الفهرس 
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Abstract
SUMMARY
eonatal sepsis is one of the most challenging problems despite the ongoing progress in diagnosis and treatment. Neonatal sepsis is the single most important cause of neonatal deaths in the community, accounting for over half of them.
Early-onset sepsis is associated with acquisition of microorganisms from the mother. Transplacental infection or an ascending infection from the cervix may be caused by organisms that colonize the mother‘s genitourinary (GU) tract; the neonate acquires the microorganisms as it passes through the colonized birth canal at delivery.
Neonatal sepsis due to intestinal bacterial translocation is a major cause of morbidity and mortality.
The aim of our study was to detect the pattern of colonization of the neonatal gut with gram negative bacilli in a tertiary care hospital (Maternity Hospital, ASU) and the possible association between this colonization and the subsequent development of neonatal sepsis.
This study was conducted at Ain shams Univeristy Maternity Hospital during the period from February 2013 till February 2014.
The study was performed on 53 neonates delivered at the hospital. Of the 53 neonates, 44 were males and 9 were females.
Their age ranging from 35 wks to 41 wks and their birth weight ranging from 1500 gm to 5300 gm. Forty three were delivered by cesarean section and 10 were delivered by normal vaginal delivery.
All neonates were subjected to full perinatal history and a thorough clinical examination with assessment of Apgar score at 1 and 5 minutes, birth weight and gestational age.
Of the 53 neonates, 19 were clinically free and uncomplicated so they stayed under observation at the postnatal ward and discharged within the first 8 hrs. 34 neonates were critically ill with a diverse associated illness and causes of admission so they were admitted to the NICU. Neonates with congenital malformation, chromosomal aberrations or inborn errors of metabolism were excluded.
Among the 34 admitted neonates, 21 neonates were suspected for sepsis and their blood was collected for cultures before starting antibiotics. Out of the 21 clinical septic Neonates, 9 neonates with a positive blood culture were identified as blood culture proven sepsis and 12 neonates were blood culture negative sepsis.
Gastric aspirate and stool samples were isolated within 6hrs of life for all studied neonates (n=53) and at 3-7 days for 12 neonates among the group of clinical sepsis. Blood culture was done to the septic neonates before administration of antibiotics. Cultures of gastric aspirate and stool samples compared with that of the blood culture.
Our results shown that the guts of 34 neonates out of 53 (%64.15) were colonized by GNB within the first 6 hours of life. 6(11.32%) neonates had GNB in the first gastric aspirate alone (GA1), 10 (18.87%) neonates had GNB in the first stool sample alone (S1) and 18(33.96%) neonates had GNB in both gut samples (GA1&S1).of the 34 colonized by GNB in the first gut samples, 28 developed sepsis. No growth was detected in the first gut samples (GA1&S1) of 19 (35.85%) neonates.
At day 7, a second gastric aspirate & stool cultures from 12 neonates was done & revealed that 5 neonates (38.46%) had GNB in their second gastric aspirate (GA2) and 1 neonate (7.69%) had GNB in both second gut samples (GA2 & S2). 7 neonates (53.85%) showed no growth in the second gut ample.
Of GNB isolates A. baumanii was the most common, being detected in 13 neonates (22.03%) followed by x.s.maltophilia and H.alvei were found in the gut of 11 neonates (18.64%).
None of the maternal risk factors (mode of delivery, PROM, chorioamnionitis and maternal fever) were significant factor for
occurrence of GNB in both first and second gut samples (p-value >0.05).
Nasogastric feeding and intake of different antibiotics were not found to influence the gut colonization with GNB in the second gut samples (p-value >0.05).
Our study revealed that neonates of the clinical sepsis group had significantly higher incidence of PROM, maternal fever and nasogastric feeding tube (p-value <0.05) and they stayed in NICU significant longer duration compared to the non septic neonates (p-value <0.001). It was also shown that clinical sepsis group had highly significant CRP value (p-value<0.001) and significant higher TLC and lower platelet count compared to the group of no sepsis (p-value<0.05).
Neonates of clinical sepsis group had significant higher GNB in their gut compared to non septic group especially in gastric aspirate taken in first 6 hours & stool sample taken at day 7 (p-value <0.05).
Blood cultures were done for 21 neonates with clinical sepsis, 12 of them had shown no growth, while 9 had positive blood cultures, 7 gram negative bacilli and 2 gram positive cocci were isolated. K.pneumoniae was isolated from 2 neonates(9.5%) and the frequency of other bacteria was 1 neonate for each (4.8%).
Neonates with GNB in the gut had a consistently higher incidence of clinical sepsis than those without GNB (p-value=
0.008). Highly sensitive biochemical identification codal system (Microbact 12 pannel) was used to assess the relation of the isolates in the gut and those from the blood of the septic neonates. It was shown that one neonate, out of 9 (11.11%) with blood culture proven sepsis, had the same organism colonize his gut (GA1&S1) and isolated from his blood, it was E.coli inactive. This further support the association of gut colonization with subsequent sepsis.
In conclusion the results of our study established the occurrence of GNB colonization of the neonatal gut and revealed an association of gut colonization with GNB with neonatal sepsis.