Meningococcal Meningitis

Meningococcal meningitis is purulent meningitis caused by Neisseria meningitidis (Nm). The pathogen enters via the nasopharynx, bloodstream, and finally the meninges. Features are abrupt fever, headache, vomiting, petechiae/purpura, nuchal rigidity, and purulent CSF; septicemic forms may be fulminant. Nm may cause pneumonia, arthritis, pericarditis, or eye infection without meningitis. It occurs worldwide in sporadic/epidemic form, predominantly in children.

Common Symptoms

Papulomacular rash; hyperesthesia; diarrhea; Cheyne-Stokes breathing; restlessness; fatigue; cyanosis; toxemia

Causes and Pathogenesis

(1) Etiology: N. meningitidis is a Gram-negative kidney-shaped diplococcus 0.6-0.8 µm with polysaccharide capsule; outer membrane ~8 nm, periplasm ~6 nm. Human-only, found in carriers' nasopharynx and patients' blood/CSF/petechiae; aerobic, enriched by 5-10% CO2 at 35-37°C; autolyzes easily, cold/dry sensitive. Ferments glucose/maltose but not lactose/fructose/sucrose. Capsular polysaccharide defines 13 serogroups (A, B, C, D, X, Y, Z, 29E, W135, H, I, K, L); ungroupable strains (20-50% of carrier isolates) are usually avirulent. B/C are further typed by outer-membrane proteins (types 2/15 cause most disease). MLST is the gold standard (www.mlst.net); African A:ST-5/ST-7 clone complex. (2) Pathogenesis: ~1 in 1000-5000 infections is clinical; lack of specific bactericidal antibody is key. Virulence factors: antiphagocytic capsule, adhesive pili, endotoxin. Endotoxin causes small-vessel necrosis/hemorrhage (petechiae, microcirculatory failure, DIC, shock). A/B/C groups are most virulent; complement C5-C8 deficiencies, properdin deficiency, hypogammaglobulinemia, SLE, myeloma, nephrosis, and liver disease predispose; viral URI predisposes. Fulminant meningococcemia (Waterhouse-Friderichsen syndrome) is due to LPS-induced Shwartzman reaction, complement activation, microcirculatory failure, and DIC—not adrenal failure (cortisol is elevated, no post-recovery Addison disease). TNF-α correlates with severity; Nm LPS is 5-10× more potent than other Gram-negative LPS in causing petechiae. Pathology: endothelial damage, vasculitis, thrombosis, perivascular hemorrhage; fulminant cases show adrenal/pulmonary/GI/cardiac hemorrhage. Meningitic phase: leptomeningeal congestion, purulent exudate at skull base and convexities, cranial nerve damage, cerebral edema/herniation; chronic cases develop hydrocephalus.

Treatment

Drug therapy, supportive therapy

Preventive Measures

Health education; avoid crowds. 1. Early detection/isolation; emergency vaccination in outbreak areas. 2. Vaccination: group A polysaccharide vaccine gives ~90% protection lasting ≥2 years (30 µg); universal coverage 85-90% before predicted epidemics; booster annually for 6 months-2 years. Group C and ACYW135 conjugate vaccines also available. Group B OMP vaccines give ~70% protection in ages 5-21 but poor in <4 years. China has developed an A polysaccharide-B OMPC conjugate. 3. Chemoprophylaxis: rifampicin 600 mg (adults) / 10 mg/kg (children) bid ×2 days, or minocycline; sulfadiazine 4-6 g/day (adults) / 100-200 mg/kg/day (children) in 2 doses ×3 days where sensitive. Medically observe all close contacts.

Department to Visit

It is recommended to visit the Neurology department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.