Introduction
Background
Meningitis is an infection of the linings of the brain and ventricles that can be divided into 3 general categories: pyogenic, granulomatous, and lymphocytic.
Pyogenic (bacterial) meningitis is a potentially life-threatening disease that consists of inflammation of the meninges and the underlying subarachnoid cerebrospinal fluid (CSF). The specific infective agents that are involved vary among different patient age groups, and the inflammation may evolve into ventriculitis, empyema, cerebritis, and abscess formation. If not treated, bacterial meningitis may lead to lifelong debility or death.1,2
Chronic mastoiditis and epidural empyema in a patient with bacterial meningitis. This axial computed tomography scan shows sclerosis of the temporal bone (chronic mastoiditis), an adjacent epidural empyema with marked dural enhancement (arrow), and the absence of left mastoid air.
Subdural empyema and arterial infarct in a patient with bacterial meningitis. This contrast-enhanced axial computed tomography scan shows left-sided parenchymal hypoattenuation in the middle cerebral artery territory, with marked herniation and a prominent subdural empyema.
For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education articles Meningitis in Adults, Meningitis in Children, and Brain Infection.
Pathophysiology
Usually, the brain is naturally protected from the body's immune system by a barrier the meninges create between the bloodstream and the brain. Normally, this protection is an advantage because the barrier prevents the body from attacking itself. However, in meningitis, the barrier can become a problem; once bacteria or other organisms have found their way to the brain, they are somewhat isolated from the immune system and can spread. When the body tries to fight the infection, the problem can worsen; blood vessels become leaky and allow fluid, white blood cells, and other infection-fighting particles to enter the meninges and brain. This process, in turn, causes brain swelling and can eventually result in decreasing blood flow to parts of the brain, worsening the symptoms of infection.3
Pyogenic organisms may reach the leptomeninges and cause meningitis via several routes, including the following:
- Bacterial seeding usually occurs via hematogenous spread. Organisms usually enter the meninges through the bloodstream from other parts of the body. Many meningitis-causing bacteria are carried in the nose and throat, often without symptoms in the carrier.
- Bacterial seeding results in increased permeability of the blood-brain barrier, cerebral edema, and the presence of toxic mediators in the CSF. Inflammations are characterized by polymorphonuclear cell infiltration and extensive fibrinous exudation, which extends throughout the CSF, basal cisterns, and cranial nerves. Acute leptomeningitis results in congestion and hyperemia of the pia-arachnoid and distention of the subarachnoid space by the exudates.
- Local extension from contiguous extracerebral infection (eg, otitis media, mastoiditis, or sinusitis) is a common cause. Possible pathways for the migration of pathogens from the middle ear to the meninges include the following:
- A systemic route in the bloodstream
- Along preformed tissue planes (eg, posterior fossa)
- Temporal bone fractures
- The oval or round window membranes of the labyrinths
Congenital malformation of the stapedial footplate has also been implicated.
- Direct implantation of bacteria into the meninges occurs less frequently and is a complication of head and neck surgery, penetrating head injury, comminuted skull fracture, and osteomyelitic erosion. Skull fractures can tear the dura and cause a CSF fistula, especially in the region of the frontal ethmoid sinuses. Patients with any of these conditions are at risk for bacterial meningitis.
- The pathogenesis of neonatal meningitis is related to labor delivery as a result of colonized pathogens in the maternal intestinal or genital tract, immaturity, and environment.
In 50% of patients, several complications may develop in the days to weeks following infection.
- Infarction and venous thrombosis: In cerebral infarction, endothelial cells swell, proliferate, and crowd into the lumen of the blood vessel, and inflammatory cells infiltrate the blood vessel wall. Foci of necrosis develop in the arterial and venous walls and induce arterial and venous thrombosis. Venous thrombosis is more frequent than arterial thrombosis, but both arterial and venous cerebral infarctions can be seen in 30% of patients.
- Cerebritis and abscess: Inflammation often extends along the perivascular (Virchow-Robin) spaces into the underlying brain parenchyma. Commonly, cerebritis results from direct spread of infection, either from otorhinologic infection or meningitis (including retrograde septic thrombophlebitis) or from hematogenous spread from an extracranial focus of infection. Parenchymal involvement, with edema and mass effect, may be localized or diffuse. Cerebritis can evolve to frank abscess formation in the gray matter–white matter junction.
- Subdural effusions and empyema: In children with meningitis who are younger than age 1 year, 20-50% of cases are complicated by sterile subdural effusions. Most cases are transient and small to moderate in size. Of these effusions, 2% are infected secondarily and become subdural empyemas. In the empyema, infection and necrosis of the arachnoid membrane permits formation of a subdural collection.
- Ventriculitis: Ventriculitis may occur through the involvement of the ependymal lining of the ventricles in 30% of patients. This complication is especially common in neonates, with an incidence as high as 92%. The organisms enter the ventricles via the choroid plexuses. As a result of reduced CSF flow, and possibly reduced secretion of CSF by the choroid plexus, the infective organisms remain in the ventricles and multiply.
- Hydrocephalus: Ventriculomegaly can occur early or late in the course of meningitis and is usually transient and mild to moderate in severity. As a result of the subarachnoid inflammatory exudate, CSF pathways may become obstructed, leading to hydrocephalus. Exudates in the foramina of Luschka and Magendie can cause noncommunicating hydrocephalus, whereas exudates that accumulate in the basilar cisterns or over the cerebral convexity can develop into communicating hydrocephalus.
- Cerebral edema: Some degree of cerebral edema is common with bacterial meningitis. This complication is an important cause of death.
- Seizures: Seizures are a common and important complication that occur in approximately one fifth of patients. The incidence is higher in patients younger than age 1 year, reaching 40%. Approximately one half of patients with this complication have repeated seizures. Patients die as a result of diffuse CNS ischemic injury or from systemic complications.
Anyone can contract bacterial meningitis, but the disease occurs most commonly in infants and children. Meningitis is caused by various pathogens depending on the patient’s age group.4 In neonates, Group B (49%) and non-group B Streptococcus species, Escherichia coli (18%) , and Listeria monocytogenes (7%) are the most common causative organisms.4 Children and infants acquire meningitis from infection with Haemophilus influenzae (40-60%), Neisseria meningitidis (25-40%) , and Streptococcus pneumoniae (10-20%). The sources of adult meningitis include S pneumoniae (30-50%) , N meningitidis (10-35%) , Staphylococcus (5-15%), other Streptococcus species, H influenzae (1-3%), gram-negative bacilli (1-10%), and L monocytogenes.
Risk factors for bacterial meningitis include pulmonary infection, otitis media, mastoiditis, head trauma, alcoholism, splenectomy, sickle cell disease, and immunosuppression. People who have had close or prolonged contact with a patient with meningitis caused by N meningitidis or H influenzae can also be at increased risk. This includes people in the same household or daycare center or anyone who has direct contact with the oral or nasal discharges of a patient with bacterial meningitis.
Frequency
United States
With almost 8000 cases and 2000 deaths occurring annually, bacterial meningitis continues to be a significant source of morbidity and mortality.
- The incidence of neonatal bacterial meningitis is 0.25-1 case per 1000 live births. In addition, the incidence is 0.15 case per 1000 full-term births and 2.5 cases per 1000 premature births. Approximately 30% of newborns with clinical sepsis have associated bacterial meningitis.
- The frequency of H influenzae type b disease has been markedly reduced, but N meningitidis causes approximately 4 cases per 100,000 children aged 1-23 months. The risk of secondary meningitis is 1% for family contacts and 0.1% for daycare contacts. The rate of meningitis caused by S pneumoniae is 6.5 cases per 100,000 children aged 1-23 months.
- Statistics show an increased incidence in persons aged 60 years and older, independent of other factors. Annual incidences are 1.7-7.2 cases per 100,000 adults, and the mean annual incidence has been reported as 3.8 cases per 100,000 adults. Of patients with bacterial meningitis, 61% had no previous or present accompanying diseases that may have predisposed them to meningitis.
International
In parts of Africa, widespread epidemics of meningococcal meningitis occur regularly. In 1996, the biggest wave of meningococcal meningitis outbreaks ever recorded was in West Africa. An estimated 250,000 cases and 25,000 deaths occurred in Niger, Nigeria, Burkina Faso, Chad, and Mali.
Mortality/Morbidity
Bacterial meningitis can be extremely serious. Morbidity, mortality, and prognosis depend on the pathogen, the patient's age and condition, and the severity of acute illness.
- Mortality rates are highest in the first year of life, decrease in mid life, and increase again in old age. Bacterial meningitis is fatal in 1 in 10 cases, and 1 in 7 survivors is left with a severe handicap, such as deafness or brain injury. Among bacterial pathogens, pneumococcal meningitis causes the highest mortality rate, which is 20-30% in adults and 10% in children, with a morbidity rate greater than 30% in those who are affected. Patients with meningococcal meningitis have a better prognosis, with a mortality rate of 4-5%; however, patients with meningococcemia have a poor prognosis, with a mortality rate of 20-30%.
- The prognosis depends on both the severity and the cause of the meningitis. Despite effective antimicrobial and supportive therapy, mortality rates among neonates remain high, with significant long-term sequelae in survivors. Bacterial meningitis also causes long-term sequelae and results in significant mortality beyond the neonatal period. Prolonged or difficult-to-control seizures are predictors of a complication. Cerebral infarction and edema are predictors of poor outcome, as are the signs of disseminated intravascular coagulopathy and endotoxic shock.
- Advanced bacterial meningitis can lead to brain damage, coma, and death. Long-term sequelae are seen in as many as 30% of survivors and vary with etiologic agent, patient age, presenting features, and hospital course. Patients usually have subtle CNS changes. Serious complications include hearing loss, cortical blindness, other cranial nerve dysfunction, paralysis, muscular hypertonia, ataxia, multiple seizures, mental motor retardation, focal paralysis, ataxia, subdural effusions, hydrocephalus, and cerebral atrophy.
Race
Statistically, blacks appear to contract meningitis more frequently than do people of other races.
Sex
In neonates, the male-to-female ratio is 3:1. Male infants have a higher incidence of gram-negative neonatal meningitis. In adults, group B Streptococcus infection affects men and women equally.
Age
Nonepidemic meningitis is most common in neonates, infants, and children. Epidemic meningitis can occur at any age. The average age for those affected with bacterial meningitis is 25 years.
- Most patients are children younger than age 5 years, and 70% of cases occur in children younger than age 2 years.
- Rates of bacterial meningitis are highest among infants. The peak incidence is at age 3-8 months.
Anatomy
Infections of the CNS can be divided into 2 broad categories: those primarily involving the meninges (meningitis) and those primarily confined to the parenchyma (encephalitis).
The meninges are membranes that enclose the brain and spinal cord. The membrane is found in 3 layers: the dura (a tough outer layer), the arachnoid (a lacy weblike middle layer), and the subarachnoid space (a delicate, fibrous inner layer that contains many of the blood vessels that feed the brain and spinal cord).
Meningitis is anatomically divided into inflammation of the dura, sometimes referred to as pachymeningitis, which is less common, and leptomeningitis, which is more common and is defined as inflammation of the arachnoid tissue and subarachnoid space.
On the basis of the finding of abundant pus, pachymeningitis most often results from a bacterial infection (usually due to staphylococcal or streptococcal organisms) that is localized to the dura. The source of the organisms is most often a skull defect (eg, skull fracture), an infection of the paranasal sinuses, or cranial osteomyelitis. Leptomeningitis is the type of meningitis usually referred to when the term meningitis is used alone.
The most common cause of meningeal inflammation is irritation caused by bacterial or viral infections. The organisms usually enter the meninges through the bloodstream from other parts of the body. Most cases of bacterial meningitis are localized over the dorsum of the brain; however, under certain conditions, meningitis may be concentrated at the base of the brain, such as with fungal diseases and tuberculosis (TB).
Depending on the severity of bacterial meningitis, the inflammatory process may remain confined to the subarachnoid space. In less severe forms, the pial barrier is not penetrated, and the underlying parenchyma remains intact. However, in more severe forms of bacterial meningitis, the pial barrier is broken, and the underlying parenchyma is invaded by the inflammatory process. Thus, bacterial meningitis may lead to widespread cortical destruction, particularly when left untreated.
Presentation
Meningitis usually develops rapidly. The clinical presentation varies with the age of the patient, and there is a distinct difference between the signs and symptoms in neonates and young infants and those in older children and adults.5,6
Symptoms
High temperature, headache, and a stiff neck are common symptoms of meningitis in anyone older than age 2 years. These symptoms can develop over several hours or over 1-2 days. Other symptoms may include nausea, vomiting, discomfort when the patient looks into bright lights, confusion, and sleepiness. Occasionally, if the patient has been taking antibiotics for another infection, the symptoms can take longer to develop or they may be less intense.
About 85% of adults and children exhibit the classic triad (fever, headache, neck stiffness) of bacterial meningitis.4 One quarter of affected patients have a fulminant onset within 24 hours of infection, and there may be a history of a respiratory illness within the preceding 7 days (50%). Other presenting symptoms include vomiting in 35% and impaired consciousness.
Newborns and small infants may not present with the classic symptoms, or the symptoms may be difficult to detect. The infant may only appear to be slow or inactive, or he or she may be irritable, vomiting, or feeding poorly. Other symptoms in this age group include temperature instability, high-pitched crying, respiratory distress, and/or bulging fontanelles (late sign in one third of neonates).
As bacterial meningitis progresses, patients of any age may have seizures (30% of adults and children; 40% of newborns and infants).
Signs
Approximately half of affected adults show signs of meningeal irritation such as nuchal and/or spinal rigidity and a positive Kernig and/or Brudzinski sign.4 On physical examination, a skin rash caused by meningococcal meningitis (50%), H influenzae, pneumococcal meningitis, echovirus type 9, or Staphylococcus aureus may be present.4 Other neurologic signs include cranial nerve palsies, focal cerebral signs (10-20%), and papilledema (<1%).
Early diagnosis and treatment of bacterial meningitis are essential. Usually, the diagnosis is made by laboratory examination of cultured bacteria from a CSF sample. More specialized laboratory tests, which may include other cultures of CSF and blood specimens, are needed for identification of the bacteria and the serogroup, as well as the organism’s susceptibility to antibiotics.
In an analysis of retrospective, multicenter, hospital-based cohort studies, Dubos et al confirmed that measurement of the procalcitonin (PCT) level is the best biological marker to differentiate bacterial meningitis from aseptic meningitis in children in the emergency department. Sensitivity and specificity of the PCT level in distinguishing between bacterial and aseptic meningitis were 99% and 83%, respectively.7
Starting treatment early in the course of the disease is crucial. Appropriate antibiotic treatment for the most common types of bacterial meningitis should reduce the risk of death to less than 15%, although the risk is higher among elderly patients.
Preferred Examination
Acute bacterial meningitis is a clinical diagnosis that is established by the affected patient's history, physical examination findings, and laboratory results.8,9
Chronic mastoiditis and epidural empyema in a patient with bacterial meningitis. This axial computed tomography scan shows sclerosis of the temporal bone (chronic mastoiditis), an adjacent epidural empyema with marked dural enhancement (arrow), and the absence of left mastoid air.
Frontal sinusitis, empyema, and abscess formation in a patient with bacterial meningitis (same patient as in Images 3-4 in Multimedia). This contrast-enhanced, axial T1-weighted magnetic resonance image shows a right frontal parenchymal low intensity (edema), leptomeningitis (arrowheads), and a lentiform-shaped subdural empyema (arrows).
Frontal sinusitis, empyema, and abscess formation in a patient with bacterial meningitis (same patient as in Images 2 and 4 in Multimedia). This T2-weighted axial magnetic resonance image shows frontal sinusitis, a bone defect (arrow) with adjacent cortical edema (arrowhead), and right occipitoparietal subdural fluid collection (empyema).
Frontal sinusitis, empyema, and abscess formation in a patient with bacterial meningitis (same patient as in Images 2-3 in Multimedia). This T2-weighted axial magnetic resonance image shows a developing abscess formation with mass effect and bilateral subdural fluid collections (empyema).
Neuroimaging studies are typically used to monitor complications such as hydrocephalus, subdural effusion, empyema (see Images 1-5, 8-10), and infarction (see Images 8-9, 11) to exclude parenchymal abscess (see Images 4, 7, 12) and ventriculitis. Neuroimaging is indicated in patients who have evidence of head trauma, sinus or mastoid infection (see Images 1-4), skull fracture, and congenital anomalies.
Imaging studies performed in patients with acute meningitis may provide normal findings. The results of an imaging study do not exclude or prove the presence of acute meningitis; prompt diagnosis depends on an accurate clinical assessment. Lumbar puncture is the single most important diagnostic study.
Cerebritis and developing abscess formation in a patient with bacterial meningitis (same patient as in Images 6-7 in Multimedia). This contrast-enhanced, axial computed tomography scan was obtained 1 month after surgery and shows a small, ring-enhanced, hypoattenuating mass (recurrence of abscess) in the left basal ganglia and a left lentiform-shaped subdural fluid collection with enhanced meninges (arrowhead).
Cerebritis and developing abscess formation in a patient with bacterial meningitis (same patient as in Images 5 and 7 in Multimedia). This contrast-enhanced axial computed tomography scan shows leptomeningitis and parenchymal enhancement (cerebritis) with a low-attenuating area (edema) in the left basal ganglia.
Cerebritis and developing abscess formation in a patient with bacterial meningitis (same patient as in Images 5-6 in Multimedia). This contrast-enhanced axial computed tomography scan shows a ring-enhancing, lobulated, hypoattenuating mass (abscess) in the left basal ganglia.
Subdural empyema and arterial infarct in a patient with bacterial meningitis. This contrast-enhanced axial computed tomography scan shows left-sided parenchymal hypoattenuation in the middle cerebral artery territory, with marked herniation and a prominent subdural empyema.
Computed tomography (CT) scanning is often performed first to exclude contraindications for lumbar puncture. Nonenhanced CT scans and magnetic resonance images (MRIs) of patients with uncomplicated acute bacterial meningitis may be unremarkable (Image 13).
Currently, MRI is the most sensitive imaging modality because the presence and extent of inflammatory changes in the meninges, as well as complications, can be detected. MRI is superior to CT scanning in the evaluation of patients with suspected meningitis, as well as in demonstrating leptomeningeal enhancement and distention of the subarachnoid space with widening of the interhemispheric fissure, which is reported to be an early finding in severe meningitis.
Watershed and lacunar infarcts in a patient with bacterial meningitis. This axial computed tomography scan shows a left frontoparietal watershed infarct, a right basal ganglia lacunar infarct, and a bilateral subdural effusion.
Subdural empyema and diffuse cerebral edema in a patient with bacterial meningitis (same patient as in Image 11 in Multimedia). This axial computed tomography scan shows bilateral subdural effusion (empyema) and parenchymal low-attenuating areas.
Subdural empyema and diffuse cerebral edema in a patient with bacterial meningitis (same patient as in Image 10 in Multimedia). This contrast-enhanced computed tomography scan was obtained 1 week after the one in Image 10 and shows diffuse cerebral edema and lacunar infarcts in the thalamus.
Abscess in a patient with bacterial meningitis. This contrast-enhanced computed tomography scan shows a ring-enhancing, hypoattenuating mass (abscess) with peripheral edema and mass effect.
Acute bacterial meningitis (same patient as in Images 14-15 in Multimedia). This axial nonenhanced computed tomography scan shows mild ventriculomegaly and sulcal effacement.
Effusion, hydrocephalus, cerebritis, and abscess can be evaluated well with CT scanning and ultrasonography (US) in infants; however, MRI is the most effective modality for localizing the level of the pathology.
Chest radiographs may be obtained to look for signs of pneumonia or fluid in the lungs, especially in children.
Limitations of Techniques
In uncomplicated cases of purulent meningitis, early CT scans and MRIs usually demonstrate normal findings or small ventricles and effacement of sulci (see Images 13-15). The value of CT scanning in the early diagnosis of subdural empyema is limited because of the presence of bone artifact.
Acute bacterial meningitis (same patient as in Images 14-15 in Multimedia). This axial nonenhanced computed tomography scan shows mild ventriculomegaly and sulcal effacement.
Acute bacterial meningitis (same patient as in Images 13 and 15 in Multimedia). This axial T2-weighted magnetic resonance image shows only mild ventriculomegaly.
Acute bacterial meningitis (same patient as in Images 13-14 in Multimedia). This contrast-enhanced, axial T1-weighted magnetic resonance image shows leptomeningeal enhancement (arrows).
Enhancement of the meninges is seen on contrast-enhanced CT scans and MRIs in cases of bacterial meningitis (see Images 2, 6, 15-17). However, meningeal enhancement is nonspecific and may also be caused by the following 5 different etiologic subgroups:
- Infectious
- Carcinomatous meningitis
- Reactive (eg, surgery, shunt, trauma)
- Chemical (eg, ruptured dermoid and cysticercoid cysts, intrathecal chemotherapy)
- Inflammatory (eg, sarcoidosis, collagen vascular disease)
Differential Diagnoses
| Brain, Abscess | Sinusitis |
| Brain, Venous Sinus Thrombosis | Tuberculosis, CNS |
| Cerebrospinal Fluid, Leak | |
| Herpes Encephalitis | |
| Leptomeningeal Carcinomatosis |
Other Problems to Be Considered
Meningeal reaction (surgery, shunt, trauma)
Fungal meningitis
Chemical meningeal reaction (ruptured dermoid and cysticercoid cysts, intrathecal chemotherapy)
Sarcoidosis
Collagen vascular disease
HIV encephalitis
More on Meningitis, Bacterial |
 Overview: Meningitis, Bacterial |
| Imaging: Meningitis, Bacterial |
| Follow-up: Meningitis, Bacterial |
| Multimedia: Meningitis, Bacterial |
| References |
| Further Reading |
| Next Page » |
References
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Further Reading
Related eMedicine topics
Meningitis (from Infectious Diseases)
Meningitis (from Emergency Medicine)
Staphylococcal Meningitis
Meningitis, Bacterial (from Pediatrics: General Medicine)
Neonatal Meningitis
Clinical guidelines
Practice Guidelines for the Management of Bacterial Meningitis
Prevention and Control of Meningococcal Disease: Recommendations of the Advisory Committee on Immunization Practices (ACIP)
Clinical studies
Dexamethasone in Cryptococcal Meningitis
Vancomycin Concentration in Cerebrospinal Fluid during Pneumococcal Meningitis
Keywords
bacterial meningitis. pyogenic meningitis, purulent meningitis, granulomatous meningitis, lymphocytic meningitis, pachymeningitis, leptomeningitis
