الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Ventilator associated pneumonia (VAP) is pneumonia in mechanically ventilated patients that develops at or later than 48 hours after the patient has been placed on a mechanical ventilator till 48 hours after extubation. VAP is a clinically and economically important HAI and one of the most important leading causes of morbidity and mortality in NICUs. The risk of VAP is increased among newborn infants owing to several identified risk factors; awareness of the preventable risk factors can aid in VAP prevention.
Evidence-based interventions aim to decrease incidence of VAP through focusing on the prevention of aerodigestive tract colonization and of aspiration of contaminated secretions. Several strategies could be easily implemented and consequently lead to better outcomes.
The aim of the present study was to detect the source of VAP in the NICU of El-Shatby University Hospital by comparing aerodigestive tract colonizing isolates and isolates from their potential sources with isolates of BAL samples collected from neonates fulfilling the CDC criteria of clinically defined VAP and to design intervention measures based on the identified practices that impose an enhanced risk of VAP in the mechanically ventilated neonates.
All mechanically ventilated neonates were monitored for the development clinically defined VAP and microbiologically for the development of aerodigestive colonization; concurrently samples were collected from the potential sources of colonizers (hands of HCPs, inner lumen of suction tubes and condensate of ventilator circuits). The incidence of clinically defined VAP based on CDC criteria was 72.5% and 28.8 per 1000 ventilator days. Once the patient fulfilled the clinically defined VAP criteria, NB-BAL samples were obtained and processed quantitatively then the etiological agents were identified except if sampling was contraindicated. The incidence of lab confirmed VAP was 43.95% and 19.2 per 1000 ventilator days. Among the recorded VAP episodes, early onset VAP was 46.96% and late onset VAP was 53.03%.
Colonization of the oral cavity was found to be important in the pathogenesis of VAP, since 35.9% (28/78) of isolates incriminated in the pathogenesis of VAP were recovered from the oral cavity prior to the onset of VAP, while 15 (19.2%) isolates recovered from pre-feeding residuals, were subsequently recovered from BAL samples of VAP cases thereby elucidating the role of gastric colonization in the pathogenesis of VAP.
Isolates from the suction tubes were potentially incriminated in the pathogenesis of VAP in 34.6% occasions of patient related samples, while 10.3% of isolates from patient related samples incriminated in the pathogenesis of VAP obtained prior to diagnosis of clinically defined VAP were from condensate of expiratory limb of V.Cs and none of the isolates from inspiratory limb of V.Cs was incriminated in the pathogenesis of VAP. No role has been identified for the hands of the HCPs in the present study as a potential source of aerodigestive colonization.
There was no significant difference between Gram stain and AO stain in the identification of PMNLs or ICO. ICO was detected in 85 % and 90 % of Gram stained and AO stained smears from BAL samples that subsequently yielded positive cultures.
Gram negative bacteria were implicated in the etiology of 80% of VAP episodes with A. Baumannii being the predominant organism isolated (47.5%), followed by Klebsiella pneumoniae and Pseudomonas aeruginosa (27.5%) for each. In total 60% of VAP episodes were due to single pathogen and 40% were due to polymicrobial etiology.
It is unlikely that VAP occurred as a consequence of BSI as 87.9% of the blood cultures in the clinically defined VAP cases showed no growth and only 2 infants had the same organism isolated from BAL and subsequently from blood cultures suggesting secondary BSI.
Twenty nine Acinetobacter isolates (12 isolates implicated in VAP etiology and 17 from relevant patient related samples) were subjected to molecular typing using PFGE technique; PFGE typing indicated the persistence of a single PFGE type throughout the study period in the form of two PFGE Clusters with 100% similarity between isolates within the same cluster and 96.7% similarity between isolates from the two clusters.
Antimicrobial susceptibility testing was performed to all isolates from NB-BAL samples, 94.7% of Acinetobactar isolates incriminated in VAP aetiology were MDR and 5.3% were PDR, 72.7% of P.aeruginosa isolates were MDR, 72.7% of Klebsiella pneumoniae isolates were MDR, and 36.4% were ESBL +ve. 75% of Enterobacter aerogenas isolates were MDR, 25% were ESBL +ve, with no PDR isolates. 60% of E.coli isolates were ESBL +ve and MDR. One of the 2 CNS isolates from BAL samples in the present study was methicillin resistant.
In the present study some of A. baumannii isolates allocated within the same PFGE cluster showed non identical antibiotic resistance patterns, while some of isolates allocated within different PFGE clusters were found to have similar antibiotic resistance patterns. This indicated that antibiograms cannot be used alone as a typing method to identify the relatedness of isolates.