HYBRID EVENT: You can participate in person at Baltimore, Maryland, USA or Virtually from your home or work.
Brandon Lucke Wold, Speaker at Vaccine Research Conference
Baylor University, United States
Title : NLR as a diagnostic and prognostic marker for neonatal sepsis: A systemic review


Neonatal sepsis is a bloodstream infection that affects newborn infants under the age of 28 days and is a leading cause of morbidity and mortality in these children 1,2. There is little information on the prevalence of newborn sepsis, however Fleischmann-Struzek et al. estimate that there are around 2,200 instances of neonatal sepsis per 100,000 live births, with a death rate of 11 to 19 percent 3. Early-onset sepsis (EOS) and late-onset sepsis (LOS) are two types of neonatal sepsis based on when symptoms appear after birth (LOS). Sepsis in neonates that occurs before 72 hours of life (some experts use seven days) is referred to as EOS, while sepsis that occurs after 72 hours of life is referred to as LOS 4

The spread of infections from the female genitourinary system to the infant or fetus is the most common cause of early-onset sepsis (EOS) 1,2,4–6. These infections can contaminate the amniotic fluid or may ascend the vaginal canal, cervix, and uterus. As they pass through the vaginal canal in pregnancy or upon delivery, neonates can become contaminated. Group B Streptoccoci (GBS), E. coli, coagulase-negative Staphylococcus, Hemophilus influenzae, and Listeria monocytogenes are common bacterial infections associated with EOS1,2. Chorioamnionitis, GBS infection, birth before 37 weeks (premature newborns), and protracted rupture of membranes longer than 18 hours are all maternal variables that enhance the risk of neonatal sepsis 2. Prematurity and delayed treatment of newborn sepsis are linked to a variety of negative outcomes, including persistent lung illness and neurodevelopmental concerns such hearing and vision loss, cerebral palsy, and poor psychomotor and mental development 2,7. Overuse of antibiotics, for prophylactic treatment in sepsis prevention, on the other hand, can raise the risk of severe candidiasis and multidrug-resistant organisms1,2,4,5

In contrast, Late-onset sepsis (LOS) usually occurs via the transmission of pathogens from the surrounding environment after delivery, such as contact from healthcare workers or caregivers2–4. A percentage of LOS may also be caused by a late manifestation of vertically transmitted infection. Infants requiring intravascular catheter insertion, or other invasive procedures that disrupt the mucosa, are at increased risk for developing LOS1–3. Preterm neonates are at higher risk for sepsis/infection than term neonates. Mortality rates are inversely proportional to gestational age, such that preterm or younger neonates have higher mortality rates than do term neonates 2,5. E. coli has also been found to be associated with a higher mortality rate when compared with GBS - this can be attributed to the introduction of GBS intrapartum antibiotic prophylaxis which has decreased mortality rates5,8. The treatment of clinically suspected neonates with negative cultures has also significantly decreased mortality rates8.  
The immature immune system is the primary cause of increased neonatal sepsis susceptibility 2,6,8–10. Polymorphonuclear neutrophils, macrophages, and T lymphocytes are unable to carry out a complete inflammatory response in newborns due to their immature function. Furthermore, newborns have a restricted quantity of immunoglobulins at birth and are unable to mount an appropriate quantitative and/or qualitative response to pathogens 1,2,6,8,10,11. The premature infant's limited time in the uterus reduces the transfer of immune globulins to the fetus. When compared to term infants, preterm infants have a substantially higher risk of sepsis due to immunoglobulin deficiency 1,2,6


Brandon Lucke-Wold was born and raised in Colorado Springs, CO. He graduated magna cum laude with a BS in Neuroscience and distinction in honors from Baylor University. He completed his MD/PhD, Master’s in Clinical and Translational Research, and the Global Health Track at West Virginia University School of Medicine. His research focus was on traumatic brain injury, neurosurgical simulation, and stroke. At West Virginia University, he also served as a health coach for the Diabetes Prevention and Management program in Morgantown and Charleston, WV, which significantly improved health outcomes for participants. In addition to his research and public health projects, he is a co-founder of the biotechnology company Wright-Wold Scientific, the pharmaceutical company CTE cure, and was a science advocate on Capitol Hill through the Washington Fellow’s program.