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  1. Definition. Neonatal meningitis is an infection of the meninges and central nervous system (CNS) in the first month of life. This is the most common time of life for meningitis to occur.

  2. Incidence. The incidence is ~ 0.16–0.45 per 1000 live births in developed countries. The incidence may be higher in underdeveloped countries.

  3. Pathophysiology. In most cases, infection occurs because of hematogenous seeding of the meninges and CNS. In cases of CNS or spinal anomalies (eg, myelomeningocele), there may be direct inoculation by flora on the skin or in the environment. Neonatal meningitis is often accompanied by ventriculitis, which makes resolution of infection more difficult. There is also a predilection for vasculitis, which may lead to hemorrhage, thrombosis, and infarction. Subdural effusions and brain abscess may also complicate the course.

    Most organisms implicated in neonatal sepsis also cause neonatal meningitis. Some have a definite predilection for CNS infection. Group B streptococcus (GBS) (especially type III) and the Gram-negative rods (especially Escherichia coli with K1 antigen) are the most common causative agents. Other causative organisms include Listeria monocytogenes (serotype IVb), other streptococci (enterococci, Streptococcus pneumoniae), and other Gram-negative enteric bacilli (Klebsiella, Enterobacter, and Serratia spp). In the very low birthweight infant, coagulase-negative staphylococci need to be considered as a causative organisms in bacterial meningitis.

    With CNS anomalies involving open defects or indwelling devices (eg, ventriculoperitoneal shunts), staphylococcal disease (Staphylococcus aureus and Staphylococcus epidermidis) is more common, as is disease caused by other skin flora, including streptococci and diphtheroids. Many unusual organisms, including fungi and anaerobes, have been described in case reports of neonatal meningitis.

  4. Risk factors. Premature infants with sepsis have a much higher incidence (up to threefold) than term infants of CNS infection. The characteristics of some bacteria make them more virulent, especially for neonates (eg, capsular polysaccharide of GBS type III, E. coli K1, and L. monocytogenes serotype IVb all contain sialic acid in high concentrations). Infants with CNS defects necessitating ventriculoperitoneal shunt procedures also are at increased risk.

  5. Clinical presentation. The clinical presentation is usually nonspecific and indistinguishable from those caused by sepsis. Meningitis must be excluded in any infant being evaluated for sepsis or infection. Signs and symptoms of meningitis include lethargy, irritability, temperature instability, respiratory distress, abdominal distension, apnea, or cyanotic episodes. Late manifestations of meningitis are a bulging anterior fontanelle, seizures, and coma. Syndrome of inappropriate antidiuretic hormone may accompany meningitis.

  6. Diagnosis

      1. Laboratory studies. Cerebrospinal fluid (CSF) examination is critical in the investigation of possible meningitis and the only way to confirm the diagnosis. Approximately 15–50% of all infants with positive CSF cultures for bacteria have negative blood cultures. The technique for obtaining CSF fluid and CSF normal values is discussed in Chapter 32.

          1. Culture. CSF culture is the gold standard for the diagnosis of bacterial meningitis. It may be positive in association with a normal or minimally abnormal CSF analysis.

          1. CSF pleocytosis is variable. There are usually more cells with Gram-negative rods ...

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