Exposure of Staphylococcus aureus and Escherichia coli strains to different subMICs of cefodizime, cefotaxime and ceftriaxone significantly reduced the bacterial attachment to human buccal cells, but the resultant patterns of inhibition were different for S. aureus and E. coli and for the behaviour of the three cephalosporins. Morphological anomalies such as clusters of enlarged S. aureus cells and filamentation with spheroplast-like structures and bulge formations in E. coli were also present. Analogies between the different patterns of inhibition of adhesiveness and the corresponding degree of morphological changes were observed. Cefodizime behaved differently from cefotaxime and ceftriaxone and this could be attributed to the presence in the cefodizime molecule of an additional substituent, a 3-methyl-5-carboxymethyl-1,3-thiazole-2-thio group in the 3' position, not present in cefotaxime or ceftriaxone.

Anti-vaccine controversial debates have been occurring for more than a century. As the debate has moved onto social media, the issue has further developed. For anti-vaccine campaigners the use of Twitter and Facebook means giving them voice and massively amplifying their message. Yet, precisely because social media advertisements and news works on the basis of an algorithm that brings people to see similar news to those they have read before, anti-vax supporters tend to read and to always believe in the same type of news, be it fake or real. In other words, anti-vax supporters cannot discern real and fake news, as they do not realize that scientific fake news is the result of a decontextualization of the medical sources. By drawing on CDA, corpus linguistics and socio-semiotic multimodality, this paper aims at analyzing fake news discursive dynamics and strategies related to the anti-vax campaign to unveil cognitive, social and institutional constructs of misinformation.

Candidiasis is frequently localized in the mucosal epithelium which covers the vaginal and oral cavity. The pathogenicity of Candida is correlated with its ability to adhere to epithelial cells and this is the resultant of both fungal and host cell properties and their physicochemical interactions. This study was performed to investigate the ability of subinhibitory concentrations (sub-MICs) of rilopirox, a new antimycotic drug, to interfere with the adhesion of Candida albicans, Candida tropicalis and Candida glabrata to human vaginal cells, in comparison with sub-MICs of nystatin and fluconazole. The three drugs are more active on C albicans, followed by C. tropicalis and, last, C glabrata, on which fluconazole was inactive (MIC > 24 μg/ml). Rilopirox, nystatin and fluconazole have different mechanisms of action, and different molecular weights, so a comparative analysis of data was performed by means of their sub-MICs. On this basis the order of activity was nystatin = rilopirox > fluconazole. These findings can be of use for optimizing also the posologic design by regarding sub-MICs which are still active in reducing the adhesiveness of Candida to cells of the vaginal mucosa.

The entry of an antibiotic into phagocytes is a prerequisite for its intracellular bioactivity against susceptible facultative or obligatory intracellular microorganisms. Brodimoprim is a dimethoxybenzylpyrimidine that has recently entered into clinical use, and its uptake into and elimination from human polymorphonuclear neutrophils (PMNs), together with its effects on normal phagocytic and antimicrobial mechanisms, have been investigated. Brodimoprim uptake by PMNs was determined by a velocity-gradient centrifugation technique under various experimental conditions and was expressed as the ratio of the intracellular to the extracellular drug concentration (C/E) in comparison with the C/E of trimethoprim, which was used as a control drug. After incubation with 7.5 micrograms of brodimoprim per ml, PMNs accumulated brodimoprim (C/E, 74.43 +/- 12.35 at 30 min) more avidly than trimethoprim (C/E, 20.97 +/- 6.61 at 30 min). The cellular uptake of brodimoprim was not affected by temperature, 2,4-dinitrophenol, or potassium fluoride and was increased with an increase in the pH of the medium. It was reduced in formaldehyde-killed PMNs. The efflux of brodimoprim was very rapid (46% after 5 min). The liposolubility of brodimoprim was about three times that of trimethoprim, as was the uptake. Therefore, a possible passive transmembrane diffusion mechanism might be proposed. Brodimoprim did not decrease either phagocytosis or phagocyte-mediated bactericidal activity, nor did it affect oxidative burst activity, as investigated by luminol-amplified chemiluminescence. On the basis of the pharmacokinetic data for brodimoprim, the concentration of 7.5 micrograms/ml was chosen as the highest concentration attainable in serum by oral therapy, and at this concentration of brodimoprim, the amount of drug that penetrated into PMNs was able to maintain its antimicrobial activity without interfering with the functions of the PMNs.

In the present study the ability of subinhibitory concentrations (sub-MICs) of brodimoprim (a new 2,4-dimethoxybenzylpyrimidine) to interfere with some important aspects of bacterial cell function, such as surface hydrophobicity, fimbriation, motility and adhesiveness to mucosal cells, was investigated in comparison with those of trimethoprim. The inhibitory behavior of both diaminopyrimidines concerning hydrophobicity and hemagglutination (fimbriation) were essentially the same, while for adhesiveness and motility brodimoprim was more effective than trimethoprim. Diaminopyrimidines have high affinity for the bacterial enzyme dihydrofolate reductase, and this reduces the synthesis of essential purines and as a consequence of DNA and proteins. Our findings indicate that the synthesis and/or the expression of surface adhesins, which are proteins, was also affected by both brodimoprim and trimethoprim, the former being more active.