Streptococcus agalactiae (Group B
Streptococcus, GBS) is a gram positive encapsulated coccus which has the ability to invade host tissues and the host defense mechanisms, to cause systemic infections such as sepsis, pneumonia, and due to its ability of crossing the blood brain barrier, it is responsible for meningitis, being the leader in the etiology of neonatal meningitis [
1]. There are 10 serotypes identified, labeled Ia, Ib, II-IX [
2], differentiated by the arrangement of four monosaccharides: glucose, N-acetylglucosamine, galactose and sialic acid, in the repetitive unit, the last monosaccharide being known to have an antiphagocytic action. Among the factors involved in the pathogenesis, it is generally accepted the important role of β-haemolysin/cytolysin toxin in producing brain endothelial cells [
3], neuronal, astrocytal [
4] and leptomeningeal lesions. GBS meningitis occurs as early-onset disease (EoD), within 7 days postpartum, by infection in utero, by placenta infection. It can be acquired perinatal during passage through the vaginal canal. Prematurity and low birth weight are additional risk factors. Late-onset disease (LoD) is associated with serotype III, and occurs after 7 days of life [
5], up to 3 months, with 50% of infections being meningitis. GBS meningitis over 3 months (ultra-late onset disease -ULOD), represent about 6% of the cases. In Europe, serotype III is involved most often, in 70 to 81% [
6], followed by serotype I in 13% of meningitis cases [
7]. In the United States, most often are involved Ia, Ib, II, III and V serotypes in 96% of GBS meningitis cases [
8]. Regarding older children up to the age of 18, there are few references that describe these cases though the numbers are small [
9]. The host factors that should prevent the invasion of the GBS in the blood are neutrophils and macrophages, cells that ensure the bacterial clearance. Leukopenia in our case suggests a lack of defense by phagocytosis, which allowed the presence of bacteremia and subsequent the crossing of blood-brain barrier by GBS. The use of PPIs is recognized as a potential trigger of damages in the leukocytes functions, involving a decreased bactericidal activity [
10], with an increased risk of enteric infections (3 times more) [
11], including
Clostridium difficile infections, the oropharyngeal colonization and the loss of bacterial diversity [
12]. Prolonged use of PPIs is associated with pulmonary translocation of potentially pathogenic bacteria from the colonization of the gastric mucosa via the upper digestive and upper respiratory tracts and with the occurrence of community acquired pneumonia [
13‐
16] namely with
Streptococcus pneumoniae [
17]. Prolonged administration of PPIs is also associated with hypomagnesaemia [
18], iron deficiency [
19], vitamin B12 deficiency [
20,
21], osteoporosis [
22,
23], atrophic gastritis, prolonged hypergastrinemia, and carcinoid formation. Gastroesophageal reflux disease associated with PPIs use, was in our opinion, the determinant factor of the upper digestive tract colonization with GBS, which was associated with leukopenia induced by PPIs, factor that is involved in bacterial clearance in the bacteremia stage.