Thrombophilia genetic mutations and their relation to disease severity among patients with COVID-19.

OBJECTIVES: Patients with COVID-19 infection appear to develop virus-induced hypercoagulability resulting in numerous thrombotic events. The aim of the present study was to determine the relationship between the thrombophilia genes mutations (prothrombin G20210A, factor V Leiden, and methyltetrahydrofolate reductase (MTHFR)) and the severity of COVID-19 patients. DESIGN: Prospective cross-sectional study. METHOD: One hundred and forty patients (80 adults and 60 children) were included in the current study. They were divided into the severe COVID-19 group and the mild COVID-19 group, with each group comprising 40 adults and 30 children. The patients were assessed for FV R506Q, FV R2H1299R, MTHFR A1298C, MTHFR C677T, and prothrombin gene G20210A polymorphisms. CBC, D-dimer, renal and liver function tests, hs-CRP, ferritin, and LDH were also assessed. Thrombotic events were clinically and radiologically documented. RESULTS: Severe COVID-19 cases were significantly more frequent to have a heterozygous mutation for all the studied genes compared to mild COVID-19 cases (p<0.05 for all). Being mutant to gene FV R506Q carried the highest risk of developing a severe disease course (p<0.0001). Patients with abnormally high D-dimer levels were significantly more frequent to be heterozygous for FV R506Q, FV R2H1299R, and prothrombin gene G20210A (p = 0.006, 0.007, and 0.02, respectively). CONCLUSION: We concluded that there is an evident relationship between severe COVID-19 and inherited thrombophilia. In the current study, FV R506Q gene mutation carried the highest risk of developing a severe COVID-19 disease course.

Prevalence of Virulence Genes and Their Association with Antimicrobial Resistance Among Pathogenic E. coli Isolated from Egyptian Patients with Different Clinical Infections.

INTRODUCTION: Escherichia (E.) coli can cause intestinal and extra-intestinal infections which ranged from mild to life-threatening infections. The severity of infection is a product of many factors including virulence properties and antimicrobial resistance. OBJECTIVES: To determine the antibiotic resistance pattern, the distribution of virulence factors and their association with one another and with some selected resistance genes. METHODS: Virulence properties were analyzed phenotypically while antimicrobial susceptibility was tested by Kirby-Bauer agar disc diffusion method. In addition, 64 E. coli isolates were tested for 6 colicin genes, fimH, hlyA, traT, csgA, crl virulence genes and bla-CTX-M-15, bla-oxa-2 , and bla-oxa-10 resistance genes by polymerase chain reaction (PCR). RESULTS: Extra-intestinal pathogenic E. coli isolated from urine and blood samples represented a battery of virulence factors and resistance genes with a great ability to produce biofilm. Also, a significant association (P<0.05) among most of the tested colicin, virulence and resistance genes was observed. The observed associations indicate the importance and contribution of the tested factors in the establishment and the progress of infection especially with Extra-intestinal E. coli (ExPEC) which is considered a great challenging health problem. CONCLUSION: There is a need for studying how to control these factors to decrease the rate and the severity of infections. The relationship between virulence factors and resistance genes is complex and needs more studies that should be specific for each area.