Ahmed Sayed

Prof. Dr. Ahmed Sayed

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Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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23 March 2022 in PLOS ONE
Verified
Journal Article
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SEShymaa Enany
Shymaa Enany
SZSamira Zakeer
Samira Zakeer
ADAya A Diab
Aya A Diab
UBUsama Bakry
Usama Bakry
ASAhmed Sayed
Ahmed Sayed
Klebsiella pneumoniae is considered a threat to public health especially due to multidrug resistance emergence. It is largely oligoclonal based on multi-locus sequence typing (MLST); in Egypt, ST 627 was recently detected. Despites the global dissemination of this ST, there is still paucity of information about it. Herein, we used 4 K. pneumoniae ST627 for whole genome sequencing utilizing an Illumina MiSeq platform. Genome sequences were examined for resistance and virulence determinants, capsular types, plasmids, insertion sequences, phage regions, and Clustered Regularly Interspaced Palindromic Repeats (CRISPR) regions using bioinformatic analysis. The molecular characterization revealed 15 and 65 antimicrobial resistance and virulence genes, respectively. Resistance genes such as tet(D), aph(3’’)-Ib, aph(6)-Id, blaTEM-234, fosA, and fosA6; were mainly responsible for tetracycline, aminoglycoside, and fosfomycin resistance; respectively. The capsular typing revealed that the four strains are KL-24 and O1v1. One plasmid was found in all samples known as pC17KP0052-1 and another plasmid with accession no. NZ_CP032191.1 was found only in K90. IncFIB(K) and IncFII(K) are two replicons found in all samples, while ColRNAI replicon was found only in K90. Entero P88, Salmon SEN5, and Klebsi phiKO2 intact phage regions were identified. All samples harbored CRISPR arrays including CRISPR1 and CRISPR2. Our results shed light on critical tasks of mobile genetic elements in ST 627 in antibiotic resistance spreading.

7 November 2023 in BMC Medicine
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Journal Article
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NMNaydeen Mostafa
Naydeen Mostafa
ASAhmed Sayed
Ahmed Sayed
OROmar Rashad
Omar Rashad
Omar BaqalOmar Baqal
Omar Baqal
Background: Malnutrition mortality in older adults is underrepresented in scientific literature. This obscures any recent changes and hinders needed social change. This study aims to assess malnutrition mortality trends in older adults (≥ 65 years old) from 1999 to 2020 in the United States (U.S.). Methods: Mortality data from the Centers for Disease Control and Prevention’s (CDC) Wide-Ranging Online Data for Epidemiology Research (WONDER) database were extracted. The ICD-10 Codes E40 – E46 were used to identify malnutrition deaths. Crude mortality rates (CMR) and age-adjusted mortality rates (AAMR) were extracted by gender, age, race, census region, and urban–rural classification. Joinpoint regression analysis was used to calculate annual percentage changes (APC) of AAMR by the permutation test and the parametric method was used to calculate 95% confidence intervals. Average Annual Percentage Changes (AAPC) were calculated as the weighted average of APCs. Results: Between 1999 and 2020, 93,244 older adults died from malnutrition. Malnutrition AAMR increased from 10.7 per 100,000 in 1999 to 25.0 per 100,000 in 2020. The mortality trend declined from 1999 to 2006 (APC = –8.8; 95% CI: –10.0, –7.5), plateaued till 2013, then began to rise from 2013 to 2020 with an APC of 22.4 (95% CI: 21.3, 23.5) and an overall AAPC of 3.9 (95% CI: 3.1, 4.7). Persons ≥ 85 years of age, females, Non-Hispanic Whites, residents of the West region of the U.S., and urban areas had the highest AAPCs in their respective groups. Conclusion: Despite some initial decrements in malnutrition mortality among older adults in the U.S., the uptrend from 2013 to 2020 nullified all established progress. The end result is that malnutrition mortality rates represent a historical high. The burden of the mortality uptrends disproportionately affected certain demographics, namely persons ≥ 85 years of age, females, Non-Hispanic Whites, those living in the West region of the U.S., and urban areas. Effective interventions are strongly needed. Such interventions should aim to ensure food security and early detection and remedy of malnutrition among older adults through stronger government-funded programs and social support systems, increased funding for nursing homes, and more cohesive patient-centered medical care.

22 December 2021 in mSphere
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Journal Article
Open access
DJDeena Jalal
Deena Jalal
MEMariam G. Elzayat
Mariam G. Elzayat
ADAya A Diab
Aya A Diab
HEHend E. El-Shqanqery
Hend E. El-Shqanqery
OSOmar Samir
Omar Samir
ASAhmed Sayed
Ahmed Sayed
Acinetobacter baumannii represents a major health threat, in particular among immunocompromised cancer patients. The rise in carbapenem-resistant A. baumannii , and the development of resistance to the last-resort antimicrobial agent colistin, complicates the management of A. baumannii outbreaks and increases mortality rates.

5 March 2020 in Scientific Reports
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RHReem Hassan
Reem Hassan
MTMarwa Tantawy
Marwa Tantawy
NGNouran A. Gouda
Nouran A. Gouda
MEMariam G. Elzayat
Mariam G. Elzayat
SGSara Gabra
Sara Gabra
ASAhmed Sayed
Ahmed Sayed
Infection with multiple drug resistant (MDR) Escherichia coli poses a life threat to immunocompromised pediatric cancer patients. Our aim is to genotypically characterize the plasmids harbored in MDR E. coli isolates recovered from bacteremic patients of Children’s Cancer Hospital in Egypt 57357 (CCHE 57357). In this study, 21 carbapenem-resistant E. coli (CRE) isolates were selected that exhibit Quinolones and Aminoglycosides resistance. Plasmid shot-gun sequencing was performed using Illumina next- generation sequencing platform. Isolates demonstrated resistant to all beta-lactams, carbapenems, aminoglycosides and quinolones. Of the 32 antimicrobial resistant genes identified that exceeded the analysis cutoff coverage, the highest represented genes were aph(6)-Id, sul2, aph(3″)-Ib, aph(3′)-Ia, sul1, dfrA12, TEM-220, NDM-11. Isolates employed a wide array of resistance mechanisms including antibiotic efflux, antibiotic inactivation, antibiotic target replacements and antibiotic target alteration. Sequenced isolates displayed diverse insertion sequences, including IS26, suggesting dynamic reshuffling of the harbored plasmids. Most isolates carried plasmids originating from other bacterial species suggesting a possible horizontal gene transfer. Only two isolates showed virulence factors with iroA gene cluster which was found in only one of them. Outside the realms of nosocomial infections among patients in hospitals, our results indicate a transfer of resistant genes and plasmids across different organisms.

1 July 2019 in Biomedicine & Pharmacotherapy
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Journal Article
Open access
SHSalah M. Hassan
Salah M. Hassan
ATAlShaimaa Mohamed Taha
AlShaimaa Mohamed Taha
Omayma EldahshanOmayma Eldahshan
Omayma Eldahshan
ASAhmed Sayed
Ahmed Sayed
ASAhmed M. Salem
Ahmed M. Salem
This study investigated the antifibrotic effect of Prosopis juliflora leaves crude methanolic extract (PJEL) against thioacetamide (TAA)-induced liver fibrosis. The phytochemical analysis of PJEL was performed via HPLC/MS in association with evaluating its free radical scavenging and cytotoxic activities. The antifibrotic activity of PJEL was assessed by dividing Wistar rats into 8 groups: normal control, PJEL1-administered rats (2 mg/ Kg b.w.), PJEL2-administered rats (4 mg/ Kg b.w.), PJEL3-administered rats (8 mg/Kg b.w.), TAA-induced hepatic fibrosis, TTA + PJEL1, TAA + PJEL2, and TAA + PJEL3. Results indicated that PJEL crude methanolic extract is rich in polyphenolic compounds and alkaloids. PJEL exerted free radical scavenging activity with IC50 of 123.5 μg/mL and cytotoxic activity against a well-differentiated hepatocellular cell line (IC50 = 11.1 μg/mL). PJEL at a dose of 4 mg/Kg b.w. ameliorated serum ALT activity and improved serum albumin level and hepatic hydroxyproline content in association with a reduction in the fibrosis stage. PJEL elevated hepatic tumor necrosis factor-α and interleukin-6 contents with less necrosis grade. PJEL post-therapy ameliorated the relative expression of Bcl-2, Col1A1, Mmp-9, and Mmp-2 genes in liver. CONCLUSION: PJEL possesses a good therapeutic activity against TAA-induced liver fibrosis via enhancing extracellular matrix removal and stimulating hepatic regeneration to decrease hepatic necrosis.

26 November 2025 in Infectious Diseases and Therapy
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Journal Article
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DJDeena Jalal
Deena Jalal
MLMaryam Lotfi
Maryam Lotfi
GZGhada A. Ziad
Ghada A. Ziad
SMSally Mahfouz
Sally Mahfouz
YMYoussef Madney
Youssef Madney
LSLobna Shalaby
Lobna Shalaby
Introduction Carbapenem-resistant Enterobacterales (CRE) pose a major threat to immunocompromised pediatric oncology patients. However, the routes of resistance spread in this vulnerable population remain poorly understood, despite their importance for guiding infection control. Methods We analyzed 189 CRE bloodstream isolates (106 Escherichia coli, 72 Klebsiella pneumoniae, and 11 other Enterobacterales) collected at the Children’s Cancer Hospital Egypt 57357 (August 2021–October 2022). Whole genome sequencing was used to assess sequence types, resistance genes, virulence factors, plasmid content, and transmission dynamics. Results Carbapenem resistance was primarily mediated by blaNDM-5, carried on species-specific plasmids: IncFIA/IncFII in E. coli and IncFIB/IncHIB megaplasmids in K. pneumoniae, frequently co-harboring additional aminoglycoside, sulfonamide, and fluoroquinolone resistance genes. The most common sequence types were ST361, ST167, and ST405 in E. coli, and ST11, ST383, and ST147 in K. pneumoniae. Clonal clustering was observed in 62.5% of K. pneumoniae but only 17% of E. coli. Plasmid phylogenetics and patient movement data indicated extensive horizontal plasmid transfer across unrelated lineages and patients, including ICU cases. A nonfunctional rmpA variant was found in 30 K. pneumoniae isolates, but no hypermucoviscous phenotype was observed. Conclusion CRE bloodstream infections in pediatric oncology patients are driven by both clonal expansion and plasmid-mediated dissemination, with plasmids playing a dominant role, especially in E. coli. These findings highlight the limitations of strain-based surveillance and the need for integrated genomic and plasmid-level monitoring to inform infection control in high-risk hospital settings. A Graphical Abstract is available for this article. Graphical Abstract