Meningococoal disease

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Researching meningococcal disease across its epidemiology, clinical presentation, diagnosis, management, and relevant imaging/rash findings.

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Meningitis (Bacterial) and Meningococcal Disease: Recognition, Diagnosis and Management

Page 69

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Harrison's Principles of Internal Medicine, Twenty First Edition

Page 4618

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Here is a comprehensive overview of meningococcal disease:

Meningococcal Disease

Etiology

Meningococcal disease is caused by Neisseria meningitidis, a gram-negative diplococcus. It is transmitted via respiratory droplets and close contact. The organism is classified into serogroups based on its polysaccharide capsule; the clinically important ones are:

Serogroup	Key Features
A	Major cause of epidemic disease in sub-Saharan Africa ("meningitis belt")
B	Predominant in Europe, Americas, Australasia; hardest to vaccinate against
C	Common in Europe and the Americas
W	Increasing global prevalence; higher case fatality
Y	Common in North America, associated with pneumonia
X	Emerging in Africa

Epidemiology

Humans are the only reservoir; 5–25% of the population carry the organism asymptomatically in the nasopharynx.
Peak incidence: infants < 1 year, toddlers, and adolescents/young adults (dormitory settings — universities, military).
Outbreaks occur in the "meningitis belt" (sub-Saharan Africa), particularly serogroup A.
Case fatality rate: 10–15% overall; up to 40–50% in fulminant meningococcemia (purpura fulminans).

Pathophysiology

Nasopharyngeal colonization → invasion of mucosal barrier
Bacteremia → release of lipopolysaccharide (LPS/endotoxin)
Massive cytokine cascade → systemic inflammatory response
Endothelial damage → disseminated intravascular coagulation (DIC), microvascular thrombosis
Meningeal seeding → meningitis; adrenal infarction → Waterhouse-Friderichsen syndrome

Clinical Presentations

Meningococcal disease presents in several overlapping forms:

1. Meningococcal Meningitis

Headache, photophobia, neck stiffness (meningism)
Fever, nausea/vomiting
Altered consciousness
Kernig's and Brudzinski's signs

2. Meningococcemia (Septicemia)

High fever, rigors
Petechial/purpuric rash — the hallmark; begins as pinpoint petechiae, rapidly progressing to non-blanching purpura
Hypotension, shock
Multi-organ failure

3. Purpura Fulminans (Fulminant Meningococcemia)

Most severe form: rapidly spreading ecchymoses, DIC, adrenal hemorrhage
High mortality even with treatment

4. Other (less common)

Pneumonia, septic arthritis, pericarditis, conjunctivitis

The Classic Rash

The non-blanching petechial/purpuric rash is a medical emergency — presence on glass test (does not blanch under pressure) mandates immediate action.

Purpuric rash on plantar surface showing widespread petechiae and confluent ecchymoses characteristic of fulminant meningococcemia

Postmortem photograph showing widespread purpura on the plantar surface — classic purpura fulminans from invasive meningococcal disease (Neisseria meningitidis). Note the dark purple-to-black non-blanching lesions.

Diagnosis

Investigations (to be done urgently, without delaying treatment)

Test	Purpose
Blood cultures (x2)	Isolate organism, sensitivities
PCR (blood/CSF)	Rapid detection; positive even after antibiotics
Lumbar puncture (if no contraindication)	CSF analysis, culture, PCR
FBC, CRP, clotting, U&E, LFTs, lactate	Assess severity, DIC
Meningococcal throat swab	Strain typing for public health/contact management
CT head	Before LP if focal neurology, papilloedema, or GCS < 13

CSF findings in bacterial meningitis:

Turbid/purulent appearance
Raised WBC (predominantly neutrophils, > 1000 cells/µL)
Raised protein (> 1 g/L)
Low glucose (CSF:serum glucose < 0.4)

Per the NICE Guideline on Bacterial Meningitis and Meningococcal Disease, a bacterial throat swab should be taken in all suspected meningococcal cases to guide management of cases, contacts, and outbreaks. (NICE, p. 69)

Management

Immediate Pre-Hospital / Emergency

If meningococcal disease is suspected and the patient cannot be transferred immediately, administer IM/IV Benzylpenicillin (or Ceftriaxone if penicillin allergy) before transfer.
Secure IV access, resuscitation fluids for shock.
Isolate (droplet precautions) until 24h of antibiotics.

Definitive Antibiotic Treatment

Scenario	Preferred Agent	Duration
Meningococcal meningitis	IV Ceftriaxone 2g BD	7 days (3–5 days may suffice)
Meningococcal septicemia	IV Ceftriaxone 2g BD	7 days
Penicillin allergy	IV Chloramphenicol or Meropenem	7 days
Resource-limited settings	Single dose IM Ceftriaxone or oily Chloramphenicol	—

Harrison's (p. 4618): "Both meningococcal meningitis and meningococcal septicemia are conventionally treated for 7 days, although courses of 3–5 days may be equally effective... Cultures usually become sterile within 24 h of initiation of appropriate antibiotic chemotherapy."

Adjunctive Treatment

Dexamethasone IV (0.15 mg/kg QDS for 4 days) — reduces neurological sequelae; best given before or with first dose of antibiotics.
ICU care for shock: vasopressors (norepinephrine), mechanical ventilation, renal replacement therapy.
DIC management: FFP, platelet transfusion as needed.
Treat Waterhouse-Friderichsen syndrome (adrenal insufficiency) with hydrocortisone.

Complications

Short-term	Long-term
Septic shock, multi-organ failure	Sensorineural hearing loss (most common)
DIC, purpura fulminans	Neurological deficits (cognitive, motor)
Waterhouse-Friderichsen syndrome	Limb amputation (from ischemic necrosis)
Raised intracranial pressure, herniation	Skin scarring
Hydrocephalus	Psychological/PTSD

Prevention

Vaccination

Vaccine	Target	Examples
MenACWY	Serogroups A, C, W, Y	Menveo, Nimenrix — routine adolescent immunization in many countries
MenB	Serogroup B	Bexsero, Trumenba — recommended for infants and high-risk groups
MenA (polysaccharide conjugate)	Serogroup A	MenAfriVac — mass campaigns in African meningitis belt

Chemoprophylaxis for Close Contacts

Close contacts (household members, kissing contacts) should receive prophylaxis within 24 hours of case identification:

Ciprofloxacin 500mg single dose PO (adults) — preferred in most guidelines
Rifampicin 600mg BD for 2 days (alternative)
Ceftriaxone 250mg IM single dose (pregnant women)

Risk Factors for Severe/Invasive Disease

Complement deficiencies (C5–C9, properdin) — recurrent disease
Asplenia or functional hyposplenism
HIV infection
Age extremes (infants, elderly)
Crowded living conditions

Key Points Summary

Any non-blanching rash + fever = meningococcal disease until proven otherwise — treat immediately.
Do not delay antibiotics to perform investigations; LP can follow once stable.
Ceftriaxone is the antibiotic of choice; dexamethasone reduces sequelae.
Hearing loss is the most common long-term complication — arrange formal audiological assessment post-recovery.
Notify public health authorities; trace and provide prophylaxis to close contacts within 24 hours.

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