are common culprits here. The MAC is crucial for lysing these bacteria, so a deficiency leaves the host vulnerable.
Looking at the options, the correct answer should be related to Neisseria infections. The other options might include autoimmune diseases (for early deficiencies), which would be incorrect here. Also, maybe some other infections or conditions like pyogenic infections, but those are more related to other parts of the immune system, like phagocyte defects.
So, the key point is that late complement deficiencies (C5-C9) lead to susceptibility to Neisseria infections. The clinical pearl here is to remember that early vs. late complement deficiencies have different clinical manifestations. Early (C1-C4) β autoimmune; late (C5-C9) β Neisseria infections. That's a high-yield fact for exams.
**Core Concept**
Complement system deficiencies are classified as early (C1-C4) or late (C5-C9). Late deficiencies impair the membrane attack complex (MAC), which directly lyses pathogens, particularly *Neisseria* species.
**Why the Correct Answer is Right**
Deficiency in late complement factors (C5-C9) prevents the formation of the MAC, a pore-forming complex that permeabilizes bacterial cell membranes. This leads to recurrent infections with encapsulated organisms like *Neisseria meningitidis* and *Neisseria gonorrhoeae*, which evade phagocytosis but are vulnerable to direct lysis.
**Why Each Wrong Option is Incorrect**
**Option A:** Autoimmune diseases (e.g., SLE) are linked to early complement deficiencies (C1-C4), not late ones.
**Option B:** Pyogenic infections (e.g., *Staphylococcus aureus*) stem from phagocyte dysfunction, not late complement defects.
**Option C:** Chronic granulomatous disease results from NADPH oxidase deficiency, impairing reactive oxygen species production.
**Clinical Pearl / High-Yield Fact**
Remember: **"Early auto, late Neisseria"** β early complement deficiencies cause autoimmune disorders; late deficiencies cause recurrent *Neisseria* infections. This distinction is critical for NEET PG and USMLE.
**Correct Answer: C. Recurrent Neisseria infections**