Background: COVID-19 can be accompanied by acute neurological complications of both central and peripheral nervous systems (CNS and PNS). In this study, we estimate the frequency of such complications among hospital inpatients with COVID-19 in Assiut and Aswan university hospitals. Materials and Methods: We screened all patients with suspected COVID-19 admitted from 1 June to 10 August 2020 to the university hospitals of Assiut and Aswan in Upper Egypt. Clinical and laboratory tests, CT/MRI of the chest and brain, and neurophysiology study were performed for each patient if indicated. Results: 439 patients had confirmed/probable COVID-19; neurological manifestations occurred in 222. Of these, 117 had acute neurological disease and the remainder had nonspecific neuropsychiatric symptoms such as headache, vertigo, and depression. The CNS was affected in 75 patients: 55 had stroke and the others had convulsions (5), encephalitis (6), hypoxic encephalopathy (4), cord myelopathy (2), relapse of multiple sclerosis (2), and meningoencephalitis (1). The PNS was affected in 42 patients: the majority had anosmia and ageusia (31) and the others had Guillain-Barré syndrome (4), peripheral neuropathy (3), myasthenia gravis (MG, 2), or myositis (2). Fever, respiratory symptoms, and headache were the most common general symptoms. Hypertension, diabetes mellitus, and ischemic heart disease were the most common comorbidities in patients with CNS affection. Conclusion: In COVID-19, both the CNS and PNS are affected. Stroke was the most common complication for CNS, and anosmia and/or ageusia were common for PNS diseases. However, there were 6 cases of encephalitis, 2 cases of spinal cord myelopathy, 2 cases of MG, and 2 cases of myositis.

Background: Ventilator associated pneumonia (VAP) remains an area of active clinical research with little data about effect of (VAP) on outcome among patients with acute exacerbation of chronic obstructive pulmonary disease.Materials and methods: A prospective study included patients with COPD exacerbation requiring endotracheal intubation for more than 48 h. Clinical assessment and Quantitative culture done for all patients for the occurrence of VAP.Results: Out of one hundred fifty two patients 92 patients (60.5%) were with VAP diagnosis. Their mean age was 56.1 ± 15.02 (38 cases developed early while 54 cases developed late VAP). Forty eight cases were discharged (54%) while 44 cases (46%) died. In comparing mean age of both groups 45.08 ± 15.52 and 57.41 ± 16.34 with P value 0.003. Prolonged use of antibiotics, reintubation and steroid use are possible risk factors for VAP with significant P values 0.03, 0.001, 0.05 respectively. Age above vs. below 60 showed adjusted odds ratio 5.33; 95% confidence interval 1.59-7.83 with P value 0.007. Early vs. late VAP, and prolonged use of antibiotics vs. none showed significant odds ratio 0.32; 95% CI 0.13-0.76, odds ratio 2.85; 95% CI 1.07-7.59 with P values 0.01, 0.04 respectively.Conclusions: Old age, late onset VAP, re-intubation and prolonged use of antibiotics were predictors of mortality in VAP patients with AECOPD.

An antigen-capture ELISA using monoclonal antibody (MAb) 128C3/3/21 was used to detect circulating parasite-derived antigens in the sera of patients actively infected with Schistosoma haematobium (31 males and four females, 5-25 years of age). The assay had a sensitivity of 100% (35 of 35 patients with antigen levels Ͼ 80 ng/ml) and a specificity Ͼ 99%. We used this ELISA to monitor antigenemia before treatment and one, three, and six months after treatment with a single oral dose of praziquantel (PZQ) (60 mg/kg in 20 patients or 40 mg/kg in 15 patients) and compared our findings with those indicated by other measures of disease progression. Circulating antigen levels decreased drastically after PZQ treatment (P Ͻ 0.001), with a significantly higher decrease occurring after treatment with 60 mg/kg than with 40 mg/kg. Although the mean antigen level was still significantly reduced (P Ͻ 0.001) at six months after treatment, 16 patients remained antigen-positive after six months, and nine had increased levels of antigenemia, reflecting reinfection in six patients and persistence of infection in another. We observed a correlation (r ϭ 0.6, P Ͻ 0.01) between the level of circulating antigen and the intensity of infection as measured by egg count. We also found a direct relationship (P Ͻ 0.001) between antigen level and the severity of the disease as monitored by ultrasonography. We conclude that our ELISA may be a useful adjunct to other methods, such as ultrasonography, for monitoring the course of S. haematobium infection and treatment.

Background and Objectives: Clostridium difficile infection (CDI) has become a significant healthcare-associated infection throughout the world and is particularly important in developing countries. This study aimed to investigate clinical characterization and risk factors related to toxigenic C. difficile infection in adult and pediatric patients, antimicrobial susceptibility pattern. Also, to evaluate different diagnostic methods for rapid detection of C. difficile associated diarrhea (CDAD) in Egypt. Materials and Methods: Stool samples were collected from 95 pediatric patients and 37 adult patients suffering from antibiotic associated diarrhea and were subjected to direct toxin immunoassay and culture on cycloserine/cefoxitin/fructose agar. The presence of tcdA and tcdB genes was tested by PCR. Results: Toxigenic C. difficile was isolated from pediatric and adult patients at a rate of 17.89% (17/95) and 27% (10/37) respectively. The sensitivity and specificity of direct PCR from stool are (100%, 100% and 82.4%, 100%) in adult and pediatric samples respectively. The susceptibility of C. difficile to vancomycin and metronidazole were found to be 66.7% and 48.2% respectively. Conclusion: Diabetes mellitus, prior antibiotic treatment, hematological malignancy on chemotherapy, malnutrition, neutropenia and Ryle feeding are risk factors for development of CDAD. Tight restriction of unnecessary antibiotic uses is necessary in our locality. Direct detection of toxin genes in stool by PCR is sensitive and specific method for early detection of C. difficile.

Background Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. There is accumulating evidence that link gut microbiota to symptomatology and pathophysiology of PD. The aim of this study was to describe the pattern of gut microbiota and its association with PD and identify the effect of environmental factors on gut microbiota. This case–control study included 46 patients diagnosed as Parkinson’s disease (PD) and 31 healthy volunteers age and sex matched. Detailed history including age of onset, duration of disease, environmental risk factors, diet data, treatment, Unified Parkinson’s Disease Rating Scale (UPDRS), and gastrointestinal tract (GIT) domain of Non‐Motor Symptoms Scale (NMSS) were assessed. After extraction of bacterial DNA from the fecal samples, bacterial abundance was quantified by qPCR using 16S rRNA group-specific primers. Results Significant high abundance of Clostridium cluster IV, Akkermansia, Bifidobacterium, and lactic acid bacteria were found in the PD group compared with the control group (P < 0.001, 0.04, 0.02 and < 0.001, respectively), while Firmicutes were significantly less abundant in the PD group (P < 0.001) compared with the control group. The naive PD patients had significant abundance of Bifidobacterium, and lactic acid compared with control group. Interestingly, Akkermansia was more abundant in treated than untreated patients. There were significant associations between pesticide exposure and Bifidobacterium (P = 0.002), while no significant correlations between different gut microbiota and demographic, environment data, different rating scores or dominant type of PD. There was a significant negative correlation between the Bifidobacterium with the duration of illness (P = 0.012). Conclusion The present study highlighted a significant connection between PD and levels of certain types of gut microbiota, in support of a possible link between gut microbiota and a neurodegenerative cascade of PD.