Application of an antimicrobial varnish to the teeth of 33 adult volunteers resulted in the elimination of detectable mutans streptococci from the saliva of 21 of them for a mean period of 34.6 weeks (range, 4 to 89 weeks) without additional treatment. The mean number of applications of varnish required for elimination was 3.14 (range, 1 to 5). Extensive examination of 10 subjects made free of mutans streptococci on the basis of saliva examination revealed no detectable mutans streptococci in their dental plaque. In 14 of the subjects in whom mutans streptococci were eliminated, they subsequently re-appeared after a mean period of 22.7 weeks (range, 4 to 71 weeks). Four out of the five recurrences that were treated were eliminated with only one additional varnish application. The treatment failed to provide long-term elimination of detectable mutans streptococci in 12 of the 33 treated subjects. No serious adverse reactions were observed in any of the treated subjects. The results indicate that it is possible to eliminate mutans streptococci from man in a safe and effective manner.
Surfaces within healthcare play a key role in the transmission of drug-resistant pathogens. Candida auris is an emerging multi-drug resistant yeast which has the ability to survive for prolonged periods on environmental surfaces. Here we show that the ability to form cellular aggregates increases survival after 14 days, which coincides with the upregulation of biofilm-associated genes. Additionally, the aggregating strain demonstrated tolerance to clinical concentrations of sodium hypochlorite and remain viable 14 days' post treatment. The ability of C. auris to adhere and persist on environmental surfaces emphasises our need to better understand the biology of this fungal pathogen.
Candida auris is an enigmatic yeast that provides substantial global risk in health care facilities and intensive care units. A unique phenotype exhibited by certain isolates of C. auris is their ability to form small clusters of cells known as aggregates, which have been to a limited extent described in the context of pathogenic traits. In this study, we screened several nonaggregative and aggregative C. auris isolates for biofilm formation, where we observed a level of heterogeneity among the different phenotypes. Next, we utilized an RNA sequencing approach to investigate the transcriptional responses during biofilm formation of a nonaggregative and aggregative isolate of the initial pool. Observations from these analyses indicate unique transcriptional profiles in the two isolates, with several genes identified relating to proteins involved in adhesion and invasion of the host in other fungal species. From these findings, we investigated for the first time the fungal recognition and inflammatory responses of a three-dimensional skin epithelial model to these isolates. In these models, a wound was induced to mimic a portal of entry for C. auris. We show that both phenotypes elicited minimal response in the model minus induction of the wound, yet in the wounded tissue, both phenotypes induced a greater response, with the aggregative isolate more proinflammatory. This capacity of aggregative C. auris biofilms to generate such responses in the wounded skin highlights how this opportunistic yeast is a high risk within the intensive care environment where susceptible patients have multiple indwelling lines. IMPORTANCE Candida auris has recently emerged as an important cause of concern within health care environments due to its ability to persist and tolerate commonly used antiseptics and disinfectants, particularly when attached to a surface (biofilms). This yeast is able to colonize and subsequently infect patients, particularly those that are critically ill or immunosuppressed, which may result in death. We have undertaken analysis on two different phenotypic types of this yeast, using molecular and immunological tools to determine whether either of these has a greater ability to cause serious infections. We describe that both isolates exhibit largely different transcriptional profiles during biofilm development. Finally, we show that the inability to form small aggregates (or clusters) of cells has an adverse effect on the organism’s immunostimulatory properties, suggesting that the nonaggregative phenotype may exhibit a certain level of immune evasion.
Over the past century, numerous studies have used oral biofilm models to investigate growth kinetics, biofilm formation, structure and composition, antimicrobial susceptibility and host-pathogen interactions. In vivo animal models provide useful models of some oral diseases; however, these are expensive and carry vast ethical implications. Oral biofilms grown or maintained in vitro offer a useful platform for certain studies and have the advantages of low cost of establishing such models, as well being easy to reproduce and manipulate. In addition, a wide range of variables can be monitored and adjusted to mimic the dynamic environmental changes at different sites in the oral cavity, such as pH, temperature, salivary and gingival crevicular fluid flow rates, or microbial composition. This review provides a detailed insight for early-career oral science researchers into how biofilm models used in oral research have progressed and improved over the years, their advantages and disadvantages, and how such systems have contributed to our current understanding of oral disease pathogenesis and aetiology.
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