**5. Pathophysiology**

Neonates are apt to develop sepsis and meningitis more than all other individuals of all ages due to relative deficiencies in humoral and cellular immune responses. Preterm and term infants are deficient in complement in terms of quantity and quality, which leads to susceptibility to infections by encapsulated bacteria. In infants younger than 32 weeks of gestational age, transfer of maternal circulating antibodies through placenta occurs only in minute quantities. Neutrophil reserves of a neonate can easily become exhausted, since they are 20–30% of that of an average adult [15].

but vesicles may not appear in the early stages or may not occur at all through the course of the disease as is the case in 20% of the newborns with systemic HSV infection. In the absence of vesicles, it is impossible to differentiate HSV meningitis from bacterial meningitis or meningitis due to other agents [11]. Seizures are seen more often in Gram-negative bacterial meningitis rather than in meningitis caused by Gram-positive bacteria. It is inadvisable to rely on the presence of bulging anterior fontanel or nuchal rigidity, because only a few infants (25 and 15%, respectively) with meningitis demonstrate these signs [3]. Neurologic signs usually appear after the second day, whereas mainly systemic signs predominate in the first 48 h. Physical examination findings in neonatal meningitis and their frequencies are summarized

First tests to be performed include complete blood count with differentials and cultures (urine and blood). Detection of growth in urine culture could be a reflection of metastatic dissemination of the organism to the bladder, thus cannot be relied upon as a locator of infection in

Lumbar puncture (LP) is an irreplaceable diagnostic tool in neonatal meningitis. Cerebrospinal fluid (CSF) obtained through LP should be examined directly and as Gram- and Giemsastained smears under microscope, cultured, and, if needed, sent for polymerase chain reaction. Direct microscopy should be performed as soon as possible, because the later it is performed, the more likely the erythrocytes and leukocytes undergo cellular lysis and escape detection. LP should ideally precede the initiation of antimicrobial therapy, but if, delayed for any reason, such as deteriorating clinical status of the patient, empirical antibiotic therapy

Interpretation of CSF findings is more difficult in neonates than in older children, since the glucose, protein concentrations, and cell count of CSF are higher due to the high permeability

**Age Erythrocytes (μL/L) Leukocytes (μL/L) Protein (mg/dL) Glucose (mg/dL)**

Term: <7 d 9 (0–50) 5 (0–21) 60 (30–250) 54 (27–99) Term: >7 d <10 3 (0–10) 50 (20–80) 54 (27–99)

<200)

<150)

54 (27–99)

Neonatal Meningitis

89

http://dx.doi.org/10.5772/intechopen.69601

54 (27–99)

Preterm: <7 d 30 (0–333) 9 (0–30) 100 (50–290) (mostly

Preterm: >7 d 30 12 (2–70) 90 (50–260) (mostly

**Table 2.** Means and normal ranges of cerebrospinal parameters in neonates [12].

in **Table 1**.

**7. Laboratory tests**

young infants [1].

d: day(s).

should be started immediately.

of the blood-brain barrier (**Table 2**).

The causative agent of neonatal meningitis is usually transmitted to fetus vertically during labor. When the etiology is bacterial, histopathologic findings of meningitis in newborns are similar, irrespective of the specific agent. Another similarity is observed in the inflammatory responses of newborns, older children, and adults, the only exception being the paucity of plasma cells and lymphocytes in the subacute phase of meningeal reactions in newborns. The most common finding is purulent exudate in meninges and ependymal surfaces of ventricles. Perivascular inflammation is also observed in some patients. This may further proceed to arteritis of various degrees with phlebothrombosis and thrombophlebitis in the subependymal region. Hydrocephalus and encephalopathy were detected in half of the infants died from meningitis. Unlike older infants (3–12 months of age), subdural effusion is rare in neonates. Interleukin-1β is present in high concentrations in the meninges and brain tissue of the infants who have succumbed to the infection [16].
