Neonatal Meningitis

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Background   Histopathology & Immunohistochemistry

BACKGROUND AND CLINICAL INFORMATION: Head

Definition: Neonatal period is defined as the first 30 days of life. This is the period in which risk for acquiring meningitis is greater than any time thereafter. In reality, the risk factors and treatment may extend to infants who are several months old.

Clinical features:

Incidence and risk factors: 0.5% of all life birth.

Risk factors:

Pathogenesis: lack of transplacentally acquired antibodies against potential meningeal pathogens, absence of alveolar macrophages at birth, a small PMN pool with chemothactic deficiencies compared with adults, and inefficient synthesis of antibodies during the neonatal stages all add to the increased susceptibility of neonates to meningitis.

Amniotic fluid is inhibitory to the growth of E. coli and certain other organisms because of the presence of lysozyme, transferrin, and certain immunoglobulins. The amniotic fluid is no longer a hostile environment for E. coli if it contains meconium or vernix. In contrast, Group B Streptococcus can grow in "normal" amniotic fluid. Macrophages in the amniotic fluid are derived from the maternal circulation.

Infectious agents: almost half of the cases are caused by streptococci (especially group B), followed by Staphylococcus (S. epidermis, S. aureus, and S. pneumoniae), Klebsiella-Enterobacter species and then Escherichia coli (most commonly type K1).

Common pathogens and route of infection:

HISTOPATHOLOGY AND IMMUNOHISTOCHEMISTRY: Head

Arachnoiditis around the base of the brain may be particularly prominent, alternatively, the exudate may be distributed over the cerebral cortex surface.

Vasculitis is an invariable component of neonatal meningitis. Perivascular inflammatory infiltration in the adventitia with the intima spared is common in arteries; phlebitis with thrombosis and complete occlusion is common in veins; this may lead to thrombotic hemorrhagic infarction.

Pathogenesis: One of the explanation for the increase in severity of neonatal meningitis is the relatively paucity and functional immaturity of arachnoid villi in the newborn. Thus, the egress of bacteria is slower, which can lead to bacterial accumulation in the CSF. The inflammatiory exudate in the ventricular CSF drains into and "Plugs" the arachnoid villi, producing dysfunction of this exit valve and transiently increasing intracranial pressure. Choroid plexitis, ventriculitis, and glial tufts and bridges formation within the ventricles will lead to obstructive hydrocephalus.

Rhombencephalitis often associate with meningitis due to Listeria in both pediatric and adult cases [Uldry PA et al., J Neurol 1993 24:235-42]