Background: Treatment failure of sepsis caused by Escherichia coli (E. Coli) is a leading cause of death of infants and children in intensive care units. Objective: To detect the prevalence of Extended-Spectrum Beta-Lactamase (ESBL) and carbapenemase-genes between E. coli isolates from infants and children with septicemia and to identify their antibiotic sensitivity pattern. Methods: This is a cross-sectional study performed on 88 patients with sepsis. The isolated E. coli were identified by Gram stain and biochemically by the Microscan automated system. ESBL and carbapenemase producing E. coli were isolated on double disk diffusion and EDTA double disk, respectively. Polymerase chain reaction for ESBL and carbapenemase producing E. coli genes were performed. Bacterial susceptibility to antibiotics was tested. The initial results were measured through the 30-days of hospital admission. IRB approved the study. Results: Of 88 patients with sepsis, 49 and 30 strains were ESBL producing and carbapenemase producing E. coli; respectively. Neither risk factors for infection nor clinical picture can differentiate between ESBL and carbapenemase producing E. coli. The most frequently detected gene of ESBL producing E. coli was SHV, it was more sensitive to Piperacillin/Tazobactam (90%) and cefepime (86.7%) while for carbapenemase-producing E. coli; IMP was the most frequent, its sensitivity was high to Piperacillin/Tazobactam and Ciprofloxacin (52.6% each). Conclusion: The commonest gene of ESBL producing E. coli is SHV whereas for carbapenemase-producing E. coli is IMP. Piperacillin/Tazobactam is the candidate drug to start in children with septicemia and suspected ESBL or carbapenemase-producing E. coli infection.

Background: Adenovirus is a common virus associated with acute gastroenteritis in children. There are certain genotypes that are prevalent in these infections such as genotypes 40 and 41. Objective: The aim of the present study was to investigate the incidence of adenovirus genotypes 40 and 41 in children with acute gastroenteritis by polymerase chain reaction (PCR) and also to determine the possibility of Adenovirus co-infections with Rota virus. Method: The study was cross- sectional study that included 100 children with acute gastroenteritis. The children were subjected to full history taking and clinical examination. Stool samples from the patients were subjected to detection of adenovirus and rotavirus antigens by enzyme linked immunosorbent assay (ELISA) and detection of adenovirus genotypes 40 and 41 by polymerase chain reaction (PCR). Results: The most prevalent virus by the used methods was rotavirus antigen in the stool (35%). Adenovirus antigen detection was positive in 23% of the stool samples with positive PCR for these samples in 22%. The ADv40 was detected in 13 samples and ADv41 was detected in 9 samples. One positive sample by adenovirus antigen ELISA was negative by PCR for these genotypes. Mixed rotavirus and adenovirus by ELISA were detected in 7% of the children. In patients with positive adenovirus antigen by ELISA , the most common symptoms were vomiting (54.5%) and abdominal pain (45.5%). Insignificant difference as regard fever (P=0.94) and abdominal pain (P=0.63) was detected in children infected with adenovirus compared to patients infected with other organisms. The adenovirus was detected in 68.2% of children with acute gastroenteritis ≤ 24 months. Vomiting was significantly increased in children with adenovirus (54.5%) compared to children negative for adenovirus (23.1%-P=0.004, OR 4.0, 95%CI: 1.5-10.8) Conclusion: The study highlights the presence of adenovirus genotypes 40 and 41 in stool of children with acute gastroenteritis. Combined rotavirus and adenovirus infections were detected in our study.

Background Toll-like (TLRs) play a crucial role in both adaptive and innate immunity. The aim of the present study was to assess the association of TLR5-rs5744168, TLR9-rs187084, and TLR9-rs352140 single nucleotide polymorphisms (SNPs) with susceptibility to systemic lupus erythematosus (SLE) and lupus nephritis (LN) in Egyptian patients. Results The C allele and homozygous CC genotype of the TLR9-rs352140 in co-dominant and recessive models were more prevalent in SLE patients than controls (P = 0.047, P = 0.017, and P = 0.005 respectively). In contrast, allelic and genotyping distribution of TLR5-rs5744168 and TLR9-rs187084 SNPs showed no association with the risk of SLE. The T allele of the TLR5-rs5744168 was more prevalent in LN patients than controls (P = 0.021). The homozygous TT genotype of TLR5-rs5744168 SNP was more prevalent in LN patients in the co-dominant and the recessive models than controls (P = 0.036 and P = 0.011 respectively). The C allele of the TLR9-rs352140 was more prevalent in LN patients than controls (P = 0.015). The homozygous CC genotype of the TLR9-rs352140 SNP was more prevalent in LN than controls in co-dominant and recessive models (P = 0.002 and P < 0.001). In the recessive model of the TLR5-rs5744168 SNP, the TT genotype was found in 3.2% of the SLE patients while none of the SLE patients without LN or controls had TT genotype (P = 0.036). Also, in the recessive model of the TLR9-rs352140 SNP, the CC genotype was significantly more frequent in SLE patients with LN than without LN (44.4% vs 29.9%, P = 0.045). Conclusion Our results support the potential role of TLR5-rs5744168 SNP and TLR9-rs3532140 SNP not only in increasing the risk for development of SLE, but also in increasing the risk of LN in SLE patients among the Egyptian population.

Background:The rs3761548 polymorphism (3279 C> A) of the FOXP3 gene is associated with several autoimmune disorders. Its role in vitiligo has not been well studied.We sought to investigate whether rs3761548 polymorphism is associated with vitiligo in Egyptian subjects. Methods:Case-control study where genomic DNA was isolated from blood samples of 100 patients and 100 control subjects and genotyping was done by allele-specific primers. Given that FOXP3 is an X-linked marker, data analysis was done for the entire cohort and then stratified based on the gender. Results:The genotype frequencies differed significantly from patients to control subjects showing that AC genotype was significantly higher in the patient group than control subjects (risky genotype ) despite of the protective nature of CC genotype which observed in our study. According to the alleles , the A allele was higher in the patient than in the control group .Insignificant results were reported according to the association between FOXP3 (rs3761548) promoter polymorphism and clinical data of patients and their response to phototherapy.Conclusions: The rs3761548 of FOXP3 gene may be associated with susceptibility to vitiligo because of altered expression.Both the A allele and AC genotype were significantly associated with vitiligo .

Background Rheumatoid arthritis (RA), is a chronic inflammatory autoimmune disease, characterized by dysregulated T cell immune response.. Objective To investigate the Tim-3 surface expression on peripheral blood CD4+ and CD8+ T cells in RA patients concerning disease activity. Methods A cross-sectional case-controlled study involving 157 RA patients who were categorized by disease activity score 28 (DAS28) into 4 groups; patients with remission and low, moderate, and high RA activity groups. The assessment of Tim-3 expression on peripheral CD4 and CD8 T cells of patients and controls using flow cytometry was done. Results The peripheral expression of Tim-3 on CD4 + and CD8 + T cells was significantly higher in RA patients as compared to controls (for CD4 + T cells, 3.55 ± 1.12% in remission group vs. 1.21 ± 0.52 in control group, p < 0.001; for CD8 + T cells, 5.95 ± 1.49% in remission group vs. 1.80 ± 0.73% in control group, p < 0.001). There was an inverse correlation between percentages of both peripheral Tim-3 + CD4 + and Tim-3 + CD8 + T cell and RA DAS28, (r = − 0.425, p = 0.001) and (r= − 0.597, p = < 0.001) respectively. Conclusion The upregulated Tim-3 expression on peripheral CD4 + and CD8 + T-cells suggests a potential role of this immune checkpoint receptor in T cell immune dysregulation in RA. Tim-3 expression was negatively correlated with disease progression. Tim-3 could be a useful biomarker in determining the rheumatoid disease activity, progression, and represents an important target for inhibitors intervention in RA.

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