Sociodemographic Disparities Increase Neonatal Sepsis Mortality: A Nationwide Study

2016 ◽  
Vol 223 (4) ◽  
pp. S90-S91
Author(s):  
Fredrick J. Bohanon ◽  
Deepak Adhikari ◽  
Hemalkumar B. Mehta ◽  
Omar Nunez Lopez ◽  
Xiaofu Wang ◽  
...  
2020 ◽  
Vol 87 (10) ◽  
pp. 880-880
Author(s):  
Chand Wattal ◽  
Neelam Kler ◽  
J. K. Oberoi ◽  
Anurag Fursule ◽  
Anup Kumar ◽  
...  

2005 ◽  
Vol 133 (5) ◽  
pp. 877-881 ◽  
Author(s):  
B. D. GESSNER ◽  
L. CASTRODALE ◽  
M. SORIANO-GABARRO

We evaluated all fatal neonatal sepsis and pneumonia cases occurring in Alaska during 1992–2000. Risk factors were evaluated using a database of all births occurring during the study period. Of 32 cases, group B streptococcus (GBS) was isolated from 21% (all <7 days of age), Candida spp. from 19% (all >7 days of age), non-GBS Gram-positive bacteria from 50% (53% <7 days of age), and Gram-negative infections from 38% (58% <7 days of age). Infants born at <37 weeks gestation accounted for 72% of cases and had an increased risk of GBS [rate ratio (RR) 9·1, 95% confidence interval (CI) 2·0–41] and non-GBS (RR 40, 95% CI 16–101) disease. Neonatal sepsis mortality has become an outcome concentrated among pre-term infants. Aetiologies include GBS during the early neonatal period, Candida spp. during the late neonatal period, and other bacteria during both periods.


2016 ◽  
Vol 113 (19) ◽  
pp. E2627-E2635 ◽  
Author(s):  
James Lawrence Wynn ◽  
Chris S. Wilson ◽  
Jacek Hawiger ◽  
Philip O. Scumpia ◽  
Andrew F. Marshall ◽  
...  

Interleukin (IL)-18 is an important effector of innate and adaptive immunity, but its expression must also be tightly regulated because it can potentiate lethal systemic inflammation and death. Healthy and septic human neonates demonstrate elevated serum concentrations of IL-18 compared with adults. Thus, we determined the contribution of IL-18 to lethality and its mechanism in a murine model of neonatal sepsis. We find that IL-18–null neonatal mice are highly protected from polymicrobial sepsis, whereas replenishing IL-18 increased lethality to sepsis or endotoxemia. Increased lethality depended on IL-1 receptor 1 (IL-1R1) signaling but not adaptive immunity. In genome-wide analyses of blood mRNA from septic human neonates, expression of the IL-17 receptor emerged as a critical regulatory node. Indeed, IL-18 administration in sepsis increased IL-17A production by murine intestinal γδT cells as well as Ly6G+myeloid cells, and blocking IL-17A reduced IL-18–potentiated mortality to both neonatal sepsis and endotoxemia. We conclude that IL-17A is a previously unrecognized effector of IL-18–mediated injury in neonatal sepsis and that disruption of the deleterious and tissue-destructive IL-18/IL-1/IL-17A axis represents a novel therapeutic approach to improve outcomes for human neonates with sepsis.


2019 ◽  
Vol 87 (2) ◽  
pp. 117-121 ◽  
Author(s):  
Chand Wattal ◽  
Neelam Kler ◽  
J. K. Oberoi ◽  
Anurag Fursule ◽  
Anup Kumar ◽  
...  

2018 ◽  
Vol 37 (7) ◽  
pp. e178-e184 ◽  
Author(s):  
Fredrick J. Bohanon ◽  
Omar Nunez Lopez ◽  
Deepak Adhikari ◽  
Hemalkumar B. Mehta ◽  
Yesenia Rojas-Khalil ◽  
...  

2018 ◽  
Vol 54 (5) ◽  
pp. 963-974 ◽  
Author(s):  
Beverley Lim Høeg ◽  
Christoffer Johansen ◽  
Jane Christensen ◽  
Kirsten Frederiksen ◽  
Susanne Oksbjerg Dalton ◽  
...  

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