Neisseria meningitidis

1. GC 051 (Meningitis lecture): "Close contacts of patients suffering from H. influenzae type B and Neisseria meningitidis require chemoprophylaxis (e.g. rifampicin or ciprofloxacin)." Mortality 80% if untreated. Benefit of adjunctive dexamethasone remains inconclusive. ^[2] — This is directly examinable: dexamethasone is proven for pneumococcal meningitis but NOT conclusively for meningococcal.

2. AOS Microbio: Eculizumab (anti-C5 monoclonal antibody) blocks MAC formation → most common pathogen is Neisseria meningitidis. ^[10] — This complement-drug-bug link has appeared verbatim in past papers.

3. Jerry's immunodeficiencies notes (from Phillip Li lecture): Terminal complement deficiency (C5-C9) → low CH50, low AH50 → susceptibility to encapsulated bacteria, specifically Pneumococcus, Neisseria meningitidis, and Hemophilus influenzae. ^[5] — Expect a vignette with a young adult presenting with recurrent meningococcal infections → check complement levels.

4. Splenectomy lecture: 4 pre-operative vaccines include Meningococcus. OPSI most commonly caused by S. pneumoniae ( > 50%), but N. meningitidis and H. influenzae also important. ^[9] — Post-splenectomy + purpuric rash + rapid deterioration = OPSI; blood smear showing Howell-Jolly bodies is the clue to functional asplenia.

5. Gen Clerk Microbiology Summary: Post-exposure prophylaxis for meningococcal disease = single-dose oral ciprofloxacin; single-dose IM ceftriaxone if ciprofloxacin contraindicated (children, pregnant). ^[8]

6. Ryan Ho Neurology: Empirical meningitis Rx = 3G cephalosporin (ceftriaxone/cefotaxime); add vancomycin for pneumococcus; add ampicillin if Listeria risk. Duration ≥7d for H. influenzae, 10–14d for S. pneumoniae. ^[7] — Meningococcal meningitis generally requires the shorter end (7d).

• N. meningitidis vs N. gonorrhoeae: Both are G−ve oxidase + diplococci. Key discriminator: maltose fermentation (meningitidis +, gonorrhoeae −). Meningitidis has a prominent capsule; gonorrhoeae does not (no vaccine possible for gonorrhoea due to antigenic variation of pili).
• Meningococcal purpura vs HSP: Meningococcal rash is non-blanching, irregular, ± necrotic centre, with systemic toxicity/shock. HSP rash is palpable purpura on buttocks/extensor surfaces with IgA-mediated vasculitis, abdominal pain, arthralgia, and haematuria — typically well-looking child.
• Complement deficiency vignette: Young patient with recurrent Neisseria infections → check CH50 and AH50 (both low in terminal complement deficiency).
• Eculizumab trap: Students may pick Cryptococcus (a capsulated organism) — but Cryptococcus killing depends on cell-mediated immunity (T-cells, macrophages), NOT MAC. MAC is specifically critical for Neisseria killing.
• Dexamethasone pitfall: Proven benefit in S. pneumoniae and S. suis meningitis only. For meningococcal meningitis, benefit is inconclusive per GC 051 lecture — do not state it is "standard" for meningococcus.

1. 2023 Fourth Summative MCQ Q84 ^[11]

"Eculizumab is a monoclonal antibody therapeutic that inhibits the complement pathway by binding to C5 and preventing formation of membrane attack complex. Infections by which of the following pathogens is expected to be the MOST COMMON in patients on eculizumab? A. Cryptococcus neoformans B. Influenza virus C. Neisseria meningitidis D. Varicella zoster virus"

Answer: C. Neisseria meningitidis. Rationale: MAC (C5b-C9) is the principal complement effector for killing Neisseria spp. due to their outer membrane structure. Blocking C5 eliminates MAC formation → dramatically increases susceptibility to N. meningitidis. Cryptococcus relies on T-cell/macrophage killing; influenza and VZV are intracellular pathogens cleared by interferon/cytotoxic T-cells, not complement. This question also appears verbatim in AOS Microbio Q4 ^[10].

2. 2021 Fourth Summative Assessment MCQ Q21 (EMQ — Investigating a child with fever and rash) ^[12]

"An 18-month-old boy presented with fever, vomiting, neck stiffness, and a reddish-purple rash for 2 days. Examination revealed a septic and dull-looking kid with purpuric rash."

Answer: B. Blood culture. Rationale: The clinical picture is classic meningococcal septicaemia/meningitis (purpuric rash + meningism + septic child). Blood culture is the most useful initial investigation to confirm the causative organism in meningococcaemia. LP may also be done but may be deferred if the child is haemodynamically unstable.

3. 2021 Fourth Summative SAQ Q12(c) ^[13]

"He did not come back for routine vaccination after transplantation for 1 year. Four years after the transplant, he had a sudden onset of high fever, hypotension, purpuric skin rash and died within 24 hours after hospitalisation. His peripheral blood smear showed Howell Jolly bodies. List three organisms found in blood cultures which may account for this clinical picture."

Answer: S. pneumoniae, N. meningitidis, H. influenzae (encapsulated organisms causing OPSI). Rationale: Howell-Jolly bodies indicate functional hyposplenism (post-BMT with chronic GVHD or splenic dysfunction). The fulminant presentation with purpuric rash, shock, and death within 24 hours is classic OPSI. The three encapsulated bacteria are the canonical answers ^[9][13].

4. 2019 Fourth Summative MCQ EMQ Q1-series (Dermatological conditions) ^[14]

Option D in the stem list is "Meningococcal septicaemia" — while the specific question matched to it is not fully indexed, the inclusion of this option confirms it is a testable dermatological vignette discriminator. Expect a purpuric, non-blanching rash in a febrile, toxic patient as the clue pointing to meningococcal septicaemia (vs other causes of purpura in the option list such as HSP).