Objectives An increased incidence of acute invasive fungal sinusitis associated with the recent COVID‐19 pandemic has been observed, which is considered a public health concern. This study aims to detect the incidence, risk factors, causative agents, clinical presentations, outcomes, and susceptibility rate of various antifungals. Methods In this cross‐sectional cohort study, a total of 30 patients showing acute invasive fungal rhinosinusitis following a COVID‐19 infection were investigated. Histopathological biopsies, culture identification, and molecular confirmation of the causative agents were conducted. The demographic data, risk factors, clinical presentations, treatment regimen and its outcomes, and efficacy of antifungals were listed and analyzed. Results A total of 30 cases with a mean age of 59.6 ± 11.9 years were included. Diabetes mellitus was the most recorded comorbidity with a rate of 86.7%, whereas most of the patients received corticosteroids. The mycological examination confirmed the existence of Mucor (Rhizopus oryzae) and Aspergillus (Aspergillus niger) in 96.7% and 3.3% of the cases, respectively. Various stages of sinonasal involvement (ethmoid, maxillary, sphenoid, and inferior turbinate) represented 100%, 83.3%, 66.7%, and 86.7% of the cases, respectively. Headache and facial pain, ophthalmoplegia, visual loss, and blindness represented 100%, 66.7%, 90%, and 53.3% of the cases, respectively. All the cases were simultaneously treated with surgical debridement and amphotericin B. Moreover, R. oryzae was susceptible to it, whereas A. niger was sensitive to voriconazole, resulting in a survival rate of 86.7% (26/30). The R. oryzae and A. niger isolates were proven to be sensitive to acetic acid, ethyl alcohol, formalin, and isopropyl alcohol. Conclusions In patients with COVID‐19, the diagnosis of acute invasive fungal sinusitis and prompt treatment with antifungal medicine and surgical debridement are important in achieving better outcomes and survival rates. Level of Evidence 4

Background: One-third of the world’s population is infected with Mycobacterium tuberculosis. Difference in clinical outcome of infection implies that host genetics may be implicated in such variability. Investigations of Toll-like receptors (TLRs) revealed new information regarding the immunopathogenesis of tuberculosis. Toll-like receptor 2 (TLR2) mediates crucial immune response against Mycobacterium tuberculosis. There is argument that Toll-like receptor (TLR10) participate in tuberculosis susceptibility by acting as a signaling modulator for TLR2. Objectives: The aim of this study was investigating the relationship between TLR 10 SNP 720A/C (rs11096957) and increase susceptibility to tuberculosis. Methodology: Eighty patients with radiological, microbiological and clinical proven active pulmonary tuberculosis (T.B) were included in this study. (TLR10) polymorphisms and allele distributions were compared between these 80 patients and 70 healthy control subjects. Peripheral blood samples were taken from all patients and controls. Genotyping was accomplished by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: When we compare T.B cases with controls, a statistically significant association was observed between T.B susceptibility and SNP 720A/C (rs11096957) in (TLR10). Allele (A) was more frequent in tuberculous cases while allele (C) was more common in controls. It was reported that the AA genotype of (TLR10) SNP rs11096957 was considerably related to the increased risk of developing pulmonary T.B. Homozygosity (AA) has been associated with predisposition to disease by comparing cases to controls (P = 0.045; OR = 2.0; 95% C.I. = 1.0- 4.0). A/C heterozygosity was considerably different in tuberculous cases than in healthy controls with lower risk of developing tuberculosis (P = 0.044; OR = 0.5; 95% C.I. = 0.26 –0.98). Conclusion: TLR10 SNP rs11096957 polymorphism is a risk factor for tuberculosis infection.

Background: Inflammatory bowel disease (IBD) is a chronically relapsing disease. It includes ulcerative colitis (UC) and crohn's disease (CD). Symptoms of IBD could be conflicting sometimes with irritable bowel syndrome (IBS) of diarrheal type. The ideal marker for IBD/IBS diagnosis has not yet been identified. B2 microglobulin (B2-M) is a low molecular weight protein released by activated T and B lymphocytes. It has been shown to increase in several chronic inflammatory conditions. Objectives: Assessment of the diagnostic role of (B2-M) in IBS cases presented with diarrhea (IBS-D type) and UC cases. Methodology: This case control study was conducted at Gastroenterology Unit in Tropical Medicine Department, Ain- Shams University Hospitals, Cairo, Egypt. Forty patients with UC, and twenty patients with IBS in addition to twenty healthy persons as control were included. Results: There was a higher mean of B2-M values among U.C group (1.93)(mean B2-M in Active UC was 2.26 and 1.61 in inactive disease) compared to the other two groups(1.51 in IBS and 1.43 in control group) and the difference was highly statistically significant(P=0.000).Using ROC curve analysis of different cut off values of (B2-M) for detection of UC cases among IBS cases, we found that at a cut off value of <1.5 , we got sensitivity, specificity, PPV, NPV and accuracy of 75 %, 70 %, 83.3%, 58.3 %, and 0.753% respectively and this was the best cut off value. Conclusion: B2-M level may have a diagnostic and differentiating utility between UC cases and IBS-D type as well as a potential indicator of disease activation in UC patients.

Emerging of tigecycline resistant Acinetobacter baumannii (A. baumannii) is a critical global health problem as tigecycline is considered the last-line antibiotic for treatment of carbapenem resistant A. baumannii infections. Overexpression of efflux pumps is a leading mechanism of antibiotic resistance in A. baumannii. Objectives:Detection of the presence of three efflux pump genes; adeB, adeJ and adeG and determination of their expression level in Tigecycline Resistant A. baumannii collected from Benha University Hospital. Methodology: Thirty A. baumannii strains were collected and tested for antibiotic susceptibility. Presence of adeB, adeJ and adeG genes was detected by conventional PCR and their expression levels were assessed by RT-PCR. Results: Tigecycline susceptibility showed 60% (18/30) resistance and 40% (12/30) sensitivity. In tigecycline resistant strains, adeB gene was identified in 13/18 (72.2%) and adeJ gene in 12/18 (66.7%) with statistically significant association (P= 0.023). In tigecycline sensitive isolates adeB and adeJ genes were identified in 7/12 (58.3%) and 2/12 (16.7%) strains respectively. The adeG gene was not identified in any of the isolated strains. Combined adeB and adeJ genes were identified in 50% of tigecycline resistant isolates and only in 8.3% of (tigecycline sensitive) isolates with statistical significance difference (P= 0.018). Comparing adeB and adeJ gene expression revealed that transcription level was increased significantly and associated with tigecycline resistance. Conclusion: This study revealed wide spread of tigecycline resistant A. baumannii strains in Benha University Hospital and elucidated the significant role of (adeB and adeJ) genes in their emergence.

During the past decade, Candida glabrata (C. glabrata) has emerged as an important cause of fungemia. Objectives: The aim of this study is to isolate strains of C. glabrata, determine its incidence and antifungal susceptibility in ICU patients attending Benha University Hospital. Methodology: This study was carried out in the period from January 2016 to December 2018. Blood culture was done to patients with suspected blood stream infections. Isolation of candida and identification of C. glabrata by phenotypic and genotypic methods then antifungal susceptibility testing was done. Results: Fourty three strains of candida were detected of which 9 strains were C. glabrata (21%). our study shows that the most common underlying risk factors in our institution were neutropenia (7cases), malignancy (6 cases), respiratory diseases (3cases), treatment with central venous catheter (3cases), receipt of parenteral nutrition (2cases) and exposure to surgery (2cases). C. glabrata was highly sensitive to caspofungin 7 (77.8%) followed by amphotricin B 6 (66.7%), fluconazol 2 (22.2%) with the least sensitivity to voriconazol 1 (11.1%). Conclusion: C. glabrata is a common cause of candidemia in our ICU. Neutropenia, malignancy, respiratory disease and treatment with central venous catheter are risk factors for its acquisition.