Background Diarrhoea, affecting children in developing countries, is mainly caused by diarrheagenic Escherichia coli (DEC). This study principally aimed to determine the prevalence of DEC pathotypes and Extended-spectrum β-lactamase (ESBL) genes isolated from children under 5 years old with diarrhea. Methods A total of 320 diarrhoea stool samples were investigated. E. coli isolates were investigated for genes specific for enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroaggregative E. coli (EAEC), enteroinvasive E. coli (EIEC) and enterohemorrhagic E. coli (EHEC) using polymerase chain reaction (PCR). Furthermore, antimicrobial susceptibility testing, detection of antibiotic resistance-genes and phylogenetic typing were performed. Results Over all, DEC were isolated from 66/320 (20.6%) of the children with diarrhoea. EAEC was the predominant (47%), followed by typical EPEC (28.8%) and atypical EPEC (16.6%). Co-infection by EPEC and EAEC was detected in (7.6%) of isolates. However, ETEC, EIEC and EHEC were not detected. Phylogroup A (47%) and B2 (43.9%) were the predominant types. Multidrug-resistance (MDR) was found in 55% of DEC isolates. Extended-spectrum β-lactamase (ESBL) genes were detected in 24 isolates (24 blaTEM and 15 blaCTX-M-15). Only one isolate harbored AmpC β-lactamase gene (DHA gene). Conclusion The study concluded that, EAEC and EPEC are important causative agents of diarrhoea in children under 5 years. MDR among DEC has the potential to be a big concern.

Autism Spectrum Disorder (ASD) and learning disabilities are neurodevelopmental disabilities characterized by dramatically increasing incidence rates, yet the exact etiology for these disabilities is not identified. Impairment in tryptophan metabolism has been suggested to participate in the pathogenesis of ASD, however, further validation of its involvement is required. Additionally, its role in learning disabilities is still uninvestigated. Our objective was to evaluate some aspects of tryptophan metabolism in ASD children (N = 45) compared to children with learning disabilities (N = 44) and healthy controls (N = 40) by measuring the expression levels of the MAOA, HAAO and AADAT genes using real-time RT-qPCR. We also aimed to correlate the expression patterns of these genes with parental ages at the time of childbirth, levels of serum iron, and vitamin D3 and zinc/copper ratio, as possible risk factors for ASD. Results demonstrated a significant decrease in the expression of the selected genes within ASD children (p < 0.001) relative to children with learning disabilities and healthy controls, which significantly associated with the levels of our targeted risk factors (p < 0.05) and negatively correlated to ASD scoring (p < 0.001). In conclusion, this study suggests that the expression of the MAOA, HAAO and AADAT genes may underpin the pathophysiology of ASD.

Objective: Zinc, copper and selenium are essential for normal development and function of the central nervous system. This study aimed at assessment of serum levels of zinc, copper and selenium in children with severe acute malnutrition (SAM) with & without cerebral palsy both before and after nutritional rehabilitation. Methods: A prospective case control study involved 2 groups (Group I); included160 children with SAM of both sex, aged 6e59 months, this group was subdivided into 2equal subgroups; subgroup A: SAM without cerebral palsy, subgroup B: SAM with cerebral palsy. Group II (control group) included 96 apparently healthy children matching age and sex with the first group. Both groups were subjected to a detailed history including nutritional history. Anthropometric measurements were recorded and laboratory assessment for serum levels of (copper, zinc, & selenium) before and after nutritional rehabilitation were performed for all children. Results: Group I (A&B) showed a significant decrease in anthropometric measurements, serum zinc, serum selenium but normal copper level before nutritional rehabilitation in comparison to

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