Meningococcemia: A Detailed Guide

Last Updated on September 9, 2026 by Nurseslab.in Editorial Team

Overview

Meningococcemia, also called meningococcal septicaemia, is an invasive bloodstream infection caused by Neisseria meningitidis. Once the bacteria enter the blood, they can multiply rapidly and release potent endotoxin. The resulting inflammatory and coagulation response damages blood vessels, makes capillaries leak, reduces blood flow to organs and limbs, and can trigger disseminated intravascular coagulation. The classic purpuric rash reflects bleeding into the skin, but it is a late or absent sign in some patients.

Meningococcemia is one manifestation of meningococcal disease. The same organism can cause meningitis, pneumonia, septic arthritis, pericarditis, or a combination of meningitis and bloodstream infection. A patient with severe septicaemia may have no headache or neck stiffness. Recognition must therefore focus on sepsis, circulation, skin changes, pain, and mental state rather than waiting for a classic meningitis picture.

The Organism and Its Virulence

Neisseria meningitidis is a Gram-negative diplococcus carried in the human nose and throat. Its polysaccharide capsule helps it evade immune clearance. Serogroups A, B, C, W, X, and Y cause most invasive disease worldwide, with distribution varying by age, geography, vaccination, and outbreak. Surface proteins help the organism attach to mucosa, cross barriers, survive in blood, and acquire iron.

Outer-membrane lipooligosaccharide acts as endotoxin. High bacterial and endotoxin burden activates complement, cytokines, coagulation, and the endothelium. Capillary leakage causes low circulating volume and tissue oedema. Microvascular thrombosis and bleeding occur at the same time. Myocardial depression, adrenal haemorrhage, metabolic acidosis, and mitochondrial dysfunction can make shock profound and resistant to treatment.

How Disease Develops

  1. Meningococci colonise the nasopharynx, usually without symptoms.
  2. In a susceptible person, bacteria cross the mucosal surface and enter the bloodstream.
  3. The capsule and other factors allow rapid multiplication despite immune defences.
  4. Endotoxin activates an extreme inflammatory response and injures blood-vessel lining.
  5. Fluid leaks from capillaries, blood pressure falls, and oxygen delivery to tissues declines.
  6. Coagulation becomes dysregulated, producing microvascular clots, consumption of platelets and clotting factors, and bleeding.
  7. Skin, kidneys, lungs, heart, brain, adrenal glands, and limbs may fail as shock progresses.

Transmission, Carriage, and Incubation

  • Carriage: Many healthy people temporarily carry meningococci without illness. Carriage is not the same as invasive infection.
  • Spread: Respiratory and throat secretions transmit the organism during close or prolonged contact.
  • Higher-risk contact: Household residence, intimate kissing, shared sleeping space, direct saliva exposure, or unprotected airway procedures.
  • Lower-risk contact: Brief casual contact, passing someone at school or work, or sharing a building generally does not qualify for prophylaxis.
  • Incubation: Usually about three to four days, with a recognised range of approximately two to ten days.
  • Infectious period: Effective antibiotics rapidly reduce carriage; hospitals use droplet precautions for the locally specified period after treatment begins.

Risk Factors

  • Infancy, adolescence and young adulthood, and older age.
  • Close living in dormitories, military accommodation, boarding schools, shelters, or crowded households.
  • Missing or incomplete meningococcal vaccination.
  • Absent or poorly functioning spleen.
  • Deficiency of terminal complement components, properdin, factor D, or factor H.
  • Complement-inhibitor medicines such as eculizumab or ravulizumab; vaccination does not eliminate this risk.
  • HIV infection or another immune disorder.
  • Recent viral respiratory infection, smoking, or second-hand smoke exposure.
  • Occupational exposure to meningococcal isolates in a microbiology laboratory.
  • Travel to an outbreak area or the African meningitis belt, including selected mass gatherings.
  • Membership of a population linked epidemiologically to an outbreak.

Clinical Presentation and Stages

The illness may begin with non-specific fever, chills, fatigue, headache, muscle pain, nausea, vomiting, diarrhoea, or sore throat. Over several hours, severe limb pain, cold hands and feet, mottled colour, tachycardia, rapid breathing, reduced urine, drowsiness, and a petechial rash may appear. The patient may deteriorate before blood pressure falls; compensated shock can preserve an apparently normal pressure while circulation is already critically impaired.

  • Early infection: Fever, rigors, malaise, headache, nausea, vomiting, diarrhoea, general aches, and irritability.
  • Early sepsis: Severe muscle or limb pain, cold extremities, pale or mottled skin, fast breathing, fast heart rate, anxiety, and reduced urine.
  • Microvascular injury: Pinpoint petechiae, purpura, bruising, skin tenderness, and reduced limb perfusion.
  • Decompensated shock: Hypotension, confusion, collapse, weak pulses, prolonged capillary refill, acidosis, and organ dysfunction.
  • Fulminant disease: Disseminated coagulation, adrenal haemorrhage, myocardial failure, respiratory failure, kidney injury, coma, and limb or skin necrosis.

Symptoms in Babies and Young Children

  • Poor feeding, vomiting, or reduced wet nappies.
  • Unusual irritability, a high-pitched cry, or distress when handled.
  • Floppiness, stiffness, abnormal movements, or seizures.
  • Marked sleepiness, reduced interaction, or difficulty waking.
  • Fever or an abnormally low temperature.
  • Rapid breathing, grunting, pauses in breathing, or blue colour.
  • Pale, mottled, or blotchy skin; cold hands and feet; or a non-blanching rash.
  • A bulging fontanelle when meningitis is also present, although it may be absent.

The Rash and Purpura Fulminans

Petechiae are tiny red, purple, brown, or black spots caused by bleeding beneath the skin. Purpura are larger lesions; purpura fulminans describes rapidly progressive skin haemorrhage and necrosis associated with severe coagulation failure. Lesions may begin in pressure areas and spread quickly. On darker skin, colour change may be easier to see on the palms, soles, conjunctivae, inside the mouth, or less pigmented areas.

A clear glass pressed firmly over a lesion can help identify non-blanching marks that do not fade under pressure. The test is not a rule-out tool: early lesions can blanch, the rash may be absent, and emergency care must never be delayed while waiting for it to develop.

Diagnostic Evaluation

  1. Immediate physiological assessment: Airway, breathing, circulation, oxygenation, mental state, temperature, heart rate, blood pressure, capillary refill, pulse quality, skin perfusion, urine output, and blood glucose are assessed at once.
  2. Focused history: Symptom onset and progression, rash, pain, vomiting or diarrhoea, headache, neck stiffness, vaccination, immune status, complement-inhibitor use, close contact, travel, and recent antibiotics are documented.
  3. Whole-body examination: Inspect all skin, including palms, soles, mucosa, and pressure areas; assess limb warmth, pulses, swelling, tenderness, and compartment pressure concerns.
  4. Blood cultures: Obtain before antibiotics when this can occur immediately without delaying treatment.
  5. Whole-blood PCR: Nucleic-acid testing can detect meningococcal DNA after antibiotic exposure and supports confirmation.
  6. Routine laboratory studies: Full blood count, C-reactive protein, electrolytes, glucose, kidney and liver function, lactate, blood gas, calcium, magnesium, and phosphate assess severity and guide treatment.
  7. Coagulation studies: Platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, and D-dimer evaluate disseminated intravascular coagulation.
  8. Cardiac assessment: Electrocardiography, troponin, natriuretic peptide, and echocardiography may identify myocardial depression or guide vasoactive support.
  9. Lumbar puncture: Perform only when meningitis is suspected and the patient is stable without a bleeding or intracranial-pressure contraindication. It is often unsafe during shock or severe coagulopathy.
  10. Cerebrospinal-fluid testing: When obtained, analyse cell count, glucose with paired blood glucose, protein, Gram stain, culture, and PCR.
  11. Microbiology from other sites: Culture or PCR of joint, pericardial, pleural, or purpuric-lesion specimens may help in unusual presentations.
  12. Serogrouping and susceptibility: Public-health laboratories characterise the isolate, support outbreak investigation, and identify resistance relevant to treatment or prophylaxis.
  13. Imaging: Chest imaging, brain imaging, vascular studies, or limb imaging is selected for complications; imaging should never delay antibiotics or resuscitation.

Differential Diagnosis

  • Pneumococcal, staphylococcal, streptococcal, or Gram-negative sepsis.
  • Severe invasive group A streptococcal disease or toxic shock syndrome.
  • Viral infection with rash, dengue, severe malaria, rickettsial infection, or leptospirosis.
  • Immune thrombocytopenia, thrombotic microangiopathy, acute leukaemia, vasculitis, or another cause of purpura.
  • Severe anaphylaxis, adrenal crisis, myocarditis, or metabolic shock.
  • Meningitis without bloodstream collapse and encephalitis with systemic illness.
  • Non-accidental or accidental bruising; the sick patient with systemic signs requires sepsis exclusion first.

Immediate Antibiotic Treatment

  • Give antibiotics immediately: Suspected meningococcemia requires prompt intravenous bactericidal therapy.
  • Empirical choice: An extended-spectrum cephalosporin such as ceftriaxone or cefotaxime is standard in many guidelines.
  • Do not delay: Culture, PCR, imaging, transfer, or lumbar puncture must not create an avoidable delay.
  • Targeted therapy: Penicillin G or ampicillin may replace the cephalosporin only when meningococcal susceptibility is confirmed and local guidance supports it.
  • Severe allergy: Alternative therapy requires immediate microbiology or infectious-disease advice.
  • Duration: Determined by clinical response, meningitis involvement, metastatic infection, and local protocol.
  • Carriage eradication: If the treatment regimen does not reliably eliminate nasopharyngeal carriage, additional eradication therapy is required before discharge.

Resuscitation and Critical Care

  • Airway and breathing: Give oxygen, monitor ventilation, and intubate when consciousness, respiratory failure, or shock threatens the airway.
  • Vascular access: Obtain rapid intravenous or intraosseous access without delaying antibiotics.
  • Fluids: Give balanced, carefully reassessed boluses for poor perfusion while watching for pulmonary oedema and myocardial dysfunction.
  • Vasoactive support: Start norepinephrine, epinephrine, or another age-appropriate agent promptly when shock persists despite initial fluid resuscitation.
  • Monitoring: Follow mental state, lactate, blood pressure, urine output, capillary refill, central temperature, blood gases, and organ function repeatedly.
  • Myocardial support: Bedside echocardiography can direct inotropes and fluid strategy when cardiac depression is present.
  • Respiratory support: Mechanical ventilation may reduce work of breathing and oxygen demand in severe shock.
  • Kidney support: Manage electrolytes and acid–base disturbance; continuous renal replacement therapy may be needed.
  • Refractory shock: Expert centres may consider advanced haemodynamic support, including extracorporeal life support, in selected patients.

Management of Coagulation, Skin, and Limb Injury

  • Disseminated intravascular coagulation: Treat the underlying infection and shock. Platelets, plasma, cryoprecipitate, or fibrinogen concentrate are considered for clinically significant bleeding, procedures, or profound deficiency—not laboratory abnormalities alone.
  • Purpura fulminans: Photograph and map lesions, protect skin, relieve pressure, and involve dermatology, plastic surgery, vascular surgery, orthopaedics, and wound specialists early.
  • Compartment syndrome: Increasing pain, swelling, tense compartments, reduced sensation, or impaired circulation requires urgent surgical assessment.
  • Necrotic tissue: Debridement or amputation may be delayed until circulation stabilises and tissue boundaries become clearer, unless immediate surgery is needed for infection or compartment pressure.
  • Adrenal haemorrhage: Consider stress-dose corticosteroids when refractory shock and adrenal failure are suspected.
  • Pain control: Severe skin and limb injury requires structured analgesia while maintaining neurological monitoring.

Infection Control and Public-Health Actions

  • Use droplet precautions until effective antibiotics have been given for the locally required interval.
  • Notify public-health authorities immediately where required.
  • Identify the infectious period and eligible close contacts.
  • Provide clear information without naming the patient unnecessarily.
  • Send isolates or specimens for serogrouping, susceptibility, and molecular typing.
  • Assess whether the case is part of a school, university, workplace, institutional, or community outbreak.

Management of Close Contacts

Antibiotic prophylaxis eradicates throat carriage and reduces secondary disease. It should be given as soon as possible, ideally within 24 hours of identifying the index case. Public-health professionals determine eligibility; vaccination does not replace prophylaxis after a qualifying exposure.

  • Usually eligible: Household members, intimate partners, childcare-room contacts, and people directly exposed to oral or respiratory secretions.
  • Healthcare exposure: Unprotected mouth-to-mouth ventilation, intubation, suctioning, or close airway procedures may qualify; routine care usually does not.
  • Drug options: Rifampicin, ceftriaxone, ciprofloxacin, or—where resistance guidance indicates—azithromycin may be used according to age, pregnancy, contraindications, interactions, and local susceptibility.
  • Not usually eligible: Casual classmates, co-workers, transport passengers, and social contacts without direct secretion exposure.
  • Ongoing vigilance: Prophylaxis is not fully protective; contacts with symptoms need emergency assessment.

Vaccination

Vaccination is the primary long-term prevention strategy. Conjugate vaccines protect against serogroups A, C, W, and Y; protein-based vaccines protect against serogroup B; combined products are available in some settings. No vaccine covers every strain, and schedules differ by country.

  • Follow routine infant, adolescent, or young-adult vaccination schedules.
  • Use risk-based vaccination for asplenia, complement deficiency, complement-inhibitor therapy, HIV where recommended, microbiology exposure, travel, or outbreak risk.
  • Give booster doses while increased risk continues.
  • Check destination-specific requirements before Hajj, Umrah, or travel to epidemic areas.
  • Seek urgent care for compatible symptoms even when fully vaccinated.
  • Use strain-specific public-health vaccination during outbreaks when indicated.

Complications

  • Septic shock: Persistent hypotension, severe acidosis, and inadequate tissue oxygen delivery.
  • Disseminated intravascular coagulation: Simultaneous microvascular clotting and bleeding.
  • Purpura fulminans: Extensive skin haemorrhage, necrosis, scarring, and tissue loss.
  • Limb ischaemia: Digital loss, compartment syndrome, growth-plate injury, contractures, or amputation.
  • Organ failure: Acute kidney injury, respiratory failure, myocardial dysfunction, liver injury, and encephalopathy.
  • Waterhouse–Friderichsen syndrome: Bilateral adrenal haemorrhage with adrenal failure and refractory shock.
  • Neurological complications: Meningitis, seizures, stroke, hearing loss, cognitive impairment, or motor disability.
  • Psychological consequences: Post-traumatic symptoms, depression, anxiety, grief, altered body image, and survivor guilt.
  • Death: Fulminant disease can be fatal despite rapid treatment.

Recovery and Rehabilitation

Recovery ranges from rapid improvement after early uncomplicated treatment to prolonged intensive care, repeated surgery, and years of rehabilitation. Fatigue, weakness, pain, poor sleep, concentration difficulty, and emotional distress can continue after organ function appears to recover. Children may reveal learning, hearing, growth, or behavioural effects only later.

  • Audiology for hearing loss following meningitis or intensive-care illness.
  • Neurology and neuropsychology for seizures, cognition, behaviour, and school or work function.
  • Physiotherapy and occupational therapy for weakness, endurance, balance, mobility, self-care, and return to activity.
  • Plastic, vascular, orthopaedic, prosthetic, and wound services for skin and limb injury.
  • Renal, cardiac, respiratory, and endocrine follow-up after organ failure.
  • Pain and rehabilitation medicine for neuropathic pain, scar sensitivity, contracture, and phantom-limb symptoms.
  • Psychological and social support for patients, siblings, caregivers, and bereaved families.
  • A structured review within weeks of discharge and longer surveillance according to complications.

Prognosis

Outcome is strongly influenced by bacterial burden, time to effective antibiotics, age, immune status, shock severity, lactate and coagulation abnormalities, myocardial depression, neurological involvement, and access to critical care. Current public-health information commonly reports death in approximately 10% to 15% of invasive meningococcal cases and long-term disability in about one in five survivors. Fulminant septicaemia with shock and purpura generally carries greater immediate risk than meningitis without circulatory collapse.

A normal appearance early in illness does not guarantee a mild course, and a survivor who initially seems well can later show hearing, cognitive, psychological, renal, skin, or musculoskeletal consequences. Planned follow-up is part of treatment, not an optional extra.

Prevention Beyond Vaccination

  • Practise hand and respiratory hygiene and dispose of tissues promptly.
  • Avoid sharing drinks, toothbrushes, smoking or vaping devices, lip products, and utensils contaminated with saliva.
  • Reduce tobacco-smoke exposure.
  • Ensure eligible close contacts receive prophylaxis rapidly.
  • Keep vaccinations and risk-based boosters current.
  • People taking complement inhibitors should carry medical information, follow any prescribed antibiotic prevention plan, and seek immediate care for symptoms even when vaccinated.
  • Laboratories should follow biosafety and post-exposure protocols when handling meningococcal isolates.

Common Misconceptions

  • “There must be a rash.” False. Shock can develop before any skin lesion.
  • “A normal blood pressure rules out shock.” False. Children and young adults may compensate until late.
  • “Neck stiffness must be present.” False. Pure bloodstream infection may have no meningitis symptoms.
  • “Vaccination makes disease impossible.” False. Vaccines do not cover every strain and breakthrough disease occurs.
  • “Everyone in the school needs antibiotics.” False. Public health defines close exposure; casual contacts usually do not qualify.
  • “Tests should confirm the diagnosis before treatment.” False. Antibiotics and resuscitation must begin on clinical suspicion.

Nursing Care of a Patient with Meningococcemia

Overview

Meningococcemia is a life-threatening bloodstream infection caused by Neisseria meningitidis. It may occur with or without meningitis and can progress rapidly to sepsis, septic shock, disseminated intravascular coagulation, purpura fulminans, multi-organ failure, adrenal haemorrhage, limb ischaemia, and death. Common features include fever, chills, malaise, severe weakness, leg pain, cold extremities, tachycardia, hypotension, altered mental status, and a petechial or purpuric rash. Nursing care focuses on rapid recognition, immediate escalation, droplet precautions, prompt antibiotics, sepsis management, haemodynamic support, skin and limb monitoring, family education, and public-health coordination.

Emergency Nursing Assessment

  • Assess airway, breathing, circulation, disability, and exposure immediately, and activate emergency, sepsis, or critical-care response according to facility policy.
  • Monitor vital signs frequently, including temperature, heart rate, respiratory rate, blood pressure, oxygen saturation, capillary refill, skin temperature, urine output, and level of consciousness.
  • Inspect the entire skin surface for petechiae, purpura, non-blanching rash, mottling, bruising, limb colour changes, cool extremities, pain, swelling, or signs of tissue ischaemia.
  • Assess for sepsis and shock: hypotension, tachycardia, tachypnoea, confusion, reduced urine output, delayed capillary refill, weak pulses, cold clammy skin, rising lactate, or worsening perfusion.
  • Assess neurological status, including headache, neck stiffness, photophobia, irritability, drowsiness, seizures, Glasgow Coma Scale, pupils, and signs of meningitis or raised intracranial pressure.
  • Review diagnostic results and urgent tests, including blood cultures, complete blood count, coagulation profile, platelets, electrolytes, renal and liver function, glucose, lactate, blood gas, C-reactive protein or procalcitonin if ordered, and cerebrospinal fluid studies if lumbar puncture is performed safely.
  • Identify high-risk history, such as close contact with a case, dormitory or crowded living, complement deficiency, asplenia, HIV, immunosuppression, travel, outbreak exposure, or incomplete meningococcal vaccination.

Priority Nursing Diagnoses

  • Risk for septic shock related to invasive meningococcal bloodstream infection and systemic inflammatory response.
  • Ineffective tissue perfusion related to hypotension, capillary leak, vasodilation, disseminated intravascular coagulation, or microvascular thrombosis.
  • Hyperthermia related to acute bacterial infection.
  • Risk for bleeding related to thrombocytopenia, disseminated intravascular coagulation, or coagulation abnormalities.
  • Risk for impaired skin integrity related to purpura, tissue ischaemia, oedema, immobility, or poor perfusion.
  • Risk for ineffective cerebral tissue perfusion related to meningitis, sepsis, shock, seizures, or raised intracranial pressure.
  • Deficient knowledge related to disease severity, isolation precautions, antibiotics, prophylaxis for contacts, vaccination, and follow-up care.

Nursing Interventions

  • Place the patient on droplet precautions immediately for suspected or confirmed meningococcal disease, along with standard precautions, and follow facility policy for duration of isolation.
  • Notify the healthcare provider, sepsis team, infection prevention team, and public-health authorities according to local reporting requirements.
  • Support prompt blood culture collection if this does not delay treatment, and ensure prescribed empiric antibiotics such as ceftriaxone or cefotaxime are administered urgently.
  • Provide oxygen as prescribed, monitor respiratory status, and prepare for ventilatory support if respiratory distress, altered consciousness, shock, or severe sepsis develops.
  • Establish intravenous access, administer prescribed isotonic fluids, vasopressors, antipyretics, analgesics, corticosteroids, blood products, or electrolyte replacement, and monitor response closely.
  • Monitor for disseminated intravascular coagulation by trending platelets, coagulation studies, bleeding, bruising, oozing from lines, haematuria, gastrointestinal bleeding, and expanding purpura.
  • Assess limb perfusion and skin integrity frequently, including colour, temperature, capillary refill, pulses, pain, swelling, sensation, movement, and progression of purpuric lesions.
  • Maintain strict intake and output measurement, monitor urine output, daily weight when ordered, renal function, lactate, blood pressure, and signs of fluid overload or worsening shock.
  • Implement seizure, fall, aspiration, pressure-injury, and delirium precautions for patients with altered mental status, seizures, weakness, immobility, or critical illness.
  • Provide emotional support to the patient and family, explain urgent procedures briefly, and coordinate contact tracing, post-exposure prophylaxis, and vaccination guidance through public health.

Patient and Family Education

  • Explain that meningococcemia is a medical emergency caused by meningococcal bacteria in the bloodstream and can worsen quickly without urgent treatment.
  • Teach family members to seek emergency care for fever with a non-blanching rash, severe headache, neck stiffness, confusion, severe weakness, cold hands or feet, rapid breathing, persistent vomiting, seizure, fainting, or extreme drowsiness.
  • Explain droplet precautions and the importance of masks, hand hygiene, respiratory etiquette, and limiting close exposure until the healthcare team says precautions can stop.
  • Teach that close contacts may need post-exposure antibiotics even if they feel well, and public-health staff may help identify who needs prophylaxis.
  • Encourage vaccination review for the patient and close contacts according to local recommendations, including meningococcal vaccines when indicated.
  • Review the need to complete prescribed antibiotics and attend follow-up appointments for hearing, neurological function, skin or limb healing, kidney function, emotional recovery, and rehabilitation if needed.
  • Encourage survivors and families to report persistent fatigue, pain, mood changes, nightmares, concentration problems, hearing changes, weakness, skin wounds, or difficulty returning to school, work, or normal activity.

Expected Outcomes

  • The patient receives urgent antibiotics and sepsis-directed treatment without avoidable delay.
  • The patient maintains adequate airway, oxygenation, blood pressure, tissue perfusion, urine output, and mental status.
  • Fever, rash progression, lactate, coagulation abnormalities, renal function, and signs of shock improve or stabilize according to the treatment plan.
  • The patient remains free from preventable aspiration, falls, pressure injury, uncontrolled bleeding, limb injury, severe dehydration, and avoidable neurological deterioration.
  • Close contacts receive appropriate public-health advice, post-exposure prophylaxis, and vaccination guidance when indicated.
  • The patient and family explain warning signs, isolation precautions, medication use, follow-up needs, and recovery support resources.

Evaluation

Evaluate nursing care by reviewing time to antibiotics, vital signs, oxygenation, perfusion, urine output, neurological status, rash progression, pain, temperature, lactate, blood cultures, renal function, coagulation results, platelet count, bleeding signs, skin integrity, limb perfusion, isolation compliance, contact prophylaxis, family understanding, and follow-up planning. Revise the care plan if shock worsens, bleeding or purpura progresses, respiratory failure develops, seizures occur, renal function declines, limb ischaemia appears, or the patient requires intensive care, surgery, rehabilitation, or additional psychosocial support.

REFERENCES

  1. Domingo, P., Barquet, N. (2001). Meningococcemia. In: Rello, J., Valles, J., Kollef, M.H. (eds) Critical Care Infectious Diseases Textbook. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1679-8_28
  2. Barlam TF. Approach to the Acutely Ill Infected Febrile Patient. In: Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson J, eds. Harrison’s Principles of Internal Medicine. 21st ed. McGraw Hill; 2022.
  3. Mbaeyi SA, Joseph SJ, Blain A, Wang X, Hariri S, MacNeil JR. Meningococcal Disease Among College-Aged Young Adults: 2014-2016Pediatrics. 2019 Jan;143(1):e20182130. doi:10.1542/peds.2018-2130
  4. Centers for Disease Control and Prevention (U.S.). Meningococcal Disease (https://www.cdc.gov/meningococcal/index.html) (Multiple pages accessed). Last reviewed 2/7/2022.
  5. Thompson MJ, Ninis N, Perera R, et al. Clinical recognition of meningococcal disease in children and adolescents (https://pubmed-ncbi-nlm-nih-gov.ccmain.ohionet.org/16458763/)Lancet. 2006 Feb 4;367(9508):397-403.

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