Meningococcal Disease

Etiology & Microbiology

Neisseria meningitidis is a Gram-negative diplococcus that is the causative agent. It is classified into 13 serogroups based on capsular polysaccharide; the clinically significant ones are A, B, C, W, X, and Y.

Serogroup A: historically dominant in sub-Saharan Africa's "meningitis belt," with epidemic waves every 8-12 years
Serogroups C (~60%) and B (~29%): responsible for most outbreaks in the US and Europe over the past 50 years
Serogroups W135, X, C: emerging pathogens in Africa (e.g., a large serogroup C outbreak in Nigeria, 2016-2017)

Humans are the only natural reservoir. The organism colonizes the nasopharynx asymptomatically in ~10% of healthy adults (carrier state). Transmission is via respiratory droplets or direct contact.

Pathophysiology

Following nasopharyngeal colonization, the organism can invade the bloodstream (bacteremia/meningococcemia) and/or spread to the meninges. Key pathogenic mechanisms include:

Endotoxin (lipooligosaccharide) release → massive systemic inflammatory response (cytokine storm with IL-1, IL-6, TNF-α)
Disseminated intravascular coagulation (DIC) → microvascular thrombosis and hemorrhage → purpuric/petechial rash and purpura fulminans
Hypovolemic shock (from vasodilation and capillary leak) — the most common cause of death
Raised intracranial pressure — in meningitis predominant forms

Clinical Presentations

Meningococcal disease manifests in several overlapping syndromes:

Syndrome	Key Features
Meningococcemia (bacteremia)	Fever, rash (petechiae → purpura), hypotension, DIC, shock
Meningococcal meningitis	Fever, headache, neck stiffness, photophobia, altered consciousness
Mixed (most common)	Features of both meningitis and septicemia
Purpura fulminans	Fulminant DIC, large ecchymoses, limb ischemia — highest mortality
Waterhouse-Friderichsen syndrome	Bilateral adrenal hemorrhage, adrenal insufficiency

Rash is present in ~75% of bacteremic patients and is the cardinal sign — initially blanching maculopapular, rapidly progressing to non-blanching petechiae and purpura. This is a medical emergency.

Classic purpuric rash of meningococcemia:

Purpura fulminans – postmortem plantar view showing classic dark purple/blue-black petechiae and confluent ecchymoses of invasive meningococcal disease

Plantar surface demonstrating widespread purpuric lesions — pinpoint petechiae and confluent ecchymoses typical of fulminant meningococcemia (purpura fulminans). Harrison's, p. 3690.

Diagnosis

Immediate clinical recognition is paramount — do not delay treatment for diagnostic workup.

Blood cultures (before antibiotics if feasible, but never delay antibiotics)
Lumbar puncture (LP): CSF shows cloudy fluid, elevated WBC (neutrophilic pleocytosis), elevated protein, low glucose; Gram stain and culture; PCR for N. meningitidis
CBC: leukocytosis (or leukopenia in severe sepsis), thrombocytopenia
Coagulation studies: PT/aPTT prolongation, elevated D-dimer, low fibrinogen (DIC)
Serum lactate, electrolytes, LFTs, renal function
Skin biopsy of petechiae: Gram stain and PCR can be diagnostic even after antibiotics
Meningococcal PCR (blood/CSF): highly sensitive, unaffected by prior antibiotic therapy

If raised ICP is suspected (papilledema, focal neuro signs, GCS <12), perform CT head before LP. Do not delay antibiotics for CT.

Management

(Harrison's, p. 4617)

1. Stabilization (ABCs)

Airway: secure if GCS is depressed due to shock or raised ICP
Oxygen for hypoxia (pulmonary edema/oligemia in meningococcemia)
IV access: aggressive fluid resuscitation for hypovolemic shock
Vasopressors (norepinephrine) for refractory shock

2. Antibiotics — Start Immediately

First-line: Benzylpenicillin (Penicillin G) IV/IM — if organism confirmed susceptible
Empirical (before results): Ceftriaxone 2g IV q12h (adults) or 80–100 mg/kg/day in children — covers both meningitis and septicemia
Alternative: Cefotaxime; Chloramphenicol in penicillin allergy
Duration: typically 5–7 days for meningococcal meningitis/septicemia

3. Adjunctive Therapy

Dexamethasone 0.15 mg/kg IV q6h × 4 days: given before or with the first antibiotic dose to reduce neurological sequelae in bacterial meningitis
DIC management: fresh frozen plasma, platelets, cryoprecipitate as needed
Adrenal insufficiency: consider hydrocortisone in hemodynamically unstable patients
ICU admission for all severe cases

Prevention & Vaccination

Chemoprophylaxis (close contacts)

All household/close contacts (within 7 days of exposure) require prophylaxis within 24 hours:

Rifampicin 600 mg PO q12h × 2 days (adults)
Ciprofloxacin 500 mg PO single dose (preferred in many guidelines due to simplicity)
Ceftriaxone 250 mg IM single dose (preferred in pregnancy)

Vaccines

Vaccine Type	Serogroups Covered	Key Use
MenACWY (conjugate)	A, C, W, Y	Routine adolescent immunization; travelers to endemic areas
MenB (protein-based)	B	Adolescents/young adults; outbreak control
MenA conjugate (MenAfriVac)	A	Mass vaccination campaigns in sub-Saharan Africa

High-risk groups requiring vaccination: asplenic patients, complement deficiencies (C5-C9, properdin), HIV, college freshmen in dormitories, military recruits, Hajj pilgrims, travelers to the meningitis belt.

Complications & Prognosis

Mortality: 10–15% overall; up to 40–60% in fulminant meningococcemia
Neurological sequelae (in survivors of meningitis): hearing loss (~10%), cognitive impairment, seizures
Limb loss: ischemic necrosis from purpura fulminans may require amputation
Waterhouse-Friderichsen syndrome: adrenal crisis
Obstructive hydrocephalus, subdural empyema (rare)

Early antibiotic therapy and aggressive ICU management are the key determinants of outcome. Delayed recognition is the leading preventable cause of death. (Harrison's, p. 4617)

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