Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Neonatal Meningitis Clinical Presentation

  • Author: David C Dredge, MD; Chief Editor: Amy Kao, MD  more...
 
Updated: Dec 14, 2015
 

History and Physical Examination

Regardless of the specific pathogen involved, neonatal meningitis is most often caused by vertical transmission during labor and delivery. It occurs most frequently in the days following birth and is more common in premature infants than in term infants.[4] It is closely associated with sepsis.

Risk factors for the development of meningitis include low birth weight (< 2500 g), preterm birth (< 37 weeks’ gestation), premature rupture of membranes, traumatic delivery, fetal hypoxia, and maternal peripartum infection (including chorioamnionitis).

In evaluating a neonate for meningitis, the following 3 key points should be kept in mind:

  • It is important to remain vigilant for maternal infection “setups” (eg, prolonged rupture of membranes, fever, and chorioamnionitis) while remembering that asymptomatic maternal infection is always a possibility even with screening
  • Early-onset and late-onset bacterial infections have distinctive clinical courses (see below)
  • In herpes simplex virus (HSV) infections, the presence of skin lesions in a meningitic neonate is the exception rather than the rule

Bacterial meningitis

Early onset

Symptoms appearing in the first 48 hours of life are referable primarily to systemic illness rather than to meningitis. Such symptoms include temperature instability, episodes of apnea or bradycardia, hypotension, feeding difficulty, hepatic dysfunction, and irritability alternating with lethargy.[1] Respiratory symptoms can become prominent within hours of birth in group B streptococcal (GBS) infection; however, the symptom complex also is seen with infection by E coli or Listeria species.

Late onset

Late-onset bacterial meningitis (ie, symptom onset after 48 hours of life) is more likely to be associated with neurological symptoms. Most commonly seen are stupor and irritability, which Volpe describes in more than 75% of affected neonates. Between 25% and 50% of neonates will exhibit the following neurological signs:

  • Seizures
  • Bulging anterior fontanel
  • Extensor posturing or opisthotonos
  • Focal cerebral signs including gaze deviation and hemiparesis
  • Cranial nerve palsies

Nuchal rigidity is the least common sign in neonatal bacterial meningitis, occurring in fewer than 25% of affected neonates.[1]

HSV meningitis

Early features of HSV meningitis may mimic those associated with bacterial meningitis, including pallor, irritability, high-pitched cry, respiratory distress, fever, or jaundice, progressing to pneumonitis, seizures, hepatic dysfunction, and disseminated intravascular coagulopathy (DIC).[16]

Next

Complications

Regardless of etiology, meningitis in neonates can progress rapidly to serious complications, including cerebral edema, hydrocephalus, hemorrhage, ventriculitis (especially with bacterial infection), abscess formation, and cerebral infarction.

Cerebral edema, hydrocephalus, and hemorrhage each may cause increased intracranial pressure, with potential for secondary ischemic injury to the brain because of decreased brain perfusion:

  • Cerebral edema results from vasogenic changes, cytotoxic cell injury, and, at times, inappropriate antidiuretic hormone (ADH) secretion
  • Hydrocephalus results from debris obstructing the flow of cerebrospinal fluid (CSF) through the ventricular system or from dysfunction of arachnoid villi; it occurs in as many as 24% of neonates with bacterial meningitis [22]
  • Hemorrhage occurs in regions of infarction or necrosis and should be suspected in a neonate with new focal neurological findings or clinical deterioration

Ventriculitis results in sequestration of infection to areas that are poorly accessible to systemic antimicrobial drugs. Inflammation of the ependymal lining of ventricles often obstructs CSF flow. Thus, all of these complications are interactive, making effective management difficult. Ventriculitis occurs in as many as 20% of infected neonates.[23] Failure to respond to appropriate antibiotic therapy and signs of elevated intracranial pressure (ICP) may suggest the diagnosis.[24] Intraventricular administration of antibiotics may be necessary in cases of ventriculitis.

Cerebral abscess occurs in as many as 13% of neonates with meningitis.[22] New seizures, signs of elevated ICP, or new focal neurological signs suggest the diagnosis. Brain imaging with contrast is essential for making the definitive diagnosis. Surgical intervention may be required.

Cerebral infarction, both focal (arterial) and diffuse (venous), may complicate recovery. Autopsy studies have found evidence of infarction in 30-50% of specimens studied.[1] Imaging studies suggest that the actual incidence of infarction may be even higher.[25] Meningitis has been shown to be associated with 1.6% of all cases of neonatal arterial stroke and 7.7% of venous infarcts.[26]

Necrotizing lesions secondary to HSV meningitis can be deleterious to the developing brain.

Other, longer-term complications that may develop include residual epilepsy, cognitive impairment, hearing loss, visual impairment, spastic paresis, and microcephaly. Some of these disorders may be difficult to detect during infancy.

Hearing, for example, is difficult to evaluate without the child’s cooperation, and even then, assessment may be limited to behavioral response to sounds. Brainstem auditory evoked response (BAER) testing does not evaluate all dimensions of hearing, but this test, which can be performed reliably in sedated infants, only slightly overestimates hearing loss, which occurs in 30% of survivors of bacterial meningitis and 14% of survivors of nonbacterial meningitis.[27] Subtle impairment of sound discrimination may not be readily apparent.

Similarly, cognitive impairment may not be evident until the child has started school or advanced into higher grades where more complex analysis of information is necessary.[20] Careful screening for neurological, cognitive, and developmental deficits must be conducted as part of routine pediatric care over a period of many years, and the responsible physician should be attentive to possible problems with perception, learning, or behavior that may result from neonatal infection.

Previous
 
 
Contributor Information and Disclosures
Author

David C Dredge, MD Attending Physician, Pediatric Neurology, Baystate Children's Hospital; Assistant Professor of Pediatrics, Tufts University Medical School

David C Dredge, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, Child Neurology Society, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Kalpathy S Krishnamoorthy, MD Associate Professor of Pediatrics and Neurology, Harvard Medical School; Consulting Staff, Division of Pediatric Neurology, Massachusetts General Hospital

Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Have stock from Cellectar Biosciences; have stock from Varian medical systems; have stock from Express Scripts.

Acknowledgements

Sarah M Barnett, MD, MPH Fellow in Neonatal Neurology, Division of Pediatric Neurology, Massachusetts General Hospital

Sarah M Barnett, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Public Health Association, Child Neurology Society , and Massachusetts Medical Society

Disclosure: Nothing to disclose.

David A Griesemer, MD Professor, Departments of Neuroscience and Pediatrics, Medical University of South Carolina

David A Griesemer, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Neurology , American Epilepsy Society, Child Neurology Society, and Society for Neuroscience

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Volpe JJ. Bacterial and fungal intracranial infections. Neurology of the Newborn. 5th. Philadelphia, Pa: Saunders Elsevier; 2008. 916-56.

  2. Volpe JJ. Viral, protozoal, and related intracranial infections. Neurology of the Newborn. 5th. Philadelphia, Pa: Saunders Elsevier; 2008. 851-915.

  3. Krebs VLJ, Costa GAM. Clinical outcome of neonatal bacterial meningitis according to birth weight. Arq. December 2007. 65:1149-1153. [Medline].

  4. Davies PA, Rudd PT. Incidence; The Developing Brain. Neonatal Meningitis. Cambridge, England: Cambridge University Press; 1994. Ch 1.

  5. Klinger G, Chin CN, Beyene J, et al. Predicting the outcome of neonatal bacterial meningitis. Pediatrics. 2000 Sep. 106(3):477-82. [Medline].

  6. Heath PT, Nik Yusoff NK, Baker CJ. Neonatal meningitis. Arch Dis Child Fetal Neonatal Ed. 2003 May. 88(3):F173-8. [Medline].

  7. Tiskumara R, Fakharee SH, Liu C-Q, Nuntnarumit P, Lui K-M, Hammoud M, et al. Neonatal infections in Asia. Arch Dis Child Fetal Neonatal Ed. March 2009. 94:F144-8. [Medline].

  8. Zaidi AK, Thaver D, Ali SA, Khan TA. Pathogens associated with sepsis in newborns and young infants in developing countries. Pediatr Infect Dis J. 2009 Jan. 28(1 Suppl):S10-8. [Medline].

  9. Puopolo KM, Madoff LC, Eichenwald EC. Early-onset group B streptococcal disease in the era of maternal screening. Pediatrics. 2005 May. 115(5):1240-6. [Medline].

  10. CDC. Trends in perinatal group B streptococcal disease - United States 2000-2006. Morb Mortal Wkly Rep. February 2009. 58:109-112. [Medline].

  11. CDC. Enterovirus surveillance--United States, 2002-2004. MMWR Morb Mortal Wkly Rep. 2006 Feb 17. 55(6):153-6. [Medline].

  12. Tebruegge M, Curtis N. Enterovirus infections in neonates. Semin Fetal Neonatal Med. March 2009. 1-6. [Medline].

  13. Levorson RE, Jantausch BA, Wiedermann BL, Spiegel HM, Campos JM. Human parechovirus-3 infection: emerging pathogen in neonatal sepsis. Pediatr Infect Dis J. 2009 Jun. 28(6):545-7. [Medline].

  14. Selvarangan R, Nzabi M, Selvaraju SB, Ketter P, Carpenter C, Harrison CJ. Human parechovirus 3 causing sepsis-like illness in children from midwestern United States. Pediatr Infect Dis J. 2011 Mar. 30(3):238-42. [Medline].

  15. Hunter JH, Petrosyan M, Ford HR, Prasadarao NV. Enterobacter sakazakii: An emerging pathogen in infants and neonates. Surg Infect (Larchmt). October 2008. 9:533-539.

  16. Kimberlin D. Herpes simplex virus, meningitis, and encephalitis in neonates. Herpes. 2004. 11 Supp 2:65A-76A. [Medline].

  17. Thaver D, Zaidi AK. Burden of neonatal infections in developing countries: a review of evidence from community-based studies. Pediatr Infect Dis J. 2009 Jan. 28(1 Suppl):S3-9. [Medline].

  18. de Louvois J, Halket S, Harvey D. Effect of meningitis in infancy on school-leaving examination results. Arch Dis Child. 2007 Nov. 92(11):959-62. [Medline].

  19. Chang CJ, Chang HW, Chang WN, Huang LT, Huang SC, CHang YC. Seizures complicating infantile and childhood bacterial meningitis. Pediatr Neurol. September 2004. 32:165-171. [Medline].

  20. Stevens JP, Eames M, Kent A, et al. Long term outcome of neonatal meningitis. Arch Dis Child Fetal Neonatal Ed. 2003. 88:F179-184. [Medline].

  21. Bedford H, de Louvois J, Halket S, et al. Meningitis in infancy in England and Wales: follow up at age 5 years. BMJ. 2001 Sep 8. 323(7312):533-6. [Medline].

  22. Pong A, Bradley JS. Bacterial meningitis and the newborn infant. Infect Dis Clin North Am. 1999 Sep. 13(3):711-33, viii. [Medline].

  23. Unhanand M, Mustafa MM, McCracken Gh, Nelson JD. Gram-negative enteric bacillary meningitis: a twenty-one year experience. J Pediatr. January 1993. 122:15-21. [Medline].

  24. Miyairi I, Causey KT, DeVincenzo JP, Buckingham SC. Group B streptococcal ventriculitis: a report of three cases and literature review. Pediatr Neurol. May 2006. 34:395-399. [Medline].

  25. Ment LR, Ehrenkranz RA, Duncan CC. Bacterial meningitis as an etiology of perinatal cerebral infarction. Pediatr Neurol. September/October 1986. 2:276-279. [Medline].

  26. Fitzgerald KC, Golomb MR. Neonatal arterial ischemic stroke and sinovenous thrombosis associated with meningitis. J Child Neurol. July 2007. 22:818-822. [Medline].

  27. Bao X, Wong V. Brainstem auditory-evoked potential evaluation in children with meningitis. Pediatr Neurol. 1998 Aug. 19(2):109-12. [Medline].

  28. Committee on Medical Liability, American Academy of Pediatrics. Berger JE ed, Deitschel CH Jr ed. Medical Liability for Pediatricians. 6th ed. 2004. 163, 169.

  29. Malbon K, Mohan R, Nicholl R. Should a neonate with possible late onset infection always have a lumbar puncture?. Arch Dis Child. 2006 Jan. 91(1):75-6. [Medline].

  30. Garges HP, Moody MA, Cotten CM, et al. Neonatal meningitis: what is the correlation among cerebrospinal fluid cultures, blood cultures, and cerebrospinal fluid parameters?. Pediatrics. 2006 Apr. 117(4):1094-100. [Medline].

  31. Shah DK, Daley AJ, Hunt RW, Volpe JJ, Inder TE. Cerebral white matter injury in the newborn following Escherichia coli meningitis. Eur J Paediatr Neurol. 2005. 9:13-17. [Medline].

  32. Malik GK, Trivedi R, Gupta A, Singh R, Prasad KN, Gupta RK. Quantitative DTI assessment of periventricular white matter changes in neonatal meningitis. Brain Dev. May 2008. 30:334-341. [Medline].

  33. Klinger G, Chin CN, Otsubo H, et al. Prognostic value of EEG in neonatal bacterial meningitis. Pediatr Neurol. 2001 Jan. 24(1):28-31. [Medline].

  34. Poblano A, Gutierrez R. Correlation between the neonatal EEG and the neurological examination in the first year of life in infants with bacterial meningitis. Arq Neuropsiquiatr. September 2007. 65:576-580. [Medline].

  35. Stoll BJ, Hansen N, Fanaroff AA, et al. To tap or not to tap: high likelihood of meningitis without infection in very low birthweight infants. Pediatrics. 2004. 113:1181-6. [Medline].

  36. Alarcon A, Pena P, Salas S, Sancha M, Omenaca F. Neonatal early onset Escherichia coli sepsis: trends in incidence and antimicrobial resistence in the era of intrapartum antimicrobial prophylaxis. Pediatr Infect Dis J. April 2004. 23:295-299. [Medline].

  37. Pickering LD, ed. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006.

  38. Thaver D, Ali SA, Zaidi AK. Antimicrobial resistance among neonatal pathogens in developing countries. Pediatr Infect Dis J. 2009 Jan. 28(1 Suppl):S19-21. [Medline].

  39. Chaudhuri A. Adjunctive dexamethasone treatment in acute bacterial meningitis. Lancet Neurol. 2004 Jan. 3(1):54-62. [Medline].

  40. Wellman MB, Sommer DD, McKenna J. Sensorineural hearing loss in postmeningitic children. Otol Neurotol. 2003 Nov. 24(6):907-12. [Medline].

 
Previous
Next
 
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).
Meninges of the central nervous parts
Neisseria meningitidis
Neonate with a lumbar myelomeningocele with an L5 neurologic level. Note the diaphanous sac filled with cerebrospinal fluid and containing fragile vessels in its membrane. Also, note the neural placode plastered to the dorsal surface of the sac. This patient underwent closure of his back and an untethering of his neural placode. The neural placode was circumnavigated and placed in the neural canal. A dural sleeve was fashioned in such a way to reconstruct the neural tube geometry.
This anteroposterior skull radiograph demonstrates the craniolacunia or Luckenschadel seen in patients with myelomeningocele and hydrocephalus. Mesodermal dysplastic changes cause defects in the bone. The thin ovoid areas of calvaria are often surrounded by dense bone deposits. They are most likely the result of defective membranous bone formation typical of neural tube defects and not increased intracranial pressure as once thought. These characteristic honeycomb changes are seen in about 80% of the skulls in children with myelomeningocele and hydrocephalus
Sagittal T1-weighted MRI image of a child after closure of his myelomeningocele. Child is aged 7 years. Note the spinal cord ends in the sacral region far below the normal level of T12-L1. It is tethered at the point in which the neural placode was attached to the skin defect during gestation. The MRI showed dorsal tethering, and the child complained of back pain and had a new foot deformity on examination. By definition, all children with a myelomeningocele have a tethered cord on MRI, but only about 20% of children require an operation to untether the spinal cord during their first decade of life, during their rapid growth spurts. Thus, the MRI must be placed in context of a history and examination consistent with mechanical tethering and a resultant neurologic deterioration.
Sagittal T1 MRI image of a child with a myelomeningocele and associated Chiari II malformation. Note the cerebellar vermis and part of the brainstem has herniated below the foramen magnum and into the cervical canal (arrow). This patient had multiple brainstem symptoms and findings to include stridor and cranial nerve paresis (cranial nerves III, VI, IX, X) despite having a well-functioning ventricular-peritoneal shunt. He required a posterior fossa decompression of his hindbrain in order to relieve the symptoms of hindbrain herniation and brainstem compression. A minority of myelomeningocele patients require a Chiari II decompression. Those that do usually present in their first year of life with similar symptoms, stridor and cranial nerve paresis. A functioning shunt is imperative prior to exploring the posterior fossa in these children. Often times, especially in older children, a shunt revision may alleviate some of the symptoms of hindbrain compression. Tube Defects in the Neonatal Period
Neonate with a large occipital encephalocele lying in the prone position prior to surgical intervention. Note the large skin-covered sac that represents a closed neural tube defect. Often called cranium bifidum, it is a more serious condition that represents a failure of the anterior neuropore to close. In this patient, a defect in the skull base (basicranium) was associated with this large sac filled with cerebrospinal fluid and a small, disorganized remnant of brain. The patient fared satisfactorily after the surgery in which the encephalocele was excised. However, the patient needed placement of a ventricular-peritoneal shunt to treat the resultant hydrocephalus, which is not uncommon. At age 5 years, the child was doing well and had only moderate developmental delay.
Autopsy specimen on a child with anencephaly. This is one of the most common CNS malformations in the West. The neonate, like almost all with such a severe forms of neural tube defects, did not survive more than a few hours or days. This malformation represents a failure of the anterior neuropore to close. This photograph also reveals an absence of the calvaria and posterior bone elements of the cervical canal, as well as the deficiency in the prosencephalon. Photo courtesy of Professor Ron Lemire.
Ventral view of a child with anencephaly that, like the previous picture, shows the loss of cranium and enclosed nervous tissue. In addition to the primary defect in development, a secondary destruction of nervous tissue occurs. Direct exposure to the caustic amniotic fluid causes progressive destruction of the remaining neural structures and secondary proliferation of a thin covering of vascular and glial tissue. Photo courtesy of Professor Ron Lemire.
These 2 photographs depict the lumbar regions on 2 different children with closed neural tube defects. Both children have lipomyelomeningocele. The child in the left has a dorsal lipoma that is pedunculated. The child on the right has a more common-appearing lipomatous mass that is heaped up beneath the skin. Both lipomas lead from the subcutaneous tissue, through the dura and into the intradural space, where they are attached to the spinal cord. Photos courtesy of Professor J.D. Loeser.
Photograph of a child undergoing a neurosurgical procedure in which the spinal cord is being detached (untethered) from the intradural and extradural lipomatous mass that fixes it to the subcutaneous tissue. The white arrow shows the laser char on the lipoma that has been shaved off the spinal cord and was connected to the extradural mass. The black arrow shows the extradural lipoma, which crept through the dura and attached to the spinal cord, thereby firmly fixing the spinal cord at too low and too dorsal a location in the sagittal plane.
The lumbar region of a newborn baby with myelomeningocele. The skin is intact, and the placode-containing remnants of nervous tissue can be observed in the center of the lesion, which is filled with cerebrospinal fluid (CSF).
Axial T1-weighted MRI scan of an 8-week-old girl who presented with enlarging head circumference. Considerable ventricular dilatation is shown on the lateral and third ventricles. Periventricular lucency is observed around the frontal horns, indicating raised intraventricular pressure.
Sagittal T1-weighted MRI scan of an 8-week-old girl who presented with enlarging head circumference. The third and lateral ventricles are dilated, whereas the fourth ventricle is of normal size. Aqueductal stenosis is shown. The appearance is typical of this condition.
Phase-contrast MRI scan of an 8-week-old girl who presented with enlarging head circumference, obtained 3 months after endoscopic third ventriculostomy. A large signal void is shown in the prepontine region, corresponding to the flow through the stoma in the floor of the third ventricle, indicating that the ventriculostomy is functioning well.
Axial T1-weighted MRI scan of a 15-year-old girl who was born with thoracic myelomeningocele, hydrocephalus, and Arnold-Chiari II syndrome. She was treated with a ventriculoperitoneal shunt. The ventricular system has a characteristic shape, with small frontal and large occipital horns, which are typical in patients with spina bifida. The shunt tube is shown in the right parietal region.
Sagittal T1-weighted MRI scan of a 15-year-old girl who was born with thoracic myelomeningocele, hydrocephalus, and Arnold-Chiari II syndrome. Significant hindbrain hernia and low-lying fourth ventricle are shown in the context of the Arnold-Chiari II syndrome. Damaged shunt valve removed during shunt revision from a 22-year-old woman with hydrocephalus and spina bifida. The material of the valve has dramatically disintegrated.
Damaged shunt valve removed during shunt revision from a 22-year-old woman with hydrocephalus and spina bifida. The material of the valve has dramatically disintegrated.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.