In 1661, Thomas Willis wrote an epidemiological report on meningitis, describing the patients as having “inflammation of the meninges with a continual fever.” However, despite breakthroughs in diagnosis, treatment, and vaccination, in 2015 there were 8.7 million reported cases of meningitis worldwide with 379,000 subsequent deaths.
Meningitis is defined as an infection that causes inflammation of the meninges. The meninges are the three membranes (the dura mater, arachnoid mater, and pia mater) that line the vertebral canal and skull and enclose the brain and spinal cord). Encephalitis is inflammation of the brain itself.
The causative agents of meningitis include bacteria, viruses, and fungi.
In the United States, the annual incidence of bacterial meningitis in the is approximately 2.5 cases/100,000 population with a case fatality rate of 14.3%, despite appropriate therapy.
The bacterial pathogens causing meningitis most commonly in the United States are:
Many viruses can cause meningitis, but the rates are unknown given that most cases are self-limited and go unreported. Of note, there is an increased incidence in summer from enteroviruses and picornaviruses.
The rates of survival for viral meningitis are far better than bacterial meningitis. Complications can be systemic such as orchitis and pancreatitis, but these are typically self-limited. One serious consequence of viral meningitis is viral encephalitis. This is characterized by altered mental status and coma. HSV encephalitis is associated with an approximately 30% mortality rate (with antiviral treatment), and long-term complications such as temporal lobe seizures, motor deficits, and change in mentation.
Less common organisms such as Staphylococcus aureus and Mycobacterium tuberculosis should be considered in susceptible populations such as post-op patients, the immuno-compromised.
Fungal meningitis typically is associated with an immunocompromised host (HIV/AIDS, chronic steroid therapy, cancer patients).
Fungi causing meningitis include:
Meningitis typically occurs through two routes of inoculation:
Direct Contiguous Spread
Viruses can penetrate the central nervous system (CNS) via retrograde transmission along neuronal pathways or by hematogenous seeding.
Infection typically begins with bacterial colonization of the nasopharynx and subsequent mucosal invasion. Once in the bloodstream, the bacteria causing meningitis have a polysaccharide capsule preventing neutrophilic phagocytosis and complement-mediated bactericidal activity.
Bloodborne bacteria cross the blood-brain barrier at the intra-ventricular choroid plexus by directly infecting the choroid plexus epithelial cells. Once there, the bacteria can proliferate given that normal CSF is devoid of host immune defenses.
The bacterial-induced immune-mediated reaction in the CSF along with bacterial cell lysis by antibiotics leads to a massive inflammatory response. This inflammatory response leads to vasogenic edema, interstitial edema, hydrocephalus, increased intracranial pressure and brain herniation.
Meningitis can have a varied clinical presentation. Classic symptoms include fever, neck pain, and petechiae/purpura. These symptoms along with signs of increased intracranial pressure (altered mental status, neurologic deficits, and seizures) portend a poor prognosis. More non-specific symptoms can include a headache, dizziness and nausea/vomiting.
The following risk factors should increase clinical suspicion:
The physical exam is centered on identifying focal neurologic deficits, characteristic skin lesions (petechiae and purpura) and meningeal irritation (Brudzinski and Kernig signs).
Absence of the above does not rule out meningitis.
The CSF findings expected in bacterial, viral and fungal meningitis are listed in the chart: Expected CSF Findings in Bacterial versus Viral versus Fungal Meningitis 2.
Obtaining a sample of CSF can be very difficult and/or take significant amounts of time, thus when the diagnosis of bacterial meningitis is seriously considered, antibiotics should be initiated before performing the LP.
Computed Tomography (CT) of the Head Before Lumbar Puncture
There is controversy regarding the adage that the lumbar puncture is the inciting event causing brain herniation and death in the setting of increased intracranial pressure caused by acute bacterial meningitis.
Currently, guidelines recommend empiric antibiotics and supportive care, while forgoing the lumbar puncture if there is clinical suspicion of increased intracranial pressure or impending brain herniation.
Signs and symptoms of impending herniation include:
It is important to note that a normal head CT does not preclude increased intracranial pressure or impending brain herniation. If the clinical symptoms are consistent with impending herniation, regardless of whether or not the CT head is normal, avoid the LP and start treatment.
Managing the airway, maintaining oxygenation, giving sufficient intra-venous fluids while providing fever control are parts of the foundation of sepsis management.
The type of antibiotic is based on the presumed organism causing the infection. The clinician must take into account patient demographics and past medical history in order to provide the best antimicrobial coverage.
Current Empiric Therapy
Neonates - Up to 1 month old
More than 1 month old
Adults (18 to 49 years old)
Adults older than 50 years old and the immunocompromised
Meningitis associated with foreign body (post-procedure, penetrating trauma)
Meningitis with severe penicillin allergy
Fungal (Cryptococcal) meningitis
Administration of dexamethasone 10 mg IV before or with the first dose of antibiotics has been shown to reduce the risk of morbidity and mortality, especially in the setting of S. pneumoniae infection.
It is important to note; the Infectious Disease Society of America recommends against dexamethasone if the patient has already received antibiotics.
Increased Intracranial Pressure
If the patient develops clinical signs of increased intracranial pressure, interventions to maintain cerebral perfusion include:
The transmission rate of N. meningitidis is 5% for close contacts, but chemoprophylaxis within 24 hours decreases that by 89%. Thus, chemoprophylaxis is indicated for close contacts of a patient suspected of having bacterial meningitis.
Close contacts include housemates, significant others, those who have shared utensils and health care providers in proximity to secretions (providing mouth-to-mouth resuscitation, intubating without a facemask).
Antibiotic chemoprophylaxis options include:
Differentiating between bacterial, viral, and fungal meningitis may be difficult. CSF analysis may not be conclusive, and cultures do not immediately yield an answer. Given the morbidity and mortality, it is prudent to initiate empiric antibiotic therapy and admit all those with suspected meningitis to the hospital on droplet precautions.
Meningitis is a serious disorder with very high morbidity and mortality. The majority of patients with meningitis first present to the emergency room and a streamlined multidisciplinary approach is vital if one wants to lower the high morbidity. The triage nurse must be fully aware of the signs and symptoms of the illness and refer the patient immediately to the ER physician. Other specialists who are usually involved in the care of these patients are neurologists, pediatricians, intensivists, infectious disease specialists, and pharmacists. If bacterial meningitis is suspected, prompt antibiotics should be started even in the absence of laboratory results. To prevent this infection, education of the public is vital.
The nurse should educate the parents on ensuring that the children are vaccinated against N.meningitidis. The pharmacists should also educate the family about the need for prophylaxis when there is a family member with Neisseria meningitis. All contacts should be educated about the signs and symptoms of the infection and when to return to the emergency room. (Level I)
For patients treated promptly, the prognosis is good. However, patients who present with an altered state of consciousness have a high morbidity and mortality. Some patients may develop seizures during the illness, which are very difficult to control or are prolonged. Any patient with a residual neurological deficit after meningitis treatment is also left with a disability. Patients art the greatest risk for death usually have the following features:
Serious complications in survivors include:
The mortality is highest for children less than 12 months of age and decreases in middle age. However, the mortality rates increase with advancing age. Overall, 10% of patients will die from bacterial meningitis. The mortality is highest when the infection is caused by streptococcus and listeria. Patients with meningococcal meningitis do respond well to treatment, but if the presentation is late with meningococcemia, the mortality rates are nearly 30%. (level II)