Prevalence and antibiotic resistance pattern of extended spectrum beta lactamase producing Escherichia coli isolated from urinary tract infection

Introduction: Urinary tract infection (UTI) due to extended spectrum beta-lactamase (ESBL)-producing bacteria including Escherichia coli has become widespread. Studies have shown a trend toward higher mortality, longer hospitalization, greater hospital expenses and reduced rates of clinical and microbiologic response in ESBL UTI. Objectives: The aim of this study is to determinate the prevalence and antibiotic resistance pattern of ESBL producing E. coli isolated from UTI. Patients and Methods: This cross-sectional study was conducted on 3126 samples. Urine specimens were cultured on Eosin Methylene Blue (EBM) and blood agar. The disk diffusion standard method (Kirby Bauer) was used to test the susceptibility of the drug on Muller- Hinton agar plates and results were reviewed based on Clinical and Laboratory Standards Institute (CLSI) criteria. The reviewing of ESBL-producing uropathogens was carried out using Combined Disk Test (CDT) by using cefotaxime (CTX; 30 μg) and cefotaximeclavulanic acid (CTX; 30 μg /CA:10 μg) disks and CLSI protocol. Results: Out of 291 E. coli isolates, 108 (37.11) are ESBL-producer and 183 (62.89) are non-ESBL-producer. Among ESBL-producing E. coli, the highest antibiotic resistance was observed with cefotaxime (100), amoxicillin (97.22) and piperacillin (96.3) and the highest antibiotic sensitivity was observed with meropenem (93.5), nitrofurantoin (81.48) and gentamicin (55.56). Conclusion: We recommended that cephalosporins, penicillins and cotrimoxazole are not suggested in the treatment of ESBL-producing E. coli. On the other hand, carbapenems as a first line and aminoglycosides as the next step in the treatment of ESBL-producing E. coli are recommended. © 2019 The Author(s)

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Partial Loss of USP9X Function Leads to a Male Neurodevelopmental and Behavioral Disorder Converging on Transforming Growth Factor beta Signaling

BACKGROUND: The X-chromosome gene USP9X encodes a deubiquitylating enzyme that has been associated with neurodevelopmental disorders primarily in female subjects. USP9X escapes X inactivation, and in female subjects de novo heterozygous copy number loss or truncating mutations cause haploinsufficiency culminating in a recognizable syndrome with intellectual disability and signature brain and congenital abnormalities. In contrast, the involvement of USP9X in male neurodevelopmental disorders remains tentative.METHODS: We used clinically recommended guidelines to collect and interrogate the pathogenicity of 44 USP9X variants associated with neurodevelopmental disorders in males. Functional studies in patient-derived cell lines and mice were used to determine mechanisms of pathology.RESULTS: Twelve missense variants showed strong evidence of pathogenicity. We define a characteristic phenotype of the central nervous system (white matter disturbances, thin corpus callosum, and widened ventricles); global delay with significant alteration of speech, language, and behavior; hypotonia; joint hypermobility; visual system defects; and other common congenital and dysmorphic features. Comparison of in silico and phenotypical features align additional variants of unknown significance with likely pathogenicity. In support of partial loss-of-function mechanisms, using patient-derived cell lines, we show loss of only specific USP9X substrates that regulate neurodevelopmental signaling pathways and a united defect in transforming growth factor signaling. In addition, we find correlates of the male phenotype in Usp9x brain-specific knockout mice, and further resolve loss of hippocannpal-dependent learning and memory.CONCLUSIONS: Our data demonstrate the involvement of USP9X variants in a distinctive neurodevelopmental and behavioral syndrome in male subjects and identify plausible mechanisms of pathogenesis centered on disrupted transforming growth factor beta signaling and hippocampal function.Genetics of disease, diagnosis and treatmen