Laboratory features
Laboratory features that are characteristic of neonatal bacterial meningitis include:
Isolation of a bacterial pathogen from the cerebrospinal fluid by culture and/or visualization by Gram stain
Increased cerebrospinal fluid white blood cell count (typically >1000 white blood cells/μL, but may be lower, especially with Gram-positive bacteria), usually with a predominance of neutrophils
Elevated cerebrospinal fluid protein concentration (>150 mg/dL in preterm (premature birth) and >100 mg/dL in term infants)
Decreased cerebrospinal fluid glucose concentration (<20 mg/dL [1.1 mmol/L] in preterm (premature birth) and <30 mg/dL [1.7 mmol/L] in term (on time) infants)

Causes
Neonatal meningitis is caused by group B streptococci Streptococcus agalactiae (39%-48% of cases), Escherichia coli (30%-35%), other Gram-negative rods (8%-12%), Streptococcus pneumoniae (about 6%), and Listeria monocytogenes (5%-7%). Meningitis is typically caused from either a bacterial or viral infection, however, it can be caused by fungal, parasitic, or amebic infections as well. Even more rare, Meningitis can be caused by some cancers, Lupus, specific drugs, head injuries, and brain surgeries. Most neonatal meningitis results from bacteremia (bacterial infection of the blood) with hematogenous spread to the central nervous system (CNS). Early-onset
In early-onset neonatal meningitis, acquisition of the bacteria is from the mother either before the baby is born or during birth. The most common bacteria found in early-onset are Streptococcus agalactiae, Escherichia coli, and Listeria monocytogenes. In developing countries, Gram-negative enteric (gut) bacteria are responsible for the majority of early onset meningitis. Late-onset
Late-onset meningitis may be caused by other Gram-negative bacteria and staphylococcal species. In developing countries, Streptococcus pneumoniae accounts for most cases of late onset.
Combined oral contraceptive
Noretynodrel (and norethisterone) were subsequently discovered to be contaminated with a small percentage of the estrogen mestranol (an intermediate in their synthesis), with the noretynodrel in Rocks 1954–5 study containing 4–7% mestranol. When further purifying noretynodrel to contain less than 1% mestranol led to breakthrough bleeding, it was decided to intentionally incorporate 2.2% mestranol, a percentage that was not associated with breakthrough bleeding, in the first contraceptive trials in women in 1956. The noretynodrel and mestranol combination was given the proprietary name Enovid.The first contraceptive trial of Enovid led by Celso-Ramón García and Edris Rice-Wray began in April 1956 in Río Piedras, Puerto Rico. A second contraceptive trial of Enovid (and norethisterone) led by Edward T. Tyler began in June 1956 in Los Angeles. On January 23, 1957, Searle held a symposium reviewing gynecologic and contraceptive research on Enovid through 1956 and concluded Enovids estrogen content could be reduced by 33% to lower the incidence of estrogenic gastrointestinal side effects without significantly increasing the incidence of breakthrough bleeding.While these large-scale trials contributed to the initial understanding of the pill formulations clinical effects, the ethical implications of the trials generated significant controversy. Of note is the apparent lack of both autonomy and informed consent among participants in the Puerto Rican cohort prior to the trials. Many of these participants hailed from impoverished, working-class backgrounds.