Traditional descriptions of bacterial meningitis in childhood have stratified causative pathogens on the basis of age. Meningitis in children older than 60 days, called ‘pediatric bacterial meningitis’ is often caused by encapsulated bacteria that colonize the nasopharynx and other body sites. Meningitis in children younger than 60 days, called ‘young infant bacterial meningitis’ is further stratified by gestational age and timing of onset of infection. In general, infections that occur within the first 7 days of life of a term neonate are described as early onset disease, whereas infections occurring from 7 to 60 days after birth are described as late-onset disease.
Causes of Early Onset Meningitis:
Early onset disease is caused predominantly by bacteria transmitted at the time of parturition, whereas late-onset disease is caused by members of the microbiome transmitted at birth or through exposures after birth, such as maternal contact or method of feeding.
Streptococcus agalactiae (Group B Streptococcus, or GBS) is the most frequently identified pathogen from cases of young infant bacterial meningitis, followed in incidence by other organisms, including Escherichia coli and Listeria monocytogenes.
Two sites of colonization likely contribute to cases of late-onset meningitis. The gastrointestinal tract serves as a frequent site of colonization for coli, GBS, and L. monocytogenes, and all of these pathogens have essential factors that allow for epithelial adherence and invasion.
GBS is readily transmitted from mother to neonate; 29–85% (mean rate of approximately 50%) of infants born to a GBS-positive mother become colonized.
The second potential site of colonization is the urinary tract, which may harbor asymptomatic bacteriuria.
Ascending infection can lead to seeding of the kidney, bacteremia, and then meningitis, as around 13.2% of febrile young infants will present with a urinary tract infection, and a smaller subset will have simultaneous evidence of bacteriuria, bacteremia, and meningitis.
In premature infants, bacteremic events can be preceded by colonization of the gut by the causative pathogen. Recent analysis of the microbiome has shown dynamic colonization of the neonatal gut, and one potential factor in colonization is the population of bacteriophage. There is an essential relationship between bacteriophages and development of the gut bacterial microbiome, in which the bacteriophage population guides the diversity of the bacterial population.
The immature immune system compounds the meningitis infection:
The relatively immature immune system of the neonate also contributes to the invasive risk of bacterial pathogens. Defects in phagocytic cell function, chemotaxis, cytokine production, complement pathways, Toll-like receptor responses, and antibody production are further conducive to invasive disease. These defects also include adaptive immunity in response to viral infections, including lymphocyte proliferation and antibody responses. Though significant, these immune defects are transient, likely contributing to the decreased incidence of serious bacterial infections with increasing age.