Meningococcal Meningitis

Resumen

Meningococcal meningitis (MM), a form of invasive meningococcal disease (IMD), is a type of meningitis caused by a human-specific bacterium known as Neisseria meningitidis (N. meningitidis), or meningococcus.¹ Meningitis is characterized by inflammation of the membranes (meninges) around the brain or spinal cord. This inflammation can begin suddenly (acute) or develop gradually (subacute). Symptoms may include fever, headache and a stiff neck, sometimes with aching muscles. Additional symptoms include, but are not limited to, nausea, vomiting, altered mental status and sensitivity to light (photophobia).² Skin rashes occur in about half of all individuals with MM.³ Severe complications of MM may include blood clot formation (thrombosis), brain swelling (cerebral edema) and septic shock.⁴

MM is still associated with a high mortality rate and persistent neurological defects, particularly among infants and young children. While the most effective preventative measure for meningococcal disease is vaccination, MM without antibiotic therapy is uniformly fatal.^1,5,6 In addition to proper antibiotic treatment, early detection and early hospital admission are essential to improve patient outcomes.⁴ Patients who receive treatment have a mortality rate of 10-14%, with those who do not receive treatment have a mortality rate of up to 50%.⁷

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Sinónimos

• bacterial meningococcal meningitis
• epidemic cerebrospinal meningitis

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Signos y Síntomas

MM is one of the three most common types of bacterial meningitis, and it progresses more rapidly than any other acute form. MM involves the central nervous system, specifically targeting the meninges–the membranes surrounding the brain and spinal cord. The time between exposure and symptoms (incubation period) averages 3-4 days (range 1-10 days. MM evolves when the bacteria N. meningitidis, progresses from the nose and throat (nasopharyngeal) mucosa to invasion of the deeper mucosal layers (the submucosa). Bacteria may be found in the throat and nose for 2-4 days and even 24 hours after taking antibiotics.⁴ These bacteria rapidly multiply and can lead to a mild (subclinical) infection. Adults may become seriously ill within hours, but the course of infection for children may be even shorter.⁸ Because the initial infection may present as an array of nonspecific symptoms with a fever; the disease may progress rapidly and lead to death of patients within 12-24 hours after onset if left untreated.⁹

Timeline of MM Symptoms in Adolescents and Adults

1. Early (prodromal) phase – hours to 1 day⁷

Symptoms may be vague and flu-like:

• Sore throat
• Fatigue/malaise
• Low-grade fever or chills and rigors
• Nasal congestion/mild headache
• Muscle aches (myalgia)

2. Rapid progression – within 12–24 hours⁷

Sudden escalation of symptoms:

• sudden onset, high-grade fever (103°F (39.4°C) or higher)
• Severe headache
• Nausea and vomiting
• Photophobia
• Neck stiffness
• Chills and rigors
• Leg pain or cold extremities
• Non-blanching petechial rash (in meningococcemia)

This is the “classic meningitis phase” and may overlap with bloodstream infection (meningococcemia).

3. Late or severe phase – 24–48 hours (if untreated)^{10, 11}

Critical symptoms develop:

• Altered mental status/confusion
• Seizures
• Signs of shock (rapid heartbeat [tachycardia]/low blood pressure [hypotension])
• Coma
• Blood clotting problems including purpura fulminans and disseminated intravascular coagulation (DIC)
• Multiorgan failure

The course of MM is less predictable in infants between three months and two years of age. Since the incidence of most types of meningitis is highest among this age group, any unexplained symptoms, particularly fever, need to be closely monitored.

Timeline of MM Symptoms in Infants and Children

Phase 1: early (0–12 hours)

Symptoms may be subtle, vague, and easily mistaken for a viral illness:

• Fever (or sometimes low body temperature in infants)
• Irritability or inconsolable crying
• Poor feeding or refusal to eat
• Sleepiness, drowsiness, or difficulty waking
• Vomiting
• Pale, blotchy, or cool hands and feet
• Floppiness or weak muscle tone (hypotonia)
• Bulging fontanelle (soft spot) in infants
• High-pitched cry

Phase 2: rapid progression (12–24 hours)

More recognizable and serious signs emerge:

• High fever
• Neck stiffness (less common in infants)
• Seizures (may be subtle: eye twitching, body jerks)
• Rapid breathing or grunting
• Leg pain or refusal to walk
• Lethargy, extreme fatigue
• Cold extremities, mottled or bluish skin
• Non-blanching rash (petechiae or purpura)

This is the critical phase when urgent hospital care is needed.

Phase 3: severe or late (24–48+ hours if untreated)

Life-threatening complications may develop:

• Confusion or unresponsiveness
• Coma
• Severe skin bruising from bleeding under the skin (purpura fulminans)
• Signs of septic shock (low blood pressure, rapid heart rate)
• Multiorgan failure
• Death (can occur rapidly without treatment)

Affected people may have neurological problems and other lifelong complications due to brain and nerve cell damage caused by MM including:

• hearing loss/potential deafness
• epilepsy
• spasticity (stiff or rigid muscles) in areas that control movement
• paralysis
• attention deficits
• intellectual disability
• behavioral problems ^11,12
• swelling or inflammation of the brain (cerebral edema or ventriculitis)
• accumulation of fluid in the brain cavity (hydrocephalus)

Dehydration is a common and dangerous complication of (MM) and meningococcemia. It results from high fever, vomiting, poor oral intake, rapid breathing (tachypnea) and fluid leakage into tissues due to vascular injury.¹ Dehydration can rapidly worsen the patient’s status, contributing to low blood volume and shock, exacerbating the risk of organ failure if not urgently corrected with intravenous fluids.^1,2

When the bacterium enters the bloodstream (septicemia), it can trigger Waterhouse-Friderichsen syndrome (WFS), one of the most devastating complications of invasive meningococcal disease.³ WFS, also called fulminant meningococcemia, is characterized by: ³

• Small red or purple skin lesions (petechial hemorrhages)
• Adrenal gland hemorrhage, leading to sudden adrenal failure
• Circulatory collapse resulting in septic shock

Bloodstream infection (meningococcemia) occurs in approximately 10–20% of people with MM.⁴ It typically precedes the onset of meningitis by 24–48 hours.⁴ This systemic form is marked by severe vascular injury and disseminated intravascular coagulation (DIC) — a dangerous disorder of abnormal clotting and bleeding.^4,6

The pathophysiology of meningococcemia includes:⁵

• Formation of clots inside blood vessels (intraluminal thrombosis)
• Hemorrhage around blood vessels (perivascular bleeding)
• Destruction of the blood vessel lining (endothelial necrosis)

In addition, meningococcal infection may present as meningococcal pneumonia, a less common but serious manifestation. Patients with meningococcal pneumonia often exhibit:

• Fever
• Cough
• Shortness of breath (dyspnea)⁶

Recognizing these different clinical syndromes — meningococcal meningitis, meningococcemia and meningococcal pneumonia — is critical for timely diagnosis and appropriate treatment.

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Causas y Herencia

MM is caused by a bacterium known as N. meningitidis, the second leading cause for bacterial meningitis in the United States.¹⁵ There are many different identified serotypes, or groups, of N. meningitidis based on differences in their protective outer layer called a meningococcal polysaccharide capsule.^15,16 Serotypes A, B, C, W, X, and Y cause the majority of human disease.⁷ Groups A and C cause the most epidemic outbreaks; Group B, on the other hand, is typically responsible for sporadic disease.⁹ Most affected individuals in the United States are in groups B and C, while group A is most common in Asia and Africa.⁴

The bacterium is spread by droplets in the air or close contact with an infected person. It collects in the nasopharynx, or post-nasal space, that connects the nasal cavities with the throat. Although it most typically colonizes in the naso- and oropharynx, it can also colonize in other areas of the body such as the anal mucosa, conjunctiva of eyes and urogenital tracts.¹⁵ The urogenital tract and anal canal can also be a habitat for meningococci, meaning N. meningitidis can also be sexually transmitted.⁴ The bacterium is transported to the membranes (meninges) around the brain or spinal cord by the blood. It usually spreads from nearby infected areas such as the nasal sinuses or from the cerebrospinal fluid.¹⁷ Asymptomatic transmission of meningococci is possible and affects about 5-10% of the population.¹⁸

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Frecuencia

U.S. cases of meningococcal disease have increased sharply since 2021 and now exceed pre-pandemic levels. In 2024, 503 confirmed and probable cases were reported based on preliminary data. This is the largest number of U.S. meningococcal disease cases reported since 2013.¹⁹ While people of all ages are at risk of contracting MM, it primarily affects infants, children and young adults. This can be because of their diminishing maternal antibodies, as well as the elevated levels of nasopharyngeal (top region of the throat) bacteria colonization.¹⁵ However, there is an increased incidence rate among adolescents and college-aged young adults. In general, there is a higher rate of infection among males than females.¹⁵ A 2022 outbreak in Florida proved meningococcal bacteria subgroup C to be typical among males who have sex with males. Other members of the public can be affected, since the bacteria can be spread via direct contact and respiratory droplets.⁴

Vaccines can help control meningitis epidemics caused by groups A, B, C, Y, or W.²⁰ Public health officials recommend that all college students take the MM immunization. In particular, those who live in close quarters (dormitories, fraternities and sororities) seem to be the population at the most increased risk due to the close proximity, which allows for faster spread of infection.³ Furthermore, those who frequent bars, consume alcohol, smoke, or are regularly around smokers are at higher risk and should consider vaccination. Students traveling to high-risk areas of the world (e.g., sub-Sahara Africa) should consider vaccination. This is because N. meningitidis is responsible for endemic and epidemic outbreaks of bacterial meningitis in sub-Saharan Africa, also known as the meningitis belt.⁷ In addition, the CDC recommends that immunocompromised individuals, the LGBTQ community, healthcare professionals, microbiologists exposed to N. meningitidis and military recruits to take the vaccine. Patients with HIV, sickle cell disease, complement component deficiency, asplenia (absence of spleen or normal spleen function), individuals taking medications for blood disorders like eculizumab or ravulizumab, and pregnant patients are also urged to take the vaccine.²¹

Other vulnerable communities include those who are affected by rural-to-urban migration, fundamental structural problems in slum or squatter settlements and people who use overpopulated transportation methods.¹

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Enfermedades con síntomas similares

Symptoms of the following disorders may resemble those of MM. Differential diagnosis should account for neurological diseases such as:

Meningitis is characterized by inflammation of the membranes (meninges) around the brain or spinal cord. This inflammation may be caused by different types of bacteria, viruses, fungi, malignant tumors, or reactions to certain injections into the spinal canal.²²

Encephalitis refers to inflammation of the brain. There are different types of this disorder that are caused by different types of viruses. Encephalitis may also be caused by hypersensitivity initiated by a virus or proteins foreign to the body. Symptoms may include headache, drowsiness, hyperactivity and/or general weakness. This disorder may have some symptoms similar to those of meningitis such as a stiff neck, altered reflexes, confusion, speech disorders, convulsions, paralysis and coma.

Other relevant differential diagnosis include:

Tetanus, otherwise known as lockjaw, is a serious bacterial infection caused by the bacterium Clostridium tetani that affects the nervous system and muscles. This bacterium, often found in soil, dust and animal bites, enters the body via wound-sites such as cuts, burns, or deep puncture wounds. Symptoms of a tetanus infection that coincide with MM include muscle stiffness (particularly in the jaw and neck), fever, seizures or sweating.²³

Rabies refers to a disorder transmitted by the saliva of an animal infected with the virus Neurotropic lyssavirus. It affects all warm-blooded species, including humans. Symptoms resembling MM in rabies include fever, headache, chills, paralysis of the limbs and stiffness in the back of the neck.²⁴

As previously mentioned, MM may potentially progress to meningococcemia, resulting in a purpuric rash that becomes difficult to differentiate from:

Rocky Mountain Spotted Fever is an acute infectious disorder transmitted to humans through the bite of an infected tick, usually in wooded areas of the Midwest, Eastern, and Southeastern United States. Fever and rash are among major symptoms. The rash may not develop in all people, possibly making diagnosis difficult. Swelling (edema), headaches, chills, weakness and muscle pains may also occur. Severe headaches, lethargy, confusion, delirium, focal neurological deficits, increased pressure in the skull leading to pressure on and swelling of the optic disk (papilledema), seizures and/or coma may occur in untreated individuals as the nervous system is progressively affected. Some individuals may have a stiff neck due to muscle pain (myalgia) or irritation of membranes surrounding the brain and spinal cord tissue (meningismus).²⁵

Thrombotic thrombocytopenic purpura refers to a blood disorder that results in symptoms such as a diminished number of blood platelets (thrombocytopenia) and red blood cell destruction (hemolytic anemia). It resembles MM in its ability to cause small clots that form in the smallest arteries.²⁶

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Diagnóstico

Patients with meningitis often display the Brudzinski sign (patient flexes both the knees and hips upon passively flexing the neck forward) and Kernig sign (inability to completely extend the knee when lying down) and further testing should immediately be done if these clinical signs are present in the patient.⁴ Physicians should test for N. meningitidis when a patient presents with a sudden fever accompanied by a rash, rapidly progressing infection and early signs of sepsis.⁷ Testing for MM may include imaging techniques such as CT scans or magnetic resonance imaging (MRI).  Computed tomography (CT) scans are often preferred to examine patients who are older than 60 or present with focal neurological deficits, altered mental status, immunodeficiency, papilledema, a history of central nervous system disease, or a new-onset of seizures.¹⁵ Other testing may include examination of the blood and/or skin via culture or PCR to test for the N. meningitidis.⁴ For a definitive diagnosis, cerebral spinal fluid can be extracted via a lumbar puncture, also known as a spinal tap, and tested for the presence of N. meningitidis via laboratory examination.²²

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Tratamiento

Treatment

Vaccine administration is the best protective method against MM.²⁰ As of October 2024, there are 5 meningococcal vaccines that are licensed for use in the United States for prevention of meningococcal disease from 6 of the currently identified 13 serogroups.^19,15 Menveo and MenQuadfi are classified as MenACWY vaccines, as they protect against serogroups A, C, W, and Y that result in meningococcal disease. Bexsero and Trumenba are classified as MenB vaccines, since they protect against serogroup B of meningococcal vaccine. Penbraya is the only pentavalent vaccine, meaning that it offers preventative measures against 5 serogroups: A, B, C, W, and Y. As per the CDC, it is recommended that all children aged 11-12 take the meningococcal conjugate vaccine.²⁰ Adolescent patients with medical conditions are at greater risk for contracting MM and are advised to receive a 2-dose primary series of the MenACWY immunization 8 weeks apart. Booster doses are recommended at age 16, but anyone who receives their initial dose of the MenACWY vaccine after age 16 does not need a booster.²⁰ See the Affected Populations section above for specific recommendations on who should receive the vaccine.

While awaiting bacterial meningitis culture, a preventative treatment of a 3rd-generation cephalosporin, such as cefotaxime or ceftriaxone, should be started.⁷ This antibiotic administration approach is also often accompanied with a steroid, dexamethasone, as well as broad-spectrum antibiotics like vancomycin and ampicillin, particularly for people who are over 50 years old.^7,4 However, dexamethasone should be discontinued once MM is identified, as there is no therapeutic benefit.⁷ In addition to antibiotic administration, it is imperative that isolation restrictions are followed, precautionary steps during contact are used, management of symptoms in the intensive care unit (ICU) occurs, and those at risk who may have been exposed to the infectious bacteria are identified promptly to minimize spread.⁷

Upon confirmation of MM, antibiotics that are effective and recommended for the elimination of N. meningitidis should be started instead.⁹ While ciprofloxacin is intended for adults only, rifampicin is intended for use in every age group but can induce the metabolism of many medications (i.e. anticoagulants), so dosages should be adjusted accordingly. Although it is less convenient due to possible pain upon intramuscular administration, patients who are pregnant or on birth control are recommended to use ceftriaxone. Chloramphenicol is the choice of treatment during MM epidemics, or if the patient is unable to tolerate beta-lactam antibiotics such as penicillin or cephalosporin.¹⁵

If the meningococcal infection becomes severe, there may be a need for resuscitation efforts such as administering fluids and electrolytes intravenously to aid the body’s recovery of balance and improve organ perfusion (blood delivery).¹⁵ Fluid resuscitation may also be used in conjunction with vasopressors as needed to increase blood pressure. Other forms of treatment for severe MM may involve blood transfusions, platelet replacement, or coagulation factor replacement (replacing missing factors to help blood clot properly).⁷

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Investigaciones

Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. Government funding, and some supported by private industry, are posted on this government website.

For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:

Tollfree: (800) 411-1222

TTY: (866) 411-1010

Email: [email protected]

Some current clinical trials also are posted on the following page on the NORD website:
https://rarediseases.org/living-with-a-rare-disease/find-clinical-trials/

For information about clinical trials sponsored by private sources, contact:
www.centerwatch.com

For information about clinical trials conducted in Europe, contact:
https://www.clinicaltrialsregister.eu/

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Referencias

1. Chhabria D, Anjankar A. An Overview of Meningococcal Disease’s Recent Diagnostic and Treatment Model. Cureus. 2023;15(11):e48509. Published 2023 Nov 8. doi:10.7759/cureus.48509

2. Borrow R, Findlow J. The important lessons lurking in the history of meningococcal epidemiology. Expert Review of Vaccines. 2024;23(1):445-462. doi:https://doi.org/10.1080/14760584.2024.2329618

3. Meningococcal Disease. Centers for Disease Control and Prevention (CDC) Feb 1, 2024. https://www.cdc.gov/meningococcal/about/index.html Accessed Oct 1, 2025.

4. Shaheen N, Mohamed A, Soliman Y, et al. Up-to-Date Review of Meningococcal Meningitis: Global Challenges and Recommendations. Dubai Medical Journal. Published online January 19, 2023:1-13. doi:https://doi.org/10.1159/000527855

5. Bennett JC, Plum F. Cecil Textbook of Medicine. W.B. Saunders Co.; 1996.

6.Ragunathan L, Ramsay M, Borrow R, Guiver M, Gray S, Kaczmarski EB. Clinical Features, Laboratory Findings and Management of Meningococcal Meningitis in England and Wales: Report of a 1997 Survey. Journal of Infection. 2000;40(1):74-79. doi:https://doi.org/10.1053/jinf.1999.0595

7. Rausch-Phung EA, Hall WA, Ashong D. Meningococcal Disease (Neisseria meningitidis Infection) [Updated 2025 Jun 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549849/ Accessed Oct 1, 2025.

8. Kastenbauer S, Grabein B, Pfister HW. Prophylaxe der Meningokokken Meningitis. Der Nervenarzt. 2000;71(2):134-137. doi:https://doi.org/10.1007/s001150050020

9. Łyczko K, Borger J. Meningococcal Prophylaxis(Archived) [Updated 2023 May 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537338/ Accessed Oct 1, 2025.

10. Girgis NI, El-Ella A, Farid Z, Haberberger RL, Woody JN. Ceftriaxone Alone Compared to Ampicillin and Chloramphenicol in the Treatment of Bacterial Meningitis. Chemotherapy. 1988;34(1):16-20. doi:https://doi.org/10.1159/000238642

11. What is Meningococcal Meningitis. WebMD. March 28, 2024. https://www.webmd.com/children/meningococcal-meningitis-symptoms-causes-treatments-and-vaccines Accessed Oct 1, 2025.

12. Orphanet. Meningococcal meningitis. https://www.orpha.net/en/disease/detail/33475?name=meningococcal%20meningitis&mode=name Accessed Oct 6, 2025.

13. Chang KH, Han MH, Roh JK, Kim IO, Han MC, Kim CW. Gd-DTPA-enhanced MR imaging of the brain in patients with meningitis: comparison with CT. AJNR Am J Neuroradiol.1990;11(1):69-76.
14. Deghmane AE, Taha S, Taha MK. Global epidemiology and changing clinical presentations of invasive meningococcal disease: a narrative review. Infectious Diseases. 2021;54(1):1-7. doi:https://doi.org/10.1080/23744235.2021.1971289

15. Yadav S, Rammohan G. Meningococcal Meningitis(Archived) [Updated 2023 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560591/ Accessed Oct 27, 2025.

16. van Soest TM, Chekrouni N, van Sorge NM, Bijlsma MW, Brouwer MC, van de Beek D. Epidemiology, clinical features and outcome of adults with meningococcal meningitis: a 15-year prospective nationwide cohort study. The Lancet Regional Health – Europe. 2023;30:100640. doi:https://doi.org/10.1016/j.lanepe.2023.100640

17. de Assis Aquino Gondim F. Meningococcal Meningitis. Medscape. Updated Feb 6, 2025. https://emedicine.medscape.com/article/1165557-overview Accessed Oct 27, 2025.

18. CDC Yellow Book 2024: Health Information for International Travel. April 4,2023.

19. Meningococcal Disease Surveillance and Trends. Centers for Disease Control and Prevention (CDC). May 9, 2025. https://www.cdc.gov/meningococcal/php/surveillance/index.html Accessed Oct 15, 2025.

20. CDC. Types of Meningococcal Vaccines. Meningococcal Disease. Published July 1, 2025. https://www.cdc.gov/meningococcal/vaccines/types.html Accessed Oct 27, 2025.

21. CDC. Chapter 14: Meningococcal Disease. Epidemiology and Prevention of Vaccine- Preventable Diseases. April 25, 2024. https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-14-meningococcal-disease.html Accessed Oct 27, 2025.

22. Meningitis. National Organization for Rare Disorders. 2009. https://rarediseases.org/rare- diseases/meningitis/ Accessed Oct 27, 2025.

23. Tetanus. National Organization for Rare Disorders. tetanus – National Organization for Rare Disorders Accessed Oct 27, 2025.

24. Rabies. National Organization for Rare Disorders. 2009. https://rarediseases.org/rare-diseases/rabies Accessed Oct 27, 2025.

25. Rocky Mountain Spotted Fever. National Organization for Rare Disorders. 2009. https://rarediseases.org/rare- diseases/rocky-mountain-spotted-fever/ Accessed Oct 27, 2025.

26. Thrombotic Thrombocytopenic Purpura. National Organization for Rare Disorders. 2025. https://rarediseases.org/rare-diseases/thrombotic-thrombocytopenic-purpura/ Accessed Oct 27, 2025.

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