Phenotypic Assays to Determine Virulence Factors of Uropathogenic Escherichia coli (UPEC) Isolates and their Correlation with Antibiotic Resistance Pattern

Objectives

Urinary tract infection caused by uropathogenic Escherichia coli (UPEC) strains is one of the most important infections in the world. UPEC encode widespread virulence factors closely related with pathogenesis of the bacteria. The purpose of this study was to evaluate the presence of different phenotypic virulence markers in UPEC isolates and determine their correlation with antibiotic resistance pattern.

Methods

UPEC isolates from patients with different clinical symptoms of UTI were collected and screened for biofilm and hemolysin production, mannose resistant, and mannose sensitive hemagglutination (MRHA and MSHA, respectively). In addition, antimicrobial resistance pattern and ESBL-producing isolates were recorded.

Results

Of the 156 UPEC isolates, biofilm and hemolysin formation was seen in 133 (85.3%) and 53 (34%) isolates, respectively. Moreover, 98 (62.8%) and 58 (37.2%) isolates showed the presence of Types 1 fimbriae (MSHA) and P fimbriae (MRHA), respectively. Our results also showed a relationship between biofilm formation in UPEC isolated from acute cystitis patients and recurrent UTI cases. Occurrence of UTI was dramatically correlated with the patients'' profiles. We observed that the difference in antimicrobial susceptibilities of the biofilm and nonbiofilm former isolates was statistically significant. The UPEC isolates showed the highest resistance to ampicillin, tetracycline, amoxicillin, and cotrimoxazole. Moreover, 26.9% of isolates were ESBL producers.

Conclusion

This study indicated that there is a relationship between the phenotypic virulence traits of the UPEC isolates, patients'' profiles, and antibiotic resistance. Detection of the phenotypic virulence factors could help to improve understanding of pathogenesis of UPEC isolates and better medical intervention.     

α-tocopherol supplementation prevents lead acetate and hypoxia-induced hepatic dysfunction

Objective:Lead (Pb) is a long-known poison of environment and industrial origin. Its prolonged exposure affects cellular material and alters cellular genetics and produces oxidative damages. In this study, we investigated the exposure of chronic sustained hypoxia or lead acetate alone or in combination with or without supplementation of α-tocopherol on hepatic oxidative and nitrosative stress in rats.Results:Exposure of both lead and hypoxia showed decreased body weight, altered serum lipid profile, oxidant and enzymatic antioxidants status, serum HIF-1α and VEGF concentrations. Simultaneous α-tocopherol supplementation showed beneficial effects to all these alterations. Histopathological observations also showed hepatic degenerative changes after lead or hypoxia exposure either alone or in combination, but remarkable improvement has been noticed after α-tocopherol supplementation.Conclusion:Supplementation of α-tocopherol is beneficial to counter both lead acetate and hypoxia induced hepatic cytotoxicities possibly by reducing oxidative and nitrosative stress.KEY WORDS: α-tocopherol, hypoxia, lead acetate, nitrosative stress, oxidative stress     

Update on the efficacy of statins in primary and secondary prevention of atrial fibrillation

Atrial fibrillation is the most common arrhythmia in adults and its prevalence is growing rapidly. It has been shown that AF is associated with increased risk of heart failure, ischemic and hemorrhagic stroke, and mortality. Hence, there is growing interest among researchers in seeking preventive and therapeutic interventions regarding AF. In recent decades, it has been suggested that statins may decrease the incidence of AF and may also decrease its recurrence after cardioversion and catheter ablation. These effects are thought to be mediated by different mechanisms such as modulating inflammation, altering the properties of transmembrane ion channels, interfering with activation of matrix metalloproteinases, and acting on endothelial function. In this article, we review and update current knowledge about the role of statins in primary and secondary prevention of AF in general and specific populations.     

Thrombotic complications in 2928 patients with COVID-19 treated in intensive care: a systematic review

A prothrombotic state is reported with severe COVID-19 infection, which can manifest in venous and arterial thrombotic events. Coagulopathy is reflective of more severe disease and anticoagulant thromboprophylaxis is recommended in hospitalized patients. However, the prevalence of thrombosis on the intensive care unit (ICU) remains unclear, including whether this is sufficiently addressed by conventional anticoagulant thromboprophylaxis. We aimed to identify the rate of thrombotic complications in ICU-treated patients with COVID-19, to inform recommendations for diagnosis and management. A systematic review was conducted to assess the incidence of thrombotic complications in ICU-treated patients with COVID-19. Observational studies and registries reporting thrombotic complications in ICU-treated patients were included. Information extracted included patient demographics, use of thromboprophylaxis or anticoagulation, method of identifying thrombotic complications, and reported patient outcomes. In 28 studies including 2928 patients, thrombotic complications occurred in 34% of ICU-managed patients, with deep venous thrombosis reported in 16.1% and pulmonary embolism in 12.6% of patients, despite anticoagulant thromboprophylaxis, and were associated with high mortality. Studies adopting systematic screening for venous thrombosis with Duplex ultrasound reported a significantly higher incidence of venous thrombosis compared to those relying on clinical suspicion (56.3% vs. 11.0%, p?<?0.001). Despite thromboprophylaxis, there is a very high incidence of thrombotic complications in patients with COVID-19 on the ICU. Systematic screening identifies many thrombotic complications that would be missed by relying on clinical suspicion and should be employed, with consideration given to increased dose anticoagulant thromboprophylaxis, whilst awaiting results of prospective trials of anticoagulation in this cohort.

     

The effect of Crocin on TFAM and PGC-1α expression and Catalase and Superoxide dismutase activities following cholestasis-induced neuroinflammation in the striatum of male Wistar rats

Metabolic Brain Disease - Bile secretion is a physiological function that is disrupted following Bile Duct Ligation (BDL) and induces cholestasis. Cholestasis is a bile flow reduction that induces...     

Paediatric gastrointestinal disorders in SARS-CoV-2 infection: Epidemiological and clinical implications

The coronavirus disease 2019 (COVID-19) pandemic is a threat worldwide for individuals of all ages, including children. Gastrointestinal manifestations could be the initial presenting manifestation in many patients, especially in children. These symptoms are more common in patients with severe disease than in patients with non-severe disease. Approximately 48.1% of patients had a stool sample that was positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral RNA. Children typically form 1%-8% of all laboratory-confirmed cases of SARS-CoV-2. Gastrointestinal manifestations of COVID-19 in children are not rare, with a prevalence between 0 and 88%, and a wide variety of presentations, including diarrhoea, vomiting, and abdominal pain, can develop before, with or after the development of respiratory symptoms. Atypical manifestations such as appendicitis or liver injury could also appear, especially in the presence of multisystem inflammatory disease. In this review, we discussed the epidemiology of COVID-19 gastrointestinal diseases in children as well as their implications on the diagnosis, misdiagnosis, prognosis, and faecal-oral transmission route of COVID-19 and the impact of gastrointestinal diseases on the gut microbiome, child nutrition, and disease management.     

Effect of cilazapril on regional left ventricular wall thickness and chamber dimension following acute myocardial infarction: in vivo assessment using MRI.

The primary goal of the current study was to assess in situ, using magnetic resonance imaging, the effect of a new angiotensin-converting enzyme inhibitor, cilazapril, in reducing left ventricular remodeling after acute myocardial infarction. Three groups of animals were investigated: (1) sham-operated rats (n = 19); (2) infarcted rats receiving no treatment (n = 23); and (3) infarcted rats receiving cilazapril (100 mg/L drinking water, n = 20). Treatment with cilazapril began on the third day postocclusion and continued for 3 to 4 months. Myocardial infarction was produced by ligation of the left coronary artery, and electrocardiographic (ECG)-gated short-axis images were acquired 3 to 4 months later. Sham-operated animals were subjected to the same procedure but the left coronary artery was not ligated. From the image acquired in the middle of the left ventricle (equatorial slice), left ventricular wall thicknesses, chamber diameters, and surface area measurements of the cavities were determined. At autopsy examination, infarct size and tissue water content were determined. The results demonstrate that magnetic resonance imaging has the potential to assess in situ the alterations of left ventricular dimensions and mass after acute myocardial infarction and can be used to document the influence of therapeutic interventions. Cilazapril provided protection against the deleterious remodeling changes such as ventricular dilation and wall thinning consequent to acute myocardial infarction.     

Delineation of acute myocardial infarction with dysprosium DTPA-BMA: influence of dose of magnetic susceptibility contrast medium.

OBJECTIVES. The contrast enhancement of acutely infarcted myocardium produced by the nonionic magnetic susceptibility-enhancing agent dysprosium diethylenetriamine pentaacetic acid-bis-methylamide (DyDTPA-BMA [S-043 Injection]) was assessed in the current study to establish the lowest dose that would yield optimal contrast between normal and acutely infarcted myocardium. BACKGROUND. Magnetic susceptibility contrast agents enhance differences between normal and ischemic tissue by reducing the signal of the normally perfused tissue to which they distribute. METHODS. Acute myocardial infarctions were produced by ligation of the left coronary artery. At 3 to 4 h after occlusion, a dose of 0.1, 0.3 or 0.5 mmol/kg of DyDTPA-BMA was injected intravenously into eight rats each in group 1, 2 or 3, respectively; a fourth group of seven rats served as a control group. Nuclear magnetic resonance (NMR) transverse relaxation time (T2)-weighted images (electrocardiographically gated to every 5th beat, echo delay time [TE] = 60 ms) were acquired before and for 1 h after administration of contrast agent. RESULTS. Images obtained before the injection of contrast agent showed moderate differences in signal intensity between normal and infarcted myocardium (p < 0.05). The contrast enhancement and the duration of delineation between infarcted and normal myocardium produced by this agent were dose dependent. At doses of 0.1, 0.3 and 0.5 mmol/kg, DyDTPA-BMA produced signal loss in normal myocardium: 63 +/- 5%, 41 +/- 4% and 28 +/- 4% of the baseline values, respectively, without any significant reduction in signal intensity of the infarcted region. The reduction in signal of normal myocardium and delineation of the infarct persisted for 5 min at a dose of 0.1 mmol/kg, for 20 min at a dose of 0.3 mmol/kg and for 40 min at a dose of 0.5 mmol/kg. No change in signal intensity or signal intensity ratio between normal and infarcted myocardium was observed in the control group during the same observation period. CONCLUSIONS. These results suggest that low doses of this agent, comparable to those of longitudinal relaxation time (T1)-enhancing agents, can delineate acutely infarcted myocardium. A dose of 0.3 mmol/kg of DyDTPA-BMA (S-043 Injection) provides reasonably persistent demarcation of acute myocardial infarction. Because this dose dramatically suppresses the NMR signal of normal myocardium, it shows the infarcted region as a region of high intensity (bright spot) on NMR images.     

High sustained response to daily dosing of interferon with ribavirin in chronic hepatitis C patients naïve to therapy

Background : Viral kinetics suggests that daily administration of α‐interferon (IFN) will clear hepatitis C virus (HCV) RNA earlier and more frequently compared with standard t.i.w. To reduce the likelihood of viral replication, mutation and subsequent development of resistance, daily dosing with IFN may be appropriate. To determine the safety and efficacy of daily IFN with ribavirin in chronic HCV infection we performed a prospective study. Methods : Thirty‐five naïve adult HCV‐positive patients (25 male/10 female) were treated with IFN‐α2b; 5 MU daily for 2 weeks followed by 3 MU daily for 22 weeks and ribavirin 800–1200 mg/day depending on weight. Liver biopsy, performed in 25 patients, showed mild to moderate activity in 19 patients (76%) and severe activity in six patients (24%). Two patients showed staged IV fibrosis. Serotyping was performed in 29 patients by an enzyme immunoassay‐based Murex assay. Type 3 was the predominant serotype, present in 14 cases. Hepatitis C virus RNA was measured by the Chiron bDNA assay. Results : Mean baseline HCV‐RNA level was 14.2 ± 18.7 MEq/mL (median 6.09; range 0.2–92.5), which became undetectable in all but three patients at week 4. Normalization of alanine aminotransferase (ALT) at week 4 was seen in 27 patients. Three patients withdrew due to non‐compliance. Thirty‐two patients completed 24 weeks of therapy as per the protocol. At the end of treatment, the HCV‐RNA level was negative in 29 of 32 patients (90.6%) and ALT was normal in 31 of 32 patients (97%). Sustained viral response at 6 months follow up was seen in 28 of 32 patients (88%). The ALT level was normal in 28 of 32 patients (88%). Conclusion : Daily administration of IFN with ribavirin is well tolerated in the majority of patients. There is rapid elimination of virus with normalization of ALT and a significantly high sustained viral response. © 2002 Blackwell Publishing Asia Pty Ltd