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Pediatric Bacterial Meningitis

  • Author: Martha L Muller, MD; Chief Editor: Russell W Steele, MD  more...
 
Updated: Aug 19, 2015
 

Practice Essentials

Pediatric bacterial meningitis is a life-threatening illness that results from bacterial infection of the meninges and leaves some survivors with significant sequelae. Therefore, meticulous attention must be paid to appropriate treatment and monitoring of patients with this disease.

Essential update: Study indicates that heparin and aspirin may discourage stroke in pediatric bacterial meningitis

In a retrospective study of children with bacterial meningitis complicated by stroke, treatment with heparin or aspirin appeared to be safe and to discourage stroke recurrence, with heparin possibly being the more effective of the two medications. Sixteen patients were treated with heparin (6 patients) or aspirin (10 patients), either after an initial infarction or following a recurrence. None of the heparin patients had a stroke following treatment, while four of the aspirin patients (40%) did. However, the 14 patients who received no antithrombotic therapy after an initial stroke had the greatest incidence of infarction, with eight of them (57%) suffering an additional stroke. None of the treated patients experienced an intracranial hemorrhage.[1]

Signs and symptoms

The 3 classic symptoms (less likely in younger children):

  • Fever
  • Headache
  • Meningeal signs

Symptoms in neonates:

  • Poor feeding
  • Lethargy
  • Irritability
  • Apnea
  • Listlessness
  • Apathy
  • Fever
  • Hypothermia
  • Seizures
  • Jaundice
  • Bulging fontanelle
  • Pallor
  • Shock
  • Hypotonia
  • Shrill cry
  • Hypoglycemia
  • Intractable metabolic acidosis

Symptoms in infants and children:

  • Nuchal rigidity
  • Opisthotonos
  • Bulging fontanelle
  • Convulsions
  • Photophobia
  • Headache
  • Alterations of the sensorium
  • Irritability
  • Lethargy
  • Anorexia
  • Nausea
  • Vomiting
  • Coma
  • Fever (generally present, although some severely ill children present with hypothermia)

See Clinical Presentation for more specific information on the signs and symptoms of pediatric bacterial meningitis.

Diagnosis

Definitive diagnosis is based on the following:

  • Bacteria isolated from the CSF obtained via lumbar puncture
  • Meningeal inflammation demonstrated by increased pleocytosis, elevated protein level, and low glucose level in the CSF

Bacterial meningitis score

Components of the bacterial meningitis score[2] are as follows:

  • Positive CSF Gram stain
  • CSF absolute neutrophil count 1000/µL or higher
  • CSF protein level 80 mg/dL or higher
  • Peripheral blood absolute neutrophil count 10,000/µL or higher
  • History of seizure before or at the time of presentation

Specific hematologic, radiographic (eg, computed tomography [CT] and magnetic resonance imaging [MRI]), and other studies assist in diagnosis. CT and MRI may reveal ventriculomegaly and sulcal effacement (see the image below).

Acute bacterial meningitis. This axial nonenhanced Acute bacterial meningitis. This axial nonenhanced CT scan shows mild ventriculomegaly and sulcal effacement.

See Workup for more specific information on testing and imaging modalities for pediatric bacterial meningitis.

Management

IV antibiotics are required; if cause is unknown, agents can be based on child’s age, as follows:

  • < 30 days, ampicillin and an aminoglycoside or a cephalosporin
  • 30-60 days, ampicillin and a cephalosporin; because Streptococcus pneumoniae may occur in this age range, consider vancomycin instead of ampicillin
  • In older children, a cephalosporin or ampicillin plus chloramphenicol with vancomycin (needs to be added secondary to the possibility of S pneumoniae)

Guidelines and recommendations

Infectious Diseases Society of America:

  • Vancomycin plus either ceftriaxone or cefotaxime [3]
  • Duration of therapy:
    • Neisseria meningitidis - 7 days
    • Haemophilus influenzae - 7 days
    • Streptococcus pneumoniae - 10-14 days
    • S agalactiae (GBS) - 14-21 days
    • Aerobic gram-negative bacilli - 21 days or 2 weeks beyond the first sterile culture (whichever is longer)
    • Listeria monocytogenes - 21 days or longer

American Academy of Pediatrics:

  • Duration of therapy should not be shorter than 5 days for meningococcus, 10 days for H influenzae, and 14 days for S pneumoniae [4]

Prevention

Preventive therapy has been shown to reduce mortality and morbidity and consists of the following:

  • Chemoprophylaxis: Rifampin, ceftriaxone, ciprofloxacin; ciprofloxacin and ceftriaxone are more effective against resistant strains of Neisseria meningitidis up to 4 weeks after treatment
  • Haemophilus influenzae type b (Hib): Rifampin chemoprophylaxis for contacts of index cases of invasive Hib disease; MenHibrix provides immunization against Hib and meningococcal serogroups C and Y
  • Neisseria meningitidis: Quadrivalent (ie, A, C, Y, W-135) meningococcal conjugate vaccine recommended for high-risk groups

See Treatment and Medication for more specific information on pharmacologic and other therapies for pediatric bacterial meningitis.

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Background

Pediatric bacterial meningitis is a life-threatening illness that results from bacterial infection of the meninges. Because bacterial meningitis in the neonatal period has its own unique epidemiologic and etiologic features, it will be discussed separately in this article as necessary.

Beyond the neonatal period, the 3 most common organisms that cause acute bacterial meningitis are Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b (Hib). Since the routine use of Hib, conjugate pneumococcal, and conjugate meningococcal vaccines in the United States, the incidence of meningitis has dramatically decreased.

Although S pneumoniae is now the leading cause of community-acquired bacterial meningitis in the United States (1.1 cases per 100,000 population overall), the rate of pneumococcal meningitis is 59% lower than it was before the introduction of the conjugate pneumococcal vaccine in 2000. The incidence of disease caused by S pneumoniae is highest in children aged 1-23 months and in adults older than 60 years.

Predisposing factors include respiratory infection, otitis media, mastoiditis, head trauma, hemoglobinopathy, human immunodeficiency virus (HIV) infection, and other immune deficiency states.

Meningitis is a life-threatening illness and leaves some survivors with significant sequelae. Therefore, meticulous attention must be paid to appropriate treatment and monitoring of these patients. Patients require hospitalization for antibiotic therapy and appropriate support. Adequate fluid administration is necessary to maintain perfusion, especially cerebral perfusion. Fluid restrictions (to prevent cerebral edema) may be more harmful because patients may be under resuscitated. Antibiotics must be promptly administered.

The emergence of penicillin-resistant S pneumoniae has resulted in new challenges in the treatment of bacterial meningitis.

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Pathophysiology

Bacteria reach the subarachnoid space via a hematogenous route and may directly reach the meninges in patients with a parameningeal focus of infection.

Once pathogens enter the subarachnoid space, an intense host inflammatory response is triggered by lipoteichoic acid and other bacterial cell wall products produced as a result of bacterial lysis. This response is mediated by the stimulation of macrophage-equivalent brain cells that produce cytokines and other inflammatory mediators. This resultant cytokine activation then initiates several processes that ultimately cause damage in the subarachnoid space, culminating in neuronal injury and apoptosis.

Interleukin (IL)–1, tumor necrosis factor alpha (TNF-a), and enhanced nitric oxide production play critical roles in triggering inflammatory response and ensuing neurologic damage. Infection and inflammatory response later affect penetrating cortical vessels, resulting in swelling and proliferation of the endothelial cells of arterioles. A similar process can involve the veins, causing mural thrombi and obstruction of flow. The result is an increase in intracellular sodium and intracellular water.

The development of brain edema further compromises cerebral circulation, and this effect can result in increased intracranial pressure (ICP) and uncal herniation. Increased secretion of antidiuretic hormone (ADH), resulting in the syndrome of inappropriate antidiuretic hormone secretion (SIADH), occurs in most patients with meningitis and causes further retention of free water. These factors contribute to the development of focal or generalized seizures.

Severe brain edema also causes midline structures to shift caudally and become entrapped in the tentorial notch or foramen magnum. Caudal shifts produce herniation of the parahippocampal gyri, cerebellum, or both. These intracranial changes appear clinically as an alteration of consciousness and postural reflexes. Caudal displacement of the brainstem causes palsy of the third and sixth cranial nerves. If untreated, these changes result in decortication or decerebration and can progress rapidly to respiratory and cardiac arrest.

Neonatal meningitis

Bacteria from the maternal genital tract colonize the neonate after rupture of membranes, and specific bacteria, such as group B streptococci (GBS), enteric gram-negative rods, and Listeria monocytogenes, can reach the fetus transplacentally and cause infection. Furthermore, newborns can also acquire bacterial pathogens from their surroundings, and several host factors facilitate a predisposition to bacterial sepsis and meningitis.

Bacteria reach the meninges via the bloodstream and cause inflammation. After arriving in the central nervous system (CNS), bacteria spread from the longitudinal and lateral sinuses to the meninges, the choroid plexus, and the ventricles.

IL-1 and TNF-a also mediate local inflammatory reactions by inducing phospholipase A2 activity, initiating the production of platelet-activating factor and the arachidonic acid pathway. This process results in production of prostaglandins, thromboxanes, and leukotrienes. Activation of adhesion-promoting receptors on endothelial cells by these cytokines attracts leukocytes, and the release of proteolytic enzymes from the leukocytes results in altered blood-brain permeability, activation of the coagulation cascade, brain edema, and tissue damage.

Inflammation of the meninges and ventricles produces a polymorphonuclear response, an increase in cerebrospinal fluid (CSF) protein content, and utilization of glucose in CSF. Inflammatory changes and tissue destruction in the form of empyema and abscesses are more pronounced in gram-negative meningitis. Thick inflammatory exudate causes blockage of the aqueduct of Sylvius and other CSF pathways, resulting in both obstructive and communicating hydrocephalus.

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Etiology

Causes in different age groups

Neonates

Bacteria are often acquired from the maternal vaginal flora. Gram-negative enteric flora and GBS are the dominant pathogens. In premature newborns who receive multiple antibiotics, those on hyperalimentation, and those who undergo various surgical procedures, Staphylococcus epidermidis and Candida species are uncommon but are reported in greater frequency in neonates. L monocytogenes is another well-known but fairly uncommon causative pathogen.

Early-onset GBS meningitis occurs during the first 7 days of life as a consequence of maternal colonization and the absence of protective antibody in the neonate; it is often associated with obstetric complications. The disease is seen most often in premature or low-birth-weight babies. Pathogens are acquired before or during the birth process.

Late-onset meningitis is defined as disease occurring after 7 days of life. Causes include perinatally acquired and nosocomial pathogens. Streptococcus agalactiae (GBS) is classified into 5 distinct serotypes: Ia, Ib, Ic, II, and III. Although these serotypes occur with almost equal frequency in the early onset of disease, serotype III causes 90% of late-onset disease.

Use of respiratory equipment in the nursery increases the risk of infection caused by Serratia marcescens,Pseudomonas aeruginosa, and Proteus species. Invasive devices predispose infants to the infections caused by S epidermidis and Pseudomonas, Citrobacter, and Bacteroides species.

Infection with Citrobacter diversus, Citrobacter koseri, Salmonella species, and Proteus species, though uncommon, carries a high mortality. These patients often develop brain abscesses, particularly those with Citrobacter, in whom meningitis produces brain abscesses in 80-90% of cases.

Infants and children

In children older than 4 weeks, S pneumoniae and N meningitidis are the most common etiologic agents. Hib has essentially disappeared in countries where the conjugate vaccine is routinely used.

Causative organisms

Streptococcus pneumoniae

S pneumoniae is a gram-positive, lancet-shaped diplococcus that is the leading cause of meningitis. Of the 84 serotypes, numbers 1, 3, 6, 7, 14, 19, and 23 are the ones most often associated with bacteremia and meningitis. Children of any age may be affected, but the incidence and severity are highest in very young and elderly persons.

In patients with recurrent meningitis, predisposing factors are anatomic defects, asplenia, and primary immune deficiency. Often, the history includes recent or remote head trauma. This organism also has a predilection for causing meningitis in patients with sickle cell disease, other hemoglobinopathies, and functional asplenia. Immunity is type-specific and long-lasting.

S pneumoniae colonizes the upper respiratory tract of healthy individuals; however, disease often is caused by a recently acquired isolate. Transmission is person-to-person, usually via direct contact; secondary cases are rare. The incubation period is 1-7 days, and infections are more common in winter, when viral respiratory disease is prevalent. The disease often results in sensorineural hearing loss, hydrocephalus, and other central nervous system (CNS) sequelae. Prolonged fever despite adequate therapy is common with S pneumoniae meningitis.

Effective antimicrobial therapy can eradicate the organism from nasopharyngeal secretions within 24 hours. However, pneumococci have developed resistance to a variety of antibiotics; this development is seen worldwide. Rates of resistance to penicillin range from 10% to 60%. Multicenter surveillance of pneumococci isolated from the cerebrospinal fluid (CSF) has found resistance rates of 20% to penicillin and 7% to ceftriaxone.

Penicillin resistance in pneumococci is due to alterations in enzymes necessary for growth and repair of the penicillin-binding proteins; thus, beta-lactamase inhibitors offer no advantage. Penicillin-resistant pneumococci are often resistant to trimethoprim-sulfamethoxazole, tetracyclines, chloramphenicol, and macrolides. However, selected third-generation cephalosporins (eg, cefotaxime and ceftriaxone) do exhibit activity against most penicillin-resistant pneumococcal isolates.

At present, all pneumococcal isolates remain susceptible to vancomycin and various oxazolidinones. Several of the fluoroquinolones (eg, levofloxacin), though contraindicated in children, have excellent activity against most pneumococci and achieve adequate CNS penetration.

Tolerance, a trait distinct from resistance, is the term used to characterize bacteria that stop growing in the presence of antibiotic yet do not lyse and die. Pneumococci that are tolerant of penicillin and vancomycin have been described in literature, and a subsequent link to recrudescent meningitis was described in 1 child. The overall incidence and clinical impact of such bacterial strains are unknown. However, the possibility of tolerance should be kept in mind in cases of recurrent pneumococcal meningitis.

Neisseria meningitidis

N meningitidis is a gram-negative, kidney bean–shaped organism that is frequently found intracellularly. Organisms are grouped serologically on the basis of capsular polysaccharide; A, B, C, D, X, Y, Z, 29E, and W-135 are the pathogenic serotypes. In developed countries, serotypes B, C, Y, and W-135 account for most childhood cases. Group A strains are most prevalent in developing countries and have resulted in epidemics of meningococcal meningitis throughout the world, as well as outbreaks in military barracks.

The upper respiratory tract frequently is colonized with meningococci, and transmission is person-to-person via direct contact with infected droplets of respiratory secretions, often from asymptomatic carriers. The incubation period is generally less than 4 days (range, 1-7 days).

Most cases occur in infants aged 6-12 months; a second, lower peak occurs among adolescents. A petechial or purpuric rash frequently is seen. Mortality is significant in patients who have a rapidly progressive fulminant form of the disease. Normocellular CSF also has been reported in patients with meningococcal meningitis. Most deaths occur within 24 hours of hospital admission in patients who have features associated with poor prognosis, such as the following:

  • Hypotension
  • Shock
  • Neutropenia
  • Extremes of age
  • Petechiae and purpura of less than 12 hours’ duration
  • Disseminated intravascular coagulation (DIC)
  • Acidosis
  • Presence of the organism in white blood cells (WBCs) on peripheral smear
  • Low erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) level
  • Serogroup C disease

Higher rates of fatality and physical sequelae (eg, scarring and amputation) are reported in survivors of serogroup C disease. Long-term sequelae are rare in patients who have an uneventful hospital course.

Haemophilus influenzaetype b (Hib)

Hib is a pleomorphic gram-negative rod whose shape varies from a coccobacillary form to a long curved rod. Hib meningitis occurs primarily in children who have not been immunized with Hib vaccine; 80-90% of cases occur in children aged 1 month to 3 years. By age 3 years, a significant number of nonimmunized children acquire antibodies against the capsular polyribophosphate of Hib, which are protective.

The mode of transmission is person-to-person via direct contact with infected droplets of respiratory secretions. The incubation period generally is less than 10 days. Current mortality is less than 5%. Most fatalities occur during the first few days of the illness.

Plasmid-mediated resistance to ampicillin due to the production of beta-lactamase enzymes by bacterium is increasingly being reported: 30-35% of Hib isolates are now ampicillin-resistant. As many as 30% of cases may have subtle long-term sequelae. Administration of dexamethasone early in treatment reduces morbidity and sequelae.

Listeria monocytogenes

L monocytogenes causes meningitis in newborns, immunocompromised children, and pregnant women. The disease also has been associated with the consumption of contaminated foods (eg, milk and cheese). Most cases are caused by serotypes Ia, Ib, and IVb. Signs and symptoms in patients with listerial meningitis tend to be subtle, and diagnosis often is delayed. In the laboratory, this pathogen can be misidentified as a diphtheroid or a hemolytic streptococcus.

Other organisms

S epidermidis and other coagulase-negative staphylococci frequently cause meningitis and CSF shunt infection in patients with hydrocephalus or those who have undergone neurosurgical procedures. Immunocompromised children can develop meningitis caused by Pseudomonas, Serratia,Proteus, and diphtheroids.

Risk factors

Risk factors for bacterial meningitis include the following:

  • Age
  • Low family income
  • Attendance at day care
  • Head trauma
  • Splenectomy
  • Chronic disease
  • Children with facial cellulitis, periorbital cellulitis, sinusitis, and septic arthritis have an increased risk of meningitis.
  • Maternal infection and pyrexia at the time of delivery are associated with neonatal meningitis

Use of Hib and pneumococcal vaccines decreases the likelihood of infection from these agents.

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Epidemiology

United States statistics

The advent of vaccine has changed the incidence of pediatric bacterial meningitis. Before the routine use of the pneumococcal conjugate vaccine, the incidence of bacterial meningitis in the United States was about 6000 cases per year; roughly half of these were in pediatric patients (≤18 years). N meningitidis caused about 4 cases per 100,000 children (aged 1-23 months). The rate of S pneumoniae meningitis was 6.5 cases per 100,000 children (aged 1-23 months). Today, disease caused by H influenzae, S pneumoniae, and N meningitidis is much less common.

The advent of universal Hib vaccination in developed countries has led to the elimination of more than 99% of invasive disease. Protection continues even when Hib is coadministered with other vaccines. Just as important, the vaccine continues to confer immunity into later childhood.

A similar effect occurs with pneumococcal vaccine. Given at ages 2, 4, and 6 months, this vaccine has reduced invasive disease by more than 90%. Age groups most affected are those younger than 2 years and those aged 2-5 years. This was proven in a surveillance study in Louisville, Kentucky.[5] Nearly half of cases of pneumococcal disease are caused by nonvaccine serotypes.[6, 7]

Vaccine for Neisseria, however, has not been efficacious in younger children. This is due to poor immunogenic response. Current recommendations target immunization for children older than 2 years and high-risk patients with asplenic and terminal complement deficiencies. In addition, young adults living in close quarters, such as dormitories or military barracks, will benefit.

A study analyzing reported cases of bacterial meningitis among residents in 8 surveillance areas of the Emerging Infections Programs Network during 1998-2007 found a 31% decrease in meningitis cases during this period and an increase in median patient age from 30.3 years in 1998-1999 to 41.9 years in 2006-2007; the case fatality rate did not change significantly.[8] Overall, approximately 4100 cases of bacterial meningitis occurred annually in the United States from 2003 to 2007, with approximately 500 deaths.[8]

A study that reported on the epidemiology of infant meningococcal disease in the United States from 2006 to 2012 found that an estimated 113 cases of culture-confirmed meningococcal disease occurred annually among infants aged <1 year in the United States from 2006 through 2012, for an overall incidence of 2.74 per 100,000 infants. Among these cases, an estimated 6 deaths occurred. Serogroup B was responsible for 64%, serogroup C for 12%, and serogroup Y for 16% of infant cases. Based on the expanded data collection forms, a high proportion of infant cases (36/58, 62%) had a smoker in the household and the socioeconomic status of the census tracts where infant meningococcal cases resided was lower compared with the other Active Bacterial Core surveillance areas and the United States as a whole.[9]

The incidence of neonatal bacterial meningitis is 0.25-1 case per 1000 live births (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.

After the initiation of intrapartum antibiotics in 1996, the national incidence of early-onset GBS infection decreased substantially, from approximately 1.8 cases per 1000 live births in 1990 to 0.32 case per 1000 live births in 2003.

International statistics

Worldwide, the use of H influenzae type B and pneumococcal vaccines is increasing at a rate faster than that observed with the use of hepatitis B vaccines.[10]

In a survey by the Hib and Pneumococcal Working Group, the incidence of meningitis in 2000 varied in different regions of the world. The overall incidence of pneumococcal meningitis was 17 cases per 100,000, with the highest incidence in Africa, at 38 cases per 100,000, and the lowest incidence in Europe, at 6 cases per 100,000.[11] The overall death rate was 10 cases per 100,000. The death rate was highest in Africa, at 28 cases per 100,000, and lowest in Europe and Western Pacific regions, at 3 cases per 100,000.

A similar trend was identified for Hib meningitis.[12] The overall incidence of Hib meningitis in 2000 was 31 cases per 100,000. The African region had the highest rate, at 46 cases per 100,000, and Europe had the lowest, at 13 cases per 100,000. The overall death rate was 13 cases per 100,000. The highest death rate was in Africa, at 31 cases per 100,000, and the lowest was in Europe, at 4 cases per 100,000.

Age-, sex-, and race-related demographics

Pediatric bacterial meningitis is most common in children younger than 4 years, with a peak incidence in those aged 3-8 months.

Male infants have a higher incidence of gram-negative neonatal meningitis. Female infants are more susceptible to L monocytogenes infection. S agalactiae (GBS) affects both sexes equally.

Bacterial meningitis occurs more frequently in black, Native American, and Hispanic children; this is thought to be related to socioeconomic rather than racial factors.

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Prognosis

Mortality and morbidity depend on the infectious agent, the age of the child, the child’s general health, and the promptness of diagnosis and treatment. Despite improvements in antibiotic and supportive therapy, death and complication rates remain significant.

Overall mortality for bacterial meningitis is 5-10% and varies according to the causative organism and the patient’s age. In neonates, mortality is 15-20%, whereas in older children, it is 3-10%. Of the meningitides caused by the most common pathogens, S pneumoniae meningitis has the highest mortality, at 26.3-30%; Hib meningitis has the next highest, at 7.7-10.3%; and N meningitidis has the lowest, at 3.5-10.3%.

As many as 30% of children have neurologic sequelae. This rate varies by organism, with S pneumoniae being associated with the highest rate of complications. One study indicated that the complication rate from S pneumoniae meningitis was essentially the same for penicillin-sensitive strains as for penicillin-resistant strains; this study also showed that dexamethasone did not improve outcomes.[13]

Prolonged or difficult-to-control seizures, especially after hospital day 4, are predictors of a complicated hospital course with serious sequelae. On the other hand, seizures that occur during the first 3 days of illness usually have little prognostic significance.

Approximately 6% of affected infants and children show signs of DIC and endotoxic shock. These signs are indicative of a poor prognosis.

Studies have documented the development of profound bilateral hearing loss, which may occur in as many as 4% of all bacterial meningitis cases.[14] Sensorineural hearing loss is one of the most frequent problems. Children at greatest risk for hearing loss include those with evidence of increased ICP, those with abnormal findings on computed tomography (CT), males, those with low CSF glucose levels, those with S pneumoniae infection , and those with nuchal rigidity.

Because many of the children affected are very young and lack mature cognitive and motor skills, some of the sequelae may not be recognized for years. In a study that followed children who recovered from meningitis for 5-10 years, 1 of every 4 school-aged meningitis survivors had either serious and disabling sequelae or a functionally important behavior disorder or neuropsychiatric or auditory dysfunction that impaired their performance in school.

For tuberculous meningitis, morbidity and mortality are related to the stage of the disease. The rate of significant morbidity is 30% for stage I, 56% for stage II, and 94% for stage III.

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Patient Education

Because of the high incidence of sequelae, parents should be cautioned from the beginning that even with appropriate medical care, the child may have some complications. Respond promptly to parents’ concerns with adequate documentation.

Careful neurologic examination and visual and hearing screening tests (brainstem evoked potentials) should be obtained and reviewed with parents so that parents are aware of any deficits. Early detection of deficits should result in initiating appropriate physical and occupational therapy and in acquiring other devices or modalities required by the patient to achieve the maximum possible benefit.

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Contributor Information and Disclosures
Author

Martha L Muller, MD Associate Professor of Pediatrics, Division of Infectious Diseases, University of New Mexico School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa

Disclosure: Received research grant from: Pfizer;GlaxoSmithKline;AstraZeneca;Merck;American Academy of Pediatrics<br/>Received income in an amount equal to or greater than $250 from: Sanofi Pasteur;Astra Zeneca;Novartis<br/>Consulting fees for: Sanofi Pasteur; Novartis; Merck; Astra Zeneca.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Robert Allan Felter, MD, FAAP, CPE, FACPE Professor of Clinical Pediatrics, Department of Pediatrics, Georgetown University School of Medicine; Medical Director, Pediatric Emergency Medicine and Inpatient Services, Inova Loudoun Hospital

Robert Allan Felter, MD, FAAP, CPE, FACPE is a member of the following medical societies: American Academy of Pediatrics and American College of Physician Executives

Disclosure: Nothing to disclose

Jeffrey Hom, MD, MPH, FACEP, FAAP Assistant Professor, Department of Pediatrics/Emergency Services and Department of Emergency Medicine, New York University School of Medicine

Jeffrey Hom, MD, MPH, FACEP, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David Jaimovich, MD Chief Medical Officer, Joint Commission International and Joint Commission Resources

David Jaimovich, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Garry Wilkes, MBBS, FACEM Director of Emergency Medicine, Calvary Hospital, Canberra, ACT; Adjunct Associate Professor, Edith Cowan University, Western Australia

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

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Acute bacterial meningitis. This axial nonenhanced CT scan shows mild ventriculomegaly and sulcal effacement.
Acute bacterial meningitis. This axial T2-weighted MRI shows only mild ventriculomegaly.
Acute bacterial meningitis. This contrast-enhanced, axial T1-weighted MRI shows leptomeningeal enhancement (arrows).
Table 1. Antibiotic Dosages for Neonatal Bacterial Meningitis, Adjusted by Weight and Age
Antibiotic Route Dosage
Birth Weight < 2000 g, Age 0-7 Days Birth Weight >2000 g, Age 0-7 Days Birth Weight < 2000 g, Age >7 Days Birth Weight >2000 g, Age >7 Days
Penicillins
Ampicillin IV, IM 50 mg/kg q12h 50 mg/kg q8h 50 mg/kg q8h 50 mg/kg q6h
Penicillin G IV 50,000 U/kg q12h 50,000 U/kg q8h 50,000 U/kg q8h 50,000 U/kg q6h
Oxacillin IV, IM 50 mg/kg q12h 50 mg/kg q8h 50 mg/kg q8h 50 mg/kg q6h
Ticarcillin IV, IM 75 mg/kg q12h 75 mg/kg q8h 75 mg/kg q8h 75 mg/kg q6h
Cephalosporins
Cefotaxime IV, IM 50 m mg/kg g q12h 50 mg/kg q8h 50 mg/kg q8h 50 mg/kg q6h
Ceftriaxone IV, IM 50 mg/kg qd 50 mg/kg qd 50 mg/kg qd 75 mg/kg qd
Ceftazidime IV, IM 50 mg/kg q12h 50 mg/kg q8h 50 mg/kg q8h 50 mg/kg q8h
Table 2. Antibiotics for Neonatal Bacterial Meningitis That Must Be Dosed According to Serum levels
Antibiotic Route Desired Serum level, µg/mL Dosage
Birth Weight < 2000 g, Age 0-7 Days* Birth Weight >2000 g, Age 0-7 Days* Birth Weight < 2000 g, Age >7 Days* Birth Weight >2000 g, Age >7 Days*
Aminoglycosides
Amikacin† IV, IM 20-30 (peak), < 10 (trough) 7.5 mg/kg q12h 10 mg/kg q12h 10 mg/kg q8h 10 mg/kg q8h
Gentamicin† IV, IM 5-10 (peak), < 2.5 (trough) 2.5 mg/kg q12h 2.5 mg/kg q12h 2.5 mg/kg q8h 2.5 mg/kg q8h
Tobramycin† IV, IM 5-10 (peak), < 2.5 (trough) 2.5 mg/kg q12h 2.5 mg/kg q12h 2.5 mg/kg q8h 2.5 mg/kg q8h
Glycopeptide
Vancomycin*† IV, IM 20-40 (peak), < 10 (trough) 15 mg/kg q12h 15 mg/kg q8h 15 mg/kg q8h 15 mg/kg q6h
*The dosage stated is the highest within the dosage range.



† Serum levels must be monitored when patient has kidney disease or is receiving other nephrotoxic drugs; adjust doses accordingly.



Table 3. Dosages and Dosing Intervals for Intravenous Antimicrobials in Infants and Children With Bacterial Meningitis
Antibiotic IV Dosage Maximum Daily Dose Dosing Interval
Ampicillin 400 mg/kg/day 6-12 g q6h
Vancomycin 60 mg/kg/day 2-4 g q6h
Penicillin G 400,000 U/kg/day 24 million U q6h
Cefotaxime 200-300 mg/kg/day 8-10 g q6h
Ceftriaxone 100 mg/kg/day 4 g q12h
Ceftazidime 150 mg/kg/day 6 g q8h
Cefepime* 150 mg/kg/day 2-4 g q8h
Imipenem† 60 mg/kg/day 2-4 g q6h
Meropenem 120 mg/kg/day 4-6 g q8h
Rifampin 20 mg/kg/day 600 mg q12h
*Experience with this agent in pediatric patients is minimal; it is not licensed for treatment of meningitis.



† Because of possible seizures, this agent must be used with caution in treating meningitis.



Table 4. Chemoprophylaxis for Bacterial Meningitis Caused by Haemophilus influenzae or Neisseria meningitidis
Causative Organism Drug Name Age of Contact Dosage
Haemophilus influenzae Rifampin Adults >600 mg PO qd for 4 days
  =1 month 20 mg/kg PO qd for 4 days; not to exceed 600 mg/dose
  < 1 month >10 mg/kg PO qd for 4 days
Neisseria meningitidis Rifampin Adults 600 mg PO q12h for 2 days
  >1 month 10 mg/kg PO q12h for 2 days; not to exceed 600 mg/dose
  =1 month >5 mg/kg PO q12h for 2 days
Ceftriaxone >15 years 250 mg IM once
  =15 years >125 mg IM once
Ciprofloxacin =18 years >500 mg PO once
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