Neonatal and young infant GBS disease can be classified into early-onset disease (EOD, onset during the first 6 days of life), and late-onset disease (LOD, onset between days 7-89 of life). It is estimated that 60.00-90.00 % of EOD occurs on the first day of life [3,4]. In the first week of life, invasive disease may appear early and frequently can cause bacteremia or pneumonia. After this period, transmission can be associated with medical care or community [5]. In most cases, it can manifests clinically as bacteremia, but also as meningitis. Both clinical forms can cause high case-fatality rate (CFR), causing often severe permanent neurological sequel [6]. The epidemiology of GBS disease considerably varies geographically and over time. A recent meta-analysis of worldwide published studies reported a mean global incidence of 0.53/1000 live births and a mean CFR of 9.60 % [7]. GBS is a Gram-positive bacterium, and there are 10 serotypes based on their capsular polysaccharide composition (Ia, Ib, II-IX). The polysaccharide capsule is a major virulence factor contributing to bacterial evasion of phagocytic clearance [8]. Serotype III is the most common invasive isolates and accounts for 30.00-50.00% of EOD and majority of LOD [7,9]. The bacteria colonize the human vagina, upper gastrointestinal and respiratory tract of healthy humans. The entrance door is often not obvious, but may be through the skin, genital, urinary and respiratory tract. Vertical transmission (mother to child) from colonized mothers can lead to invasive disease in their offspring. Later on, it transmission Volume 7 Issue 3-2017