Pediatric Bacterial Meningitis 

  • Author: Martha L Muller, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Jun 15, 2011
 

Background

Bacterial meningitis is a life-threatening illness that results from bacterial infection of the meninges. 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), since the introduction of the conjugate pneumococcal vaccine in 2000, the rate of pneumococcal meningitis has declined 59%. 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.

The emergence of penicillin-resistant S pneumoniae has resulted in new challenges in the treatment of bacterial meningitis. Because bacterial meningitis in the neonatal period has its own unique epidemiologic and etiologic features, it is described separately in this article.

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Pathophysiology

Bacteria reach the subarachnoid space by 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 1 (IL-1), tumor necrosis factor-alpha (TNF-α), 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, which can result in increased intracranial pressure and uncal herniation. Increased secretion of antidiuretic hormone 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 results in a caudal shift of midline structures with their entrapment 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.

Pathogenesis of 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 reaching the CNS, bacteria spread from the longitudinal and lateral sinuses to the meninges, the choroid plexus, and the ventricles.

IL-1 and TNF-α also mediate local inflammatory reactions by inducing phospholipase A2 activity, initiating the production of platelet-activating factor and arachidonic acid pathway. This process results in production of prostaglandins, thromboxanes, and leukotrienes. By activating adhesion-promoting receptors on endothelial cells, these cytokines result in attraction of leukocytes, and then release of proteolytic enzymes from the leukocytes causes alteration of blood-brain permeability, activation of 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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Epidemiology

Frequency

United States

Prior to 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 y). N meningitidis causes about 4 cases per 100,000 children (aged 1-23 mo). The rate of S pneumoniae meningitis was 6.5 cases per 100,000 children (aged 1-23 mo). This number has since declined given the routine use of conjugate pneumococcal vaccine in children. The recent introduction of conjugate meningococcal vaccine in the United States is expected to reduce the incidence of bacterial meningitis even further.

A study analyzed data on reported cases of bacterial meningitis among residents in 8 surveillance areas of the Emerging Infections Programs Network during 1998-2007. The results found a 31% decrease in meningitis cases during this period and a median age of patient increase from 30.3 years in 1998-1999 to 41.9 years in 2006-2007; the case fatality rate did not change significantly. Overall during 2003-2007, approximately 4100 cases of bacterial meningitis occurred annually in the United States, with approximately 500 deaths.[1]

Incidence of neonatal bacterial meningitis is 0.25-1 case per 1000 live births. In addition, 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.

Since the initiation of intrapartum antibiotics in 1996, a decrease has occurred in the national incidence of early-onset GBS infection from approximately 1.8 cases per 1000 live births in 1990 to 0.32 case per 1000 live births in 2003.

International

The use of H influenzae type B and pneumococcal vaccines is increasing worldwide at a rate faster than that observed with hepatitis B vaccines.[2]

Mortality/Morbidity

In general, mortality rates vary with age and pathogen, with the highest being for S pneumoniae. 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 morbidity beyond the neonatal period. Mortality rates are highest during the first year of life, decreasing in mid life and increasing again in elderly persons.

Despite advances in care for patients with bacterial meningitis, the overall case fatality remains steady at approximately 10-30%.

Race

Incidence rates are higher in black and Native American populations.

Sex

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

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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

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.

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, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

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, and Southern Medical Association

Disclosure: Nothing to disclose.

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Acute bacterial meningitis (same patient as in the other two images). This axial nonenhanced CT scan shows mild ventriculomegaly and sulcal effacement.
Acute bacterial meningitis (same patient as in the other two images). This axial T2-weighted MRI shows only mild ventriculomegaly.
Acute bacterial meningitis (same patient as in the other two images). This contrast-enhanced, axial T1-weighted MRI shows leptomeningeal enhancement (arrows).
Table 1. Antibiotic Dosages for Neonatal Bacterial Meningitis to be Adjusted by Weight and Age Dosage (mg/kg/dose or U/kg/dose for Highest Dose Within Dosage Range) and Intervals of Administration
AntibioticAdmin-istration



Route



Dose for birth weight < 2000g and age 0-7 dDose for birth weight >2000g and age 0-7 dDose for birth weight < 2000g and age >7 dDose for birth weight >2000g and age >7 d
Penicillins
AmpicillinIV, IM50 mg q12h50 mg q8h50 mg q8h50 mg q6h
Penicillin-GIV50,000 U q12h50,000 U q8h50,000 U q8h50,000 U q6h
OxacillinIV, IM50 mg q12h50 mg q8h50 mg q8h50 mg q6h
TicarcillinIV, IM75 mg q12h75 mg q8h75 mg q8h75 mg q6h
Cephalosporins
CefotaximeIV, IM50 mg q12h50 mg q8h50 mg q8h50 mg q6h
CeftriaxoneIV, IM50 mg once daily50 mg once daily50 mg once daily75 mg once daily
CeftazidimeIV, IM50 mg q12h50 mg q8h50 mg q8h50 mg q8h
Table 2. Antibiotics for Neonatal Bacterial Meningitis That Need to be Dosed According to Serum levels
AntibioticAdmin-istration RouteDesired Serum level (mcg/mL)Initial dose



for birth weight < 2000g and age 0-7 d (mg/kg / dose)*



Initial dose



for birth weight >2000kg and age 0-7 d (mg/kg / dose)*



Dose for



birth weight < 2000g and age >7 d (mg/kg / dose)*



Dose for



birth weight >2000g and age >7 d (mg/kg / dose)*



Aminoglycosides
Amikacin†IV, IM20-30 (peak), < 10 (trough)7.5 q12h10 q12h10 q8h10 q8h
Gentamicin†IV, IM5-10 (peak), < 2.5 (trough)2.5 q12h2.5 q12h2.5 q8h2.5 q8h
Tobramycin†IV, IM5-10 (peak), < 2.5 (trough)2.5 q12h2.5 q12h2.5 q8h2.5 q8h
Glycopeptide
Vancomycin*†IV, IM20-40 (peak), < 10 (trough)15 q12h15 q8h15 q8h15 q6h
*Dose stated is highest within dosage range.



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



Table 3. Dose Guidelines of Intravenous Antimicrobials in Infants and Children With Bacterial Meningitis
AntibioticDose (mg/kg/d) IVMaximum Daily DoseDosing Interval
Ampicillin4006-12 gq6h
Vancomycin602-4 gq6h
Penicillin G400,000 U24 millionq6h
Cefotaxime200-3008-10 gq6h
Ceftriaxone1004 gq12h
Ceftazidime1506 gq8h
Cefepime*1502-4 gq8h
Imipenem†602-4 gq6h
Meropenem1204-6 gq8h
Rifampin20600 mgq12h
*Minimal experience in pediatrics and not licensed for treatment of meningitis.



† Caution in use for treatment of meningitis because of possible seizures.



Table 4. Chemoprophylaxis for Contacts of Patients and Index (Case of H influenzae type b and contacts of meningococcal disease)
Drug NameAge of ContactDosage
H influenzae disease
RifampinAdults<>600 mg PO qd for 4 d
≥ 1 month20 mg/kg PO qd for 4 d;



not to exceed 600 mg/dose



< 1 month<>10 mg/kg PO qd for 4 d
N meningitidis disease
RifampinAdults600 mg PO q12h for 2 d
>1 month10 mg/kg PO q12h for 2 d;



not to exceed 600 mg/dose



≤ 1 month5 mg/kg PO q12h for 2 d
Ceftriaxone>15 years250 mg IM once
≤ 15 years125 mg IM once
Ciprofloxacin≥ 18 years500 mg PO once
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